Autoimmune retinopathy

Last updated
Autoimmune retinopathy
Specialty Immunology Ophthalmology

Autoimmune retinopathy (AIR) is a rare immunological disease in which the patient's immune system attacks proteins in the retina, leading to loss of vision. Researchers do not yet fully understand the disease, but it may be the result of cancer or cancer chemotherapy. [1] Autoimmune retinopathy is an autoimmune condition characterized by vision loss, blind spots, and visual field abnormalities. Autoimmune retinopathy can be divided into paraneoplastic (PAIR) or non-paraneoplastic (nPAIR). [2] The nPAIR division can be further divided into cancer-associated retinopathy (CAR) and melanoma-associated retinopathy (MAR). [3] The condition is associated with retinal degeneration, when autoimmune antibodies recognize retinal proteins as antigens and target them, leading to retinal degeneration. [4]

Contents

Types

Cancer-associated retinopathy

A division of AIR, cancer-associated retinopathy is a paraneoplastic syndrome, which is a disorder caused by an immune system response to an abnormality. Autoimmune antibodies target proteins in retinal photoreceptor cells. The proteins targeted as antigenic are recoverin, α-enolase and transducin. This autoimmune response leads to photoreceptor cell death. [5] It causes progressive vision loss that can lead to blindness. [3] CAR is typically associated with the anti-recoverin antibody. [3]

Melanoma-associated retinopathy

Retinal bipolar cells (cells in retina that transmit signals) react with the antibodies, leading to cell death. Although it is less prevalent than CAR, diagnosed cases of MAR continue to increase while CAR numbers decrease. [3]

Pathophysiology

Antiretinal antibodies (ARAs) likely cause the pathogenesis of AIR by targeting retinal antigens. [3] Autoimmune retinopathy is also related to molecular mimicry, in which foreign antigens and self antigens have a similar sequence, eliciting an autoimmune response. [3] In nPAIR, the molecular mimicry occurs between retinal proteins and viral/bacterial antigens, while in PAIR, it occurs between tumor antigens and retinal proteins. The most common antibodies found in CAR and nPAIR, respectively, are against recoverin (23kDa) and alpha-enolase. [3] Presence of these particular antibodies is related to symptoms and diagnosis of AIR in patients. Different subtypes of AIR cause dysfunction of varying retinal cells, resulting in varying vision impairment. Both nPAIR and CAR cause dysfunction of rods and cones, while MAR causes dysfunction of only rods. Cone dysfunction is responsible for photosensitivity, loss of color vision, and decreased visual acuity. Rod dysfunction, however, is responsible for loss of peripheral field ad prolonged darkness adaptation. [6] Many factors contribute to the pathogenesis of Autoimmune Retinopathy, contributing to it being poorly understood and requiring further research.

Immunology and Autoimmunity

The immune system is a network of cells, molecules, and organs that function to protect the body from any form of harm. In autoimmune diseases like autoimmune retinopathy (AIR), the immune system attacks the body’s own tissues and cells. In AIR, the retina, a highly specialized tissue, becomes the target of this misdirected immune response. How both innate and adaptive immunity contribute to the pathogenesis of AIR is extremely important to determining the mechanisms of the disease for future research endeavors.

Innate Immunity in Autoimmune Retinopathy

The innate immune system is the body's first line of defense and responds rapidly to infectious agents. It is nonspecific, meaning it is activated without previous exposure to the agent. However, in the context of AIR, components of the innate immune response can inadvertently contribute to tissue damage in the retina.

The innate immune response in AIR is often triggered when immune cells recognize damage-associated molecular patterns (DAMPs) released by damaged retinal cells. These signals are detected by pattern recognition receptors (PRRs) on innate immune cells such as macrophages and dendritic cells. Once activated, these cells release pro-inflammatory cytokines, which can further promote inflammation within the retina. While these inflammatory mediators can normally help to fight infections, in autoimmune diseases like AIR, they progress tissue damage by promoting the activation of both the innate and adaptive immune responses within the body.

Specialized macrophages in the retina (also known as microglia) play an important role in inflammation of the retina. In AIR, microglial cells become activated and contribute to retinal degeneration through the release of inflammatory factors. Additionally, these cells can present antigens to adaptive immune cells, initiating the transition from an innate to adaptive immune response. Although the innate immune response is critical for early detection and inflammation in AIR, it also plays a role in amplifying the autoimmune process, leading to progressive retinal damage and vision loss.

Adaptive Immunity in Autoimmune Retinopathy

The adaptive immune system is responsible for generating specific and long-lasting immune responses to pathogens. It involves T cells and B cells, which are both extremely important in the pathogenesis of AIR.

In AIR, B cells are mainly responsible for the production of autoantibodies that target retinal proteins. These autoantibodies are central to the development of the disease. Recoverin, for example, is a retinal protein, and when autoantibodies bind to it, they interfere with its function, leading to retinal cell death. These autoantibodies can trigger further immune responses that result in complement system activation, which contributes to further damage to the retina. The production of these retina-specific autoantibodies is a key factor of the disease and plays a critical role in its diagnosis.

In addition to B cells, T cells also contribute to the autoimmune response in AIR. Cytotoxic T cells, or CD8+ T cells, can directly attack retinal cells expressing antigens that have been recognized as foreign by other immune cells. These T cells are recruited to the retina through the action of pro-inflammatory cytokines, furthering the tissue damage to the retina. Helper T cells (CD4+ T cells) are also involved, aiding in the activation of B cells and cytotoxic T cells, further amplifying the immune response.

A key feature of the adaptive immune system is the development of immune system memory, which can lead to autoimmune diseases being chronic. In AIR, once the immune system has been exposed to retinal antigens, it continues to produce autoreactive antibodies and T cells even in the absence of an initial trigger. This chronic immune response is a primary factor in the long-term and progressive retinal damage observed in AIR.

The failure of immune tolerance mechanisms in AIR is another critical element in the pathogenesis of the disease. Normally, the immune system has regulatory mechanisms, such as regulatory T cells (Tregs), that maintain tolerance to self-antigens and prevent autoreactive immune responses. In AIR, however, these regulatory mechanisms are often impaired, allowing autoreactive T cells and antibodies to persist and attack retinal tissues. The impairment of tolerance to these antigens in AIR can be furthered by molecular mimicry, as mentioned previously, where foreign antigens share similar structure and properties with retinal proteins, leading to the targeting of self-tissues. [7] [8]

Signs and symptoms

Both CAR and MAR share the same symptoms. This is because they are both paraneoplastic syndromes. AIR symptoms are numerous and shared by many other diseases. [3]

Symptoms
Progressive Vision Loss
Blind Spots in Vision
Photopsia
Nyctalopia
Scotomas
Dislike/avoidance of Light
Loss of Contrast Sensitivity
Incomplete Color Blindness
Decreased Night Vision
Rod and Cone Dysfunction

[9] [10]

Diagnosis

It is difficult to diagnose AIR due to the overlap of symptoms with other disorders. There is no standardized protocol for diagnosis, leading to AIR being extremely underdiagnosed or misdiagnosed as diseases such as Retinitis Pigmentosa. [3] Examination of the fundus (inner surface of eye) can show no results or it can show narrowing of the blood vessels, abnormal colouration of the optic disc, and retinal atrophy. [3] Fundus examination results are not indicative of autoimmune retinopathy but they are used to initiate the diagnostic process. An electroretinogram (eye test used to see abnormalities in the retina) is used to detect AIR. An abnormal electroretinogram (ERG) with respect to light and dark adaptations indicates AIR. [3] The ERG also allows differentiation between cancer-associated retinopathy and melanoma-associated retinopathy. [3] If the ERG shows cone responses, CAR can be prematurely diagnosed. [3] If the ERG shows a significant decrease in b-wave amplitude, MAR can be prematurely diagnosed. [3] [11] To confirm, analysis for anti-retinal antibodies through Western blotting of serum collected from the patient, immunohistochemistry (IHC), or enzyme-linked immunosorbent assay (ELISA). [3] Since AIR is an autoimmune disease, it is likely related to a family history of autoimmune disease, which can be used to make a tentative diagnosis. While diagnosis of AIR is typical in patients >60 years of age, it can present in younger patients as well, especially those with nPAIR. [3]

Autoimmune Retinopathy vs. Retinitis Pigmentosa

One of the challenges in diagnosing autoimmune retinopathy (AIR) is its overlap of symptoms with other retinal diseases, particularly retinitis pigmentosa (RP). Both conditions share similar symptoms, such as progressive vision loss, night blindness, and blind spots. However, they have different underlying causes. RP is a hereditary disorder caused by mutations that lead to the degeneration of photoreceptor cells, typically starting with peripheral vision loss and progressing to central vision loss over time. In contrast, AIR is an acquired condition where the immune system attacks retinal cells, often leading to more rapid vision deterioration and additional symptoms such as photophobia and color vision loss.

While both conditions affect the retina, AIR tends to progress faster and can be associated with a history of cancer or systemic inflammation. RP, on the other hand, is usually a lifelong, slowly progressing disorder with a genetic basis. [3] [12]

Risk Factors

With Autoimmune retinopathy being so understudied, complex, and misdiagnosed, risk factors are important in determining its diagnosis. These risk factors include age, gender, and history of cancer. Other factors such as bacterial/viral infections, environmental factors, and heredity could be linked to the development of autoimmune retinopathy, but this is not proven.

Age and Gender

Autoimmune retinopathy is most commonly diagnosed in those over the age of 60, but can occur at any age. Non-paraneoplastic autoimmune retinopathy, especially, is more prevalent at younger ages, as it does not have a connection to cancer and can be linked to a known autoimmune condition. Gender also plays a role, as autoimmune conditions are known to be more common in women. With AIR specifically, this is suggested by studies as well. [3]

History of Cancer

A major risk factor for AIR is a history of cancer, especially in paraneoplastic autoimmune retinopathy, where the autoimmune response is triggered by cancerous cells and cancer treatments. Cancer-associated retinopathy is commonly linked with cancers such as lung cancer and breast cancer, which trigger an autoimmune response due to malignant cells. In these cases, the immune system produces antibodies targeting retinal proteins, leading to retinal degeneration and overall vision loss. Melanoma-associated autoimmune retinopathy, another form of paraneoplastic autoimmune retinopathy, is associated with melanoma, resulting in antibodies targeting other varieties of retinal cells. Treatment for cancers such as chemotherapy and radiation is also considered a risk factor for development of autoimmune retinopathy, as chemotherapies and other cancer-treatment components have been proven to elicit autoimmune responses. [3]

Treatment

Due to the difficulty of diagnosis, managing this disease is a challenge. For this reason, there is no established treatment for AIR. Clinicians try to reduce and control the autoimmune system attack to prevent any irreversible retinal damage. [3] Methods of treatment include intravenous immunoglobulin (IVIG), plasmapheresis, and corticosteroids. [3] In PAIR, treatment of cancerous bodies are typically used such as tumor removal, chemotherapy, or radiation. For nPAIR, treatment is more experimental with the use of systemic or local corticosteroids. Another form of treatment currently in the clinical trial stage is with intravitreal dexamethasone implant (IDI), which has shown promising results. [13] The overall goal of these treatments, however, is not to reverse the damage done by AIR, but to inhibit progression patient vision loss. [3] Future research in AIR and treatment possibilities is crucial to identifying appropriate and effective therapeutic methods.

Immunoglobulin

Immunoglobulin samples are obtained from a large pool of healthy, matched donors (10000 - 20000). [6] The immunoglobulin mixture is then administered through IV at a rate of 0.4g/kg/day for 5 days. [3] Antibodies in the IVIG mixture interact with binding sites of the disease-associated antibodies (such as anti-recoverin antibodies). [6] This prevents binding to proteins targeted as antigenic and reduces disease activity. [6] Treatment responses vary and depend on whether the patient has been diagnosed with cancer. [14] Patients who respond positively show improvement in the clarity of their vision and their visual field. [6]

Plasmapheresis

Plasmapheresis involves separating blood into two parts - blood cells and plasma. [15] The blood plasma components, such as the antibodies, are treated outside of the body. After removal of the disease-associated antibodies, the blood cells and plasma are transfused back into the body. [15] Response to this treatment depends on how much retinal damage has been done. Patients who respond positively show significant visual gains. [3]

Corticosteroids

Corticosteroids are administered through IV or orally. They cause lymphocytopenia, a condition where white blood cell levels are abnormally low. [16] Corticosteroids cause white blood cell death, lowering their numbers throughout the body. [16] They also cause white blood cells to recirculate away from the area of damage (the retina). [16] This minimizes damage caused by the antibodies produced by the white blood cells. Often, this treatment is combined with plasmapheresis. [3] Instead of treating the plasma and blood cells, they are replaced with a healthy donor mixture. Patients who respond positively show improved visual fields and an almost complete disappearance of anti-retinal antibodies. [17]

Management

Since AIR is a chronic, rare, and often misunderstood disease, there is not yet a standardized management protocol and most are only in preliminary stages. Once a confirmed diagnosis is made for AIR, there is not much can can be done to impact the final outcome, which depends on type of antibody present. However, there are some management methods that suggest to be successful. Immunosuppression therapy uses corticosteroids and other immunomodulatory drugs to stabilize the disease. In some cases though, this therapy has shown minor visual recovery. Plasmapheresis, which is used to decrease photoreceptor damage, has been used in combination with immunomodulators and showed some improvement in visual properties. While using immunosuppression therapy, antioxidant supplementation can prevent against retinal degeneration by providing necessary vitamins and minerals for retinal health. Overall, there is no standardized management protocol, but studies suggest that a combination of methods would be the most successful. The primary issue with AIR diagnosis is acceptance of progressive vision loss and navigation of its effect on daily life. [3]

Related Research Articles

<span class="mw-page-title-main">Diabetic retinopathy</span> Diabetes-induced damage to the retina of the eye

Diabetic retinopathy, is a medical condition in which damage occurs to the retina due to diabetes. It is a leading cause of blindness in developed countries and one of the lead causes of sight loss in the world, even though there are many new therapies and improved treatments for helping people live with diabetes.

<span class="mw-page-title-main">Autoimmunity</span> Immune response against an organisms own healthy cells

In immunology, autoimmunity is the system of immune responses of an organism against its own healthy cells, tissues and other normal body constituents. Any disease resulting from this type of immune response is termed an "autoimmune disease". Prominent examples include celiac disease, diabetes mellitus type 1, Henoch–Schönlein purpura, systemic lupus erythematosus, Sjögren syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's disease, rheumatoid arthritis, ankylosing spondylitis, polymyositis, dermatomyositis, and multiple sclerosis. Autoimmune diseases are very often treated with steroids.

<span class="mw-page-title-main">Antinuclear antibody</span> Autoantibody that binds to contents of the cell nucleus

Antinuclear antibodies are autoantibodies that bind to contents of the cell nucleus. In normal individuals, the immune system produces antibodies to foreign proteins (antigens) but not to human proteins (autoantigens). In some cases, antibodies to human antigens are produced; these are known as autoantibodies.

<span class="mw-page-title-main">Uveitis</span> Inflammation of the uvea of the eye

Uveitis is inflammation of the uvea, the pigmented layer of the eye between the inner retina and the outer fibrous layer composed of the sclera and cornea. The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is described anatomically, by the part of the eye affected, as anterior, intermediate or posterior, or panuveitic if all parts are involved. Anterior uveitis (iridocyclitis) is the most common, with the incidence of uveitis overall affecting approximately 1:4500, most commonly those between the ages of 20–60. Symptoms include eye pain, eye redness, floaters and blurred vision, and ophthalmic examination may show dilated ciliary blood vessels and the presence of cells in the anterior chamber. Uveitis may arise spontaneously, have a genetic component, or be associated with an autoimmune disease or infection. While the eye is a relatively protected environment, its immune mechanisms may be overcome resulting in inflammation and tissue destruction associated with T-cell activation.

<span class="mw-page-title-main">Pemphigus</span> Blistering autoimmune diseases

Pemphigus is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes. The name is derived from the Greek root pemphix, meaning "blister".

An autoantibody is an antibody produced by the immune system that is directed against one or more of the individual's own proteins. Many autoimmune diseases are associated with such antibodies.

<span class="mw-page-title-main">Birdshot chorioretinopathy</span> Medical condition

Birdshot chorioretinopathy, now commonly named birdshot uveitis or HLA-A29 uveitis, is a rare form of bilateral posterior uveitis affecting both eyes. It causes severe, progressive inflammation of both the choroid and retina.

Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken. Contrary to cold autoimmune hemolytic anemia which happens in cold temperature (28–31 °C), WAIHA happens at body temperature.

Paraneoplastic cerebellar degeneration (PCD) is a paraneoplastic syndrome associated with a broad variety of tumors including lung cancer, ovarian cancer, breast cancer, Hodgkin’s lymphoma and others. PCD is a rare condition that occurs in less than 1% of cancer patients.

<span class="mw-page-title-main">Autoimmune pancreatitis</span> Type of chronic pancreatitis

Autoimmune Pancreatitis (AIP) is an increasingly recognized type of chronic pancreatitis that can be difficult to distinguish from pancreatic carcinoma but which responds to treatment with corticosteroids, particularly prednisone. Although autoimmune pancreatitis is quite rare, it constitutes an important clinical problem for both patients and their clinicians: the disease commonly presents itself as a tumorous mass which is diagnostically indistinguishable from pancreatic cancer, a disease that is much more common in addition to being very dangerous. Hence, some patients undergo pancreatic surgery, which is associated to substantial mortality and morbidity, out of the fear by patients and clinicians to undertreat a malignancy. However, surgery is not a good treatment for this condition as AIP responds well to immunosuppressive treatment. There are two categories of AIP: Type 1 and Type 2, each with distinct clinical profiles.

A paraneoplastic syndrome is a syndrome that is the consequence of a tumor in the body. It is specifically due to the production of chemical signaling molecules by tumor cells or by an immune response against the tumor. Unlike a mass effect, it is not due to the local presence of cancer cells.

Autoimmune hypophysitis is defined as inflammation of the pituitary gland due to autoimmunity.

<span class="mw-page-title-main">Autoimmune inner ear disease</span> Medical condition

Autoimmune inner ear disease (AIED) was first defined by Dr. Brian McCabe in a landmark paper describing an autoimmune loss of hearing. The disease results in progressive sensorineural hearing loss (SNHL) that acts bilaterally and asymmetrically, and sometimes affects an individual's vestibular system. AIED is used to describe any disorder in which the inner ear is damaged as a result of an autoimmune response. Some examples of autoimmune disorders that have presented with AIED are Cogan's syndrome, relapsing polychondritis, systemic lupus erythematosus, granulomatosis with polyangiitis, polyarteritis nodosa, Sjogren's syndrome, and Lyme disease.

<span class="mw-page-title-main">Autoimmune disease</span> Disorders of adaptive immune system

An autoimmune disease is a condition that results from an anomalous response of the adaptive immune system, wherein it mistakenly targets and attacks healthy, functioning parts of the body as if they were foreign organisms. It is estimated that there are more than 80 recognized autoimmune diseases, with recent scientific evidence suggesting the existence of potentially more than 100 distinct conditions. Nearly any body part can be involved.

Paraneoplastic pemphigus (PNP) is an autoimmune disorder stemming from an underlying tumor. It is hypothesized that antigens associated with the tumor trigger an immune response resulting in blistering of the skin and mucous membranes.

White dot syndromes are inflammatory diseases characterized by the presence of white dots on the fundus, the interior surface of the eye. The majority of individuals affected with white dot syndromes are younger than fifty years of age. Some symptoms include blurred vision and visual field loss. There are many theories for the etiology of white dot syndromes including infectious, viral, genetics and autoimmune.

<span class="mw-page-title-main">Anti-SSA/Ro autoantibodies</span> Type of anti-nuclear autoantibodies

Anti-SSA autoantibodies are a type of anti-nuclear autoantibodies that are associated with many autoimmune diseases, such as systemic lupus erythematosus (SLE), SS/SLE overlap syndrome, subacute cutaneous lupus erythematosus (SCLE), neonatal lupus and primary biliary cirrhosis. They are often present in Sjögren's syndrome (SS). Additionally, Anti-Ro/SSA can be found in other autoimmune diseases such as systemic sclerosis (SSc), polymyositis/dermatomyositis (PM/DM), rheumatoid arthritis (RA), and mixed connective tissue disease (MCTD), and are also associated with heart arrhythmia.

<span class="mw-page-title-main">Autoimmune autonomic ganglionopathy</span> Medical condition

Autoimmune autonomic ganglionopathy is a type of immune-mediated autonomic failure that is associated with antibodies against the ganglionic nicotinic acetylcholine receptor present in sympathetic, parasympathetic, and enteric ganglia. Typical symptoms include gastrointestinal dysmotility, orthostatic hypotension, and tonic pupils. Many cases have a sudden onset, but others worsen over time, resembling degenerative forms of autonomic dysfunction. For milder cases, supportive treatment is used to manage symptoms. Plasma exchange, intravenous immunoglobulin, corticosteroids, or immunosuppression have been used successfully to treat more severe cases.

Anti-Hu associated encephalitis, also known as Anti-ANNA1 associated encephalitis, is an uncommon form of brain inflammation that is associated with an underlying cancer. It can cause psychiatric symptoms such as depression, anxiety, and hallucinations. It can also produce neurological symptoms such as confusion, memory loss, weakness, sensory loss, pain, seizures, and problems coordinating the movement of the body.

Cancer Associated Retinopathy (CAR) also known as Carcinoma Associated Retinopathy is an immune-mediated disease affecting the retina of the eye. It is a paraneoplastic type autoimmune retinopathy associated with cancer that can cause blindness. It can be seen in association with various types of cancers. It can be treated with a combination of chemotherapy and immunosuppression.

References

  1. ↑ Grange, Landon; Dalal, Monica; Nussenblatt, Robert B.; Sen, H. Nida (February 2014). "Autoimmune Retinopathy". American Journal of Ophthalmology. 157 (2): 266–272.e1. doi:10.1016/j.ajo.2013.09.019. PMC   3946999 . PMID   24315290.
  2. ↑ Canamary, AM; Takahashi, WY; Sallum, JMF (January 2018). "Autoimmune retinopathy: A Review". Int J Retina Vitreous. 4 (1). doi: 10.1186/s40942-017-0104-9 . PMC   5759752 . PMID   29340169.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 Braithwaite, T.; Vugler, A.; Tufail, A. (2012-01-01). "Autoimmune retinopathy". Ophthalmologica. 228 (3): 131–142. doi:10.1159/000338240. ISSN   1423-0267. PMID   22846442. S2CID   19694235.
  4. ↑ Adamus, Grazyna; Ren, Gaoying; Weleber, Richard G (June 2004). "Autoantibodies against retinal proteins in paraneoplastic and autoimmune retinopathy". BMC Opthamology. 4 (5). doi: 10.1186/1471-2415-4-5 . PMID   15180904.
  5. ↑ Weixler, Benjamin; Oertli, Daniel; Nebiker, Christian Andreas (2015-12-20). "Cancer-associated retinopathy as the leading symptom in colon cancer". Clinical Case Reports. 4 (2): 171–176. doi:10.1002/ccr3.463. ISSN   2050-0904. PMC   4736525 . PMID   26862417.
  6. 1 2 3 4 5 Pyne, D.; Ehrenstein, M.; Morris, V. (2002-04-01). "The therapeutic uses of intravenous immunoglobulins in autoimmune rheumatic diseases". Rheumatology. 41 (4): 367–374. doi: 10.1093/rheumatology/41.4.367 . ISSN   1462-0324. PMID   11961165.
  7. ↑ Pawestri, A.R.; Arjkongharn, N.; Suvannaboon, R. (2021). "Autoantibody profiles and clinical association in Thai patients with autoimmune retinopathy". Scientific Reports. 11 (15047). doi:10.1038/s41598-021-94377-0. PMID   34294798.
  8. ↑ Smith, D A (Oct 1999). "Germolec". D R. 107 (5): 661–665. doi:10.1289/ehp.99107s5661. PMC   1566249 . PMID   10502528.
  9. ↑ Larson, T. A.; Gottlieb, C. C.; Zein, W. M.; Nussenblatt, R. B.; Sen, H. N. (2010-04-17). "Autoimmune Retinopathy: Prognosis and Treatment". Investigative Ophthalmology & Visual Science. 51 (13): 6375. ISSN   1552-5783.
  10. ↑ Abazari, Azin; Allam, Souha S.; Adamus, Grazyna; Ghazi, Nicola G. (2016-11-21). "Optical Coherence Tomography Findings in Autoimmune Retinopathy". American Journal of Ophthalmology. 153 (4): 750–756.e1. doi:10.1016/j.ajo.2011.09.012. ISSN   0002-9394. PMC   3495560 . PMID   22245461.
  11. ↑ "The Absent-Minded Professor: An Unusual Complication of Melanoma". www.cancernetwork.com. 2008-12-01. Archived from the original on 2017-01-06. Retrieved 2016-11-21.
  12. ↑ Hamel, Christian (October 2011). "Retinitis Pigmentosa". Orphanet Journal of Rare Diseases. 1 (40): 40. doi: 10.1186/1750-1172-1-40 . PMC   1621055 . PMID   17032466.
  13. ↑ Hou, Si-Meng; Liu, Qian; Peng, Xiao-Yan; Li, Yi-Bin; Li, Zhi-Hua; Zing, Hui-Yang (Dec 2022). "Management of autoimmune retinopathy treated with intravitreal dexamethasone implant". Graefes Arch Clin Exp Ophthalmol. 261 (5): 1381–1389. doi:10.1007/s00417-022-05941-x. PMC   9789510 . PMID   36565329.
  14. ↑ Adamus, Grazyna; Ren, Gaoying; Weleber, Richard G. (2004-01-01). "Autoantibodies against retinal proteins in paraneoplastic and autoimmune retinopathy". BMC Ophthalmology. 4: 5. doi: 10.1186/1471-2415-4-5 . ISSN   1471-2415. PMC   446200 . PMID   15180904.
  15. 1 2 Lobo, David R; García-Berrocal, Jose Ramon; Ramírez-Camacho, Rafael (2014-06-26). "New prospects in the diagnosis and treatment of immune-mediated inner ear disease". World Journal of Methodology. 4 (2): 91–98. doi: 10.5662/wjm.v4.i2.91 . ISSN   2222-0682. PMC   4202484 . PMID   25332908.
  16. 1 2 3 Hall, Bruce M. (1999). "Corticosteroids in autoimmune diseases". Australian Prescriber. 22: 9–11. doi: 10.18773/austprescr.1999.008 .
  17. ↑ Bursztyn, Lulu L. C. D.; Belrose, Jillian C.; Coupland, Stuart G; Fraser, J. Alexander; Proulx, Alain A. (2015). "Remission of Nonparaneoplastic Autoimmune Retinopathy After Minimal Steroid Treatment". Retinal Cases & Brief Reports. 9 (2): 173–176. doi:10.1097/ICB.0000000000000131. PMID   25764315. S2CID   10353381.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.