Eye

Autoimmune eye disorders: Ocular Manifestations of Autoimmune Disease

Autoimmune Diseases That Affect the Eyes

An autoimmune disease occurs when the natural defense system of a body is not able to differentiate its own cells from foreign cells. As a result, the immune system mistakenly attacks normal cells. Nearly every part of the body – including the eyes – can take the brunt of autoimmune diseases.

In this article, a reputable eye clinic takes a closer look at some of the autoimmune diseases that can heavily affect the eyes, the common symptoms of these conditions and their risk factors.

Autoimmune Diseases That Are Linked to Vision Health

There are more than 80 types of autoimmune diseases that affect a wide range of body parts, from nerves and joints to eyes. Some autoimmune diseases that typically affect the eyes are:

Behcet Disease
This rare autoimmune disease characterized by ocular lesions, skin lesions and genital ulcers is a leading case of blindness in some parts of the world. It can affect the anterior and posterior portions of the eye.

Crohn’s Disease
This type of inflammatory bowel disease causes swelling of the tissues in the digestive tract. The main eye-related problem that can occur with Crohn’s disease is episcleritis, a common and benign cause of red eye.

Diabetes
A potential effect of diabetes is swelling of the eye lens. If blood sugar levels change from low to normal too quickly, the shape of the eye lens can be affected, leading to blurred vision. High blood sugar can also damage the blood vessels in the retina, the light-sensitive part of the eye.

Lupus
Inflammation caused by lupus can affect many systems of the body, including the skin, brain, heart and lungs. The effects of lupus in and around the eyes include inflammation of the white outer layer of the eyeball, changes in the skin around the eyelids and damage to nerves controlling eye movement.

Multiple Sclerosis
This is a lifelong condition that can affect the brain and spinal cord. Optic neuritis or inflammation of the optic nerve is a common symptom of this disease. It usually occurs in one eye and can cause blurred vision, loss of color vision and pain with eye movement.

Psoriasis
A common chronic skin disease, psoriasis causes rashes with itchy, scaly patches all over the body, most typically on the scalp, knees and elbows. Some types of psoriasis are linked to a heightened risk of developing inflammatory eye conditions, such as conjunctivitis or inflammation of the eyelid.

Reactive Arthritis
Formerly known as Reiter’s syndrome, reactive arthritis is a condition that causes redness and swelling in various joints of the body. Many people with this condition also develop conjunctivitis.

Rheumatoid Arthritis
This is an autoimmune and inflammatory disease that causes painful swelling in affected parts of the body. Its most common eye-related symptom is dryness of the sclera, which, if left untreated, can cause damage to the cornea, the clear surface that helps the eye focus.

Sjogren’s Syndrome
A disorder of the immune system, Sjogren’s syndrome is identified by its two most common symptoms: dry eyes and a dry mouth. Because of the decrease in tear production, the eyes may feel extremely dry, itchy or burning.

Thyroid Diseases
This is a group of autoimmune diseases that result in high or low thyroid function. It increases the risk of developing glaucoma, a condition that causes high pressure inside the eye. With Graves’ disease, for instance, tissues build up around the eye and increase pressure. With low-thyroid disorders, on the other hand, pressure builds up because the eye is not able to effectively circulate its fluids.

Uveitis
This is an autoimmune disease that directly affects the middle layer of tissue in the eye wall called uvea. Its common symptoms include eye redness, pain and blurred vision. It can affect one or both eyes and can cause vision loss if left untreated by an eye specialist.

Risk Factors of Autoimmune Diseases

While the exact cause of autoimmune diseases is unknown, some people are more likely to develop an autoimmune disease than others. Risk factors that increase the chances of developing autoimmune diseases include:

Genetics: Certain autoimmune diseases like lupus and multiple sclerosis do tend to run in families, meaning that certain genes make some people more likely to develop them. Viruses, chemicals and other things in the environment can trigger an autoimmune disease if the body already possesses the genes for it.

Weight: Obesity increases the risk of developing rheumatoid arthritis or psoriatic arthritis. This could be due to heavier weight putting significant strain on the joints or fat tissues producing substances that encourage inflammation.

Smoking: Research has also linked smoking to the development of several immune and autoimmune diseases, such as lupus, rheumatoid arthritis, hyperthyroidism and multiple sclerosis. Smoking has wide-reaching effects on the immune system, including increasing inflammation levels and allergic conditions.

Medications: Some blood pressure medications or antibiotics can trigger drug-induced lupus, a generally milder version of the idiopathic disorder. Specific medications used to lower cholesterol can also trigger statin-induced myopathy, a rare autoimmune disease causing muscle weakness.

Medicines That Can Help Treat Eye Symptoms of Autoimmune Diseases

Fortunately, there are over-the-counter medicines that can help alleviate the eye-related symptoms of autoimmune diseases. These include artificial tears, lubricating gels and ointments, all of which can help with dry eyes. These medicines bring moisture back to the surface of the eye. Other inflammatory conditions are sometimes treated with oral non-steroidal anti-inflammatory drugs that are available over the counter. Patients who do not respond to oral medications should be referred to an ophthalmologist for possible treatment with immunosuppressive medications.

The Importance of Getting Regular Eye Examinations

Aside from eating a balanced diet and leading a healthy lifestyle, one of the most critical steps to preserve eyesight is to regularly attend appointments with an ophthalmologist. According to the American Academy of Ophthalmology, all adults should undergo eye screening at age 40 to maintain healthy vision, especially if they have not seen an eye specialist previously. Generally, however, adults aged 18 to 60 should get a comprehensive eye exam at least every two years.

If you happen to be affected by an autoimmune disease:

  • You should not wait until you are 40 years old to get a vision health screening. If you have not been to an ophthalmologist in the past year, it will be for your own benefit to see one now.

  • Make sure you talk to your doctor about how often you need a vision screening. If you are experiencing symptoms related to vision health issues, then you will definitely need to get screened more frequently. Some patients get screened as often as every six months, but this is for severe cases.

  • It is also important to get regular eye examinations if you are taking medications for autoimmune disease treatment, such as hydroxychloroquine, which can cause ocular toxicity to various parts of the eye. Other medications for autoimmune diseases that can have negative effects on vision health include corticosteroids, which can increase the risk of cataracts and glaucoma when used long-term.

Most autoimmune diseases can be managed with medication, although serious eye damage and, in some cases, blindness can happen if they are not treated. An eye doctor and an autoimmune specialist should work closely together to effectively treat eye symptoms that occur with autoimmune diseases.

Neuromyelitis optica: MedlinePlus Genetics

Description

Neuromyelitis optica is an autoimmune disorder that affects the nerves of the eyes and the central nervous system, which includes the brain and spinal cord. Autoimmune disorders occur when the immune system malfunctions and attacks the body’s own tissues and organs. In neuromyelitis optica, the autoimmune attack causes inflammation of the nerves, and the resulting damage leads to the signs and symptoms of the condition.

Neuromyelitis optica is characterized by optic neuritis, which is inflammation of the nerve that carries information from the eye to the brain (optic nerve). Optic neuritis causes eye pain and vision loss, which can occur in one or both eyes.

Neuromyelitis optica is also characterized by transverse myelitis, which is inflammation of the spinal cord. The inflammation associated with transverse myelitis damages the spinal cord, causing a lesion that often extends the length of three or more bones of the spine (vertebrae). In addition, myelin, which is the covering that protects nerves and promotes the efficient transmission of nerve impulses, can be damaged. Transverse myelitis causes weakness, numbness, and paralysis of the arms and legs. Other effects of spinal cord damage can include disturbances in sensations, loss of bladder and bowel control, uncontrollable hiccupping, and nausea. In addition, muscle weakness may make breathing difficult and can cause life-threatening respiratory failure in people with neuromyelitis optica.

There are two forms of neuromyelitis optica, the relapsing form and the monophasic form. The relapsing form is most common. This form is characterized by recurrent episodes of optic neuritis and transverse myelitis. These episodes can be months or years apart, and there is usually partial recovery between episodes. However, most affected individuals eventually develop permanent muscle weakness and vision impairment that persist even between episodes. For unknown reasons, approximately nine times more women than men have the relapsing form. The monophasic form, which is less common, causes a single episode of neuromyelitis optica that can last several months. People with this form of the condition can also have lasting muscle weakness or paralysis and vision loss. This form affects men and women equally. The onset of either form of neuromyelitis optica can occur anytime from childhood to adulthood, although the condition most frequently begins in a person’s forties.

Approximately one-quarter of individuals with neuromyelitis optica have signs or symptoms of another autoimmune disorder such as myasthenia gravis, systemic lupus erythematosus, or Sjögren syndrome. Some scientists believe that a condition described in Japanese patients as optic-spinal multiple sclerosis (or opticospinal multiple sclerosis) that affects the nerves of the eyes and central nervous system is the same as neuromyelitis optica.

Frequency

Neuromyelitis optica affects approximately 1 to 2 per 100,000 people worldwide. Women are affected by this condition more frequently than men.

Causes

No genes associated with neuromyelitis optica have been identified. However, a small percentage of people with this condition have a family member who is also affected, which indicates that there may be one or more genetic changes that increase susceptibility. It is thought that the inheritance of this condition is complex and that many environmental and genetic factors are involved in the development of the condition.

The aquaporin-4 protein (AQP4), a normal protein in the body, plays a role in neuromyelitis optica. The aquaporin-4 protein is found in several body systems but is most abundant in tissues of the central nervous system. Approximately 70 percent of people with this disorder produce an immune protein called an antibody that attaches (binds) to the aquaporin-4 protein. Antibodies normally bind to specific foreign particles and germs, marking them for destruction, but the antibody in people with neuromyelitis optica attacks a normal human protein; this type of antibody is called an autoantibody. The autoantibody in this condition is called NMO-IgG or anti-AQP4.

The binding of the NMO-IgG autoantibody to the aquaporin-4 protein turns on (activates) the complement system, which is a group of immune system proteins that work together to destroy pathogens, trigger inflammation, and remove debris from cells and tissues. Complement activation leads to the inflammation of the optic nerve and spinal cord that is characteristic of neuromyelitis optica, resulting in the signs and symptoms of the condition.

The levels of the NMO-IgG autoantibody are high during episodes of neuromyelitis optica, and the levels decrease between episodes with treatment of the disorder. However, it is unclear what triggers episodes to begin or end.

Inheritance

Neuromyelitis optica is usually not inherited. Rarely, this condition is passed through generations in families, but the inheritance pattern is unknown.

Other Names for This Condition

  • Devic disease
  • Devic neuromyelitis optica
  • Devic syndrome
  • Devic’s disease
  • Optic-spinal MS
  • Opticospinal MS

Additional Information & Resources

Genetic and Rare Diseases Information Center

  • Neuromyelitis optica spectrum disorder

Patient Support and Advocacy Resources

  • Disease InfoSearch
  • National Organization for Rare Disorders (NORD)

Research Studies from ClinicalTrials.

gov

  • ClinicalTrials.gov

Catalog of Genes and Diseases from OMIM

  • AQUAPORIN 4

Scientific Articles on PubMed

  • PubMed

References

  • Hinson SR, Pittock SJ, Lucchinetti CF, Roemer SF, Fryer JP, Kryzer TJ, Lennon
    VA. Pathogenic potential of IgG binding to water channel extracellular domain in
    neuromyelitis optica. Neurology. 2007 Dec 11;69(24):2221-31. doi:
    10.1212/01.WNL.0000289761.64862.ce. Epub 2007 Oct 10. Citation on PubMed
  • Mata S, Lolli F. Neuromyelitis optica: an update. J Neurol Sci. 2011 Apr
    15;303(1-2):13-21. doi: 10.1016/j.jns.2011.01.002. Citation on PubMed
  • Matiello M, Kim HJ, Kim W, Brum DG, Barreira AA, Kingsbury DJ, Plant GT, Adoni
    T, Weinshenker BG. Familial neuromyelitis optica. Neurology. 2010 Jul
    27;75(4):310-5. doi: 10.1212/WNL.0b013e3181ea9f15. Citation on PubMed or Free article on PubMed Central
  • Matiello M, Schaefer-Klein JL, Hebrink DD, Kingsbury DJ, Atkinson EJ,
    Weinshenker BG; NMO Genetics Collaborators. Genetic analysis of aquaporin-4 in
    neuromyelitis optica. Neurology. 2011 Sep 20;77(12):1149-55. doi:
    10.1212/WNL.0b013e31822f045b. Epub 2011 Sep 7. Citation on PubMed
  • National Institute of Neurological Disorders and Stroke: Neuromyelitis Optica Information Page
  • Sato DK, Lana-Peixoto MA, Fujihara K, de Seze J. Clinical spectrum and
    treatment of neuromyelitis optica spectrum disorders: evolution and current
    status. Brain Pathol. 2013 Nov;23(6):647-60. doi: 10.1111/bpa.12087. Citation on PubMed
  • Takahashi T, Fujihara K, Nakashima I, Misu T, Miyazawa I, Nakamura M, Watanabe
    S, Shiga Y, Kanaoka C, Fujimori J, Sato S, Itoyama Y. Anti-aquaporin-4 antibody
    is involved in the pathogenesis of NMO: a study on antibody titre. Brain. 2007
    May;130(Pt 5):1235-43. doi: 10.1093/brain/awm062. Epub 2007 Apr 19. Citation on PubMed
  • Veszeli N, Fust G, Csuka D, Trauninger A, Bors L, Rozsa C, Nagy Z, Jobbagy Z,
    Eizler K, Prohaszka Z, Varga L, Illes Z. A systematic analysis of the complement
    pathways in patients with neuromyelitis optica indicates alteration but no
    activation during remission. Mol Immunol. 2014 Feb;57(2):200-9. doi:
    10.1016/j.molimm.2013.09.010. Epub 2013 Oct 26. Citation on PubMed

Features of ophthalmic pathology in autoimmune diseases | Lukashenko

1. Basantsova N.Yu., Zinchenko Yu.S., Starshinova A.A., Yablonsky P.K. Features of the diagnosis of neuropathy of small fibers in various diseases (literature review) // Pediatrician, 2018. V. 9, No. 6. P. 101-110.

2. Vizel A.A. Sarcoidosis: monograph. M.: Atmosfera, 2010. 416 p.

3. Godzenko A.A. Prospects for the treatment of uveitis in rheumatic diseases // Modern Rheumatology, 2011. V. 2, No. 37. C. 42.

4. Zaitseva N.S., Katsnelson L.A. Uveitis. Moscow: Medicine, 1984. 318 p.

5. Kansky D. Clinical ophthalmology: a systematic approach. Per. from English. M.: Logosfera, 2006. P. 744.

6. Plekhanov A.N., Fomina A.S., Sverkunova O.P., Ivanova Yu.V. Autoimmune uveitis. Review // Ophthalmology, 2019. V. 16, No. 1. P. 5-11.

7. Polunin G.S., Safonova T.N., Polunina E.G. Features of the clinical course of various forms of dry eye syndrome – the basis for the development of adequate methods of treatment // Bulletin of the ophthalmologist, 2006. V. 102, No. 5. P. 17-20.

8. Roit A, Brostoff J, Meil ​​D. Immunology. Per. from English. M.: Mir, 2000. 208 p.

9. Ustinova E.I. Endogenous uveitis (selected lectures for ophthalmologists). St. Petersburg: Eco-Vector, 2017. 204 p.

10. Shishkin A.N. Diffuse diseases of connective tissue / Systemic pathology of connective tissue. Ruk. For doctors / Ed. Yu.I. Stroeva, L.P. Churilova. St. Petersburg: Elbi-SPb, 2014. S. 282-313.

11. Akiki R.K., Statler B., Greenberg P.B., Janigian R.H. Unilateral birdshot chorioretinopathy in an elderly patient. R.I. Med. J., 2019Vol. 102, no. 1, pp. 60-61.

12. Alhatem A., Cavalcanti B., Hamrah P. In vivo confocal microscopy in dry eye disease and related conditions. Semin. Ophthalmol., 2012, Vol. 27, no. 5-6, pp. 138-148.

13. Avichezer D., Chan C.C., Silver P.B., Wiggert B., Caspi R.R. Residues 1-20 of IRBP and whole IRBP elicit different uveitogenic and immunological responses in interferon gamma deficient mice. Exp. Eye Res, 2000, Vol. 71, no. 2, rr. 111-118.

14. Becker M.D., Adamus G., Davey M.D., Rosenbaum J.T. The role of T-cells in autoimmune uveitis. Ocul. Immunol. Inflam., 2000, Vol. 8, no. 2, rr. 93-100.

15. Benitez-Del-Castillo J.M., Acosta M.C., Wassfi M.A., Díaz-Valle D., Gegúndez J.A., Fernandez C., GarcíaSánchez J. Relation between corneal innervation with confocal microscopy and corneal sensitivity with noncontact esthesiometry in patients with dry eye. Invest. Ophthalmol. Vis. Sc., 2007, Vol. 48, no. 1, pp. 173-181.

16. Bose T., Diedrichs-Möhring M., Wildner G. Dry eye disease and uveitis: A closer look at immune mechanisms in animal models of two ocular autoimmune diseases. J. Autoimmun. Rev., 2016, no. 15 (12), pp. 1181-1192.

17. Boulton A.J., Malik R.A., Arezzo J.C., Sosenko J.M. Diabetic somatic neuropathies. Diabetes Care, 2004, Vol. 27, no. 6, rr. 1458-1486.

18. Coulon C., Kodjikian L., Rochepeau C., Perard L., Jardel S., Burillon C., Broussolle C., Jamilloux Y., Seve P. Ethnicity and association with ocular, systemic manifestations and prognosis in 194 patients with sarcoid uveitis. Graefes. Arch. Clin. Exp. Ophthalmol., 2019, Vol. 257, no. 11, pp. 2495-2503.

19. Cruzat A., Qazi Y., Hamrah P. In vivo confocal microscopy of corneal nerves in health and disease. Ocul. Surf., 2017, Vol. 15, no. 1, pp. 15-47.

20. Davatchi F. Behcet’s disease. J. Int. Rheum. Dis., 2014, Vol. 17, no. 4, pp. 355-357.

21. Davatchi F., Shahram F., Chams-Davatchi C., Shams H., Nadji A., Akhlaghi M., Faezi T., Ghodsi Z., Faridar A., ​​Ashofteh F., Abdollahi B.S. Behcet’s disease: from east to west. Clin. Rheumatol., 2010, Vol. 29, no. 8, pp. 823-833.

22. Direskeneli H. Behçet’s disease: infectious aetiology, new autoantigens, and HLA-B51. Ann. Rheum. Dis., 2001, Vol. 60, no. 11, pp. 996-1002.

23. Kernel A., Dedorsson I., Johansson B., Wickstrom C.P., Ludvigsson J., Tuvemo T., Neidemd J., Sjostrom K., Malmgreen K., Kanulf P., Mellvig Gjotterberg M., Sule J., Persson L.A., Larsson L.I., Aman J., Dahlquist . Prevalence of diabetic retinopathy in children and adolescens with IDDM. A population-based multicentre study. Diabetologia, 1997, Vol. 40, no. 3, pp. 307-310.

24. Malik R.A, Kallinikos P., Abbott C.A., van Schie C.H.M., Morgan P., Efron N., Boulton A.J.M. Corneal confocal microscopy: a noninvasive surrogate of nerve fiber damage and repair in diabetic patients. Diabetology, 2003, Vol. 46, pp. 683-688.

25. Malik R.A., Veves A., Walker D., Siddique I., Lye R.H., Schady W., Boulton A.J. Sural nerve fiber pathology in diabetic patients with mild neuropathy: relationship to pain, quantitative sensory testing and peripheral nerve electrophysiology. Acta Neuropathol., 2001, Vol. 101, pp. 367-374.

26. Messmer E.M., Schmid-Tannwald C., Zapp D., Kampik A. In vivo confocal microscopy of corneal small fiber damage in diabetes mellitus. Graefs Arch. Clin. Exp. Ophthalmol., 2010, Vol. 248, no. 9, rr. 1307-1312.

27. Messmer E.M. The pathophysiology, diagnosis, and treatment of dry eye disease. Dtsch Arztebl. Int., 2015, Vol. 112, no. 5, pp. 71-81.

28. Morgan J.P., Robins R.A., Dua H.S., Tighe P.J. S antigen specific effector T cell activation detected by cytokine flow cytometry. Br. J. Ophthalmol., 2002, Vol. 86, no. 5, pp. 517-520.

29. No authors listed. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop. Ocul. Surf., 2007, Vol. 5, no. 2, rr. 75-92.

30. Pasadhika S., Rosenbaum J.T. Ocular Sarcoidosis. Clin. Chest. Med., 2015, Vol. 36, no. 4, pp. 669-683.

31. Pascolini D., Mariotti S.P.M. Global estimates of visual impairment: 2010. Br. J. Ophthalmol., 2012, Vol. 96, no. 5, pp. 614-618.

32. Raizman M. Corticosteroid therapy of eye diseases. Arch. Ophthalmol., 1996, Vol. 114, no. 8, rr. 1000-1001.

33. Rosenberg M.E., Tervo T.M., Immonen I.J., Müller L.J., Grönhagen-Riska C., Vesaluoma M.H. Corneal structure and sensitivity in type 1 diabetes mellitus. Invest. Ophthalmol. Vis. Sc., 2000, Vol. 41, no. 2, rr. 2915-2921.

34. Sakane T., Takeno M., Suzuki N., Inaba G. Behçet’s disease. N. Engl. J. Med., 1999, Vol. 341, no. 17, pp. 1284-1291.

35. Sherman M.A., Ardashev I.V. A case of recurrent Devic’s optiomyelitis. J. Nevrol. Psychiatr. Im. S.S. Korsakova, 2015, Vol. 115, no. 2, Pt. 2, pp. 38-44.

36. Tuisku I.S., Konttinen Y.T., Konttinen L.M., Tervo T.M. Alterations in corneal sensitivity and nerve morphology in patients with primary Sjogren’s syndrome. Exp. Eye Res., 2008, Vol. 86, no. 6, rr. 879-885.

37. Tuisku I.S., Lindbohm N., Wilson S.E., Tervo T.M. Dry eye and corneal sensitivity after high myopic LASIK. J. Refract. Surg., 2007, Vol. 23, no. 4, pp. 338-342.

38. Tuominen I.S., Konttinen Y.T., Vesaluoma M.H., Moilanen J.A., Helintö M., Tervo T.M. Corneal innervation and morphology in primary Sjögren’s syndrome. Invest. Ophthalmol. Vis. Sc., 2003, Vol. 44, no. 6, rr. 2545-2549.

39. Villani E., Baudouin C., Efron N., Hamrah P., Kojima T., Patel S.V., Pflugfelder S.C., Zhivov A., Dogru M. In vivo confocal microscopy of the ocular surface: from bench to bedside. Curr. Eye, 2014, Vol. 39, no. 3, pp. 213-231.

40. Yazici H. The place of Behçet’s syndrome among the autoimmune diseases. Int. Rev. Immunol., 1997, Vol. 14, no. 1, pp. 1-10.

41. Zierhut M., Schlote T., Tomida J., Stiemer R. Immunology of uveitis and ocular allergy. Acta Ophthalmol., 2000, Vol. 78, pp. 22-25.

Eye and autoimmune rheumatic diseases

  • 1
    Rheumatoid arthritis

  • 2
    Systemic lupus erythematosus

  • 3
    scleroderma

  • 4
    Hashimoto’s thyroiditis

  • 5
    Seronegative spondyloarthropathies

  • 6
    Eye damage in rheumatic diseases

  • 7
    Sjögren’s syndrome

  • 8
    cicatricial pemphigoid

  • 9
    Steven-Johnson Syndrome

  • 10
    Graft-versus-host disease

Most rheumatic diseases are immunological in nature, attacking one’s own tissues, this is what we know as an autoimmune reaction, and it can affect various parts of the body, including the eyes, so it is important to know this connection between rheumatic diseases and eye damage.

In this article, we will consider the most common rheumatic and autoimmune processes that can affect the eyes, as well as the form of manifestation at the eye level:

Rheumatoid arthritis abilities. Sometimes its behavior is extra-articular in nature and can affect various organs and systems, such as the eyes, lungs and pleura, heart and pericardium, skin or blood vessels. Although the cause of the disease is unknown, autoimmunity plays an important role in the chronic course of the disease.

At the eye level of the crisis, uveitis (inflammation of the middle membrane of the eye: iritis, when located anteriorly and choroiditis, when it affects the back region). Another form of manifestation is episcleritis, scleritis or dry eye syndrome due to damage to the lacrimal glands and the ocular surface (cornea and conjunctiva).

Articular deformity of the hand in rheumatoid arthritis

Systemic lupus erythematosus

This is a chronic autoimmune disease affecting the connective tissue, characterized by inflammation and tissue damage mediated by the immune system, in particular due to the binding of antibodies to body cells and the deposition of antigen-antibody complexes. It can affect any part of the body, although the most common sites are the reproductive system, joints, skin, lungs, blood vessels, kidneys, liver (the first organ it usually affects), and the nervous system. . The course of the disease is unpredictable, periods of crises alternate with remissions. It is nine times more common in women than in men. The first manifestations of the disease are more often observed between the ages of 15 and 44 years.

Erythema of the wings of a butterfly in systemic lupus erythematosus. Erythema and inflammation of the skin in systemic lupus erythematosus.

Eye involvement can also be in the form of uveitis scleritis, conjunctivitis o Dry eye syndrome.

Scleroderma

Scleroderma (“roughening of the skin”), also called progressive systemic sclerosis and CREST syndrome, is a diffuse connective tissue disease characterized by changes in the skin, blood vessels, skeletal muscles, and internal organs. The causes of this disease are unknown.

Scleroderma causes thickening and hypertrophy of the connective tissue, increasing its volume. It can also cause swelling or pain in muscles and joints.

Hands in claws due to sclerosis of the skin in scleroderma

At the eye level, they often appear conjunctivitis, non-infectious diseases that are difficult to diagnose, as well as ocular dryness and inflammation of the internal structures of the eye: retinal vasculitis and uveitis.

Hashimoto’s thyroiditis

This is an autoimmune disease (due to antithyroid autoantibodies) that causes inflammation of the thyroid gland. It is a common cause of primary subclinical hypothyroidism due to thyroiditis, goiter, or severe hypothyroidism. The clinical picture is the same as in any condition of hypothyroidism, so the treatment is thyroid hormone replacement therapy. The disease is more common in women than in men (in a ratio of 14:1), usually manifests or is detected between the ages of 20 and 30 years.

Enlargement of the thyroid gland in Hashimota thyroiditis

At the ocular level, non-infectious conjunctivitis and dryness syndrome due to hyposecretion of lacrimal fluid and drying of the ocular surface are common, since these patients usually have altered, less frequent and incomplete blinking.

Seronegative spondyloarthropathies

Spondyloarthropathies are autoimmune inflammatory diseases of the spine, spine and especially the sacroiliac joints. The term seronegative spondyloarthropathy comes from the fact that a blood test or serological test called rheumatic factor is negative. This group includes diseases such as ankylosing spondylitis, psoriatic arthropathy, Reiter’s syndrome (or reactive arthritis), Crohn’s disease, uveitis, etc. From 60% to 90% of people with this disease have the HLA-B27 antigen, but only 8% of the population have this antigen.

Inflammation and pain in the lumbosacral spine in seronegative spondyloarthropathies Mucocutaneous manifestations and conjunctivitis Sx. Reiter

These patients commonly present with multiple ocular changes, especially uveitis, scleritis, conjunctivitis, and even corneal involvement. keratitis y ulcers that can reduce vision in a very important way.

Eye affection in rheumatic diseases

All these diseases have a great influence at eye level. They cause inflammatory processes that can affect the most superficial layers of the eye, such as simple conjunctivitis, or deeper layers, causing episcleritis, scleritis, uveitis, and vasculitis in the vessels of the eye. retina. It is important to know this connection between rheumatic and ocular diseases, as a correct diagnosis of ocular manifestations can help to identify a systemic process and vice versa. In people suffering from a rheumatic process involving the eyes, the latter will not resolve unless the former is properly treated. This is why it is essential that an ophthalmologist be first and foremost a physician and thus work alongside other specialists. At the level of the ocular surface, it is worth mentioning Sjögren’s syndrome, a frequent pathology in immunological diseases.

Sjögren’s syndrome

It can be primary or secondary, in primary forms it usually has an idiopathic cause and appears in women between the 4th. and 5th. decade of life. In secondary forms, it is associated with autoimmune diseases: rheumatoid arthritis, lupus erythematosus, scleroderma, Hashimoto’s thyroiditis, etc. The age of manifestation varies greatly, more often in women.

The eye condition is characterized by the development of dryness and atrophy of the conjunctiva and cornea, causing this condition: Keratoconjunctivitis dry. What causes a feeling of sand, burning, itching, hyperemia, decreased tearing, which leads to the accumulation of thick stripes in the inner corner of the eye, photosensitivity and blurred vision. Secondary infections, ulcers and iridocyclitis.

Leukoma and neovascularization of the cornea in the advanced stages of Sjögren’s syndrome

cicatricial pemphigoid

This is an idiopathic, chronic and progressive process, more common in older people and women. It is characterized by the presence of recurrent subepithelial pots and vesicles on the skin and mucous membranes with a tendency to scarring.

In the eyes, papillary conjunctivitis may debut and later form subconjunctival vessels, which, when opened, leave ulcers and pseudomembranes. The most dangerous eye complications are: severe dryness of the eyes, conjunctival adhesions, palpebral adhesions, cicatricial eversion of the eyelid (eversion of the eyelid outwards).

Simblepharon in cicatricial pemphigoid

Steven-Johnson syndrome

Disease of the mucous membranes with the formation of amphipods and vesicles, acute and severe course, usually self-limiting. It is more common in healthy young people and men.

Causes that can provoke the disease are hypersensitivity reactions to drugs, infections caused by Mycoplasma Pneumoniae and herpes simplex virus.

At the ocular level, it may present with papillary conjunctivitis, which may heal without sequelae or cause complications such as: keratinization and fibrosis of the conjunctiva, metaplastic inlays, obstruction of the lacrimal ducts, ectropion (eyelid eversion outwards) and inversion cicatricial (eversion of the eyelids inward).

Blefaritis associated with conjunctivitis with purulent discharge in Stevens-Johnson Sx

Graft-versus-host disease

In GVHD, the immune response originates from the donor tissue (usually bone marrow) and is produced against the recipient, who is usually immunosuppressed.