About all

Label the organs of the endocrine system: Illustrations of Anatomy, Function, Glands $ Organs


Organs of the Endocrine System Tutorial

Video Transcription

Download PDF

Welcome to this lesson today on organs of the endocrine system. Today we are just going to be giving a brief overview of the various organs and the hormones that they secrete that are all associated with the endocrine system.

So we are actually going to start by labeling the hypothalamus. And the hypothalamus is in a region of the brain right up here. So the hypothalamus, basically its role is that it secretes hormones such as ADH and oxytocin. So ADH is also known as the antidiuretic hormone. And oxytocin is a hormone that plays a role in childbirth, among other aspects as well.

And so a gland that we have that’s very closely associated with the hypothalamus is the pituitary gland. So the pituitary gland is a gland that works very closely with the hypothalamus. So the pituitary gland, basically it stores and releases hormones that were produced in the hypothalamus.

So the hypothalamus will produce some hormones. And then those hormones will be stored and released by the pituitary gland. And in addition to that, the pituitary gland also makes and secretes some of its own hormones, such as growth hormone, luteinizing hormone, and follicle stimulating hormone, for example.

So another part of the endocrine system that we’re going to label is the pineal gland. So the pineal gland is a gland that secretes melatonin. And basically melatonin is a hormone that plays a role in our sleep and wake cycles. So that’s what the pineal gland is responsible for.

So moving on from there, we have our thyroid gland, which is located in the neck. And our thyroid gland has a couple of different roles. It releases thyroid hormone, abbreviated TH, which plays a role in metabolism. And it also releases calcitonin. And calcitonin is a hormone that plays a role in bone remodeling. So those are kind of the two main hormones released by the thyroid gland.

And then the parathyroid, actually found on the thyroid gland, also plays a role in bone remodeling. So there are actually four parathyroid glands. And they release parathyroid hormone, or PTH. So as I mentioned, that also plays a role in bone remodeling.

So moving on from there, we have our thymus gland. And the thymus gland releases thymosins. And so the thymus gland is also where T-cells, which are a part of our immune system, they’re a type of white blood cell, that’s where these T-cells are actually stored and allowed to mature. So it does play a role in those T-cells being stored and matured, which plays a role in our immune system.

Moving on from there, we have the pancreas. So the role of the pancreas then is to make and secrete insulin and glucagon. So insulin is a hormone that lowers blood sugar levels. And glucagon is a hormone that raises blood sugar levels. So somebody who is diabetic, for example, their body doesn’t create or secrete the hormone insulin. So they have take insulin injections in order to make up for that to help lower blood sugar levels in their body.

The adrenal glands, we have two of them, one here and one here, found on top of the kidneys are the next organ of the endocrine system we’re going to talk about. So these adrenal glands, basically what they do is they secrete the hormones epinephrine and norepinephrine, which create kind of that fight or flight response that prepare the body for different types of situations. If you’re in a dangerous situation, you get that rush of adrenaline. That’s coming from those adrenal glands. It also really says out cortisol and aldosterone.

So if we move on to male- and female-specific organs of the endocrine system, for the females we have the ovaries. So the ovaries basically release progesterone and estrogen. Those are its two main hormones, again, that are female-specific. And male-specific, we have the testes, which make and secrete testosterone. So testosterone is a male-specific hormone.

So this lesson has been an overview on the various organs of the endocrine system, as well as the different hormones that those organs create and secrete.

14: The Endocrine System – Medicine LibreTexts

Structures of the Endocrine System

The endocrine system consists of cells, tissues, and organs that secrete hormones as a primary or secondary function. The endocrine gland is the major player in this system. The primary function of these ductless glands is to secrete their hormones directly into the surrounding fluid. The interstitial fluid and the blood vessels then transport the hormones throughout the body. The endocrine system includes the pituitary, thyroid, parathyroid, adrenal, and pineal glands (Figure 14.1). Some of these glands have both endocrine and non-endocrine functions. For example, the pancreas contains cells that function in digestion as well as cells that secrete the hormones insulin and glucagon, which regulate blood glucose levels. The hypothalamus, thymus, heart, kidneys, stomach, small intestine, liver, skin, female ovaries, and male testes are other organs that contain cells with endocrine function. Moreover, adipose tissue has long been known to produce hormones, and recent research has revealed that even bone tissue has endocrine functions.

Figure 14.1 Endocrine System Endocrine glands and cells are located throughout the body and play an important role in homeostasis.

The ductless endocrine glands are not to be confused with the body’s exocrine system, whose glands release their secretions through ducts. Examples of exocrine glands include the sebaceous and sweat glands of the skin. As just noted, the pancreas also has an exocrine function: most of its cells secrete pancreatic juice through the pancreatic and accessory ducts to the lumen of the small intestine

Download for free at http://cnx.org/contents/[email protected]


 On the person, draw and label the following endocrine organs:

  • Thyroid
  • Adrenals
  • Pancreas
  • Ovaries
  • Hypothalamus
  • Pituitary



Identify this organ and related structures Label the following: Thyroid, parathydroid























  1. Obtain a slide of each of the tissues listed below from the slide box at your table.
  2. Follow the checklist above to set up your slide for viewing.
  3. View the slide on the objective which provides the best view. Find the representative object.
  4. In the circle below the name, draw a representative sample of the tissue, taking care to correctly and clearly draw their true shape in the slide. If it is a stratified epithelium draw all the layers. Draw your structures proportionately to their size in your microscope’s field of view.
  5. Fill in the blanks next to your drawing and identify the structures listed on the last page under, “Histology”

Repeat this for each of the tissue types seen below.
















MODELS: Torso, Mid-Sagittal Head

Found on models:

 Hypothalamus

 Pituitary gland

  • Infundibulum

     Pancreas

     Pineal gland

     Adrenal glands

     Testis

     Ovary

     Thyroid gland

  • Ithsmus


 Pituitary

Endocrine system quiz questions, diagrams and study tools

Molly Smith DipCNM, mBANT

Dimitrios Mytilinaios MD, PhD
Endocrine system diagram

First things first – you’ll need to know which organs the endocrine system is comprised of! Organs like the thyroid, pancreas and adrenal glands are the guys doing all of the important work behind the scenes, like synthesizing and releasing hormones. Once you know which organs are which, you can start the business of learning exactly what it is that they do.

Want to revise the endocrine system in half the time? Flashcard-style quizzes are the way to go.

Overview about the organs of the endocrine system

Start by observing the labeled endocrine system diagram above. Spend some time familiarizing yourself with the location and appearance of each organ, then try labeling each one yourself using the unlabeled version of the diagram below. This endocrine system practice test is a great way to set yourself up for the next stage of your studies: using our spaced repetition endocrine quizzes! 

Download PDF Worksheet (blank) Download PDF Worksheet (labeled)

First, though, you might like to watch our video overview of the endocrine system. This will take you through its main organs as well as their various functions in the body. 

Quizzes: Questions and practice test

At Kenhub, we have quizzes to suit every level, from beginner through to advanced. If you’re just starting out learning about the endocrine system, quizzes on basic identification would be a great place to begin.  

If you fancy more of a challenge, try our advanced identification or clinical question bank questions. These endocrine quizzes are set up to emulate the same types of questions you’ll find in your exam, making them the perfect preparation tool. 

Ready to get started? Have a browse through our selection of endocrine quizzes below. P.S. As you progress through the quiz, our intelligent algorithm learns which endocrine system questions you could do with more practice on based on your answers. For those areas, you’ll automatically get tested on them more frequently. Which quiz will you take first? 

Are you enjoying using our quizzes and labeled diagrams to learn anatomy? Check out our anatomy practice quizzes and diagrams on every topic! 

Glandular tissue: The Histology Guide

What is a Gland?

An organised collection of secretory epithelial cells.
Most glands are formed during development by proliferation of
epithelial cells so that they project into the underlying connective
tissue. Some glands retain their continuity with the surface via
a duct and are known as EXOCRINE GLANDS. Other
glands lose this direct continuity with the surface when their
ducts degenerate during development. These glands are known as

This is the parotid gland, a type of salivary
gland. Can you identify the secretory acini and the ducts in this
typical exocrine gland. The intensity of staining should tell you
that the secretory cells of this gland are serous. This gland secretes
thin watery secretions, which are rich in enzymes and antibodies,
and the ducts open onto surface of oral mucosa.

Exocrine Glands

Exocrine glands have ducts
– and they secrete onto a surface: examples of exocrine glands
are: sebaceous and sweat glands (in the skin), salivary glands
(oral), Brunner’s glands. So, we have covered their basic structure
and function in tissue types, and we have looked at several examples
of exocrine glands in other topics.

Exocrine glands can be Unicellular – Goblet cells, or
Multicellular – and the basis of their classification was
covered in the topic on epithelia.

Endocrine Glands

Hormones co-ordinate, integrate and regulate interdependent processes
around the body. These hormones are secreted by the endocrine

Endocrine glands do not have ducts. Their secretions
(hormones) are secreted into the blood stream. Because of this,
the hormones can act over long distances, and reach any organ
in the body to co-ordinate activity. Often there is a specific
‘target’ organ that the hormone acts on. This long range activity
is also often called neuroendocrine – as it is
somewhat analogous to the co-ordinating activity of neurones.Some
short range endocrine activity also occurs in the digestive system
– and this is known as paracrine activity – for
example enteroendocrine cells of the gut respond to activity by
secreting peptides of monoamines that act locally.

The secretory cells of endocrine glands are therefore always
found in close proximity to a capillary bed, and have a rich network
of blood vessels.

The signalling molecules released – hormones, are
usually released by exocytosis, by the secretory cells, into the
interstitial spaces and pass through fenestrated cpaillaries to
enter the blood stream and move to target organs. The target organs
will have specific receptors for the hormone, and can respond
when the hormone binds. This means you should know the gland,
hormone, target organ/cells and response to the hormone.

How the endocrine glands are classified

Discrete Endocrine Glands – these include the pituitary
(hypophysis), thyroid, parathyroid, adrenal and pineal glands.
Endocrine component of Glands with both an Endocrine and an Exocrine
These include the kidney, pancreas and gonads. And
finally, there is a Diffuse Neuroendocrine system, which includes
APUD cells.

This topic only covers the Discrete Endocrine Glands;
pituitary, thyroid parathyroid and adrenal glands.
Other endocrine glands are covered in their respective topics.

The pineal gland – a small gland 6-8mm long
is found in the brain, close to the hypothalamus, and is a photoreceptor
organ, which is stimulated by information received via the retina,
that secretes the hormone melatonin, which appears to regulate
the circadian rhythms of the body. Secretions of this hormone
at night, cause a hypnotic effect. Its structure is not covered

Lab Content


The term “endocrine” implies secretion into the internal milieu of a multicellular organism. In contrast to exocrine tissues, where the secretory products are discharged into the external space – the outer surface of the body, mucosal surfaces, duct systems – the endocrine organs and cells secrete their products into the vascular system. The blood vessels then serve as conduits for these secretions to travel to their target tissues.

Endocrine tissues function according to a basic model. Individual cell types respond, via surface receptors, to different signals. They produce a very limited spectrum of secretory products, called hormones, that themselves function as signaling molecules for specific cell populations. These hormones are effective at exceedingly low concentrations. Because of this, relatively few cells are sufficient for the integrative function of large, multicellular organisms. Therefore, endocrine tissues are characteristically present in small quantities.

Pituitary Gland

The pituitary gland, or hypophysis, is a collection of different cell types that control the activity of other endocrine organs. It is governed by the hypothalamus, which sends both electrical and hormonal signals to the pituitary, and by feedback regulation (both positive and negative) through the secretions of its target glands. This slide shows a section of the human pituitary. In the anterior pituitary (pars distalis), you can see cords of cuboidal cells with a wide range of nuclear to cytoplasmic volume ratios. The posterior pituitary (pars nervosa) is connected to the hypothalamus by the pituitary stalk – this is easily visualized because the nervous tissue appears continuous between the two glands.

Anterior Pituitary

The anterior pituitary contains cells that, when viewed under the light microscope, appear as acidophils, basophils, or chromophobes. This slide displays the three cell types of the anterior pituitary under H&E stain. The acidophils appear as cells with pink cytoplasm and dark nuclei. These cells secrete protein hormones like growth hormone and prolactin. The basophils appear as darker cells with purple cytoplasm. These cells secrete glycoprotein hormones such as adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), and leutenizing hormone (LH). Finally, a few chromophobes are visible in this section; these cells are non-secretory and serve as support cells or precursors to the acidophils and basophils.

Posterior Pituitary

The posterior pituitary is mostly composed of unmyelinated axonal processes and terminals of the supraoptic and paraventricular nuclei of the hypothalamus. The pituitary stalk connects the two glands. The posterior pituitary has characteristic Herring bodies, focal axonal swellings that are packed with secretory granules. Pituicytes are the glial cells of the pituitary gland; the nuclei that are visible in sections of posterior pituitary belong to these cells, as well as cells of the vasculature. A third section of the pituitary, the intermediate lobe, is vestigial in man.

Adrenal Gland

The adrenal gland has two distinct parts, the cortex and medulla, which differ in structure and function. The cortex secretes hormones produced from cholesterol and can be functionally and histologically divided into three zones: glomerulosa, fasciculata, and reticularis. The adrenal medulla is the innermost portion of the gland and shares an embryological origin with the sympathetic nervous system.

The zona glomerulosa is the thin outer layer of the adrenal cortex. Its cells are pale staining and organized in ovoid clusters that are separated by capillaries. The cells of the zona glomerulosa produce mineralocorticoid hormones like aldosterone, which regulates salt and water balance.

The zona fasciculata comprises the thick middle layer of the cortex. Its cells are extensively vacuolated because of the presence of lipid droplets. The cells of this region produce glucocorticoids like cortisol, which has metabolic effects.

The zona reticularis is the innermost layer of the adrenal cortex. The border between it and the zona fasciculata is less distinct than that between the previous two zones. Cells in the zona reticularis stain deeply and are less vacuolated. This region produces androgens, which supplement sex hormones produced by the gonads.

The medulla primarily secretes catecholamines, including adrenaline and noradrenaline. Its cells possess abundant cytoplasmic granules that contain stored peptide hormones and catecholamines. These cells are frequently called chromaffin cells because they can be stained with chromium salts. Preganglionic sympathetic fibers traverse the adrenal cortex and synapse directly on chromaffin cells, where they release acetylcholine to stimulate the exocytosis of catecholamine granules during a sympathetic response.


The thyroid is located in the neck and stores large amounts of inactive hormone within extracellular compartments. The thyroid consists of structural units called follicles, which are composed of secretory epithelial cells called principal cells that are adjoined by junctional complexes and surrounded by a basement membrane. Follicles vary in size, but each displays a central lumen containing colloid. Colloid consists of the glycoprotein thyroglobulin, which is secreted by the principal cells and serves as a precursor to thyroid hormone. The height of the principal cells varies according to their level of secretory activity; in hypothyroidism, the cells are squamous or cuboidal, whereas in hyperthyroidism, they are columnar.

Also visible in this slide are a few C-cells, or parafollicular cells, scattered in the spaces between follicles. C-cells secrete calcitonin, which serves as a fine control for calcium homeostasis.


The parathyroid glands are closely associated with the thyroid. They consist of closely packed groups of two cell types:

  • Chief (principal) cells, which have prominent central nuclei surrounded by pale cytoplasm. Chief cells produce parathyroid hormone (PTH), which is the most important regulator of calcium metabolism in humans.
  • Oxyphilic cells, which are large and fewer in number, have small, dark nuclei and an acidophilic cytoplasm with many mitochondria. The function of these cells is unknown, but they increase in abundance as a person ages.

Endocrine Pancreas

The endocrine portion of the pancreas is comprised of the islets of Langerhans. During development, the cells of the islets migrate away from the duct system and aggregate around capillaries. The islets contain three important cell types:

  • Alpha cells produce glucagon, which increases the plasma glucose concentration. They are primarily located around the periphery of the islets.
  • Beta cells produce insulin, which decreases plasma glucose by promoting uptake by liver, skeletal muscle, and adipose tissue. Beta cells are typically located in the center of the islets.
  • D-cells produce somatostain, which has broad effects on gastrointestinal function and inhibits insulin and glucagon secretion. Delta cells are scattered throughout the islets.

Functions of the Endocrine System


  • 2

  • 462


The biological role of the endocrine system is closely linked to that of the nervous system; the two together coordinate the functions of the other (in some cases widely separated) organs and organ systems. The distinguishing feature of the endocrine system is that its influence is exerted by way of a number of substances, the hormones. Chemically, the hormones are a nonuniform group; the range of compounds represented includes steroids, amino-acid derivatives, peptides and proteins. Their common characteristic is that they are produced in special organs, the endocrine glands (glands without secretory ducts) or in circumscribed groups of cells — for example, the islet cells of the pancreas, Leydig’s interstitial cells in the testes, and cell groups in the duodenal mucosa (secretin) and the hypothalamus (ADH, oxytocin, etc.) — and are transported in the blood to more or less distant organs. They have specific actions on these target organs, actions that as a rule cannot be produced by any other substance. The word “specific” also indicates that the action of each hormone is exerted only on its particular functional systems or organs, the “effector organs.” A further characteristic is that the endocrine glands and cell groups are occupied exclusively with the formation and secretion of their hormones.


Growth Hormone Luteinizing Hormone Brown Adipose Tissue Corpus Luteum Adrenal Cortex 

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

This is a preview of subscription content,

log in

to check access.


Unable to display preview. Download preview PDF.


Textbooks and Handbooks

  1. 1.



    , R.O., A


    , E.B. (Eds.) Handbook of Physiology. Section 7: Endocrinology, Volumes I-VII. Washington, D. C.: American Physiological Society 1972–76

    Google Scholar

  2. 2.





    , L.J. (Ed.) Endocrinology, Volumes I-III. New York-San Francisco-London: Grune & Stratton 1979

    Google Scholar

  3. 3.



    , R.H. (Ed.) Textbook of Endocrinology. Philadelphia-London-Toronto: Saunders 1974

    Google Scholar

  4. 4.



    , B.T.: Mammalian Neuroendocrinology. London: McGraw Hill Pubi. Co. Ltd. 1970

    Google Scholar

  5. 5.



    , L.S., H


    , J.S.M. The Endocrine Hypothalamus. London-New York-San Francisco: Academic Press 1978

    Google Scholar

  6. 6.



    , P.: Mechanisms of Hormone Action. Stuttgart: Thieme 1965

    Google Scholar

  7. 7.



    , R.O. (Ed.) Reproductive Physioloqy II. In: Int. Rev. Physiol. Vol. 13 (G


    , A.C. Ed.). Baltimore-London-Tokyo: Univ. Park Press 1977

    Google Scholar

  8. 8.



    , C.T.: The Hormones. Endocrine Physiology. London: Churchill 1969

    Google Scholar

Research Reports and Reviews

  1. 9.



    , R. P. (Ed.) Human Reproductive Physiology. Oxford-London-Edinburgh-Melbourne: Blackwell Scientific Publications 1979

    Google Scholar

  2. 10.



    , E.F.: General and specific characteristics of physiological adaptations. Amer. J. Physiol.


    ,18 (1956)

    PubMedGoogle Scholar

  3. 11.



    , N.: Actions of growth hormone on carbohydrate metabolism. In: Handbook of Physiology, Vol. IV, Part 2 (see Ref. 1)

    Google Scholar

  4. 12.



    , B.: Central nervous and hormonal interaction in temperature regulation of the goat. In: Physiological and Behavioral Temperature Regulation (J.D. H


    , A.P. G


    , J.A.J. Stolwijk, Eds.), p. 634. Springfield, 111.: Ch. C. Thomas 1970

    Google Scholar

  5. 13.



    , B.: Receptors subserving hunger and thirst. In: Handbook of Sensory Physiology, Vol.III/1: Enteroceptors (E. Neil, Ed.), p. 187. Berlin-Heidelberg-New York: Springer 1972

    Google Scholar

  6. 14.



    , A.: Hypothalamic gonadotropin releasing hormone and reproduction. In: see Ref. 7

    Google Scholar

  7. 15.



    , J.: The pineal gland: A neurochemical transducer. Science


    ,1341 (1974)

    PubMedCrossRefGoogle Scholar

  8. 16.



    , S.B., K


    , H.M.: Metabolism of tissues excised from thyroxine-injected rats. Amer. J. Physiol.


    ,81 (1952)

    PubMedGoogle Scholar

  9. 17.

    Brück, K.: Non-shivering thermogenesis and brown adipose tissue in relation to age, and their integration in the thermoregulatory system. In: Brown Adipose Tissue (O. Lindberg, Ed.), p. 117. New York: Amer. Elsevier Publ. 1970

    Google Scholar

  10. 18.



    , W.B.: Die Notfallsfunktionen des sympathicoadrenalen Systems. Ergebn. Physiol


    ,380 (1928)

    CrossRefGoogle Scholar

  11. 19.



    , C. D., S


    , W. E.: Endocrine optic pathways to the hypothalamus. In: Anatomical Neuroendocrinolgy (W.E. S


    , C. D. Grant, Eds.). Basel: Karger 1975

    Google Scholar

  12. 20.



    , B. A., D


    , R.E.J.: Central pathways for neurohypophysial hormone release. In: Handbook of Physiology, Vol. IV, Part 1, The Pituitary Gland (see Ref. 1)

    Google Scholar

  13. 21.



    , H. W., H


    , A.C. P


    , L.S.: The regulation of growth by endocrines. Ann. Rev. Physiol.


    ,211 (1975)

    CrossRefGoogle Scholar

  14. 22.



    , J.O.: Regulation of aldosteron secretion. In: Handbook of Physiology, Vol. VI, Adrenal Gland (see Ref. 1)

    Google Scholar

  15. 23.



    , J.O., F


    , R.H.: Mechanisms regulating renin release. Physiol. Rev.


    ,1 (1976)

    PubMedGoogle Scholar

  16. 24.



    , R. G., D


    , R. E. J.: Evidence for a direct effect of LRF and TRF on single unit activity in the rostral hypothalamus. Nature


    , 486(1974)

    Google Scholar

  17. 25.



    , I. S., Ismall-B


    , F.: Thyroid thermogenesis and active sodium transport. In: Recent Progress in Hormone Research (R.O. Greep, Ed.). New York-London: Academic Press 1974

    Google Scholar

  18. 26.



    , U. S.: Adrenal medullary secretion and its neural control. In: Neuroendocrinology, Vol. II (C. M


    , W.F. Ganong, Eds.), p. 283. New York-London: Academic Press 1967

    Google Scholar

  19. 27.



    , J.T.: The Physiology of Thirst and Sodium Appetite. London-New York-Melbourne: Cambridge Univ. Press 1975

    Google Scholar

  20. 27 a.



    , T., K


    , S., Yui, R, I


    , T.: Evolution of neurons and paraneurons. Hormones, Adaptation and Evolution (S. Ishii et al., eds.), pp. 35–43, Japan Sci. Soc. Press, Tokyo, Berlin: Springer-Verlag 1980

    Google Scholar

  21. 28.



    , C.C.: Neuroendocrine aspects of thermoregulation. Ann. Rev. Physiol.


    ,391 (1973)

    CrossRefGoogle Scholar

  22. 29.



    , W. F., F


    , P. H.: Adenohypophysis and adrenal cortex. Ann. Rev. Physiol.


    ,579 (1960)

    CrossRefGoogle Scholar

  23. 30.



    , F. J., A


    , O. , N


    , P. E.: Über einen osmorecepto- risch tätigen Mechanismus in der Leber. Pflügers Arch. ges. Physiol.


    ,73 (1965)

    Google Scholar

  24. 31.



    , J. N.: Neural control of the posterior pituitary. Ann. Rev. Physiol.


    ,191 (1975)

    CrossRefGoogle Scholar

  25. 32.



    , J. N., V


    , J. D.: Osmosensitive single neurons in the hypothalamus of unanesthetized monkeys. J. Physiol. (Lond.)


    , 947(1970)

    Google Scholar

  26. 33.



    , R.I.: The role of adrenal corticosteroids in sensory processes. In: Handbook of Physiology, Vol. VI, Chap. 15 (see Ref. 1)

    Google Scholar

  27. 34.



    , H. Brück, K., R


    , P.: Homeothermic Organisms. In: Temperature and Life (H. P


    , J. C


    , H. H


    , W.Larcher, Eds.), p.505. Berlin-Heidelberg-New York: Springer 1973

    Google Scholar

  28. 35.



    , A. C. C, P


    , C. W, L


    , K. M, T


    , K. W.: Circulatory and metabolic effects of noradrenaline in cold-adapted rats. Fed. Proc.


    , 1205 (1966)

    PubMedGoogle Scholar

  29. 36.



    , D.C.: The pineal gland: A model of neuroendocrine regulation. In: The Hypothalamus (S. R


    , R.J. B


    , J. B. Martin, Eds.), pp. 303–327. New York: Raven Press 1978

    Google Scholar

  30. 37.



    , E.: On the control of gonadotropin secretion in the Rhesus monkey. In: Recent Progress in Hormone Research (R.O. Greep, Ed.), Vol. 30. New York-London: Academic Press 1974

    Google Scholar

  31. 38.



    , J., V


    , A.: Thyroxine and noradrenaline on noradrenaline sensitivity, cold resistance and brown fat. Amer. J. Physiol.


    ,1 742(1970)

    Google Scholar

  32. 39.



    , G. P.: Physiological mechanisms controlling secretory activity of adrenal medulla. In: Handbook of Physiology, Vol. VI, Adrenal Gland, pp. 309–319 (see Ref. 1)

    Google Scholar

  33. 40.



    , J.B., T


    , G., W


    , J.O., R


    , L.P., B


    , P.: Functions of the central nervous system in regulation of pituitary GH secretion. In: Hypothalamic Hormones (M. M


    , P.G. C


    , L. Martini, Eds.). London-New York: Academic Press 1975

    Google Scholar

  34. 41.



    , R.P.: The effects of hormones on sexual behavior in female cat and Rhesus monkey. In: Handbook of Physiology, Vol. II, Female Reproductive System, Part I, pp. 187–222 (see Ref. 1)

    Google Scholar

  35. 42.



    , N.C.: Adrenergic receptors. In: Handbook of Physiology, Vol. VI, Adrenal Gland, pp. 447–472 (see Ref. 1)

    Google Scholar

  36. 43.



    , P. W.: Endocrine mechanisms of parturition. Ann. Rev. Physiol.


    ,411 (1978)

    CrossRefGoogle Scholar

  37. 44.



    , R. A.: Excitatory action of TRH on spinal motoneurons. Nature


    ,242 (1977)

    PubMedCrossRefGoogle Scholar

  38. 45.



    , A.: Circumventricular structures and pituitary functions. Proc. 4th Int. Congr. Endocrinology, Washington. Amsterdam: Excerpta Medica 1972

    Google Scholar

  39. 46.



    , A., H


    , H. G.: Photoneuroendocrine systems and the third ventricle. In: Brain-endocrine interaction II (K.M. Krigge et al., Eds.), pp. 40–53. Basel: Karger 1975

    Google Scholar

  40. 46 a.



    , A. G. E.: The diffuse neuroendocrine system and the APUD concept: related “endocrine” peptides in brain, intestine, pituitary, placenta, and anuran cutaneous glands. Medical Biology


    , pp. 115–125 (1978)

    Google Scholar

  41. 47.



    , E.R.: Corticosteroids and skeletal muscle. In: Handbook of Physiology, Vol. VI, Adrenal Gland, Chapter 17 (see Ref. 1)

    Google Scholar

  42. 48.



    , L. P., M


    , J. P., M


    , J. B., B


    , O.: Depressant action of TRH, LH-RH and somatostatin on activity of central neurons. Nature


    ,233 (1975)

    CrossRefGoogle Scholar

  43. 49.



    , H.: The physiology and pathology of exposure to stress. Montreal: Acta Inc. Medical Publ. 1950

    Google Scholar

  44. 50.



    , K., L


    , J.H.: The thyroid and its control. Ann. Rev. Physiol.


    ,349 (1977)

    CrossRefGoogle Scholar

  45. 51.



    , R. V., M


    , R. A.: Physiological role of parathyroid hormone. In: Handbook of Physiology, Vol.VII, Parathyroid Gland (see Ref. 1)

    Google Scholar

  46. 52.



    , W., R


    , C., B


    , M.: Regulatory peptides of the hypothalamus. Ann. Rev. Physiol.


    ,473 (1977)

    CrossRefGoogle Scholar

  47. 53.



    , E.B.: The antidiuretic hormone and factors which determine its release. Proc. roy. Soc. B


    ,25 (1947)

    CrossRefGoogle Scholar

  48. 54.



    , S. C., P


    , D.: Neural control of the endocrine pancreas. Physiol. Rev.


    ,596 (1974)

    PubMedGoogle Scholar

  49. 55.



    , W., A


    , P., B


    , D., C


    , O., L


    , S., T


    , W.: Circulating hormones, EEG and performance in psychological tests of women with and without oral contraceptives. Psychoneuroendocrinology 1,141 (1975)

    PubMedCrossRefGoogle Scholar

  50. 56.



    , W. S., B


    , J. R, (Eds.): Physiological Controls and Regulations. Philadelphia-London: Saunders 1965

    Google Scholar

  51. 57.



    , F. E., M


    , J. W.: Stimulation and inhibition of adrenocor- ticotropin release. In: Handbook of Physiology, Vol. IV, The Pituitary Gland, Part 2 (see Ref. 1)

    Google Scholar

Copyright information

© Springer-Verlag Berlin · Heidelberg 1983

Authors and Affiliations

There are no affiliations available

Endocrine System Organs, Glands | Hormones and Metabolism

The endocrine system is one of two systems that control and coordinate many functions to keep our bodies working in balance, called homeostasis. While our nervous system uses electrical impulses, the endocrine system uses chemicals called hormones. Hormones usually work more slowly than nerves, but can have longer lasting effects.

The endocrine system is made of 9 major glands located throughout our body. Together, these glands make dozens of chemical messengers called hormones and release them directly into the blood stream that surrounds the glands. Using chemicals, our endocrine system regulates a number of functions including our metabolic rate, growth rate, and how our body develops. Lab tests are used to diagnose and manage health conditions caused by imbalances in hormones and chemicals.

Endocrine Glands

Glands are a group of cells that produce and release hormones directly into our blood stream in a process called secretion. There are 2 types of glands. Exocrine glands have ducts or channels which secrete chemicals such as saliva or sweat. Endocrine glands do not have ducts; they secrete hormones directly into the blood stream.

Organs of the Endocrine System


The hypothalamus is located in the brain and links the nervous and endocrine systems to each other. It secrets hormones that put the pituitary gland into action.

Pineal Gland

The pineal gland is a small, pine-cone shaped endocrine gland in the brain. It produces melatonin, a derivative of serotonin, a hormone that affects wake/sleep patterns and seasonal functions.

Pituitary gland

The pituitary gland, or hypophysis, is an endocrine gland about the size of a pea. It weighs less than an ounce and is one of the most important organs in the body. It is located at the base of the brain and is closely connected to the hypothalamus. The pituitary gland secretes nine hormones that regulate homeostasis by stimulating other endocrine glands to produce and secrete their own hormones.

This particular gland has two components: the anterior (front) pituitary (or adenohypophysis) and the posterior (back) pituitary (neurohypophysis).  The anterior lobe makes up most of the gland and releases the majority of the hormones. The smaller posterior lobe stores hormones but does not make them. It links the endocrine system with the nervous system by way of the hypothalamus.

The pituitary gland is known as the ‘master’ endocrine gland. The hypothalamus controls the production of hormones in both lobes. The pituitary gland produces many important hormones, some of which act on other glands to make them produce hormones. The pituitary gland releases at least 9 hormones that have important effects on the body—these include the thyroid stimulating hormone (TSH), adrenocorticotrophic hormone  stimulates the adrenal glands.


The butter-fly shaped thyroid gland is one of the largest endocrine glands. The thyroid gland is in the front of the neck, just below the thyroid cartilage or “Adam’s apple”. The isthmus bridges the two lobes of the thyroid and is located below the cricoid cartilage.

The thyroid gland controls how quickly the body uses energy (metabolism), calcium levels in the blood, how the body makes proteins, and how sensitive the body is to other hormones. It produces thyroid hormones, the principal ones being triiodothyronine (T3), thyroxine which can sometimes be called tetraiodothyronine (T4) and calcitonin. These hormones regulate the heart rate, the rate of metabolism and affect the growth and rate of function of many other systems in the body. T3 and T4 are made from iodine and tyrosine. Calcitonin slows down the rate at which bone is broken down decreasing the amount of calcium dissolved in the blood.

Parathyroid Gland

The parathyroid gland controls calcium levels in the blood. The parathyroid is a small of glands around by the thyroid gland. They produce the parathyroid hormone or PTH, which increases the rate at which broke bone is broken down. As a result, more calcium is released into the blood. Parathyroid hormone works in partnership with calcitonin from the thyroid gland. The 2 hormones have the opposite effect. Through negative feedback they keep the calcium level in the blood stable.

Hormonal output from the thyroid is regulated by the thyroid-stimulating hormone (TSH) produced by the anterior pituitary, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus. The thyroid gets its name from the Greek word for “shield” because of its shape. The most common problems of the thyroid gland are overactive thyroid gland, called hyperthyroidism, and an underactive thyroid gland, called hypothyroidism.


The thymus is a specialized organ of the immune system. The thymus “educates” T-lymphocytes (T cells), which are critical cells of the adaptive immune system.

Adrenal Glands

The small, triangular adrenal glands (also known as suprarenal glands) sit atop the kidneys. Each is divided into two distinct anatomic and functional organs. The adrenal cortex (the outer region which secretes corticosteroid hormones that affect metabolism (that is how food is stored and used), chemicals in the blood, and characteristics such as body shape and hairiness. The smaller, inner region—the adrenal medulla (which is part of the sympathetic nervous system)—is the body’s first line of defense against physical and emotional stress.

They are mainly responsible for releasing hormones in response to stress through the synthesis of corticosteroids such as cortisol and catecholamines such as epinephrine (adrenaline) and norepinephrine. They also produce androgens. The adrenal glands affect kidney function through the secretion of aldosterone, a hormone that helps regulate the osmolarity of blood plasma. The adrenal glands help us deal with dress and as well as maintain homeostasis.

Disorders of the adrenal glands include congenital defects such as adrenal hyperplasia, tumors, autoimmune disorders, infection, and impaired blood supply.

Adrenal cortex

When looked at under a microscope, the adrenal cortex is made up of 3 distinct zones. The outermost zone secretes the hormone aldosterone, which inhibits the amount of sodium excreted in the urine, maintaining blood pressure and blood volume. The inner and middle zones together secrete hormones hydrocortisone, also called cortisol, corticosterone, as well as small amounts of androgen hormones. The rate of release and amount of secretion is controlled by other hormones made in the hypothalamus and pituitary.

Adrenal medulla

The adrenal medulla is closely related to nervous tissue and secretes the hormone epinephrine and norepinephrine in response to stimulation by sympathetic nerves. These nerves are most active at times of stress. The release of these hormones increases the heart rate in order to pump more blood to the large skeletal muscles. The airways in the lungs are increased so that more oxygen can be taken in. As more blood is sent to the active organs less blood is sent to the internal organs.


The pancreas is a gland organ in the digestive system and endocrine system. It is both an endocrine gland—producing several important hormones, including insulin, glucagon, somatostatin, and pancreatic polypeptide—and a digestive organ—secreting pancreatic juice containing digestive enzymes that help with the absorption of nutrients and digestion in the small intestine. These enzymes help to break down the carbohydrates, proteins, and fats.


The ovary is an ovum-producing reproductive organ, often found in pairs in the female reproductive system. Ovaries in women are analogous to testes in males—they are both gonads and endocrine glands. Our ovaries produce estrogen, progesterone, relaxin and inhibin.


The testicle is the male gonad. Like the ovaries in women to which they are homologous, testes are components of both the reproductive system and the endocrine system. The primary functions of the testes are to produce inhibin, sperm (spermatogenesis) and androgens, primarily testosterone.


Hormones are powerful chemical messengers that our endocrine system uses to control various processes in our body. Hormones can be fat-soluble or water-soluble. Endocrine glands secrete hormones into the blood stream near them; the hormones then travel in our bloodstream until it reaches its destination, called a target cell, in distance parts of the body. In the target tissue, hormones lock onto the target’s plasma membrane, called the receptor site. This chemical changes inside the target cells and adjusts the rate at which a specific action happens, such as a contraction of the muscle. Hormones can have one target or several targets. Hormones are released when they get feedback from triggers. Some hormones work on specific cells while other hormones work throughout the body. The level of hormones in the body are controlled by feedback. It is important that the amount of hormones in our body is kept at the right level. If hormone levels get too high or too low, they can make us sick. Although hormones come in contact with many cells in the body, they only react with target cells. A hormone can have more than one target cell, and can have different effects on different targets.

Luteininzing Hormone

This is a pituitary hormone that helps regulate the function of the reproductive organs. It stimulates ovulation to release the egg in the woman’s ovaries. In men it triggers the testes to produce male reproductive hormones.


This is a pituitary hormone that stimulates the production of milk in the breast. It is one of several hormones that stimulate milk production or lactation. Breast-feeding stimulates the pituitary gland to make more prolactin so that milk is made for as long as the baby breastfeeds.


Oxytocin is a pituitary hormone that stimulates muscle contractions in the uterus during childbirth. These contractions cause the release of more oxytocin. This is a positive feedback reaction that makes the cycle continue until the baby is born. Oxytocin also stimulates the breasts to release milk when the baby feeds.


The hormone glucagon increases the level of sugar in the blood. It plays a vital part in maintaining the correct blood sugar level. It is made by the pancreas, a gland that is part of the endocrine system and the digestive system. The pancreas releases glucagon when the blood sugar level starts to fall. Glucogon makes cells release glucose, and helps convert glycogen, the form of glucose stored in the liver, back to glucose. As a result the blood sugar level rises. Your blood has enough glucose to keep you alive for just 15 min. However, as glucose is used up, more is released to take its place.

Reproductive Hormones

Reproductive hormones control the reproductive development of boys and girls. The development of primary and secondary characteristics and regulate all reproductive related processes such as sperm and egg production. Primary reproductive characteristics are the development of the major reproductive organs. There are 3 main types of reproductive hormones—androgens, estrogen, and progesterone.

Female Reproductive Hormone

Estrogen is the female hormone made mainly in the ovaries. It not only makes the girl reproductive organs develop, and controls her monthly menstrual cycle. Progesterone is the female hormone that prepares the girls uterus for pregnancy every month. Some contraceptive pills have estrogen in them to prevent the ovaries from releasing their egg cells.

Male Reproductive Hormone

The male reproductive system consists of the penis, scrotum, and the 2 testes. A male reproductive system creates sperm cells that combined with a female egg to create a new human life. The testes and scrotum hang outside the body where it is cooler because it improves sperm production. Sperm cells look like microscopic tadpoles. Sperm is made in the testes, which are inside the scrotum. Sperm cells leave the testes through epididymis. The epididymis connects to the vas deferens. Glands called seminal vesicles lie along the vas deferens and add fluids and nutrients to the sperm. The male reproductive system also produces the reproductive hormones needed to make sperm and for a boy to develop at puberty. The male reproductive hormone testosterone also stimulates bone and muscle growth


Epinephrine is a hormone that works with out nervous system to prepare our body to cope with danger or stress. If you’re suddenly scared, your heart pounds, your breathing becomes steep and rapid. These are just two of the effects of epinephrine, also called adrenaline. Epinephrine is a very fast acting hormone that prepares our body for emergency action—also called the fight or flight reflex. It speeds up our breathing and heart rate and diverts extra blood to the muscles. At the same time it slows down digestion and makes the liver release glucose into the bloodstream so more fuel is available for the muscles to contract.


Insulin is a hormone that reduces the level of sugar in our blood. Insulin is a protein made by the pancreas. It is released when the blood sugar level rises and reduces the sugar in 2 ways. First it makes insulin take up the glucose. 2nd in makes the liver store glucose by turning it into glycogen. Insulin and glucagon have opposite effects. Together they form a negative feedback system that keep sugar levels within set limits. In people with diabetes this control system does not work properly and they made may need daily injections of insulin to keep their blood glucose levels within safe limits.

Growth Hormone

The growth hormone is a pituitary hormone that controls the body’s growth by stimulating cell division. It also increases the blood glucose level. If your body has too little growth hormone, the body fails to grow normally. Too much growth hormone can cause the body to grow more than usual.

Thyroid-stimulating Hormone

The thyroid stimulating hormone makes the thyroid gland produce thyroid hormones.

Adrenocorticotrophic Hormone

This hormone stimulates the adrenal glands to produce other hormones.

Antidiuretic Hormone

This pituitary hormone increases the amount of water in the blood. A diuretic is a substance that stimulates the body to produce urine by taking water out of the blood stream. The antidiuretic hormone or vasopressin, have the opposite effect. It increases the amount of water that the kidneys return to the blood and makes arterioles constrict. As a result, more fluid is squeezed into a smaller space and blood pressure rises.

Follicle-stimulating Hormone

This hormone and the Luteininzing Hormone are used in reproduction in both men and women. They also affect the production of reproductive hormones.

Growth Hormone

The growth hormone encourages growth in children and teenagers, makes our bones stronger, and helps build muscle. Growth is controlled by hormones produced by the pituitary gland.

Oxytocin Hormone

Oxytocin encourages childbirth and makes the breasts release milk when breast-feeding a baby.

Prolactin Hormone

Prolactin is produced during and after pregnancy and helps the breasts produce milk for breast-feeding.

Disorders of the Endocrine System

  • Hashimoto’s Thyroiditis
  • Hyperthyroidism
  • Graves’ disease
  • Hypothyroidism
  • Type I diabetes
  • Type II diabetes
  • Gestational diabetes
  • Hypopituitaryism
  • Pituitary tumors
  • Thyroid carcinoma
  • Acromegaly
  • Cushing’s syndrome
  • Addison’s disease
  • Calcium metabolism disorders

90,000 Lesson 3: labeling of plastics and disposal of hazardous waste :: RBC Trends

Reducing your environmental impact without sacrificing personal comfort and family budget is easy. Join the sustainable consumption course and incorporate new habits into your daily life

“Ten Steps to Conscious Consumption” – a joint course of RBC Trends and the High Sedge project.

The first lesson is about sustainable consumption.

The second lesson is about the separate collection of recyclable materials.

From the last lesson, we learned that not all plastic can be handed over with peace of mind to a separate collection point and be sure that it will not end up in a landfill or incineration plant. In this lesson, we will learn how to distinguish recyclable from non-recyclable plastic, find out why this material is dangerous, and at the same time figure out what to do with very dangerous waste.

You can also save the list below as a memo (.pdf).

Types of plastics and markings

Plastic that is accepted for recycling wherever there is separate collection of waste:

1 – PET (E) or PET – polyethylene terephthalate

Most often we meet with him.

It contains, for example, soft and dairy drinks, ready-made sauces, cosmetics, powders. PET is easily recognizable by the raised point at the bottom of the bottle.

Photo: Pixabay

Attention: vegetable oil bottles are also made from “one”, but they are rarely taken (oil penetrates into plastic and makes processing difficult).

Such containers can be used only once: when reused, the material releases phthalate – a toxic substance that negatively affects the liver, kidneys, reproductive organs, endocrine and nervous systems.

2 – PEHD (HDPE) or HDPE – high density polyethylene

This plastic is found in solid or film form.

From it, for example, rustling bags, bottles for cosmetics, buckets, children’s toys are made. Products made of this type of plastic are easily recognizable by the characteristic longitudinal seam on the bottom.

Photo: DRIVE2.RU

Such containers can be used several times, but the material can emit formaldehyde – a colorless gas that negatively affects the respiratory system, skin and nervous system.

Accepted for processing, but not everywhere:

4 – LDPE or PEBD – low density polyethylene

Almost all bags are made of it, including garbage, cling film, part of packaging for household appliances.

The material is almost harmless, but when heated and decomposed, it releases formaldehyde.

5 – PP – polypropylene

It is used to make cups for yoghurts, bags for bread and cereals, baby pacifiers, packaging for baby food, diapers, food containers, straws for drinks, jars for pills, syringes, children’s toys.

The material is almost harmless, but it releases formaldehyde when heated and decomposed.

6 – PS – polystyrene

It is used for making, for example, foamed pads for slices, vegetables and fruits, egg packaging, styrofoam, audio tapes and CD boxes, children’s toys.

It is recommended to use it only once: upon repeated use, heating or in contact with some products, it releases styrene, which adversely affects the function of the liver and kidneys, the circulatory and nervous systems.

Not accepted for processing:

3 – PVC or PVC – polyvinyl chloride

For example, food containers and cling film, children’s toys, plastic windows, stretch ceilings, furniture parts, pipes, tablecloths and bathroom curtains, linoleum and artificial leather, containers for technical liquids are made of it.

Contraindicated for food, but still used. Can be reused for other purposes.

Invisible evil: bisphenol A, vinyl chloride, phthalates, and possibly cadmium. When burned, it releases dioxin – a highly toxic substance that negatively affects the reproductive and immune systems, causes hormonal disorders and cancer.

7 – O or OTHER – everything else

It is used for making, for example, baby bottles and toys, transparent disposable devices, reusable water bottles and bottles for a cooler, CD and DVD, combined packaging.

After frequent washing or heating, it releases bisphenol A or luorene-9-bisphenol (BHPF), which negatively affects the brain, reproductive and endocrine systems.

As you can see, plastic labeling is a whole science. Complicated by the fact that:

  1. Not all plastic products have markings;
  2. in Russia there is no legislation that regulates labeling and, moreover, controls its compliance with the material;
  3. recycling is an energy-intensive process that usually consumes non-renewable energy sources;
  4. Plastic recycling does not completely eliminate household waste.Sooner or later, the material reaches the stage where it can no longer be recycled.

Disposal of hazardous household waste

Such wastes include:

  • batteries,
  • disposable lighters,
  • household appliances, electronics, gas stoves,
  • cylinders for household aerosols and paints;
  • unused or expired drugs,
  • glass and double-glazed windows, mirrors,
  • mercury thermometers;
  • halogen lamps, incandescent lamps, fluorescent lamps;
  • 90,097 leftovers or expired household chemicals;

    90,097 garden chemicals;

  • water filters and printer cartridges;
  • 90,097 fireworks;

  • car tires and batteries;
  • oil and fat.

You can find the nearest separate collection point for everyday and hazardous household waste on the RecycleMap.

Video from Greenpeace about plastic sorting, and at the same time a repetition of the previous lesson about storage and preparation of recyclable materials


1.Which of these materials is considered the least harmful?

  • PET (E) (1)
  • PEHD (HDPE) (2)
  • PVC or PVC (3)
  • LDPE or PEBD (4)
  • PP (5)
  • PS (6)
  • O or OTHER (7)

2. Which of these items are hazardous household waste?

  • medicines
  • mirrors
  • mercury thermometers
  • plastic buckets
  • plastic toys for children
  • batteries
  • car tires

3.Select the correct statements:

  • Russia has legislation regulating the use of markings.
  • Phthalate is released from PET containers when reused.
  • Oil and grease are classified as hazardous household waste.

4. Mark the material (by number), which can be recognized by the characteristic outlet point on the bottom.

5. Indicate the marking of the material (with a number), which can be recognized by the characteristic seam on the bottom.

More information and news about how business, law and society are “greening” in our Telegram channel. Subscribe.

Multiple endocrine neoplasias in children and adolescents | # 03/18

The syndrome of multiple endocrine neoplasia (MEN) is understood as the formation in two or more organs of the endocrine system of hereditary benign or malignant tumors and other (diffuse, nodular) hyperplastic processes with increased production of hormones.

Despite the relative rarity of the combination of multiple tumors in different endocrine glands, the number of publications devoted to this problem has increased in the last decade. The development and implementation into clinical practice of a wide range of modern research methods (molecular genetic, immunomorphological, hormone monitoring, etc.) contributed to a significant increase in the detection of patients with multiple endocrine neoplasia syndrome. The recognition of the importance of familial genetic screening has led to a more thorough description of this syndrome, early diagnosis and timely treatment.

The number of nosological forms of MEN syndrome is constantly expanding. Currently, it includes four genetically different familial diseases, Carney complex, Peitz – Yegers syndrome, type 1 neurofibromatosis, Hippel – Lindau syndrome, McCune – Albright – Braitsev syndrome [1].

Each of these syndromes is inherited in an autosomal dominant manner, and phenotypic traits are characterized by high penetrance, varying degrees of expressiveness, and outwardly are not always associated with the consequences of a single gene mutation.In some cases, the exact location of the mutation is not known.

Syndrome of multiple endocrine neoplasia type 1 (MEN type 1)

MEN type 1 syndrome (Vermeer’s syndrome) – includes heterogeneous hereditary diseases, the pathogenesis of which is hyperplasia or tumor transformation of several endocrine glands, mainly of neuroectodermal origin. The syndrome is characterized by tumors of the parathyroid glands, pituitary gland and islets of Langerhans pancreas.The appearance of duodenal gastrinomas, carcinoid tumors (derivatives of the anterior embryonic intestine), benign adrenal adenomas and lipomas is also possible.

Menin gene, which is located in the long arm of chromosome 11 (11q13), is the cause of type 1 MEN. These changes in the gene are identified in 70–95% of patients with this syndrome. Menin is a classic tumor suppressor that regulates the cell cycle and transcription. Insufficiency of menin leads to cell hyperplasia, and the absence of menin leads to their tumor transformation.The frequency of MEN type 1 is 1 case per 30,000 population. Among patients with primary hyperparathyroidism, type 1 MEN syndrome occurs in 2–4% [2].

Vermeer’s syndrome is characterized by high penetrance. The first clinical symptoms appear in 50% of patients by the age of 20, and at the age of over 40 – in almost 95%. The age of onset of the disease ranges from 4 to 80 years, but the peak of manifestation falls on the age of 20 to 40 years [3].

The above statistics indicate that in about 50% of cases of MEN type 1 can occur in childhood, which, in turn, requires vigilance and more careful genetic screening control of children in families with identified mutations of the meningean gene.

MEN type 1 is characterized by the variability of the combination of clinical manifestations. More than 20 different combinations of endocrine and metabolic disorders within this syndrome have been described in the literature. In about 40% of cases of MEN type 1, three endocrine glands are affected – the parathyroid gland, the pancreas and the pituitary gland. In patients with a mutation of the menin gene and damage to at least one of these three tumors characteristic of MEN type 1, there is a risk of subsequent development of either of the other two.Tumors of the parathyroid glands (in 95% of cases), gastrointestinal tract (in 30–80%), and adenohypophysis (in 15–90%) develop more often synchronously or sequentially [4].

The most characteristic neoplasms for type 1 MEN syndrome are hyperplasia or tumors of the parathyroid glands, leading to the development of primary hyperparathyroidism (PHPT) in the patient. Clinical symptoms are usually found at a young age (20–25 years). Either three or all four parathyroid glands are affected.Due to impaired calcium metabolism, patients experience a constant feeling of thirst, develop polydipsia, polyuria, urolithiasis or nephrocalcinosis, and subsequently renal failure. In half of patients with hyperparathyroidism, symptoms from the digestive system are noted – loss of appetite, nausea, vomiting, flatulence, stool disorders, weight loss, in 10% – peptic ulcers of the stomach and duodenum develop.

Islet cell neoplasms of the pancreas, which are part of the type 1 MEN syndrome, are most often gastrinoma and insulinoma (up to 60% of cases), less often – glucagonoma, somatostatinoma, PP-cell tumors, as well as accidentally detected tumors that do not have functional activity, and carcinomas (slowly growing hormone-active formations).Tumors in the pancreas in type 1 MEN syndrome are usually diagnosed at the age of 40 or more. They are characterized by multicentric (simultaneous appearance of several tumors at once) growth. In addition to the pancreas, they can also be located in the submucosa – these are multiple small gastrinomas of the duodenum [5].

Tumors of the adenohypophysis are observed in 60% of patients. Of the hormone-active tumors of the adenohypophysis, prolactinomas are most often found.However, there are frequent cases of their combination with somatotropinoma, corticotropinoma, thyrotropinoma. In childhood, hormone-inactive microadenomas are more often detected. In a large review (2230 patients with pituitary adenoma), type 1 MEN syndrome was diagnosed in 1.4% of children under the age of 11, of which only 16% had hormone-active tumors [6].

Carcinoid neoplasms (from the group of neuroendocrine tumors) are found mainly in men. This is a carcinoid tumor of the thymus, the growth of which does not show any clinical signs.For women, the presence of such tumors in the bronchial tree, producing corticotropin-releasing hormone, adrenocorticotropic hormone (ACTH), is more typical. In type 1 MEN syndrome, multiple carcinoid tumors are also found in the stomach and other parts of the digestive system (gastrinomas, etc.).

The adrenal glands are often affected in Vermeer’s syndrome. These are usually hormone-inactive tumors (incidentaloma), which are incidental findings on CT imaging.

Neoplasms on the skin are characteristic of MEN type 1 syndrome: lipomas, angiofibromas, collagenomas (nevi), which are a kind of precursors of the development of the syndrome before the formation of an obvious clinical picture of the disease.

Syndrome of multiple endocrine neoplasia type 4 (MEN type 4)

In 10–30% of patients with a phenotypic manifestation characteristic of type 1 MEN syndrome, no mutations in the type 1 MEN gene are detected. In less than 3% of these patients, mutations in the CDK1B gene, which encodes an inhibitor of cyclin-dependent kinase (p27), are found.The latter regulates cell proliferation and differentiation. In an animal experiment, a mutation in this gene causes tumor growth in endocrine organs, similar to those in MEN type 1. This option was identified in the MES of the 4th type [7].

Diagnosis of MEN type 1 syndrome consists of taking anamnesis, physical examination, laboratory, genetic and instrumental research methods. In the presence of a burdened family history, which is confirmed by genetic studies, as well as with a manifest defeat of two endocrine glands, it is necessary to investigate other organs that are prone to frequent damage in order to early detection and timely therapy.

Laboratory research is one of the important stages in the diagnosis of MEN type 1 syndrome. The diagnostic criteria for hyperparathyroidism are an increase in the concentration of ionized calcium and a decrease in the level of phosphorus and alkaline phosphatase in plasma, an increase in the level of intact parathyroid hormone in the blood, hypercalciuria and hyperphosphaturia. To detect neuroendocrine tumors, it is recommended to determine the level of gastrin and insulin in the blood on an empty stomach, as well as to assess the content of chromogranin A. In order to visualize neoplasms, as well as the size and nature of the tumor process, ultrasound examination of the parathyroid glands, abdominal organs and retroperitoneal space, magnetic resonance imaging is used brain.

Indications for carrying out a genetic study for detecting type 1 MEN gene mutations are the detection of two or more neoplasms characteristic of the type 1 MEN syndrome in patients, the identification of multiple tumors of the parathyroid glands in patients under 30 years of age, relapses of hyperparathyroidism after surgery in patients with multiple gastrinomas and pancreatic tumors. In addition, genetic testing is recommended for relatives of patients with an identified genetic mutation.

In children with detected mutations characteristic of MEN type 1, after 8 years, annual studies of the concentration of ionized calcium, phosphorus, parathyroid hormone, gastrin, prolactin, cortisol, ACTH, as well as glucose and immunoreactive insulin are prescribed on an empty stomach.

After 5 years, magnetic resonance imaging of the hypothalamic-pituitary region, ultrasound of the parathyroid, pancreas, and abdominal organs are performed once every 3 years [1].

The main goal of treatment of patients with MEN 1 type is removal of neoplasms and subsequent correction of hormonal imbalance.

Given that the parathyroid glands are most common, surgery is the treatment of choice. However, the optimal timing has not been determined, and the decision on surgical intervention is made based on the data of instrumental and laboratory studies. Subtotal parathyroidectomy (at least 3.5 glands) or total parathyroidectomy is recommended.

However, the results of treatment of tumors associated with MEN type 1 are not always successful due to the frequent extensive local spread of the tumor and the high probability of recurrence [5].

Syndrome of multiple endocrine neoplasia type 2

The syndrome of multiple endocrine neoplasia type 2 (MEN type 2) unites a group of pathological conditions characterized by the presence of a neoplasm or a hyperplastic process from the cells of the neuroectoderm that affects two or more organs of the endocrine system.

In the population, this syndrome occurs with a frequency of 1:30 000, is an autosomal dominant disease with a high risk of neuroendocrine tumors, accompanied by the emergence and accumulation in families of medullary thyroid cancer (MTC), pheochromocytoma and parathyroid hyperplasia [8].

It is characterized by high penetrance and variability of manifestations. It occurs more often in young people and in childhood. Despite the fact that the mechanism of the development of the syndrome is not fully understood, it is directly related to the development of defects in the RET proto-oncogene. The RET (Rearranged during transfection) gene is localized on chromosome 10 and consists of 20 exons. It encodes a cell surface glycoprotein belonging to the tyrosine kinase receptor class that plays a role in the development of the ganglionic plate and its derivatives.The gene functions in human tissues that are derived from the neural crest (parafollicular cells of the thyroid gland, medullary adrenal glands, and sympathetic ganglia). In the follicular cells of the thyroid gland and in the adrenal cortex, this gene does not transmit information.

MEN type 2 is subdivided into three subtypes: MEN 2A (Sipple’s syndrome), MEN 2B (Gorlin’s syndrome), and medullary thyroid cancer. In almost all cases of MEN type 2, MTC is detected.

Mutations of the extracellular domain of the RET proto-oncogene, localized in exons 10 and 11, in most cases are detected in MEN 2A and MTC syndromes.The development of MEN 2B syndrome is associated with intracellular domain mutations (exons 14-16).

According to the latest information provided by ARUP Online Scientific Resourse, 155 germline mutations of the RET gene have been reported. According to the database of this organization and the American Thyroid Association (ATA), patients with only MTC have a relatively low risk of developing aggressive forms of the tumor. In these cases, mutations are most often detected in exon 13 (codons 768, 790), exon 14 (codon 804), and exon 15 (codon 891) of the RET proto-oncogene [9].

Patients with MEN 2A syndrome have an intermediate risk of developing prognostically unfavorable forms of MTC and mutations are more often localized in exon 10 (codons 609, 611, 618, 620) and in codon 630 of exon 11 of the RET gene. The high-risk group includes patients with the classic MEN 2A syndrome. Mutations in this case are found in the 634th codon of the 11th exon of the RET proto-oncogene.

The most unfavorable prognosis group with an early age of MTC manifestation, early distant metastasis, and an aggressive nature of tumor growth include patients with MEN 2B syndrome, in which mutations are most often detected in codon 883 of exon 15 (3%) and codon 918 The 16th exon (95%) of the RET proto-oncogene [9, 10].

MEN 2A syndrome, subtype accounts for 70–80% of all cases, which combines MTC, pheochromocytoma, and damage to the parathyroid glands. MTC is the main manifestation of the disease and occurs in 70–90% of cases. It is usually diagnosed before the age of 35, while 70% of patients are already at the stage of regional lymphogenous metastasis. The second most common tumor in Sipple’s syndrome is pheochromocytoma, which is detected in 60–75% of patients, and in 50–80% of cases it is bilateral.It is accompanied by general weakness, moderate transient or persistent arterial hypertension, hyperhidrosis, hypersalivation, and polyuria. With a crisis course of pheochromocytoma, there is a high probability of ventricular fibrillation, acute heart failure, and pulmonary edema. Hyperplasia of the parathyroid glands in MEN 2A subtype occurs in 20% of cases and is characterized by a mild course [11].

MEN 2B syndrome, subtype accounts for about 5% of all cases of MEN type 2 syndrome.Unlike the other two subtypes, Gorlin’s syndrome is characterized by the presence of specific phenotypic manifestations, early manifestation and aggressive course of MTC [12]. Approximately 75% of patients have a marfan-like phenotype, suffer from kyphoscoliosis or lordosis, in some patients hypermobility of the joints and a decrease in subcutaneous fat are noted. Already in early childhood, protruding lips, submucosal nodules on the borderline of the lips draw attention to themselves. Eyelid neuromas cause thickening and outward turning of the edge of the upper eyelid [12].

In some patients, neuromas may form on the surface of the tongue, hard palate, and the posterior surface of the pharyngeal mucosa. In 40% of patients with MEN 2B syndrome, during routine examination, diffuse ganglioneuromatosis of the gastrointestinal tract is diagnosed, associated with the development of symptoms such as megacolon and diarrhea.

In a study of 19 people with MEN 2B, 84% of the authors found a lesion of the gastrointestinal tract already in early childhood [13]. Changes in the parathyroid glands with this variant of MEN 2B syndrome are not typical.

Hereditary (family) MTC accounts for 10–20% of all cases of MEN type 2 syndrome and is, as a rule, the only manifestation of the disease with a later age of disease manifestation. With this subtype, MTC is inherited over many generations. Family members do not have pheochromocytoma and PGPT. Since the RET mutation occurs in all clinical subtypes of MEN type 2, MTC can be considered as MEN 2A with reduced specificity. In this regard, molecular genetic testing is practically mandatory and is most often used to isolate sporadic cases of MTC [14].

Each of the subtypes of MEN type 2 can be suspected based on clinical signs. MEN 2A is characterized by the appearance of two or more specific endocrine tumors (MTC, pheochromocytoma, or parathyroid adenoma / hyperplasia) in one person or in close relatives. MEN 2B can be assumed in the presence of a Marfan-like appearance, mucosal lesions, and MTC [10]. In contrast to MEN 2A, with MEN 2B, there is no PGPT. MTC should be kept in mind in families when this disease is detected in several generations in the absence of pheochromocytoma and parathyroid adenoma.

If you suspect MTC, it is imperative to determine the basal and stimulated (calcium gluconate) levels of calcitonin, which in these cases rises sharply. To confirm pheochromocytoma, the content of metanephrine and normetanephrine in daily urine is determined. An increase in the secretion of parathyroid hormone is confirmed by determining its concentration, as well as the content of calcium and phosphorus ions in the blood serum.

To visualize neoplasms that form the basis of the syndrome of multiple endocrine neoplasias, ultrasound, computed and magnetic resonance imaging are used.With atypical localization of pheochromocytoma, one of the most informative methods is scintigraphy with metaiodobenzylguanidine (MIBG).

If the genetic basis of the syndrome is found, even in the absence of clinical signs, hormones – calcitonin, parathyroid hormone and catecholamines – are analyzed annually in order to early recognition of the type 2 MEN syndrome. The main goal of treatment for MEN type 2 is to get rid of tumor foci and subsequent correction of hormonal disorders.

This tactic of treatment and prevention of MTC assumes an exclusively operative pathway, which includes radical thyroidectomy with central cervical lymphadenectomy. Even with tumors less than 1 mm in size, nodal metastases are described in 50% of cases [15].

In children with a RET gene mutation, two treatment strategies can be applied. The first is based on constant monitoring of the level of calcitonin in the blood serum, before performing surgical treatment and thereby postponing its duration.However, constant screening is required, which can take into account the lack of a reliable correlation between the growth of laboratory parameters and the prevalence of the tumor process. In this regard, there is a risk of the formation of invasive and locally spread forms of cancer, which in turn will affect the volume of surgical intervention and further deterioration of the prognosis of the disease [16].

The second strategy is to carry out prophylactic thyroidectomies at an early stage, based only on the RET gene mutation.That is, these children are advised to undergo preventive thyroidectomy at an early age when there is a low likelihood of invasive MTC. Prophylactic thyroidectomy for RET gene mutations is preferable to long-term laboratory screening. The level of lymphadenectomy may be limited to the paratracheal and central group of lymph nodes. In the presence of verified metastases of other groups of lymph nodes, surgical intervention is carried out in accordance with oncological standards.

If MTC is combined with pheochromocytoma, treatment begins with removal of the adrenal tumor, namely, with adrenalectomy for unilateral lesions and removal of both adrenal glands for bilateral lesions. For prophylactic purposes, the removal of both adrenal glands is not provided.

With hyperplasia of the parathyroid glands, damage to all four glands is extremely rare at the same time, however, it is advisable to carry out their full revision. The enlarged glands are removed in whole or in part.Removal of the parathyroid glands during surgery on the thyroid gland is possible only after confirmation of hyperparathyroidism on the basis of biochemical data. Since the aggressiveness of hyperparathyroidism in the general course of type 2 MEN syndrome is low, the removal of the parathyroid glands for prophylactic purposes is not recommended [14].

Medullary thyroid cancer is insensitive to radiation therapy and chemotherapy, however, in the era of targeted therapy, the study of the effect of the drug vandetanib is extremely promising.

Vandetanib, being a selective tyrosine kinase inhibitor, inhibits the activity of vascular endothelial growth factor receptor-2 tyrosine kinase. This drug reduced tumor cell-induced angiogenesis, tumor vascular permeability, and suppressed tumor growth and metastases in human lung cancer heterograft models in athymic mice. In a clinical study involving 331 patients with inoperable locally advanced or metastatic MTC, there was a statistically significant improvement in progression-free survival with vandetanib compared with placebo [17].

There is evidence that the use of this drug in children with type 2 MEN syndrome gives a good response in metastatic forms of MTC, significantly increasing life expectancy [17].

Karni complex

Carney complex is a rare predominantly hereditary autosomal dominant syndrome characterized by the presence of lentiginosis of the skin, mix of the heart, skin, mammary glands, and endocrine tumors [18].

In 70% of patients, a heterozygous mutation was detected in the PRKAR1A gene, which is located on the 17th chromosome in the 17q22-24 region.5. It is a tumor suppressor gene that encodes protein kinase A (PKA). This mutation can occur de novo in 20% of patients. In a number of cases, mutations of the CNC2 gene were found in the 2p16 locus, which is responsible for maintaining the stability of the cell genome. Changing this gene activates cell proliferation and differentiation, which is the basis of carcinogenesis [19].

The classic manifestations of the Carney complex include spotty pigmentation (lentigo) on the face, conjunctiva, chest and shoulders, border of lips, dorsum of hands and feet, vulva, perianal region and glans penis.The pigmentation can have a tan color ranging from dark brown to black. These elements do not differ clinically from freckles, but have a different histological structure and are usually less than 5 mm in size. In addition, blue nevi, subcutaneous neurofibromas and, less commonly, melanotic schwannomas can be detected on the skin with this syndrome.

Lentigines in patients with the Carney complex are similar to those found in Peutz-Yeghers syndrome and McCune-Albright-Braitsev syndrome, but the genes in which the mutation occurs are different.

Myxomas of the heart usually occur mainly at the age of 20-30 years, in 9-22% of patients they have a tendency to embolization of blood vessels, leading to ischemic strokes, heart failure and sudden cardiac death. They can be accompanied by fever, joint pain, shortness of breath, and diastolic murmur. The literature describes a case of ischemic stroke in a 6-year-old girl with the Carney complex, as a result of embolization by particles of myxoma of the left atrium [20].

Skin myxomas most often develop on the eyelids, in the outer canal of the ear, although they can affect any part of the skin, rarely exceed sizes of more than 1 cm.These are usually small dark pink opalescent papules. In 80% of patients with myxoma of the heart, similar changes in the skin are accompanied. Multiple bilateral myxoid fibroadenomas of the mammary glands can be considered an unusual manifestation of the Carney complex [21].

Among the lesions of the endocrine system of the Carney complex, ACTH-independent Cushing’s syndrome is more often detected, caused by primary micronodular hyperplasia of the cortical layer of both adrenal glands. The test with dexamethasone confirms the peculiarity of the morphological structure of the adrenal glands – the level of cortisol increases by more than half [21].The syndrome of hypercortisolism can occur in waves with varying degrees of severity.

Skin myxomas most often develop on the eyelids, in the outer canal of the ear, although they can affect any part of the skin, rarely exceed sizes of more than 1 cm. These are, as a rule, small dark pink opalescent papules. In 80% of patients with myxoma of the heart, similar changes in the skin are accompanied. Less common in young people are large-cell calcified Sertoli cell tumors in the testicles. For them in the clinic, gynecomastia is characteristic, due to excessive aromatase activity.Described isolated cases of ovarian cysts in patients, and in men with Leydig.

The Carney complex can also include clinical manifestations of pituitary adenoma (hyperprolactinemia and growth hormone), hyperparathyroidism, benign thyroid nodules, bilateral ductal adenoma of the breast.

Genetic screening is recommended if there is a family history of complications. When genetic abnormalities are confirmed, laboratory and instrumental diagnostics are performed, which allows diagnosing the disease at an early stage and preventing the occurrence of life-threatening consequences [22].

Peutz-Jeghers syndrome

It is a rare autosomal dominant inherited syndrome with a mutation in the serine threonine kinase (STK11) gene that acts as a tumor inhibitor. Its overexpression can cause disruption of the cell cycle in the G1 phase. The role of the STK11 gene, located on chromosome 19p13.3, in the life of the cell is still being studied. Peitz-Jeghers syndrome is a hereditary hamartoma polyposis. Every first-line relative of a person with Peutz-Jeghers syndrome has a 50% chance that the syndrome will manifest itself at any stage of life.But 45% of patients with Peitz-Jeghers syndrome do not have a burdened family history.

A mutation in this gene causes a whole spectrum of phenotypic manifestations in humans.

An increased incidence of tumors in the ovaries and testicles is associated with this syndrome. In the latter, they are represented by benign tumors of Sertoli cells with calcifications. Young men develop prepubertal gynecomastia. This is due to the loss of heterozygosity at the STK11 locus in Sertoli and breast cells, which leads to an increase in aromatase expression.In some patients, tumors of the mammary glands and thyroid gland are detected [23].

Melanin pigmentation of the skin and mucous membranes is a typical symptom of the disease. It is characterized by melanin spots (lentigo), round or oval, with a diameter of 1 to 5 mm, around the mouth and eyes, on the nose, less often on the extremities, on the mucous membrane of the oral cavity, rectum and genitals. The spots on the red border of the lips are more dense than on the skin. They do not cause painful sensations, have a small size, oval shape, brown color, do not darken with prolonged exposure to the sun, do not become malignant.Spots appear at an early age, sometimes in infants. The presence of such elements may indicate an increased risk of developing cancer of the digestive and reproductive system.

The syndrome is accompanied by hamartomatous polyposis. Large intestinal polyps are usually located in the jejunum (93%) from 5 cm or more in size, on a pedicle or broad base, while small polyps are more often found in the stomach and colon. Polyps are predominantly benign adenomatous type. During histological examination, hyperchromic nuclei are determined, in the rebuilt glands, muscle fibers grow into the muscle plastic of the mucous membrane, which allows them to be considered precancerous cells.Multiple polyposis of the gastrointestinal tract for a long time does not manifest itself in anything and manifests itself in adulthood. In children, mucosal pigmentation and family history require genetic testing [24].

Neurofibromatosis type 1

Neurofibromatosis is a heterogeneous group of hereditary syndromes that lead to the development of tumors of the central and peripheral nervous system. By far the most common form is neurofibromatosis type 1 (NF1), known as von Recklinghausen’s disease or peripheral neurofibromatosis.It is an autosomal dominant disorder caused by mutation of the suppressor gene NF1 with the formation of peripheral nerve neurofibromas.

The NF1 gene contains information responsible for the synthesis of the neurofibromin protein. Due to gene damage in one of the pairs of 17 chromosomes, half of the synthesized neurofibromin becomes defective, which leads to increased cell proliferation [25].

The frequency of occurrence of NF1 is approximately 1: 2500 to 3000. If the allelic gene in the paired chromosome does not undergo mutation and protein synthesis does not stop, then the growth of benign formations increases.If the neurofibromin allelic gene is also damaged, a malignant tumor develops. Approximately 50% of mutations appear de novo in patients without a family history of NF1 [26].

The clinical picture of Recklinghausen neurofibromatosis is characterized by a significant variety of symptoms. The earliest sign that allows one to suspect a disease is the presence of more than 5 milk-coffee pigment spots in a newborn or child with a diameter of 0.5 to 15 mm or more. They are usually located on the torso and neck, but can be found on the face and limbs.Although coffee stains are a specific finding in neurofibromatosis, they can occur in 10% of the healthy population, as well as in Russell – Silver, MEN 2B, Legius, McCune – Albright – Braitsev syndromes.

Neurofibromas are diagnosed in about 60% of patients. They can appear both on the skin and in internal organs. Skin forms can be pedunculated, in the form of nodules or plaques, more often develop in late childhood, and their frequency increases in adulthood. Intraorganic neurofibromas can occur throughout the body, including periorbital, in the retroperitoneal space, along the gastrointestinal tract, in the mediastinum [27].

Plexiform (groin-like) growth of neurofibroma is pathognomonic for internal neurofibromas in NF1. Interlaced neurofibromas often develop during childhood and grow rapidly by applying intense pressure to adjacent tissues. In contrast to the cutaneous form, plexiform neurofibroma has an increased risk of transformation into a malignant tumor of the peripheral nerve sheath [27].

Patients with NF1 also have a significant predisposition to malignant tumors outside the nervous system.Children are at high risk, 7 times more likely to develop systemic malignant malignant neoplasm of hematopoiesis, especially myeloid leukemia, compared with children of their age group. Patients with NF1 have a high risk of developing breast cancer, especially in women in their 50s.

Finally, although rare, adrenal pheochromocytoma may appear in patients with NF1 up to 5% and in the general population less than 1%. In addition, many patients with NF1 are short, although their body proportions remain normal.The mechanism of the onset of skeletal deformities is still unknown, but such patients have low bone mineral density and low vitamin D concentration and, as a consequence, a high rate of recurrent fractures in children [28].

Von Hippel-Lindau disease

Hippel-Lindau disease (HDL) is an inherited disease with a dominant mode of inheritance. The reason for this fancomatosis is a mutation of the tumor suppressor gene VHL, which is localized on the short arm of the 3rd chromosome 3p25.3. In 20% of cases, mutations occur de novo . In case of illness, abnormal production of the von Hippel-Lindau protein or its complete absence occurs, thereby disrupting the regulation of cell division and the process of their regeneration. This protein has several functions, the main one being the control of angiogenesis by regulating the degradation of hypoxy-regulating transcription factors. The incidence in the population is 1:36 000. The average age of incidence is 26 years, and the youngest known patient was 5 years old [29].

The disease is characterized by the development of multiple neoplasms and cysts in various organs and systems: hemangioblastoma in the retina and central nervous system, pheochromocytoma, renal cell carcinoma, cysts of the pancreas, testicles and kidneys, pancreatic neuroendocrine tumors, cystoadenomas of the urogenital system and paraglycotic tumors.

The most common symptom is retinal angiomatosis, which accompanies up to 75% of cases.It often acts as a diagnostic marker of this pathology.

In childhood, von Hippel-Lindau disease is characterized by the appearance of neurological symptoms against the background of pre-existing visual disorders. In some cases, the disease in children manifests as subarachnoid hemorrhage [30].

Pheochromocytomas occur in 10–20% of patients. The defeat of the adrenal glands is often bilateral. Changes in the pancreas are benign in the form of small cystic degeneration.In some patients, impaired glucose tolerance is detected. Kidney involvement is represented by cysts, and renal cell carcinoma can develop in adulthood. In childhood, with a familial type of disease, polycystic kidney disease is often its only manifestation.

Most peripheral retinal tumors can be treated with laser photocoagulation (small peripheral tumors) or cryotherapy (large tumors), but these current treatments cannot be used for tumors near the optic nerve.Recently, data have been published on the positive results of the use of propranolol (a synthetic blocker of β-adrenergic receptors) in patients with proliferative vascular tumors. This drug reduced the growth of these retinal hemangioblastomas. Propranolol stopped the division of tumor cells and triggered apoptosis through the activation of the caspase cascade, induction of antiangiogenesis, and increased vasoconstriction [31].

So, the clinical criteria for the diagnosis of Hippel-Lindau disease are based on a burdened family history and / or the occurrence of regional / central hemangioblastoma, pheochromocytoma, carcinoma, renal and pancreatic parenchyma cysts.Von Hippel-Lindau disease should be assumed and excluded in each case of retinal angiomatosis during ophthalmoscopy, especially in the presence of a burdened family history.

McCune-Albright-Braitsev syndrome

It is a rare congenital disorder characterized by polyosseous fibrous bone dysplasia, coffee pigmentation of the skin and premature puberty (PPD) and other endocrinopathies. The genetic defect is caused by a mutation in the GNAS1 gene, which encodes the α-subunit of the G-protein, which is a messenger in the conversion of cAMP, which regulates the entire hormonal system.GNAS1 is located on the long arm of chromosome 20 (region 20ql3.2). Molecular changes in the protein lead to proliferation of endocrine cells and their increased function. It is assumed that this cell mutation occurs in the early stages of embryogenesis. As a result, clones of cells carrying mutant proteins are formed [32].

Fibrous dysplasia, leading to fractures, deformities, systemic bone pain, is the most severe manifestation of this disease. The process involves many bones, starting with the pelvic and femur.In bone tissue, mutant G-protein disrupts osteoblast differentiation. In the lesions, altered osteoblasts cause thinning of bone tissue, and bone trabeculae dissolve. Fibrous dysplasia, as a rule, does not appear from birth, but becomes clinically evident during the first few years of life

A shortened skeleton, fractures, often of the proximal femur, its shape in the form of a “shepherd’s staff” and scoliosis lead to a change in gait like a “duck”, respiratory failure.Disruption of phosphorus-calcium metabolism is the cause of hypophosphatemia, vitamin D-resistant rickets, osteomalacia in patients with already pronounced changes in the skeletal system.

Of the endocrine pathology for this syndrome, PPD is typical mainly in girls (80%), more often after the first year of life. As a rule, the first manifestation is uterine bleeding. They are found long before the onset of thelarch and adrenarche. Bleeding is caused by the autonomous functioning of ovarian follicular cysts, which occasionally lead to excess estrogen release.The ovaries are of normal size, but large persistent follicular cysts can be found. It is believed that the mutant protein activates adenylate cyclase at the receptors for luteinizing hormone and follicle-stimulating hormone in ovarian cells, thereby stimulating the secretion of estrogen in the absence of gonadotropic hormones. Characterized by an increase in mammary glands and accelerated growth in length. Some patients have elevated levels of gonadotropic hormones. In such cases, we can talk about the true SPR [33].

Other endocrine disorders are thyroid abnormalities, half of which occur with hyperthyroidism, less often with hypothyroidism. Excess growth hormone is less common, affecting only 15–20% of patients. In some patients, somatotropinoma was combined with prolactin hypersecretion. Hyperadrenocorticism, which is a rare pathology, occurs in the neonatal period due to primary pigmented small-nodular dysplasia or adrenal adenoma of the fetus [34].

The GNAS mutation has been identified in patients with intraductal papillary mucinous neoplasms (IPMNs) of the pancreas.Rare cases of pancreatic cancer have been identified in patients with McCune – Albright – Braitsev syndrome [32].

There is no etiotropic treatment yet, but aromatase inhibitors (tamoxifen), ketonazole, bisphosphonates are widely used as a complex correction of clinical manifestations.

So, the diagnosis of MEN syndrome presents significant difficulties for diagnosis, which is primarily associated with multi-organ damage, and the involvement of endocrine tissue leads to a variety of metabolic disorders.The first signs of MEN syndrome often occur during childhood, so it is important that pediatricians are familiar with the main symptoms of these syndromes.

Patients with MEN syndrome should be monitored in a specialized clinic that has experience in working with this pathology in order to determine the tactics of management and treatment.


  1. Dedov I.I., Peterkova V.A., Shiryaeva T. Yu. et al. Handbook of a pediatrician-endocrinologist. M .: Litterra, 2014.528 s.
  2. White M. L., Doherty G. M. Multiple endocrine neoplasia // Surgical Oncology Clinics of North America. 2008; 17: 439-459.
  3. Skarulis M. C. Clinical expression of MEN1 at NIH // Ann Intern Med. 1998; 129: 484-494.
  4. Gibril F., Schumann M., Pace A., Jensen R. T. Multiple endocrine neoplasia type 1 and Zollinger-Ellison syndrome: a prospective study of 107 cases and comparison with 1009 cases from the literature // Medicine (Baltimore).2004; 83 (1): 43–83.
  5. Brandi ML, Gagel RF, Angeli A., Bilezikian JP, Beck-Peccoz P., Bordi C., ConteDevolx, Falchetti BA, Gheri RG, Libroia A., Lips CJ, Lombardi G., Mannelli M., Pacini F. , Ponder BA, Raue F., Skogseid B., Tamburrano G., Thakker RV, Thompson NW, Tomassetti P., Tonelli F., Wells SA Jr., Marx SJ Guidelines for diagnosis and therapy of MEN type 1 and type 2 // J Clin. Endocrinol Metab. 2001; 86: 5658-5671.
  6. Mindermann T., Wilson C. B. 1995 Pediatric pituitary adenomas // Neurosurgery. 36: 259-269.
  7. Endocrinology: National Guidelines / Under. ed. I.I.Dedova, G.A.Melnichenko. 2nd ed., Rev. and add. M .: GEOTAR-Media, 2016.112 p.
  8. Allgayer H., Render H., Fulda S. Hereditary Tumors: From genes to clinical consequences. Wiley-VCH, 2009.530 p.
  9. ARUP Online Scientific Resourse. www. arup. utah. edu.
  10. Moline J., Eng C. Multiple endocrine neoplasia type 2: an overview // Genet Med. 2011, Sep; 13 (9): 755-764.
  11. Cohen M. S., Moley J. F. Surgical treatment of medullary thyroid carcinoma // J Intern Med. 2003 Jun; 253 (6): 616-626.
  12. Skinner M. A., DeBenedetti M. K., Moley J. F. et al. Medullary thyroid carcinoma in children with multiple endocrine neoplasia types 2 A and 2 B // J Pediatr Surg. 1996 Jan; 31 (1): 177-81; discussion 181-182.
  13. Wray C. J., Rich T. A., Waguespack S. G., Lee J. E., Perrier N. D., Evans D. B. Failure to recognize multiple endocrine neoplasia 2B: more common than we think? // Ann Surg Oncol. 2008; 15: 293-301.
  14. Kloos R. T., Eng C., Evans D. B. et al. Medullary thyroid cancer: management guidelines of the American Thyroid Association // Thyroid. 2009; 19: 565-612.
  15. Melvin K. E. W., Miller H. H., Tashjian A. M. Early diagnosis of medullary carcinoma of the thyroid gland by means of calcitonin assay // N Engl J Med.1971; 285: 115-120.
  16. Telander R. L., Zimmerman D., van Heerden J. A., Sizemore G. W. Results of early thyroidectomy for medullary thyroid carcinoma in children with multiple endocrine neoplasia type 2 // J Pediatr Surg. 1986; 12: 1190-1194.
  17. Fox E., Widemann B. C., Chuk M. K. et al. Vandetanib in Children and Adolescents with Multiple Endocrine Neoplasia Type 2 B Associated Medullary Thyroid Carcinoma // Clin Cancer Res. 2013; 19: 4239-4248.
  18. Casey M., Vaughan C. J., He J., Hatcher C. J., Winter J. M., Weremowicz S. et al. Mutations in the protein kinase A R1 alpha regulatory subunit cause familial cardiac myxomas and Carney complex // J Clin Invest. 2000, Sep; 106 (5): R31–38.
  19. Briassoulis G., Kuburovic V., Xekouki P., Patronas N., Keil M. F., Lyssikatos C. et al. Recurrent left atrial myxomas in Carney complex: a genetic cause of multiple strokes that can be prevented // J Stroke Cerebrovasc Dis Off J Natl Stroke Assoc.2012, Nov; 21 (8): 914. e1-8.
  20. Turhan S., Tulunay C., Altin T., Dincer I. Second recurrence of familial cardiac myxomas in atypical locations // Can. J. Cardiol. 2008; 24: 715-716.
  21. Orlova EM, Kareva MA Carni-complex – multiple endocrine neoplasia syndrome // Problems of endocrinology. 2012, vol. 58, no. 3, p. 22-30.
  22. Bertherat J. Carney complex (CNC) // Orphanet J Rare Dis. 2006; 1: 21.
  23. Wang Z.J., Churchman M., Avizienyte E. et al. Germline mutations of the LKB1 (STK11) gene in Peutz – Jeghers patients // J Med Genet. 1999; 36: 365-368.
  24. Giardiello F. M., Brensinger J. D., Tersmette A. C. et al. Very high risk of cancer in familial Peutz – Jeghers syndrome // Gastroenterology. 2000; 119: 1447-1453.
  25. Weiss S. et al. Enzinger and Weiss’s Soft Tissue Tumors. Philadelphia, PA. Elsevier Saunders; 2014.
  26. Boyd K.P., Korf B. R., Theos A. Neurofibromatosis type 1 // J Am Acad Dermatol. 2009; 61 (1): 1-14, quiz 15-16.
  27. Rosai J. et al. Rosai and Ackerman’s Surgical Pathology. 10 th ed. Philadelphia, PA: Elsevier Saunders; 2011.
  28. Hirbe A. C., Gutmann D. H. Neurofibromatosis type 1: a multidisciplinary approach to care // Lancet Neurol. 2014; 13 (8): 834-843.
  29. Huynh T. T., Pacak K., Brouwers F. M., Abu-Asab M.S., Worrell R. A., Walther M. M. et al. Different expression of catecholamine transporters in phaeochromocytomas from patients with von Hippel-Lindau syndrome and multiple endocrine neoplasia type 2 // Eur J Endocrinol. 2005; 153: 551-563.
  30. Chung S. Y., Jeun S. S., Park J. H. Disseminated Hemangioblastoma of the Central Nervous System without Von Hippel-Lindau Disease // Brain tumor research and treatment. 2014, Vol. 2, p. 96-101.
  31. Von Hippel E. Vorstellung eine patienten mit einer sehr ungewohnlieben Netzhant // Ber Ophthalmol Ges. 1985, Vol. 24, p. 269.
  32. Happle R. The McCune-Albright syndrome: a lethal gene surviving by mosaicism // Clin Genet. 1986; 29 (4): 321–324.
  33. Parvanescu A. et al. Lessons from McCune-Albright syndrome-associated intraductal papillary mucinous neoplasms: GNASactivating mutations in pancreatic carcinogenesis // JAMA Surg. 2014; 149 (8): 858-862.
  34. Brown R. J., Kelly M. H., Collins M. T. Cushing syndrome in the McCune-Albright syndrome // J Clin Endocrinol Metab. 2010; 95 (4): 1508-5115.

V. V. Smirnov 1 , Doctor of Medical Sciences, Professor
S.A. Miroshnichenko

FSBEI IN RNIMU them. N.I. Pirogova, Ministry of Health of the Russian Federation, Moscow

1 Contact information: smirnov-web @ mail.ru

Multiple endocrine neoplasias in children and adolescents / V. V. Smirnov, S. A. Miroshnichenko

For citation: Attending physician No. 3/2018; Page numbers in the issue: 25-31

Tags: insulinoma, lentigo, myxoma, angiomatosis

90,000 Rating of regions for the production of drugs for the treatment of diseases of the endocrine system and digestive organs in 2015

Based on monitoring data for 20156 federal districts were engaged in the production of drugs for the treatment of diseases of the endocrine system and digestive organs in packages.

Svetlana Romanova , “Remedium”

Production concentration

Analysis of the location structure of medical industry enterprises producing drugs for the treatment of diseases of the endocrine system and digestive organs in packages by regions of Russia showed that the leader in the number of regions producing drugs in this group is Central and Privolzhsky federal districts, where there are 7 regions produce these drugs.In Siberian district – three, in Ural and South – two regions produce these products, and in Far East – one.

Production of drugs

Location of production and production volumes of drugs for the treatment of diseases of the endocrine system and digestive organs in ampoules and packages for 2014 are presented in Table 1 and Figures 1-6.

Release of this group of medicines by medical industry enterprises in 2015amounted to 522.381 million packs, or 135.90% from the previous year.

The leaders in the production of drugs for the treatment of diseases of the endocrine system and digestive organs in packages are enterprises of the Central Federal District – 219.035 million packages, or 41.93% of the total production volume and 1.36 times higher than the production level of the previous year. In this federal district, the leader in the production of drugs in this group is the Kursk Region – 102.617 million units, or 19.64% of the total volume in the industry, and 1.25 times higher than the level of 2014.

Enterprises of Privolzhsky Federal District increased the output of drugs in this group by 1.32 times compared to the previous year and produced 149.178 million packs, or 28.56% of the total production. In this federal district, the leader in the production of drugs is the Republic of Tatarstan – 88.018 million packages, or 16.85% of the total volume in the industry, and 1.42 times higher than the level of 2014.

In Ural Federal District, 134.798 million …packages, or 25.80% of the total volume in the industry and 1.42 times higher than the production level of the previous year. Most of the production of drugs in this federal district was produced by enterprises of the Sverdlovsk region – 16.10% of the total volume in the industry.

Rating of federal districts

The effectiveness of the activities of the federal districts in saturating the pharmaceutical market with domestically produced drugs can also be assessed by the increase in the share of the federal district’s output in the total volume of Russia.

The leader in terms of the increase in the share of production in the total volume of drugs in Russia for the treatment of endocrine and digestive system diseases in packages was Urals Federal District – 1.08 points. The high figure in the federal district is due to the increase in the share of output in the total volume of enterprises in the Sverdlovsk region. The largest decrease in the share was noted in Privolzhsky Federal District – by 0.86 points.

The rating of federal districts by two criteria: the volume of production of drugs for the treatment of diseases of the endocrine system and digestive organs in packages, and an increase in the share of production of these products in the total volume of Russia showed that the leaders were: Central Federal District – 1st place, Privolzhsky Federal District – 2nd place, Uralsky – 3rd place.

1. Korolev M.A., Figurnov E.B. Statistics and economic analysis in the management of the national economy, Moscow, “Economics”, 1985.
2. Zakharova V.M., Romanova S.A. Regional location of the Russian medical industry. Remedium, 2000; 1: 54-59.


Draft Law No. 834261-7 on amendments to Article 67 of the Federal Law “On Circulation of Medicines” (in terms of improving the procedure for introducing a system for monitoring the movement of medicines for medical use) was accepted for consideration.Published on the website sozd.duma.gov.ru.

The document was prepared by the deputies of the State Duma: A.K. Isaev, S.M. Boyarsky, S.A. Zhigarev, D.A. Morozov, E.V. Panina, A.P. Petrov, A.Z. Farrakhov.

In the explanatory note, the authors of the bill note:

The monitoring system is currently being implemented as part of an experiment on drug labeling.

Considering that during the experiment, new basic principles for the functioning of a unified marking system were established, today it is difficult to formulate final user specifications.At the same time, conditions appear that radically change the entire established production process.

In addition, still do not have most IT solution providers. According to manufacturers’ estimates, depending on the supplier of the IT solution, the company’s infrastructure and the global nature of production, the development processes, data exchange with the operator’s information system, including software updates, testing and further validation on production lines, takes from 6 months to 1 years from the date of finalization of technical conditions and requirements .Only selected manufacturers who have installed the latest equipment on the lines have positive test results for applying the 44-character crypto-marking. In addition, until now technical documentation has not been approved, which is necessary for setting up equipment and production processes according to the new requirements for applying a crypto code.

However, the current situation and the readiness status of the drug labeling system using crypto coding, taking into account the number of participants registered in the system (about 15%), as well as the number of drugs for which data has been entered into the system (about 8% of the estimated volume of commodity items of all drugs circulating in the Russian Federation) raises serious concern and indicates high risks for the full-fledged industrial implementation of all stages of the monitoring system functioning at the same time for all drugs circulating on the market from January 1, 2020.

According to information from domestic drug manufacturers (264 manufacturers), out of 860 production lines, 52% are equipped with equipment, for 11% of packaging lines equipment is expected to be supplied in accordance with concluded contracts, 37% of packaging lines are in the process of equipping.

In addition, there is no objective information on the readiness to implement a monitoring system for the rest of the distribution chain (wholesalers, pharmacy and medical organizations).

It is a matter of concern that a full-scale testing of the entire drug movement monitoring system has not yet been carried out, taking into account the new requirements and the participation of all participants in the distribution chain (manufacturers, distributors, pharmacy chains, medical organizations) using a crypto code.

In order to guarantee the sustainability of drug supply to the population, to prevent disruption of the supply of drugs for medical use, the draft law proposes to establish a phased introduction of the drug labeling system, defining the period of its implementation until July 1, 2020 , and to give the Government of the Russian Federation the right to establish the procedure for implementation marking system, including the timing of its implementation.

The draft federal law provides that drugs of “high-cost nosologies” (intended to provide people with hemophilia, cystic fibrosis, pituitary dwarfism, Gaucher’s disease, malignant neoplasms of lymphoid, hematopoietic and related tissues, multiple sclerosis, persons after organ transplantation and ) fabrics) introduced into civil circulation before October 1, 2019, as well as other medicinal products for medical use introduced into civil circulation before July 1, 2020, are subject to storage, transportation, dispensing, sale, transfer, use without applying identification means until their expiration date.

The draft federal law defines the obligation of legal entities and individual entrepreneurs engaged in the circulation of medicinal products for medical use to register in the system for monitoring the movement of medicinal products for medical use.

The State Duma Council set the deadline for preparing the bill for consideration in the first reading – December 2019.

Source: sozd.duma.gov.ru.

90,000 Pharmacy 86 Plus

Set “AquaRosa +” (“AquaRosa +” Nasal spray 30 ml + Mineral rinse “AquaRosa +” 300 ml & nbsp, + additional nozzle for the oral cavity and larynx), hypertonic solution 2%

Nasal spray 30ml + Mineral rinse 300ml + Nozzle for irrigation of the oral cavity and larynx – cardboard packs

& nbsp,

INN: ——-

Dosage form : Hypertonic solution (2%) for nasal cavity care and nasopharynx in the form of a spray in a bottle of 30 ml made of polyethylene based on brine concentrate (natural salt), with an additional spare bottle of 300 ml

ATX code : ———-

Availability of the drug in the list VED: ———-

Pharmacotherapeutic group : means for irrigation and rinsing of the oral cavity and nasopharynx

Shelf life : 2 years from the date of manufacture Storage conditions

Storage conditions :

Store in a dry place protected from direct sunlight at temperatures from 0 ° C to 30 ° C and relative humidity no more than 75%.

Pharmacological action

For the prevention, maintenance and restoration of the physiological state of the mucous membrane of the nasal cavity and nasopharynx, by irrigating and washing the nasal cavity and nasopharynx.

Has a beneficial effect on the mucous membrane of the nasal cavity and nasopharynx, helps to reduce nasal congestion and restore nasal breathing. It has an anti-inflammatory and moisturizing effect, relieves irritation.

After rinsing the nasal cavity with the Means, the sections of the nasal cavity and nasopharynx are cleared of bacteria, viruses, allergens, protects against colds and allergic diseases, and local immunity increases.

Increases the therapeutic efficacy of drugs applied to the mucous membrane of the nasal cavity, reduces the duration of respiratory diseases, and reduces the risk of infection spreading to the paranasal sinuses and ear cavity.


• & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, The need for hygiene in order to prevent, maintain and restore the physiological state of the nasal mucosa.

• & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, It is used for the complex treatment of acute and chronic inflammatory diseases of the nasal cavity, paranasal sinuses and nasopharynx: acute and chronic rhinitis (runny nose), acute and chronic sinusitis, acute and chronic allergic and vasomotor rhinitis, prevention and complex treatment of acute respiratory viral infections and influenza, after surgical interventions in the nasal cavity and paranasal sinuses.

• & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, Apply within 20 days

Dosing regimen

For children under 2 years old.Rinsing the nose in a young child is carried out in the & nbsp position, lying:

– turn the child’s head to one side,

– insert the tip of the product into the nasal passage located on top, rinse the nasal cavity for a few seconds (drip the solution into the nasal passage),

– remove the remnants of the flushing liquid with an aspirator,

– sit the child up and help blow his nose.

Repeat the procedure if necessary.

Carry out the procedure with a different nasal passage.

The term of use of the opened Means is 45 days.

For children over 2 years of age and adults:

– tilt the head to one side,

– insert the tip of the products into the nasal passage located on top, rinse the nasal cavity for a few seconds,

– remove the residual rinsing fluid using an aspirator in a child / blow your nose, repeat the procedure if necessary.

Instructions for sanitization: rinse the anatomical attachment with water before and after using the medical device.

The term of use of the opened Means is 45 days.

Side effects

Side effects when using the Means were not identified.

Contraindications to use

• & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, Individual intolerance to the components of the Means.

• & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, Complete obstruction of the nasal passages.

• & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, & nbsp, Acute otitis media and exacerbation of chronic otitis media.

Use during pregnancy and lactation


Use for impaired renal function


Use in children

– ——-

Special instructions

In case of contraindications, it is recommended to consult a doctor.

It is prohibited to use the product if the consumer container has been opened or damaged.

It is prohibited to use the product after the expiration date.

Method of administration and dosage

For children under 2 years old. Rinsing the nose in a young child is carried out in the & nbsp position, lying:

– turn the child’s head to one side,

– insert the tip of the product into the nasal passage located on top, rinse the nasal cavity for a few seconds (drip the solution into the nasal passage),

– remove the remnants of the flushing liquid with an aspirator,

– sit the child up and help blow his nose.

Repeat the procedure if necessary.

Carry out the procedure with a different nasal passage.

The term of use of the opened Means is 45 days.

For children over 2 years of age and adults:

– tilt the head to one side,

– insert the tip of the products into the nasal passage located on top, rinse the nasal cavity for a few seconds,

– remove the residual rinsing fluid using an aspirator in a child / blow your nose, repeat the procedure if necessary.

Instructions for sanitization: rinse the anatomical attachment with water before and after using the medical device.

The term of use of the opened Means is 45 days.


The agent is poured into a consumer container, depending on the version, either into a bottle with a spray device and a protective cap or into a bottle with a spray device and a protective cap.

The product in consumer packaging is placed in individual packaging – a cardboard box, which contains instructions for use and attachments (in the quantity and version, depending on the configuration).

The product in consumer containers and individual packaging is placed in a shipping container – a cardboard box.


The following information is indicated on the consumer packaging and individual packaging of the product:

– the name of the manufacturer and (or) its trademark,

– the address of the manufacturer,

– the name and purpose of the product,

– number of these specifications,

– amount of funds,

– series number,

– date of manufacture (month, year),

– storage conditions,

– date before which the product can be used and / or “Best before”,

– purpose and method of product use,

– registration certificate number of the Ministry of Health of the Russian Federation,

– inscription “Sterile” and / or the corresponding symbol in accordance with GOST R ISO 15223-1,

– inscription “Store out of the reach of children “,

– composition of the product,

– age restrictions on the use of the product by patients,

– for versions of the means that include a nozzle, an image of the nozzle included in the kit must be additionally placed.

All types of packaging may additionally contain a barcode in accordance with GOST R 51294-1.