Calcium deposits under eyes. Calcium Deposits in Skin: Causes, Symptoms, and Treatments Explained

10.12.202108.06.2023 by alexxlab

What are the main types of calcium deposits in the skin. How are calcium deposits in the skin diagnosed and treated. Can calcium deposits in the skin be prevented.

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Understanding Calcium Deposits in the Skin: An Overview

Calcium deposits in the skin, also known as calcinosis cutis, occur when abnormal amounts of calcium phosphate accumulate in soft tissue. These deposits typically manifest as firm, white or yellowish bumps on the skin surface. While they may seem to appear without warning, calcium deposits can often be indicative of underlying medical conditions or tissue damage.

The primary component involved in these deposits is hydroxyapatite, a form of calcium phosphate that the body normally uses to build and strengthen bones and teeth. When this mineral accumulates abnormally in soft tissues, it leads to calcification, or calcinosis.

Key Characteristics of Calcium Deposits

Appearance: Firm, pimple-like bumps or nodules
Color: White or yellow
Size: Variable, often appearing in clusters
Common locations: Elbows, fingers, shins (can occur anywhere)
Texture: If punctured, they release a white, chalky, paste-like material
Associated symptoms: Tenderness, pain, joint stiffness (if near joints)

The Four Types of Calcium Deposits in Skin

Medical professionals classify calcium deposits into four distinct categories based on their underlying causes:

Dystrophic calcinosis cutis
Iatrogenic calcinosis cutis
Metastatic calcinosis cutis
Idiopathic calcinosis cutis

Dystrophic Calcinosis Cutis

This type of calcium deposit occurs in damaged, inflamed, or dead tissue. Various conditions can trigger dystrophic calcinosis cutis, including:

Skin injuries
Infections
Connective tissue diseases
Panniculitis
Acne
Tumors

Iatrogenic Calcinosis Cutis

Iatrogenic calcinosis is typically associated with certain medications or medical procedures. For instance, repeated blood draws from an infant’s heel can lead to this type of calcium deposit.

Metastatic Calcinosis Cutis

This form of calcinosis results from medical conditions that cause an excess of phosphorus (hyperphosphatemia) or calcium (hypercalcemia) in the body. Some conditions that can lead to metastatic calcinosis cutis include:

Kidney failure
Sarcoidosis
Paraneoplastic hypercalcemia
Hyperparathyroidism
Milk-alkali syndrome
Calciphylaxis
Excess vitamin D

Idiopathic Calcinosis Cutis

When calcium deposits form without any apparent cause, they are classified as idiopathic calcinosis cutis. In these cases:

Phosphate and calcium levels in the body are normal
There’s no evidence of previous tissue damage
The patient isn’t taking medications known to trigger calcinosis
Recent medical procedures aren’t a factor

Diagnosing Calcium Deposits in the Skin

Diagnosing calcium deposits in the skin typically involves a combination of physical examination, medical history review, and diagnostic tests. How do healthcare providers approach this process?

Physical Examination

A dermatologist or primary care physician will carefully inspect the affected areas, noting the size, shape, color, and distribution of the deposits. They may also assess whether the bumps are painful or causing any limitation in movement.

Medical History

The doctor will inquire about the patient’s medical history, including any underlying conditions, recent injuries, or medications that might contribute to calcium deposit formation.

Diagnostic Tests

To confirm the diagnosis and determine the type of calcinosis, several tests may be ordered:

Blood tests: To check calcium and phosphate levels
Skin biopsy: To examine the tissue structure and confirm the presence of calcium deposits
Imaging studies: X-rays, CT scans, or MRIs may be used to assess the extent of calcification

Treatment Options for Calcium Deposits in Skin

Treatment for calcium deposits in the skin varies depending on the underlying cause, severity, and location of the deposits. What are the primary treatment options available?

Medication-Based Treatments

Several medications can be used to manage calcium deposits:

Intralesional corticosteroids (e.g., triamcinolone acetonide): Reduce inflammation and may help shrink deposits
Calcium channel blockers (e.g., amlodipine, diltiazem): May help prevent further calcium accumulation
Antacids containing aluminum hydroxide: Can help reduce calcium absorption
Colchicine: An anti-inflammatory medication that may help in some cases
Warfarin: Used in certain types of calcinosis to prevent further calcium deposition

Procedural Treatments

For more severe or persistent cases, various procedures may be recommended:

Laser therapy: Uses light energy to dissolve calcium deposits
Iontophoresis: Employs low-level electric current to deliver medication directly to affected areas
Surgery: In some cases, surgical removal of calcium deposits may be necessary

Natural Remedies

While not always recommended by medical professionals, some people report benefits from natural treatments:

Massage with aloe vera gel or olive oil
Application of apple cider vinegar
Use of magnesium oil

It’s important to note that these natural remedies lack scientific evidence and should be discussed with a healthcare provider before use.

Preventing Calcium Deposits in the Skin

While not all cases of calcium deposits can be prevented, there are steps individuals can take to reduce their risk. How can one minimize the likelihood of developing calcium deposits in the skin?

Manage Underlying Conditions

Since many cases of calcinosis are associated with other health issues, properly managing these conditions is crucial:

Follow prescribed treatment plans for conditions like kidney disease or autoimmune disorders
Regularly monitor calcium and phosphate levels if you have a condition that affects mineral balance
Work closely with your healthcare team to keep any chronic conditions well-controlled

Maintain a Balanced Diet

A diet that supports healthy calcium and phosphate levels can help prevent abnormal deposits:

Consume calcium-rich foods in moderation
Ensure adequate vitamin D intake to support proper calcium absorption
Avoid excessive consumption of phosphate-rich foods, especially if you have kidney issues

Protect Your Skin

Since skin damage can lead to dystrophic calcinosis, taking steps to protect your skin is important:

Use sun protection to prevent skin damage from UV rays
Avoid trauma to the skin when possible
Treat skin infections promptly to prevent complications

Living with Calcium Deposits: Coping Strategies and Quality of Life

For individuals dealing with calcium deposits in the skin, the condition can impact daily life and emotional well-being. How can those affected best cope with this condition?

Pain Management

If calcium deposits cause discomfort, several strategies can help manage pain:

Over-the-counter pain relievers like ibuprofen or acetaminophen
Application of cold or warm compresses
Gentle massage of the affected areas
Physical therapy to improve mobility and reduce discomfort

Emotional Support

The visible nature of skin calcium deposits can sometimes lead to self-consciousness or anxiety. Seeking emotional support is crucial:

Join support groups for individuals with similar conditions
Consider counseling or therapy to address any emotional challenges
Communicate openly with friends and family about your condition

Lifestyle Adaptations

Depending on the location and severity of calcium deposits, some lifestyle changes may be necessary:

Choose clothing that doesn’t irritate affected areas
Modify exercise routines to accommodate any mobility limitations
Use adaptive tools if deposits affect dexterity

The Future of Calcium Deposit Treatment: Emerging Research and Therapies

As medical science advances, new treatments for calcium deposits in the skin are being explored. What promising developments are on the horizon for managing this condition?

Targeted Drug Therapies

Researchers are investigating medications that specifically target the mechanisms of calcium deposition:

Drugs that inhibit the formation of hydroxyapatite crystals
Medications that enhance the body’s ability to remove excess calcium from soft tissues
Topical treatments that can dissolve existing deposits without invasive procedures

Gene Therapy

For cases of calcinosis related to genetic factors, gene therapy holds potential:

Correcting genetic mutations that lead to abnormal calcium metabolism
Introducing genes that promote the breakdown of calcium deposits

Nanotechnology

Advancements in nanotechnology may offer new treatment options:

Nanoparticles designed to target and dissolve calcium deposits
Nanoscale delivery systems for more effective medication administration

While these emerging therapies show promise, it’s important to note that they are still in various stages of research and development. Patients should continue to work closely with their healthcare providers to manage their condition using current best practices while staying informed about new treatment possibilities.

Calcium Deposits in Skin: Causes, Symptoms, and Treatments

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Medically reviewed by Cynthia Cobb, DNP, APRN, WHNP-BC, FAANP — By Scott Frothingham — Updated on May 31, 2018

What are calcium deposits in the skin?

Your body uses hydroxyapatite to build and strengthen bones and teeth. Hydroxyapatite is a type of calcium phosphate. Calcification (calcinosis) occurs when abnormal amounts of calcium phosphate are deposited in the body’s soft tissue.

Calcinosis in the skin often appears as white or yellowish lumps.

Calcium deposits in the skin often seem to occur without warning. These bumps might be a sign or symptom of a medical condition.

The primary symptom of calcinosis is the appearance of firm, pimple-like bumps or nodules on the skin that are white or yellow. They also have the following characteristics:

The bumps can appear in various sizes and quantities.
They often appear in clusters.
They are most commonly found on the elbows, fingers, or shins, though they can appear anywhere on the body.
If punctured, this type of nodule will leak a white, chalky, paste-like material.
They can cause tenderness and even pain on the affected area
Bumps arising near joints can cause joint stiffness.

There are four different types of calcium deposits, each based on the cause of the condition:

dystrophic calcinosis cutis
iatrogenic calcinosis cutis
metastatic calcinosis cutis
idiopathic calcinosis cutis

Dystrophic calcinosis

Dystrophic calcinosis can occur in tissue that is damaged or inflamed, or has become malignant or died. Conditions that can lead to dystrophic calcinosis cutis are:

skin injury
skin infections
connective tissue diseases
panniculitis
acne
tumors

Iatrogenic calcinosis

Iatrogenic calcinosis are typically attributed to certain medications and medical procedures such as repeated drawing of blood from an infant’s heel.

Metastatic calcinosis

Metastatic calcinosis can result from any medical condition associated with excess phosphorus (hyperphosphatemia) and calcium (hypercalcemia), including:

kidney failure
sarcoidosis
paraneoplastic hypercalcemia
hyperparathyroidism
milk-alkali syndrome
calciphylaxis
excess vitamin D

Idiopathic calcinosis

Idiopathic calcinosis cutisis calcinosis that can’t be attributed to a specific cause. The typical reasons have been ruled out:

Phosphate and calcium levels in your body are normal.
There is no evidence of previous tissue damage.
You’re not taking medications that could trigger calcinosis.
You haven’t had medical procedures recently that could trigger calcinosis.

Your doctor has a number of different treatments available and will recommend the one they feel is best suited to your situation. Some of those options are:

intralesional corticosteroids, such as triamcinolone acetonide and triamcinolone diacetate
calcium channel blockers, such as amlodipine (Norvasc), diltiazem (Cardizem, Tiazac) and verapamil (Calan, Verelan)
antacids containing aluminum hydroxide, such as Gaviscon Extra Relief Formula and Acid Gone Antacid
colchicine (Colcrys), an anti-inflammatory medication
warfarin (Coumadin, Marevan), used to treat blood clots
laser therapy, the use of light energy to dissolve the calcium deposits
iontophoresis, the use of low levels of electric current to dissolve the calcium deposits by delivering medication — such as cortisone — directly to the affected areas
surgery to remove the calcium deposits

There are a few natural remedies you can try to treat calcium deposits on the skin:

Massage. Although not necessarily recommended by medical professionals, many people claim that massaging the affected area with aloe vera gel or olive oil eliminates the calcium deposits over time.
Diet. Many advocates of natural healing suggest lowering your calcium intake and avoiding foods such as dairy products can help.
Apple cider vinegar. Some believe that drinking 1 tablespoon of apple cider vinegar mixed in 8 ounces of water every day will help break down calcium deposits.
Chanca piedra. Others suggest the herb chanca piedra can break down the buildup of calcium in the body.

If you discover whitish or yellowish bumps on your skin, visit your doctor to find out if these are calcium deposits. Your doctor can determine if they should be treated or an underlying cause needs to be addressed. They will discuss options with you and recommend a treatment that best aligns with your needs.

Last medically reviewed on May 30, 2018

How we reviewed this article:

Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations. We avoid using tertiary references. You can learn more about how we ensure our content is accurate and current by reading our editorial policy.

Calcinosis: An intractable and distressing problem (slideshow). (2016).
consultqd.clevelandclinic.org/calcinosis-intractable-distressing-problem-slideshow/
Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. (1997). Calcium. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride.
ncbi.nlm.nih.gov/books/NBK109827/
Le C, et al. (2017). Calcinosis cutis. StatPearls.
ncbi.nlm.nih.gov/books/NBK448127/
Mayo Clinic Staff. (2018). Calcium channel blockers.
mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/calcium-channel-blockers/art-20047605

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Medically reviewed by Cynthia Cobb, DNP, APRN, WHNP-BC, FAANP — By Scott Frothingham — Updated on May 31, 2018

Major cause of blindness linked to calcium deposits in the eye | UCL News

Microscopic spheres of calcium phosphate have been linked to the
development of age-related macular degeneration (AMD), a major cause of
blindness, by UCL-led research.

AMD affects 1 in 5 people over 75, causing their vision to slowly
deteriorate, but the cause of the most common form of the disease remains a
mystery.* The ability to spot the disease early and reliably halt its
progression would improve the lives of millions, but this is simply not
possible with current knowledge and techniques.

The latest research, published in Proceedings
of the National Academy of Sciences, has implicated tiny spheres of
mineralised calcium phosphate, ‘hydroxylapatite’, in AMD progression. This not
only offers a possible explanation for how AMD develops, but also opens up new
ways to diagnose and treat the disease.

AMD is characterised by a build-up of mainly protein and fat containing
deposits called ‘drusen’ in the retina, which can prevent essential nutrients
from reaching the eye’s light-sensitive cells, ‘photoreceptors’. Photoreceptors
are regularly recycled by cellular processes, creating waste products, but drusen
can trap this ‘junk’ inside the retina, worsening the build-up. Until now,
nobody understood how drusen formed and grew to clinically relevant size.

The new study shows that tiny calcium-based hydroxyapatite, commonly
found in bones and teeth, could explain the origin of drusen. The researchers
believe that these spheres attract proteins and fats to their surface, which
build up over years to form drusen. Through post-mortem examination of 30 eyes
from donors between 43 and 96 years old, the researchers used fluorescent dyes
to identify the tiny spheres, just a few microns – thousandths of a millimetre
– across.

As drusen are hallmarks of AMD, then strategies to prevent build-up could potentially stop AMD from developing altogether.

Dr Imre Lengyel

“We found these miniscule hollow spheres inside all of the eyes and all
the deposits that we examined, from donors with and without AMD,” explains Dr
Imre Lengyel, Senior Research Fellow at the UCL Institute of Ophthalmology and Honorary
Research Fellow at Moorfields Eye Hospital, who led the study. “Eyes with more
of these spheres contained more drusen. The spheres appear long before drusen
become visible on clinical examination.

“The fluorescent labelling technique that we used can identify the early
signs of drusen build-up long before they become visible with current methods.
The dyes that we used should be compatible with existing diagnostic machines.
If we could develop a safe way of getting these dyes into the eye, we could
advance AMD diagnoses by a decade or more and could follow early progression
more precisely.”

Some of the mineral spheres identified in the eye samples were coated
with amyloid beta, which is linked to Alzheimer’s disease. If a technique were developed
to identify these spheres for AMD diagnosis, it may also aid early diagnosis of
Alzheimer’s. Whether these spheres are a cause or symptom of AMD is still
unclear, but their diagnostic value is significant either way. As drusen are hallmarks
of AMD, then strategies to prevent build-up could potentially stop AMD from
developing altogether.

“The calcium-based spheres are made up of the same compound that gives
teeth and bone their strength, so removal may not be an option,” says Dr
Lengyel. “However, if we could get to the spheres before the fat and protein
build-up, we could prevent further growth. This can already be done in the lab,
but much more work is needed before this could be translated into patients. ”

“Our discovery opens up an exciting new avenue of scientific research
into potential new diagnostics and treatments, but this is only the beginning
of a long road.” says Dr Richard Thompson, the main international collaborator
from the University of Maryland School of Medicine, USA.

The work was supported by the Bill Brown Charitable Trust, Moorfields Eye
Hospital, Mercer Fund from Fight for Sight, and the Bright Focus Foundation.
The UCL-led international collaboration involved researchers from the
University of Maryland School of Medicine, Imperial College London, the University
of Tübingen, George Mason University, Fairfax, and the University of Chicago.

Images

Thousands of hydroxyapatite spheres (magenta), each
just a few microns across, are found in large drusen deposits within the eye (credit: Imre Lengyel, UCL)

Media contact

Harry Dayantis

Tel: +44 (0)20 3103 3844

Email: h. dayantis [at] ucl.ac.uk

Features of eye damage in primary hyperparathyroidism | Mokrysheva

Annotation

Pathology of the organ of vision occurs in various endocrine diseases, however, information about the state of the visual apparatus in primary hyperparathyroidism (PHPT) remains limited to date. There are no large systematized studies on this problem, mainly in the literature there are descriptions of individual clinical cases, indicating non-specific changes in the eyes during the development of severe hypercalcemia. The most common manifestations of hyperparathyroid ophthalmopathy include calcification of the cornea and conjunctiva, dysfunction of the oculomotor muscles. Taking into account the predominance of mild forms of PHPT, due to early diagnosis and timely initiation of pathogenetic treatment of the disease, these disorders are rare at present. However, specific eye damage in this category of patients requires in-depth study and further research.

INTRODUCTION

Primary hyperparathyroidism (PHPT) is a disease associated with excessive production of parathyroid hormone (PTH) by the parathyroid glands and involving various organs and body systems in the pathological process, which leads to a significant decrease in the quality of life, as well as disability of patients [1] . Data on the state of the visual apparatus in PHPT still remain limited. The most common manifestations of hyperparathyroid ophthalmopathy include corneal calcification with the development of calcified band keratopathy, conjunctival calcification, and dysfunction of the oculomotor muscles [2–4]. There are no large systematized studies on the study of this problem, mainly descriptions of individual clinical cases are presented in the literature.

CALCINATED BAND KERATOPATHY

Calcified band keratopathy is a corneal change that develops as a result of chronic hypercalcemia of various etiologies. It is characterized by calcium deposits in the Bowman’s membrane, the basement membrane of the corneal epithelium, the most superficial layers of the stroma, making it opaque. Damage to superficial structures is its main difference from petrification of the cornea, an extremely rare pathology in which, as a rule, the deeper layers of the anterior part of the sclera are affected. Turbidity of white or grayish color develops in the interpalpebral region, starting from the periphery in the form of horizontal strands. It is separated from the limbus by a thin transparent zone and contains intact areas of the cornea in places where the nerves penetrate the Bowman’s membrane, giving the appearance of “Swiss cheese” [5, 6].

The exact mechanism of development of calcified band keratopathy is still unknown. The deposition of calcium salts (hydroxyapatite) in the cornea is associated with external factors, since the degenerative process develops in the area exposed to the external environment. This may be the result of tear fluid evaporation, a change in its osmolarity, an increase in pH during metabolic processes, or a local increase in the concentration of calcium and phosphate ions that exceed the solubility threshold of elements. Under physiological conditions, the pH value of the interpalpebral region is higher than in the rest of the cornea, which is associated with the release of carbon dioxide from the surface of the eye shell. The cumulative effect of several blood buffer systems prevents fluctuations in acid-base balance in places with the most developed vascularization. Probably, this mechanism explains the presence of clear transparent areas of the cornea with a developed limbal circulation. The absence of damage to the deep layers of the corneal stroma may be due to the peculiarities of local metabolism – the accumulation of lactic acid during anaerobic glycolysis and, as a result, a decrease in the pH of the medium. In addition, the anatomical structure of the basal layer of the epithelium and Bowman’s membrane is of particular importance. The difference between keratopathy in systemic hypercalcemia and degenerative and post-inflammatory changes is the primary location of calcium deposits intracellularly, and not outside epithelial cells [5].

M. Petrochelos et al. presented a case of severe PHPT in a 24-year-old woman. The disease debuted in the postpartum period with the development of severe anorexia, bilateral deafness, and decreased vision [7]. The revealed band keratopathy made it possible to suspect the presence of hypercalcemia, and histological examination of the tissues of the cornea and conjunctiva obtained by biopsy from the limbus confirmed the deposition of calcium crystals. According to laboratory analysis, there was an increase in serum calcium levels up to 4.05 mmol / l, and hypercalciuria up to 15.6-19.8 mmol/day Parathyroid adenoma 1.5×1.0 cm, removed during parathyroidectomy, was visualized. When examined one month after the operation, there was a restoration of visual acuity and hearing, a significant improvement in general well-being. The manifestations of banded keratopathy significantly regressed with the restoration of the transparency of the cornea of both eyes in the pupil area and the preservation of only limited areas of opacity of about 2 mm in the limbus area.

The development of band keratopathy quite rarely leads to visual impairment and requires treatment in some cases when there is a feeling of discomfort, a foreign body as a result of mechanical irritation of the eye membrane by excessive deposition of calcium hydroxyapatite, photophobia or the formation of corneal ulcers, a pronounced decrease in visual acuity. Various treatment approaches are being considered, including surgical removal, chelation therapy, excimer laser photorefractive keratectomy, and amniotic membrane transplantation as an additional method to ensure rapid healing and maintain the stability of the corneal surface [6].

CALCIFICATION OF THE EYE

Several papers have been published describing calcification of the mucous membrane of the eye (conjunctiva) in hyperparathyroidism. D.K. Lee and A.K. Eiferman were the first to present a clinical case of a 34-year-old woman with a long history of PHPT for 10-15 years and subsequent parathyroidectomy [3]. Within two months, the patient noted redness and a feeling of a foreign body in the eyes. With preserved visual acuity, a significant injection of the conjunctiva of the eyeballs and calcification of the marginal edge of the eyelid on both sides were detected. In addition, band keratopathy and calcium deposition in the limbus were observed. Taking into account the pronounced feeling of discomfort, the removal of calcifications of the cornea and conjunctiva was performed, and the presence of calcium salts in the subepithelial layers was confirmed by histological examination. Similar lesions of the conjunctiva of the eye have also been noted in secondary and tertiary hyperparathyroidism [8, 9].

Ph.

Finney et al. describe a 38-year-old patient who initially consulted an ophthalmologist with complaints of redness of the eyes against the background of increased fatigue and general weakness [10]. Examination revealed bilateral scleritis and retinal hemorrhages. There were no signs of infectious and inflammatory lesions of the eyes. A double biochemical blood test revealed severe hypercalcemia (3.22–3.77 mmol/l) in combination with hypophosphatemia (0.67 mmol/l), an increase in alkaline phosphatase activity up to 932 U/L (reference values 40–120). The serum parathyroid hormone level was 2770 ng/l (reference values 12–72). Thus, the diagnosis of PHPT was not in doubt. An additional examination revealed an adenoma of the left lower parathyroid gland according to ultrasound and radiological studies. After parathyroidectomy, the “red eye” syndrome regressed.

Calcium crystal deposition can also occur in the choroid, classified as sclerochoroidal calcification (SCC). In this case, flat or convex plaques are formed, outwardly similar to such formations as choroidal nevus, melanoma, lymphoma, choroidal osteoma, metastases. They are usually yellow or white in color and are located in the superior temporal quadrant or closer to the equator. In the affected area, atrophy of the choroid and retinal pigment epithelium is noted, while the presence of hemorrhages, fluid accumulations in the subretinal layers, and neovascularization are not typical. From malignant pathology, the degenerative process is distinguished by the stable nature of the course and the minimal risk of vision loss. These clinical signs of CCS were described by C.L. Shields et al. in 118 patients (mean age 69years), observed in them in the ophthalmological hospital, during the examination of 179 eyes, revealing a connection with systemic disorders of calcium metabolism. Thus, in 27% of cases, SCC was diagnosed among patients with PHPT [11].

EYE MOTOR MUSCLE DEFECT

Muscle weakness is one of the most common symptoms of parathyroid hyperfunction. In PHPT, damage to various muscles, including the eyeball, which contains skeletal muscle fibers, can develop. B.H. Forman et al. published a clinical case of a patient suffering from strabismus with the development of diplopia due to PHPT [12]. Pathology of the brain and orbits was excluded. Despite hypercalcemia of 12.5 mg/dL (3.12 mmol/L), banded keratopathy and proximal muscle weakness were absent. The researchers managed to establish a connection between a decrease in the tone of the extraocular muscles and the pathology of the parathyroid glands due to the complete regression of ocular symptoms against the background of achieving normocalcemia after parathyroidectomy.

OTHER VISUAL PATHOLOGY

The literature describes rare cases of asymmetric exophthalmos that developed in patients with PHPT and the presence of “brown tumors” of the skull bones [13, 14]. Tension or compression of the optic nerve during proptosis (exophthalmos) can potentially lead to impaired focus, color perception, or progressive loss of vision.

Ischemic optic neuropathy with a gradual decrease in visual acuity (up to counting fingers in the face) as a possible complication of hypercalcemia and hyperparathyroidism was presented by D. Chappel and K. Farrington in a 58-year-old patient with an increase in serum calcium to 3.66 mmol/l and adenoma of the left lower parathyroid gland (2.5×3.5×2.0 cm) [15]. Remission of PHPT after surgical treatment did not lead to the restoration of visual function, which is probably due to irreversible complete atrophy of the optic nerve. As possible mechanisms of ischemic damage to nerve fibers, the development of microthrombosis is considered, the risk of which is increased with hypercalcemia and concomitant dehydration, calcification of the supply vessels, arterial hypertension, and cerebral artery spasm. The direct effect of PTH on the nervous tissue is not excluded.

In 2016, H. Baser et al. a study was conducted to study the thickness of the cornea (measured in the center), the thickness of the retina and intraocular pressure in patients with PHPT. There were no significant differences compared to healthy controls. A statistically significant association between the levels of PTH and serum calcium with the indicated parameters has also not been established [16].

CONCLUSION

In severe cases of PHPT, cases of non-specific damage to various structures of the eye are described, most likely due to the development of severe hypercalcemia. However, the direct effect of PTH on the nervous and muscle tissue is not excluded. Taking into account the predominance of mild forms of PHPT, due to early diagnosis and timely initiation of pathogenetic treatment of the disease, these disorders are rare at present. Nevertheless, an in-depth study of the pathogenetic mechanisms of eye damage in patients with PHPT is required, as well as large systematic studies on this issue.

Conflict of interest. The authors declare the absence of obvious and potential conflicts of interest related to the publication of this article.

1. Mokrysheva N.G. Primary hyperparathyroidism. Epidemiology, clinic, modern principles of diagnosis and treatment: Dis. … doc. honey. Sciences – Moscow; 2011. [Mokrysheva NG. Pervichnyi hyperparathyroidism. Epidemiologiya, clinic, modern printsipy diagnostiki i lecheniya. [dissertation] Moscow; 2011. (In Russ.)] Available at: http://www.dslib.net/luch-diagnostika/pervichnyj-giperparatireoz-jepidemiologija-klinika-sovremennye-principy-diagnostiki.html Link active as of 09.04.2019.

2. Lee DB, Zawada ET, Kleeman CR. The pathophysiology and clinical aspects of hypercalcemic disorders. West J Med. 1978;129(4):278-320. PMID:362722

3. Lee DK. Ocular Calcifications in Primary Hyperparathyroidism. Arch Ophthalmol. 2006;124(1):136-137. doi: 10.1001/archopht.124.1.136

4. Jacob J, Chopra R, Chander A. The eye as a window to rare endocrine disorders. Indian J Endocrinol Metab. 2012;16(3):331-338. doi: 10.4103/2230-8210.95659

5. O’Connor GR. Calcific band keratopathy. Trans Am Ophthalmol Soc. 1972;70:58-81. PMID: 4677022.

6. Jhanji V, Rapuano CJ, Vajpayee RB. Corneal calcific band keratopathy. Curr Opin Ophthalmol. 2011;22(4):283-289. doi: 10.1097/ICU.0b013e3283477d36

7. Petrohelos M, Tricoulis D, Diamantacos P. Band keratopathy with bilateral deafness as a presenting sign of hyperparathyroidism. Br J Ophthalmol. 1977. doi: 10.1136/bjo.61.7.494

8. Berkow JW, Fine BS, Zimmerman LE. Unusual ocular calcification in hyperparathyroidism. Am J Ophthalmol. 1968;66(5):812-824. PMID: 5686911

9. Moutopoulos Canellos H, Cooper J, Paek A, Chien J. Multiple calcified deposits along the eyelid margins secondary to chronic renal failure and hyperparathyroidism. Optom – J Am Optom Assoc. 2005;76(3):181-184. doi: 10.1016/S1529-1839(05)70283-9

10. Finny P, Jacob JJ, Thomas N. Primary hyperparathyroidism presenting as redness of eyes. Eur J Intern Med. 2007;18(8):608. doi: 10.1016/j.ejim.2007.03.005

11. Shields CL, Hasanreisoglu M, Saktanasate J, Shields PW, Seibel I, Shields JA. SCLEROCHOROIDAL CALCIFICATION. retina. 2015;35(3):547-554. doi: 10.1097/IAE.0000000000000450

12. Forman BH, Ciardiello K, Landau SJ, Freedman JK. Diplopia associated with hyperparathyroidism: report of a case. Yale J Biol Med. 1995;68(5-6):215-217. PMID: 8903046

13. Block MB, Johnston H, Kartub MG. Unilateral exophthalmos: an unusual presentation of primary hyperparathyroidism. Ariz Med. 1978;35(12):785-786. PMID: 727953

14. Jahagirdar VR, Gittoes NJ. A rare presentation of primary hyperparathyroidism [abstract]. Endocr Abstr. 2015;38.P14 doi: 10.1530/endoabs.38.P14

15. Chappel D, Farrington K. Primary hyperparathyroidism presenting as unilateral visual loss. Postgrad Med J. 1991;67(787):469-470. doi: 10.1136/pgmj.67.787.469

16. Baser H, Cuhaci N, Topaloglu O, et al. Is there any association between primary hyperparathyroidism and ocular changes, such as central corneal thickness, retinal thickness, and intraocular pressure? endocrine. 2016;51(3):545-550. doi: 10.1007/s12020-015-0724-5

Corneal degenerations

Corneal degenerations

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Trufanov S.V.

Institution of the Russian Academy of Medical Sciences “Research Institute of Eye Diseases of the Russian Academy of Medical Sciences”, Moscow

Salovarova E.P.

Research Institute of Eye Diseases, st. Rossolimo, 11, A, B, Moscow, 119021, Russian Federation

Tekeyeva L.Yu.

Research Institute of Eye Diseases, st. Rossolimo, 11, A, B, Moscow, 119021, Russian Federation

Corneal degeneration

Authors:

Trufanov S.V., Salovarova E.P., Tekeeva L.Yu.

More about the authors

Magazine:

Bulletin of ophthalmology.

2018;134(5): 282-288

DOI:

10.17116/oftalma2018134051282

How to quote:

Trufanov S.V., Salovarova E.P., Tekeyeva L.Yu. Corneal degeneration. Bulletin of ophthalmology.
2018;134(5):282-288.
Trufanov SV, Salovarova EP, Tekeeva LYu. Corneal degenerations. Vestnik Oftalmologii. 2018;134(5):282-288. (In Russ.)
https://doi.org/10.17116/oftalma2018134051282

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Degeneration is a process of changing cells, their individual parts or intercellular substance, arising as a result of external influences during the life of an organism, as a result of which a gradual violation of the normal state of a tissue or organ occurs with a possible loss of its functional activity. Corneal degenerations can be the result of physiological changes during aging, associated with a certain systemic disease, local inflammatory process, or be the result of chronic toxic effects of harmful environmental factors on the eye. Corneal degenerations, unlike dystrophies, are not inherited and have a late onset. With a significant impact on visual acuity, the treatment of such conditions should be aimed primarily at eliminating the underlying disease and only then at changes in the cornea itself. It is important to remember the existence of such a pathology and timely differentiate it with acute inflammatory processes of various etiologies that require emergency treatment. Making the correct diagnosis is a key factor in choosing an effective treatment and obtaining adequate clinical results.

Keywords:

cornea

corneal degeneration

confocal microscopy

Authors:

Trufanov S.V.

Institution of the Russian Academy of Medical Sciences “Research Institute of Eye Diseases of the Russian Academy of Medical Sciences”, Moscow

Salovarova E.P.

Research Institute of Eye Diseases, st. Rossolimo, 11, A, B, Moscow, 119021, Russian Federation

Tekeyeva L. Yu.

Research Institute of Eye Diseases, st. Rossolimo, 11, A, B, Moscow, 119021, Russian Federation

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Corneal degenerations

Degeneration is a process of changing cells, their individual parts or intercellular substance, arising as a result of external influences during the life of an organism, as a result of which a gradual violation of the normal state of a tissue or organ occurs with a possible loss of its functional activity. Corneal degenerations may be the result of physiological changes with aging, associated with a certain systemic disease, a local inflammatory process, or be a consequence of chronic toxic effects of harmful environmental factors on the eye, such as ultraviolet (UV) radiation. In rare cases, the cause of degeneration may be a genetic predisposition. Since some corneal degenerations are associated with systemic diseases such as rheumatoid arthritis, Crohn’s disease, a careful medical history should be taken. Changes caused by chronic inflammation, age, or systemic disease lead to deposits, thinning, or vascularization of the corneal tissue. Corneal degenerations are characterized by a late onset, predominantly unilateral involvement in local lesions and bilateral, albeit asymmetric, involvement in systemic disorders or involutional processes. Usually degenerative changes are located closer to the periphery of the cornea.

Degenerative diseases of the cornea of the eye can be classified according to the depth of the lesion of the cornea, according to the degree of remoteness from the optical center, as involutional and non-involutional. In addition, there are forms with peripheral thinning of the cornea and with the deposition of substances. The processes of thinning are mostly of unknown etiology, even with the identification of some concomitant diseases. As a rule, in degenerations characterized by the deposition of substances, local or systemic causes of corneal involvement can be identified [1].

Age-related degeneration of the cornea

As a result of aging, the cornea gradually becomes flatter along the vertical meridian, thinner, its transparency slightly decreases and the refractive index increases. The Descemet’s membrane becomes thicker, changing from about 3 µm at birth to 10 µm in adults. It can sometimes show peripheral gutta, known as Hazal-Henle bodies. In the first 50 years of life, the number of endothelial cells normally decreases by approximately 100,000, from approximately 4000 cells/mm ² at birth up to 2500-3000 cells/mm ² in the elderly. The average rate of decline in endothelial cell density throughout adulthood is about 0.6% per year.

Age-related corneal degeneration is quite common in the elderly. They manifest themselves either as pathological thinning of the cornea or as deposits of various substances and, as a rule, do not require treatment, since they can lead to visual impairment only in isolated cases [2].

Corneal senile arch ( arcus senilis ) is the most common corneal degeneration in the elderly. In men, it can appear already after 40 years, in women about 10 years later. It is detected in 90% of people after 80 years of age. It is a bilateral but often asymmetric process. Asymmetry is especially pronounced with uneven damage to the carotid arteries (less on the side of the lesion) and chronic hypotension of the eyeball (more on the side of the lesion). Clinically, it is a circular band of extracellular lipoprotein deposition with a clear outer border separated from the limbus by a transparent cornea. Inner border arcus senilis usually looks washed out. The central sections of the cornea always remain transparent. The deposition of low-density lipids begins from above and below at the periphery with the involvement of deep stromal layers in the immediate vicinity of the Descemet’s membrane and extends to the sub-Bowman surface layers and around the circumference. Lipids enter the cornea from the limbal capillaries, but their penetration into the paracentral cornea is limited by the high mass of molecules. In addition to aging, the lipid arc can be identified in young men with hypercholesterolemia and hypertriglyceridemia ( arcus juvenilis ). Since such changes are considered a sign of cardiovascular diseases, if they are detected at a young age, a thorough examination under the supervision of a therapist is necessary [2, 3]. In addition, similar lipid changes along the periphery of the cornea are characteristic of the noncrystalline form of Schneider’s dystrophy [4].

Vogt’s limbal stripes are represented by crescent-shaped whitish lines near the limbus, which develop in the interpalpebral fissure, more often on the nasal side (Fig. 1).

Fig. 1. Vogt’s limbal bands. Limbal streaks are characterized by some thinning of the stroma, often associated with subepithelial calcium deposits. This common degenerative change in the cornea is present in 100% of subjects over 80 years of age [2, 5]. Two types of Vogt’s belt have been described: Type I is separated from the limbus by a clear zone, includes calcium deposits, and is an early form of band-like keratopathy; Type II does not have a transparent area, consists of small deposits located in the form of thin lines (usually nasal), and is a hyaline degeneration with hyperelastosis on the periphery of the Bowman’s membrane [5].

Crocodile shagreen usually occurs in the anterior stroma near Bowman’s membrane, but in some cases the posterior layers adjacent to Descemet’s membrane may be involved. Degeneration is clinically represented by mosaic, polygonal, nonintense opacities separated by clear lines that resemble crocodile skin [6]. Damage occurs in old age. It is believed that such clinical manifestations may be associated with a certain abnormal orientation of stromal fibers. Electron microscopy reveals the presence of vacuoles throughout the corneal stroma, some of which contain electron-dense material. Crocodile corneal degeneration is uncommon, may be mild, and is discovered incidentally during a routine slit lamp examination. Practically does not affect visual acuity, only in some cases with a posterior location. [7]. The family form of crocodile shagreen occurs with the dominant form of juvenile and X-linked megalocornea. Franco’s central cloudy dystrophy looks similar and is probably not a dystrophy, but crocodile shagreen [8].

Peripheral corneal gutta. Age-related changes in the corneal endothelium, as mentioned above, are associated primarily with progressive cell loss and a decrease in their density [9]. Peripheral gutta, also known as Hazal-Henle bodies, are localized deposits of abnormal collagen secreted by age-related endothelial cells. They form superimposed outgrowths on the corneal endothelium, which are predominantly localized in the middle periphery. The condition is distinct from Fuchs’ endothelial dystrophy, which begins in the center ( cornea guttata ) and spreads to the periphery, causing chronic corneal edema as it progresses [10]. The number and distribution of peripheral gutta is limited, so they do not affect the endothelial density and function of cells [2].

Degeneration with corneal thinning

Terjen’s Marginal Degeneration (TBD) is a rare, slowly progressive, painless, non-inflammatory, peripheral corneal thinning of unknown etiology, described by Terjen in 1900 g. The condition is most commonly seen in men over 40 years of age. In the early stages of development, CDT is represented by small yellowish-white subepithelial or anterior stromal opacities, consisting of lipids, separated from the limbus by a section of transparent cornea, and slight superficial vascularization (Fig. 2).

Fig. 2. Terjen’s marginal degeneration. Gradually, the stroma on the periphery becomes thinner, but the epithelium remains intact, which is typical for this degeneration. Degenerative processes, as a rule, starting in the upper nasal quadrant, spread along the periphery of the corneal circumference. The edge of thinning, located closer to the center of the cornea, is steeper than the limbal. Vessels grow to the central border of thinning in the form of a pannus, where lipid deposits often occur. The lesion is often bilateral and asymmetrical. Corneal perforation is rare and may occur spontaneously or secondary to trauma [11].

In some cases, an association with autoimmune disorders has been identified, so an autoimmune mechanism is assumed to be the basis of pathogenesis. An association with a chronic inflammatory skin condition known as erythema diutinum elevatum has also been noted [12].

The disease is asymptomatic until the development of irregular or oblique astigmatism begins to reduce visual acuity [13]. In some cases, confocal microscopy reveals signs of a minor inflammatory response that is sensitive to topical steroid treatment [14]. Histopathological studies indicate an increased activity of lysosomes along with the absence of Bowman’s membrane in places of thinning [13]. The differential diagnosis should be made with peripheral corneal lysis, Moray’s ulcer, pellucid marginal degeneration, thinning with localized desiccation ( dellen ). In rare cases, inflammatory lesions of the periphery of the cornea, resembling Terjen’s degeneration, have been noted in children and young patients, sometimes in association with scleritis and episcleritis [14, 15].

Treatment consists of optical correction of irregular astigmatism. Contact lenses are recommended in advanced forms. In cases of perforation or severe thinning, peripheral lamellar keratoplasty is the method of choice [16].

Degeneration of the cornea with deposition of substances

Saltzman nodular degeneration. In 1925, Saltzmann described this non-inflammatory, slowly progressive disease characterized by the presence of single or multiple whitish-gray sub-epithelial nodules in the cornea and associated it with keratoconjunctivitis. To date, the etiopathogenesis of degeneration remains unknown, and a relationship with chronic inflammation of the anterior surface of the eye and chronic trauma is assumed – prolonged wearing of contact lenses, recurrent erosions, as well as chemical and thermal injuries [17]. Degeneration may occur several years or decades after long-standing interstitial or phlyctenular keratitis. Saltzman’s nodular degeneration has been reported in patients with Crohn’s disease. Accordingly, a hypothesis of an association with systemic diseases was put forward [18]. However, in most cases, concomitant corneal pathology is not determined and the lesion in this case is idiopathic. It is believed that degeneration is more common in middle-aged women. It is bilateral in about 60% of cases.

In some cases, the disease is asymptomatic. Visual acuity and photophobia may be observed. Discomfort is often due to dryness and foreign body sensation. In severe forms with pronounced prominence of nodules, epithelial damage occurs with pain syndrome – recurrent erosions. Decreased visual acuity is due to the progression of astigmatism caused by nodules [19].

The typical clinical features seen under the slit lamp are single or multiple grayish-white nodules that rise above the surface of the cornea and are located on its middle periphery. Sometimes the nodules can capture the central zone, their diameter is usually about 0.5-2 mm, they are non-vascularized. When there are many nodules, they have a typical circular arrangement, in the later stages they often merge with each other. A characteristic clinical sign is the areas of normal transparent cornea between the nodules. The disease progresses slowly over many years (Fig. 3).

Fig. 3. Nodular degeneration of Saltzman.

Histopathological studies have shown that the corneal nodules are subepithelial, but may extend to one third of the thickness of the anterior stroma. They are formed by dense connective tissue with hyaline degeneration. The corneal epithelium has an uneven thickness, it is significantly thinned above the nodules. In the Bowman’s membrane, there are zones of ruptures that correspond to the localization of nodules and are quickly replaced by fibrous tissue or a substance resembling a basement membrane [20]. The found increased expression of matrix metalloproteinase-2 in patients with Salzmann’s degeneration may be the cause contributing to the disruption of the basement membrane and Bowman’s layer [20, 21].

Optical coherence tomography allows to estimate the size and depth of the nodules, which can be useful in the planned surgical treatment. [22]. Confocal microscopy reveals uneven epithelium, increased reflectance of the anterior stroma, which contains altered and activated keratocytes. Stromal light scattering is noted associated with the presence of nodules in which fibrosis occurs [23].

Therapy depends on the severity of symptoms and severity. In the early forms, treatment is aimed at reducing symptoms through conservative management, including eyelid hygiene, lubricants, and anti-inflammatory eye drops, which are often sufficient to relieve dry eye symptoms and foreign body sensation. A significant decrease in vision is an indication for surgical treatment, which consists in removing the nodules and restoring the regularity of the corneal surface. For superficial nodules, manual removal with a round knife is used. This method allows you to save a fairly homogeneous smooth surface of the cornea. In the case of a deeper ingrowth involving the anterior stroma, phototherapeutic keratectomy (PTK) may be performed after removal of the nodules. In some cases with deep ingrowth, anterior lamellar keratoplasty is required [24]. Recurrence of Saltzman’s nodes after surgical removal is likely in 18-21.9% of observations. The time period before relapse can range from 1 month to 6 years [20, 25].

Ribbon keratopathy is the deposition of calcium salts in the interpalpebral region of the cornea. May occur at any age. It begins near the corneal limbus on the periphery from the nasal and temporal sides simultaneously. Gradually, ribbon-like keratopathy spreads to the center, forming a ribbon-like whitish-gray opacity. The zone of transparent cornea separates the peripheral border of the band from the limbus. Between salt deposits in turbidity, small transparent rounded zones can occur, corresponding to the exit through the Bowman’s membrane of nerve endings (Fig. 4).

Fig. 4. Ribbon keratopathy. Visual acuity decreases with the advancement of deposits towards the center. In advanced stages, the density of calcium deposits can cause severe visual impairment. In addition, in severe lesions, deposits prominate and lead to significant discomfort due to a change in the shape of the ocular surface. Band keratopathy can affect one eye when it occurs after local diseases (such as chronic anterior uveitis, interstitial keratitis, severe trauma, chronic inflammation of the cornea), subatrophy of the eye, presence of silicone oil inside the eye, long-term use of phosphate steroids. It can be bilateral when its cause is a significant increase in plasma calcium and phosphate in systemic lesions. Such systemic diseases that underlie banded keratopathy are chronic renal failure, juvenile rheumatoid arthritis and hyperuricemia, sarcoidosis, hyperthyroidism, and impaired vitamin D metabolism [26].

Histological examination of calcium deposits in the form of hydroxyapatite salts is localized in the Bowman’s layer, the basement membrane of the epithelium and the anterior stroma of the cornea [27].

In the treatment, it is necessary to solve the main problems that are the causes of ribbon-shaped keratopathy. Combined systemic or local disorders should be identified, their adequate therapy should be prescribed. In the early stages, mechanical scraping is considered effective. It can be performed as a first step before chelation in cases of dense overgrown deposits. Chelation is carried out using a 1.5-3.0% solution of ethylenediaminetetraacetic acid for 15-20 minutes. If indicated, the corneal surface can then be further smoothed with excimer laser PTK. To stimulate the regeneration of the epithelium after the removal of deposits, in some cases, an amniotic membrane is used. Only in advanced cases with severe visual impairment is the expediency of layered keratoplasty considered [28].

Lipid keratopathy is rarely idiopathic (primary). Secondary lipid keratopathy is much more common and is usually associated with corneal vascularization from previous trauma or inflammation. With lipid keratopathy, deposits of cholesterol, fats and phospholipids are formed in the stroma (Fig. 5)

5. Lipid keratopathy. [29]. The most common cause of corneal involvement underlying secondary lipid keratopathy is herpes infection, as H erpes simplex and Herpes zoster . Accordingly, treatment should be directed first to the relief of the underlying disease. In the future, abnormal vascularization can be eliminated using argon laser photocoagulation or coagulation with a special needle. This causes lipid absorption through disruption of the afferent vessels. Corneal transplantation is considered a last resort treatment option [30].

Spheroidal keratopathy of the cornea was described by Bietti in 1955 g. There are primary, secondary corneal and conjunctival forms. The corneal forms are characterized by the deposition of oily amber globular deposits near the limbus and on the periphery of the interpalpebral part of the cornea. The lesion is more common in populations living in areas with a high degree of exposure to climatic UV radiation and wind. The severity of the lesion correlates with the exposure time. Dry eye syndrome and corneal trauma are risk factors. Secondary forms are described for corneal scars, lattice dystrophy, and glaucoma. Spheroidal keratopathy is more common in men, is bilateral, and usually does not cause visual acuity loss. Over time, corneal opacity increases and deposits spread towards the center of the cornea. In the advanced stages of damage, a local haze develops. Sometimes corneal changes coexist with similar deposits in the conjunctiva [31].

Histological examination reveals extracellular protein deposits and elastoid degeneration in the anterior corneal stroma. They are formed by UV-degradable protein materials that enter from the plasma through the vessels of the limbus. Gradually, such deposits slowly replace Bowman’s membrane. For patients with spheroidal degeneration, protection from UV damage with sunglasses is a must. In advanced stages with central involvement and impaired visual acuity, superficial keratectomy and PTK are recommended, and good clinical and visual results can be expected [32].

Vortex keratopathy also known as cornea verticillata . It is bilateral and is characterized by whitish-gray or golden-brown deposits that form whorl-like patterns in the lower half of the cornea. The typical clinical appearance makes it easily recognizable. Vortex keratopathy is a form of drug-induced lipidosis and is associated with long-term systemic therapy with amiodarone hydroxychloroquine (Cordarone) (Fig. 6),

Fig. 6. Vortex keratopathy while taking amiodarone. chloroquine, indomethacin and phenothiazine and deposition in the cornea of phospholipids that are not metabolized by lysosomal phospholipases. Vortex keratopathy is also characteristic of lipid metabolism disorders in Fabry disease, which is caused by a genetically determined enzyme deficiency. Corneal lipid deposits are localized in basal epithelial cells [33]. As a rule, the patient does not experience any visual disturbances. With prolonged drug-induced keratopathy and visual discomfort, modification of systemic therapy is advisable. Vortex keratopathy is reversible and decreases or disappears when the drug is discontinued.

Pigmentary deposit keratopathy is caused by the deposition of various pigmented substances in the layers of the cornea. The most common are epithelial iron deposits. The Hudson-Stuckley line is observed sporadically in the normal cornea of the elderly along the border of the upper two-thirds and lower thirds of the cornea. Iron deposits are usually present when the regular profile of the cornea is disturbed. This can be observed in cases of pterygium, keratoconus, previous corneal refractive surgery, corneal scars, and pronounced filtration cushion [34]. In these cases, the changes are associated with a significant violation of the shape of the cornea. In this case, deposits are usually localized in zones where such changes occur. A corneal profile disorder leads to a change in the physiological distribution of the tear film, which probably underlies this keratopathy. Histologically, the deposits are hemosiderin localized intraepithelially in basal cells. In advanced stages, iron deposits surround the advancing head of the pterygium. In this case, the deposits form the so-called Stoker line [35]. In keratoconus, circular iron deposits surround the base of the cone where there are most pronounced changes in corneal curvature. They are known as the Fleischer ring [36]. Iron deposits in the central zone of the corneal epithelium are a common side effect of refractive surgery, both incisional and excimer laser. For example, in eyes that have undergone laser refractive surgery for hypermetropia, there is a significant increase in corneal curvature in the center, leading to the formation of a pseudo-Fleischer ring. When correcting myopia, iron lines can be detected in the flattened central zone [37].

Calcium deposits under eyes. Calcium Deposits in Skin: Causes, Symptoms, and Treatments Explained

Understanding Calcium Deposits in the Skin: An Overview

Key Characteristics of Calcium Deposits

The Four Types of Calcium Deposits in Skin

Dystrophic Calcinosis Cutis

Iatrogenic Calcinosis Cutis

Metastatic Calcinosis Cutis

Idiopathic Calcinosis Cutis

Diagnosing Calcium Deposits in the Skin

Physical Examination

Medical History

Diagnostic Tests

Treatment Options for Calcium Deposits in Skin

Medication-Based Treatments

Procedural Treatments

Natural Remedies

Preventing Calcium Deposits in the Skin

Manage Underlying Conditions

Maintain a Balanced Diet

Protect Your Skin

Living with Calcium Deposits: Coping Strategies and Quality of Life

Pain Management

Emotional Support

Lifestyle Adaptations

The Future of Calcium Deposit Treatment: Emerging Research and Therapies

Targeted Drug Therapies

Gene Therapy

Nanotechnology

Calcium Deposits in Skin: Causes, Symptoms, and Treatments

Dystrophic calcinosis

Iatrogenic calcinosis

Metastatic calcinosis

Idiopathic calcinosis

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Annotation

INTRODUCTION

CALCINATED BAND KERATOPATHY

CALCIFICATION OF THE EYE

EYE MOTOR MUSCLE DEFECT

OTHER VISUAL PATHOLOGY

CONCLUSION

Corneal degenerations

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