Lupus Erythematosus, Systemic
Enzyme-Linked Immunosorbent Assay
Anemia, Hemolytic, Autoimmune
RNA, Small Cytoplasmic
snRNP Core Proteins
Receptor-Like Protein Tyrosine Phosphatases, Class 8
Diabetes Mellitus, Type 1
Mice, Inbred MRL lpr
Antibodies, Antineutrophil Cytoplasmic
Binding Sites, Antibody
Ribonucleoproteins, Small Nuclear
Fluorescent Antibody Technique, Indirect
Skin Diseases, Vesiculobullous
Fluorescent Antibody Technique
Liver Cirrhosis, Biliary
Connective Tissue Diseases
Protein Array Analysis
beta 2-Glycoprotein I
Molecular Sequence Data
Mixed Connective Tissue Disease
Epidermolysis Bullosa Acquisita
Amino Acid Sequence
Anti-Glomerular Basement Membrane Disease
Immunoglobulin Fab Fragments
Pulmonary Alveolar Proteinosis
Immunoglobulin Variable Region
Mice, Inbred Strains
Disease Models, Animal
Islets of Langerhans
Purpura, Thrombocytopenic, Idiopathic
Receptors, Adrenergic, beta-1
Receptors, Phospholipase A2
Lupus Vasculitis, Central Nervous System
Weak autoantibody reactions to antigens other than sperm after vasectomy. (1/9574)Autoantibody activity against various antigens was measured by indirect immunofluorescence in 97 men about to undergo vasectomy and 170 men who had undergone the operation up to six years earlier. There was a significantly higher prevalence of weakly positive autoantibody reactions among those who had undergone vasectomy. There was, however, no evidence that vasectomy could induce stronger autoantibody reactions such as those associated with autoimmune disease. (+info)
Anti-heart autoantibodies in ischaemic heart disease patients. (2/9574)One hundred and ninety-nine ischaemic heart disease (IHD) patients were studied with regard to the prevalence of anti-heart autoantibodies (AHA). The incidence of AHA in IHD patients was 1%: one out of 102 patients who suffered acute myocardial infarction (AMI), one out of seventy-two patients who suffered from acute coronary insufficiency (ACI), and none out of twenty-five patients with other signs and symptoms of IHD, had AHA in their sera. An additional 2% of patients who suffered from AMI developed detectable antibody levels during a follow-up period of 15 days. In comparison,, 53% of patients (eight out of fifteen) who underwent heart surgery and who had no AHA prior to operation, developed these antibodies in their sera during 1-2 weeks following operation. (+info)
Explanations for the clinical and microscopic localization of lesions in pemphigus foliaceus and vulgaris. (3/9574)Patients with pemphigus foliaceus (PF) have blisters on skin, but not mucous membranes, whereas patients with pemphigus vulgaris (PV) develop blisters on mucous membranes and/or skin. PF and PV blisters are due to loss of keratinocyte cell-cell adhesion in the superficial and deep epidermis, respectively. PF autoantibodies are directed against desmoglein (Dsg) 1; PV autoantibodies bind Dsg3 or both Dsg3 and Dsg1. In this study, we test the hypothesis that coexpression of Dsg1 and Dsg3 in keratinocytes protects against pathology due to antibody-induced dysfunction of either one alone. Using passive transfer of pemphigus IgG to normal and DSG3(null) neonatal mice, we show that in the areas of epidermis and mucous membrane that coexpress Dsg1 and Dsg3, antibodies against either desmoglein alone do not cause spontaneous blisters, but antibodies against both do. In areas (such as superficial epidermis of normal mice) where Dsg1 without Dsg3 is expressed, anti-Dsg1 antibodies alone can cause blisters. Thus, the anti-desmoglein antibody profiles in pemphigus sera and the normal tissue distributions of Dsg1 and Dsg3 determine the sites of blister formation. These studies suggest that pemphigus autoantibodies inhibit the adhesive function of desmoglein proteins, and demonstrate that either Dsg1 or Dsg3 alone is sufficient to maintain keratinocyte adhesion. (+info)
Autoantibodies to gastrin in patients with pernicious anaemia--a novel antibody. (4/9574)Autoantibodies arise when there is a breakdown in immunological tolerance. Autoantibodies to parietal cells and intrinsic factor are found in autoimmune atrophic gastritis (AAG) and are associated with elevated plasma gastrin. Endogenous gastrin autoantibodies have not been described to date. The aim of this study was to investigate the occurrence of autoantibodies to gastrin. Plasma from 50,000 patients, including more than 2000 with AAG, was tested. Gastrin was measured by radioimmunoassay (RIA) in whole plasma and the presence of autoantibody determined by using a control which omitted assay antibody. The quantity and affinity of gastrin autoantibodies was assessed. Three patients had autoantibodies to gastrin. All three had AAG and pernicious anaemia (PA). The antibodies were of low titre and relatively high affinity. Free circulating plasma gastrin levels were within the normal range, but total gastrin levels were elevated. This is the first description of autoantibodies to endogenous gastrin. The incidence of antibodies to gastrin is low, they are found in association with PA, and they may lead to falsely low measurements of plasma gastrin. (+info)
Associations of anti-beta2-glycoprotein I autoantibodies with HLA class II alleles in three ethnic groups. (5/9574)OBJECTIVE: To determine any HLA associations with anti-beta2-glycoprotein I (anti-beta2GPI) antibodies in a large, retrospectively studied, multiethnic group of 262 patients with primary antiphospholipid antibody syndrome (APS), systemic lupus erythematosus (SLE), or another connective tissue disease. METHODS: Anti-beta2GPI antibodies were detected in sera using an enzyme-linked immunosorbent assay. HLA class II alleles (DRB1, DQA1, and DQB1) were determined by DNA oligotyping. RESULTS: The HLA-DQB1*0302 (DQ8) allele, typically carried on HLA-DR4 haplotypes, was associated with anti-beta2GPI when compared with both anti-beta2GPI-negative SLE patients and ethnically matched normal controls, especially in Mexican Americans and, to a lesser extent, in whites. Similarly, when ethnic groups were combined, HLA-DQB1*0302, as well as HLA-DQB1*03 alleles overall (DQB1*0301, *0302, and *0303), were strongly correlated with anti-beta2GPI antibodies. The HLA-DR6 (DR13) haplotype DRB1*1302; DQB1*0604/5 was also significantly increased, primarily in blacks. HLA-DR7 was not significantly increased in any of these 3 ethnic groups, and HLA-DR53 (DRB4*0101) was increased in Mexican Americans only. CONCLUSION: Certain HLA class II haplotypes genetically influence the expression of antibodies to beta2GPI, an important autoimmune response in the APS, but there are variations in HLA associations among different ethnic groups. (+info)
The inhibition of myeloperoxidase by ceruloplasmin can be reversed by anti-myeloperoxidase antibodies. (6/9574)BACKGROUND: The purpose of this study was to characterize the recently reported inhibition of myeloperoxidase (MPO) by ceruloplasmin and to determine whether this may be disturbed in the presence of anti-MPO antibodies. METHODS: Specificity of the binding between ceruloplasmin and MPO was confirmed by Western blotting and enzyme-linked immunosorbent assay (ELISA), and the enzymatic activity of MPO was measured in the presence of ceruloplasmin, affinity-purified anti-MPO antibodies, or both. The affinity of the binding between MPO and ceruloplasmin and MPO and the anti-MPO antibodies was measured using a biosensor, with the results confirmed by chaotrope ELISA. RESULTS: Affinity-purified anti-MPO antibodies from patients with microscopic polyangiitis and florid renal vasculitis inhibited the binding between ceruloplasmin and MPO to a maximum of 72.9 +/- 12.8%, whereas those from patients with Wegener's granulomatosis and only minimal renal involvement inhibited the binding to a maximum of only 36.8 +/- 10.9% (P < 0. 001), with comparable reversal of the ceruloplasmin-mediated inhibition of MPO activity. Measurement of the affinity of the interactions demonstrated that binding between MPO and the anti-MPO antibodies is stronger than that between MPO and ceruloplasmin (1.61 x 107 to 1.33 x 108 vs. 7.46 x 106 m-1), indicating that binding to the autoantibody would be favored in vivo. CONCLUSIONS: This study confirms a role for ceruloplasmin as a physiological inhibitor of MPO, and demonstrates how the inhibition may be disrupted in the presence of anti-MPO antibodies. Because a majority (16 of 21) of the antibodies did not themselves inhibit MPO activity, their interference with the inhibition mediated by ceruloplasmin may be brought about by steric hindrance consequent upon the binding of the antibody to a dominant epitope at or near the active site. (+info)
Goodpasture antigen: expression of the full-length alpha3(IV) chain of collagen IV and localization of epitopes exclusively to the noncollagenous domain. (7/9574)BACKGROUND: Tissue injury in Goodpasture (GP) syndrome (rapidly progressive glomerular nephritis and pulmonary hemorrhage) is mediated by antibasement membrane antibodies that are targeted to the alpha3(IV) chain of type IV collagen, one of five alpha(IV) chains that occur in the glomerular basement membrane. GP antibodies are known to bind epitopes within the carboxyl terminal noncollagenous domain (NC1) of the alpha3(IV) chain, termed the GP autoantigen. Whether epitopes also exist in the 1400-residue collagenous domain is unknown because studies to date have focused solely on the NC1 domain. A knowledge of GP epitopes is important for the understanding of the etiology and pathogenesis of the disease and for the development of therapeutic strategies. METHODS: A cDNA construct was prepared for the full-length human alpha3(IV) chain. The construct was stably transfected into human embryonic kidney 293 cells. The purified full-length r-alpha3(IV) chain was characterized by electrophoresis and electron microscopy. The capacity of this chain for binding of GP antibodies from five patients was compared with that of the human r-alpha3(IV)NC1 domain by competitive enzyme-linked immunosorbent assay. RESULTS: The r-alpha3(IV) chain was secreted from 293 cells as a single polypeptide chain that did not spontaneously undergo assembly into a triple-helical molecule. An analysis of GP-antibody binding to the full-length r-alpha3(IV) chain showed binding exclusively to the globular NC1 domain. CONCLUSION: The full-length human alpha3(IV) chain possesses the capacity to bind GP autoantibodies. The epitope(s) is found exclusively on the nontriple-helical NC1 domain of the alpha3(IV) chain, indicating the presence of specific immunogenic properties. The alpha3(IV) chain alone does not spontaneously undergo assembly into a triple-helical homotrimeric molecule, suggesting that coassembly with either the alpha4(IV) and/or the alpha5(IV) chain may be required for triple-helix formation. (+info)
Identification of a clinically relevant immunodominant region of collagen IV in Goodpasture disease. (8/9574)BACKGROUND: The characteristic feature of Goodpasture disease is the occurrence of an autoantibody response to the noncollagenous domain of the alpha3 chain of type IV collagen [alpha3(IV)NC1] in the alveolar and glomerular basement membrane. These antibodies are associated with the development of a rapidly progressive glomerulonephritis, with or without lung hemorrhage, whereas autoantibodies specific for the other alpha chains of the heterotrimeric type IV collagen probably do not cause disease. In this study, we have investigated whether differences in fine specificity of autoimmune recognition of the alpha3(IV)NC1 correlate with clinical outcome. METHODS: For mapping of antibody binding to type IV collagen, chimeric collagen constructs were generated in which parts of the alpha3(IV)NC1 domain were replaced by the corresponding sequences of homologous nonreactive alpha1(IV). The different recombinant collagen chimeras allowed the analysis of antibody specificities in 77 sera from well-documented patients. RESULTS: One construct that harbors the aminoterminal third of the alpha3(IV)NC1 was recognized by all sera, indicating that it represents the dominant target of the B-cell response in Goodpasture disease. Seventy percent of the samples recognized other parts of the molecule as well. However, only reactivity to the N-terminus of the alpha3(IV)NC1 correlated with prognosis, that is, kidney survival after six months of follow-up. CONCLUSION: The results indicate the crucial importance of antibody recognition of this particular domain for the pathogenesis of Goodpasture disease, thereby opening new avenues for the development of better diagnostic and therapeutic procedures. (+info)
Examples of autoimmune diseases include:
1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.
The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.
The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.
There are several subtypes of LES, including:
1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.
There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.
It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.
There are several types of pemphigus, including:
1. Pemphigus vulgaris: This is the most common form of the disease and is characterized by the formation of large, painful blisters on the skin and mucous membranes.
2. Pemphigus foliaceus: This type of pemphigus is characterized by the formation of smaller, crusting sores on the skin.
3. Pemphigus erythematosus: This type of pemphigus is characterized by the formation of flat, red sores on the skin.
4. Bullous pemphigoid: This is a rare form of pemphigus that is characterized by the formation of large, fluid-filled blisters on the skin.
Treatment for pemphigus typically involves the use of corticosteroids and immunosuppressive drugs to reduce inflammation and suppress the immune system. In severe cases, hospitalization may be necessary to manage complications such as infection and fluid loss.
Prevention of pemphigus is difficult, but avoiding exposure to known triggers such as certain medications and taking steps to maintain good skin care can help reduce the risk of developing the disease. Early diagnosis and treatment are important to prevent complications and improve outcomes for patients with pemphigus.
A group of autoimmune blistering diseases that are characterized by the formation of large, tense bullae on the skin and mucous membranes. These diseases are caused by abnormal immunological responses to certain antigens, which lead to the production of autoantibodies that attack the basement membrane zone of the skin and mucous membranes, causing damage and blister formation.
There are several types of pemphigoid, bullous diseases, including:
* Pemphigoid, benign chronic
* Pemphigoid, severe
* Bullous pemphigoid
* Epidermolysis bullosa acquisita
Symptoms of pemphigoid, bullous diseases may include:
* Blisters on the skin and mucous membranes
* Redness and swelling around the blisters
* Itching or pain
Diagnosis of pemphigoid, bullous diseases is based on a combination of clinical findings, laboratory tests, and biopsy. Treatment involves the use of corticosteroids, immunosuppressive drugs, and antibiotics to manage symptoms and prevent complications.
There are two main types of systemic scleroderma: diffuse cutaneous systemic sclerosis (DCSS) and limited cutaneous systemic sclerosis (LCSS). DCSS is characterized by skin thickening and scar formation over the trunk, arms, and legs, while LCSS is characterized by skin tightening and patches of scaly skin on the hands and face.
The symptoms of systemic scleroderma can include:
* Skin hardening and tightening
* Joint pain and stiffness
* Muscle weakness
* Swallowing difficulties
* Heartburn and acid reflux
* Shortness of breath
* Raynaud's phenomenon (pale or blue-colored fingers and toes in response to cold temperatures or stress)
The exact cause of systemic scleroderma is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment options for systemic scleroderma include medications to manage symptoms such as pain, stiffness, and swallowing difficulties, as well as physical therapy and lifestyle modifications to improve quality of life.
In summary, systemic scleroderma is a chronic autoimmune disease that affects multiple systems in the body, causing skin hardening and thickening, fatigue, joint pain, and other symptoms. While there is no cure for systemic scleroderma, treatment options are available to manage symptoms and improve quality of life.
Sjögren's syndrome can affect people of all ages, but it most commonly occurs in women between the ages of 40 and 60. The exact cause of the disorder is not known, but it is believed to be an autoimmune response, meaning that the immune system mistakenly attacks the glands as if they were foreign substances.
Symptoms of Sjögren's syndrome can vary in severity and may include:
* Dry mouth (xerostomia)
* Dry eyes (dry eye syndrome)
* Joint pain
* Swollen lymph nodes
* Sores on the skin
* Numbness or tingling in the hands and feet
* Sexual dysfunction
There is no cure for Sjögren's syndrome, but various treatments can help manage the symptoms. These may include:
* Medications to stimulate saliva production
* Eye drops to moisturize the eyes
* Mouthwashes to stimulate saliva production
* Pain relief medication for joint pain
* Anti-inflammatory medication to reduce swelling
* Immunosuppressive medication to suppress the immune system
* Hormone replacement therapy (HRT) to treat hormonal imbalances.
Sjögren's syndrome can also increase the risk of developing other autoimmune disorders, such as rheumatoid arthritis or lupus. It is important for people with Sjögren's syndrome to work closely with their healthcare provider to manage their symptoms and monitor their condition over time.
The symptoms of lupus vulgaris typically include:
* Rough, scaly patches on the skin that may be dark red or purple in color
* Itching or burning sensation on the skin
* Skin thickening or hardening
* Painless ulcers or sores on the skin
* Swollen lymph nodes
* Joint pain or swelling
The diagnosis of lupus vulgaris is based on a combination of clinical findings and laboratory tests. A physical examination of the skin and mucous membranes can reveal characteristic signs of the condition, such as scaly patches or ulcers. Laboratory tests, such as blood tests or biopsies, may be performed to confirm the diagnosis and rule out other conditions.
Treatment of lupus vulgaris typically involves antibiotics, which can help to clear the infection and reduce symptoms. In severe cases, surgical debridement or laser therapy may be necessary to remove damaged tissue and promote healing. In addition, patients with lupus vulgaris may require supportive care to manage symptoms such as pain, itching, and swelling.
Overall, lupus vulgaris is a chronic skin condition that can cause significant discomfort and disfigurement if left untreated. It is important for individuals in regions where the condition is common to be aware of the signs and symptoms and seek medical attention if they suspect they may have the condition. With proper diagnosis and treatment, however, most patients with lupus vulgaris can experience significant improvement in their symptoms and quality of life.
Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.
In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.
Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.
In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.
There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:
* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.
Lupus Nephritis can cause a range of symptoms, including:
* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Joint pain
Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.
1. Polymyositis: This is an inflammatory disease that affects the muscles and can cause muscle weakness, pain, and stiffness.
2. Dercum's disease: This is a rare condition that causes fatty degeneration of the muscles, leading to muscle pain, weakness, and wasting.
3. Inflammatory myopathy: This is a group of conditions that cause inflammation in the muscles, leading to muscle weakness and pain.
4. Dermatomyositis: This is an inflammatory condition that affects both the skin and the muscles, causing skin rashes and muscle weakness.
5. Juvenile myositis: This is a rare condition that affects children and can cause muscle weakness, pain, and stiffness.
The symptoms of myositis can vary depending on the type of condition and its severity. Common symptoms include muscle weakness, muscle pain, stiffness, and fatigue. Other symptoms may include skin rashes, fever, and joint pain.
The diagnosis of myositis typically involves a combination of physical examination, medical history, and laboratory tests such as blood tests and muscle biopsies. Treatment for myositis depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy. In some cases, surgery may be necessary to remove affected muscle tissue.
Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.
Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.
The symptoms of dermatomyositis can vary in severity and may include:
* Rashes and lesions on the skin, particularly on the face, neck, and hands
* Muscle weakness and fatigue
* Joint pain and stiffness
* Swelling and redness in the affected areas
Dermatomyositis is often associated with other autoimmune disorders, such as polymyositis, and can be triggered by certain medications or infections. There is no cure for dermatomyositis, but treatment options are available to manage the symptoms and prevent complications. Treatment may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy to maintain muscle strength and flexibility.
The term "dermatomyositis" is derived from the Greek words "derma," meaning skin, "myo," meaning muscle, and "-itis," indicating inflammation. The condition was first described in the medical literature in the early 20th century, and since then has been studied extensively to better understand its causes and develop effective treatments.
In summary, dermatomyositis is a rare autoimmune disease that affects both the skin and muscles, causing inflammation and various symptoms such as rashes, weakness, and joint pain. While there is no cure for the condition, treatment options are available to manage the symptoms and prevent complications.
The term "paraneoplastic" refers to the fact that these conditions are parallel to, or associated with, neoplasms (abnormal growths) in the body. The exact cause of paraneoplastic syndromes is not fully understood, but they are believed to be related to the immune system's response to cancer cells.
Some common features of paraneoplastic syndromes include:
1. Autoantibodies: The immune system produces antibodies that attack the body's own tissues and organs.
2. Inflammation: The immune system causes inflammation in various parts of the body.
3. Nerve damage: Paraneoplastic syndromes can affect the nerves, leading to symptoms such as numbness, weakness, and pain.
4. Muscle weakness: Some paraneoplastic syndromes can cause muscle weakness and wasting.
5. Skin rashes: Some patients with paraneoplastic syndromes may develop skin rashes or lesions.
6. Eye problems: Paraneoplastic syndromes can affect the eyes, leading to symptoms such as double vision, blindness, and eye pain.
7. Endocrine dysfunction: Some paraneoplastic syndromes can disrupt the normal functioning of the endocrine system, leading to hormonal imbalances.
Examples of paraneoplastic syndromes include:
1. Lambert-Eaton myasthenic syndrome (LEMS): This is a rare autoimmune disorder that affects the nerves and muscles, leading to muscle weakness and fatigue. It is often associated with small cell lung cancer.
2. Anti-NMDA receptor encephalitis: This is a severe autoimmune disorder that affects the brain and can cause symptoms such as seizures, confusion, and memory loss. It is often associated with ovarian teratoma.
3. Paraneoplastic cerebellar degeneration (PCD): This is a rare condition that affects the cerebellum and can cause symptoms such as coordination problems, balance difficulties, and difficulty with movement. It is often associated with lung cancer or other types of cancer.
4. Stiff-person syndrome: This is a rare autoimmune disorder that affects the central nervous system and can cause symptoms such as muscle stiffness, spasms, and autonomy dysfunction. It is often associated with ovarian teratoma.
5. Polymyositis: This is a rare inflammatory condition that affects the muscles and can cause muscle weakness and wasting. It is often associated with cancer, particularly lung cancer.
6. Dercum's disease: This is a rare condition that affects the adipose tissue and can cause symptoms such as pain, swelling, and limited mobility. It is often associated with cancer, particularly breast cancer.
7. Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow and can cause symptoms such as bone pain, fatigue, and weakness. It is often associated with ovarian teratoma.
8. Painless thyroiditis: This is a rare condition that affects the thyroid gland and can cause symptoms such as thyroid gland inflammation, fatigue, and weight gain. It is often associated with cancer, particularly breast cancer.
9. Ovarian cysts: These are fluid-filled sacs that form on the ovaries and can cause symptoms such as pelvic pain, bloating, and irregular menstrual periods. They are often associated with ovarian teratoma.
10. Endometriosis: This is a condition in which tissue similar to the lining of the uterus grows outside of the uterus and can cause symptoms such as pelvic pain, heavy menstrual bleeding, and infertility. It is often associated with ovarian teratoma.
It's important to note that these conditions are rare and not all cases of ovarian teratoma are associated with them. If you suspect you may have ovarian teratoma, it's important to talk to your healthcare provider for proper diagnosis and treatment.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
Grave's disease is the most common cause of hyperthyroidism and affects about 1 in 200 people. It can occur at any age but is more common in women and tends to run in families. The exact cause of Grave's disease is not known, but it may be related to a combination of genetic and environmental factors.
Symptoms of Grave's disease can vary from person to person, but common signs include:
* Weight loss
* Nervousness or anxiety
* Irregular heartbeat (palpitations)
* Increased sweating
* Heat intolerance
* Changes in menstrual cycle in women
* Enlargement of the thyroid gland, known as a goiter
* Bulging eyes (exophthalmos)
Grave's disease can be diagnosed through blood tests and scans. Treatment options include medication to reduce the production of thyroxine, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.
It is important to seek medical attention if you experience any symptoms of Grave's disease, as untreated hyperthyroidism can lead to complications such as heart problems, osteoporosis, and eye problems. With proper treatment, most people with Grave's disease can manage their symptoms and lead a normal life.
The term "polyendocrinopathy" refers to the involvement of multiple endocrine glands, while "autoimmune" indicates that the disorder is caused by an abnormal immune response against the body's own tissues.
Examples of polyendocrinopathies, autoimmune include:
1. Type 1 diabetes with thyroiditis and adrenal insufficiency
2. Hashimoto's thyroiditis with hypophyseal and adrenal involvement
3. Addison's disease with hypothyroidism and hemolytic anemia
4. Autoimmune polyglandular syndrome type 1 (APS-1) with autoantibodies against multiple endocrine glands
5. Autoimmune polyglandular syndrome type 2 (APS-2) with autoantibodies against thyroid, adrenal, and gonadal glands.
The exact cause of polyendocrinopathies, autoimmune is not fully understood, but it is thought to involve a combination of genetic and environmental factors that trigger an abnormal immune response against endocrine tissues. Treatment varies depending on the specific disorder and may include hormone replacement therapy, immunosuppressive medications, and management of associated symptoms.
1. Bullous pemphigoid: This is a rare autoimmune disease that causes large, fluid-filled blisters to form on the skin.
2. Pemphigus: This is another group of rare autoimmune diseases that cause blisters and sores to form on the skin.
3. Impetigo: This is a highly contagious bacterial infection that causes red sores or blisters to form on the skin, often around the nose and mouth.
4. Herpes simplex: This is a viral infection that causes small, painful blisters to form on the skin, often around the mouth or genitals.
5. Molluscum contagiosum: This is a viral infection that causes small, firm bumps to form on the skin, which can become inflamed and itchy.
These conditions can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or blood tests. Treatment for skin diseases, vesiculobullous depends on the underlying cause and may include antibiotics, anti-inflammatory medications, or immunosuppressive drugs. In some cases, surgical removal of the blisters or sores may be necessary. It is important to seek medical attention if you suspect you have a skin disease, vesiculobullous, as these conditions can be difficult to diagnose and treat, and can lead to complications such as infection or scarring.
The exact cause of SPS is not known, but it is believed to be an autoimmune disorder that results in the immune system attacking healthy brain cells, leading to inflammation and damage to the nervous system. Treatment options are limited, and current therapies focus on managing symptoms and improving quality of life.
The definition of Stiff-Person Syndrome (SPS) in the medical field includes:
1. A rare and progressive neurological disorder characterized by muscle stiffness, rigidity, and spasms.
2. Associated with heightened sensitivity to external stimuli such as noise, touch, or emotional stress.
3. Cognitive impairment, anxiety, and depression are common features.
4. Believed to be an autoimmune disorder, causing inflammation and damage to the nervous system.
5. Limited treatment options, with a focus on managing symptoms and improving quality of life.
Polymyositis can affect people of all ages, but it most commonly occurs in adults between the ages of 30 and 60. It is more common in women than men, and the symptoms can vary in severity. The disease may be acute or chronic, and it can affect one or more muscle groups.
The symptoms of polymyositis include:
* Muscle weakness and fatigue
* Pain in the affected muscles
* Wasting of the affected muscles
* Difficulty swallowing (in severe cases)
* Shortness of breath (in severe cases)
The diagnosis of polymyositis is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include blood tests to check for muscle enzymes and inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Imaging studies, such as magnetic resonance imaging (MRI), can help to confirm the diagnosis and assess the extent of the disease.
There is no cure for polymyositis, but treatment can help to manage the symptoms and slow the progression of the disease. Treatment options may include:
* Corticosteroids to reduce inflammation
* Immunosuppressive drugs to suppress the immune system
* Physical therapy to maintain muscle strength and function
* Pain management with analgesics and other medications
* Plasmapheresis to remove antibodies from the blood
The prognosis for polymyositis varies, depending on the severity of the disease and the response to treatment. In general, the prognosis is better for patients who have a mild form of the disease and who respond well to treatment. However, in severe cases, the disease can be life-threatening, and mortality rates are estimated to be as high as 20% to 30%.
There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:
1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.
The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.
Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.
In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:
1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.
It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.
The condition is often caused by gallstones or other blockages that prevent the normal flow of bile from the liver to the small intestine. Over time, the scarring can lead to the formation of cirrhosis, which is characterized by the replacement of healthy liver tissue with scar tissue.
Symptoms of liver cirrhosis, biliary may include:
* Jaundice (yellowing of the skin and eyes)
* Abdominal pain
* Dark urine
* Pale stools
The diagnosis of liver cirrhosis, biliary is typically made through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, CT scans, and blood tests.
Treatment for liver cirrhosis, biliary depends on the underlying cause of the condition. In some cases, surgery may be necessary to remove gallstones or repair damaged bile ducts. Medications such as antioxidants and anti-inflammatory drugs may also be prescribed to help manage symptoms and slow the progression of the disease. In severe cases, a liver transplant may be necessary.
Prognosis for liver cirrhosis, biliary is generally poor, as the condition can lead to complications such as liver failure, infection, and cancer. However, with early diagnosis and appropriate treatment, it is possible to manage the symptoms and slow the progression of the disease.
Some common types of connective tissue diseases include:
1. Rheumatoid arthritis (RA): A chronic autoimmune disorder that causes inflammation and joint damage.
2. Systemic lupus erythematosus (SLE): An autoimmune disorder that can affect multiple systems in the body, including the skin, joints, and kidneys.
3. Sjogren's syndrome: An autoimmune disorder that causes dry eyes and mouth, as well as joint pain and swelling.
4. Fibromyalgia: A chronic condition characterized by widespread muscle pain and fatigue.
5. Myositis: Inflammatory diseases that affect the muscles, such as dermatomyositis and polymyositis.
6. Giant cell arteritis: A condition that causes inflammation of the blood vessels, particularly in the head and neck.
7. Takayasu arteritis: A condition that causes inflammation of the blood vessels in the aorta and its branches.
8. Polyarteritis nodosa: A condition that causes inflammation of the blood vessels, particularly in the hands and feet.
9. IgG4-related disease: A condition characterized by inflammation and damage to various organs, including the pancreas, salivary glands, and liver.
Connective tissue diseases can cause a wide range of symptoms, including joint pain and stiffness, fatigue, skin rashes, fever, and weight loss. Treatment options vary depending on the specific disease and its severity, but may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). In some cases, surgery or physical therapy may also be necessary.
The exact cause of autoimmune hepatitis is not fully understood, but it is believed to involve a combination of genetic and environmental factors. The condition can occur in people of all ages, although it is most common in women between the ages of 20 and 40.
Symptoms of autoimmune hepatitis may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, and yellowing of the skin and eyes (jaundice). If left untreated, the condition can lead to liver failure and even death.
Treatment for autoimmune hepatitis typically involves medications to suppress the immune system and reduce inflammation in the liver. In severe cases, a liver transplant may be necessary. Early diagnosis and treatment can improve the chances of a successful outcome.
The exact cause of MCTD is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the body. The disease is more common in women than men and typically affects people between the ages of 20 and 50.
Symptoms of MCTD can vary widely and may include:
* Skin rashes or lesions
* Joint pain and stiffness
* Raynaud's phenomenon (digits turn white or blue in response to cold or stress)
* Swollen lymph nodes
* Shortness of breath
* Chest pain
* Abdominal pain
* Weakness and wasting of muscles
There is no cure for MCTD, but treatment focuses on managing symptoms and preventing complications. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive drugs may be used to reduce inflammation and suppress the immune system. Physical therapy and exercise may also be helpful in maintaining joint mobility and strength.
The prognosis for MCTD varies depending on the severity of the disease and the presence of certain complications, such as lung or heart involvement. Some people with MCTD may experience a gradual worsening of symptoms over time, while others may experience periods of remission. With appropriate treatment, many people with MCTD are able to manage their symptoms and lead active lives.
Blisters are caused by friction or rubbing against a surface, which causes the top layer of skin to separate from the underlying layer. This separation creates a space that fills with fluid, forming a blister. Blisters can also be caused by burns, chemical exposure, or other types of injury.
There are different types of blisters, including:
1. Friction blisters: These are the most common type of blister and are caused by friction or rubbing against a surface. They are often seen on the hands, feet, and buttocks.
2. Burn blisters: These are caused by burns and can be more severe than friction blisters.
3. Chemical blisters: These are caused by exposure to chemicals and can be very painful.
4. Blisters caused by medical conditions: Certain medical conditions, such as epidermolysis bullosa (a genetic disorder that affects the skin), can cause blisters to form easily.
Blisters can be treated in several ways, depending on their size and location. Small blisters may not require treatment and can heal on their own within a few days. Larger blisters may need to be drained and covered with a bandage to prevent infection. In severe cases, surgical intervention may be necessary.
Preventing blisters is key to avoiding the discomfort and pain they can cause. To prevent blisters, it is important to:
1. Wear properly fitting shoes and clothing to reduce friction.
2. Use lubricating creams or powders to reduce friction.
3. Take regular breaks to rest and allow the skin to recover.
4. Avoid using harsh chemicals or detergents that can cause irritation.
5. Keep the affected area clean and dry to prevent infection.
In conclusion, blisters are a common and uncomfortable condition that can be caused by a variety of factors. While they can be treated and managed, prevention is key to avoiding the discomfort and pain they can cause. By taking steps to prevent blisters and seeking medical attention if they do occur, individuals can reduce their risk of developing this uncomfortable condition.
The symptoms of EBA can vary in severity and may include:
* Blisters and sores on the skin and mucous membranes
* Skin thickening and scarring
* Pain and discomfort
* Infection and inflammation
The exact cause of EBA is not known, but it is believed to be an autoimmune response, where the body's immune system mistakenly attacks its own tissues. Genetic factors may also play a role in the development of EBA.
There is no cure for EBA, but treatment options include:
* Immunosuppressive medications to reduce inflammation and suppress the immune system
* Topical and oral medications to manage pain and prevent infection
* Wound care and debridement to promote healing and reduce scarring
* Phototherapy to reduce inflammation and promote healing
The diagnosis of EBA is based on a combination of clinical findings, laboratory tests, and skin biopsy. Laboratory tests may include:
* Immunofluorescence to detect the presence of autoantibodies against the basement membrane zone
* Direct immunofluorescence to detect the presence of autoantibodies on the skin
* Indirect immunofluorescence to detect the presence of autoantibodies in the blood
The prognosis for EBA is generally poor, with a high risk of complications and a significant impact on quality of life. However, with appropriate treatment, some patients may experience improved symptoms and reduced inflammation. Early diagnosis and aggressive treatment are important to improve outcomes in patients with EBA.
1. Hypothyroidism: This is a condition where the thyroid gland does not produce enough thyroid hormones. Symptoms can include fatigue, weight gain, dry skin, constipation, and depression.
2. Hyperthyroidism: This is a condition where the thyroid gland produces too much thyroid hormone. Symptoms can include weight loss, anxiety, tremors, and an irregular heartbeat.
3. Thyroid nodules: These are abnormal growths on the thyroid gland that can be benign or cancerous.
4. Thyroid cancer: This is a type of cancer that affects the thyroid gland. There are several types of thyroid cancer, including papillary, follicular, and medullary thyroid cancer.
5. Goiter: This is an enlargement of the thyroid gland that can be caused by a variety of factors, including hypothyroidism, hyperthyroidism, and thyroid nodules.
6. Thyrotoxicosis: This is a condition where the thyroid gland produces too much thyroid hormone, leading to symptoms such as weight loss, anxiety, tremors, and an irregular heartbeat.
7. Thyroiditis: This is an inflammation of the thyroid gland that can cause symptoms such as pain, swelling, and difficulty swallowing.
8. Congenital hypothyroidism: This is a condition where a baby is born without a functioning thyroid gland or with a gland that does not produce enough thyroid hormones.
9. Thyroid cancer in children: This is a type of cancer that affects children and teenagers, usually in the form of papillary or follicular thyroid cancer.
10. Thyroid storm: This is a life-threatening condition where the thyroid gland produces an excessive amount of thyroid hormones, leading to symptoms such as fever, rapid heartbeat, and cardiac arrest.
These are just a few examples of the many conditions that can affect the thyroid gland. It's important to be aware of these conditions and seek medical attention if you experience any symptoms or concerns related to your thyroid health.
Causes: Thyroiditis can be caused by a viral or bacterial infection, autoimmune disorders, or radiation exposure.
Symptoms: Symptoms of thyroiditis may include pain and swelling in the neck, difficulty swallowing, hoarseness, fatigue, weight gain, muscle weakness, and depression.
Types: There are several types of thyroiditis, including subacute thyroiditis, silent thyroiditis, and postpartum thyroiditis.
Diagnosis: Thyroiditis is typically diagnosed through a combination of physical examination, blood tests, and imaging studies such as ultrasound or CT scans.
Treatment: Treatment for thyroiditis usually involves antibiotics to treat any underlying infection, pain relief medication to manage neck swelling and discomfort, and hormone replacement therapy to address hormonal imbalances. In some cases, surgery may be necessary to remove part or all of the affected thyroid gland.
Complications: Untreated thyroiditis can lead to complications such as hypothyroidism (underactive thyroid), hyperthyroidism (overactive thyroid), and thyroid nodules or cancer.
Prevention: Preventing thyroiditis is challenging, but maintaining good overall health, avoiding exposure to radiation, and managing any underlying autoimmune disorders can help reduce the risk of developing the condition.
Prognosis: With proper treatment, most people with thyroiditis experience a full recovery and normalization of thyroid function. However, in some cases, long-term hormone replacement therapy may be necessary to manage persistent hypothyroidism or hyperthyroidism.
The hallmark of anti-GBM disease is the presence of circulating anti-GBM antibodies and immune complexes, which are deposited in the glomeruli and lung alveoli, leading to inflammation and tissue damage. The disease can progress rapidly and lead to ESRD if left untreated.
The symptoms of anti-GBM disease vary depending on the severity of the disease and may include:
* Hematuria (blood in urine)
* Proteinuria (excess protein in urine)
* Reduced kidney function
* Weight loss
* Shortness of breath
The diagnosis of anti-GBM disease is based on a combination of clinical findings, laboratory tests, and kidney biopsy. Laboratory tests may include:
* Detection of anti-GBM antibodies in the blood
* Presence of immune complexes in the urine or lung tissue
* Abnormal liver enzymes
* Low complement levels
Treatment of anti-GBM disease typically involves a combination of steroids, immunosuppressive medications, and plasmapheresis (a process that removes harmful antibodies from the blood). In severe cases, kidney transplantation may be necessary. The prognosis for anti-GBM disease is generally poor, with a five-year survival rate of approximately 50%.
There are two main types of Addison's disease: primary and secondary. Primary Addison's disease is caused by an autoimmune disorder that destroys the adrenal glands, while secondary Addison's disease is caused by a problem with the pituitary gland, which regulates the adrenal glands.
Symptoms of Addison's disease can include fatigue, weakness, weight loss, dehydration, and changes in skin color. Treatment involves replacing the missing hormones with medication and managing symptoms. If left untreated, Addison's disease can be life-threatening.
Specialists who may be involved in treating Addison's disease include endocrinologists, primary care physicians, and surgeons. Treatment options can include medication, hydration therapy, and in some cases, surgery to remove the affected adrenal gland(s).
It is important for individuals with Addison's disease to work closely with their healthcare team to manage their condition and avoid complications. With proper treatment and self-management, most people with Addison's disease can lead active and fulfilling lives.
1. Rheumatoid arthritis (RA): An autoimmune disease that causes inflammation in the joints, leading to pain, stiffness, and swelling.
2. Osteoarthritis (OA): A degenerative condition that occurs when the cartilage in the joints wears down over time, causing pain and stiffness.
3. Psoriatic arthritis (PsA): An inflammatory disease that affects both the skin and joints, often occurring in people with psoriasis.
4. Ankylosing spondylitis (AS): A condition that causes inflammation in the spine and peripheral joints, leading to stiffness and pain.
5. Lupus: An autoimmune disease that can affect multiple systems in the body, including the joints, skin, and kidneys.
6. Juvenile idiopathic arthritis (JIA): A condition that affects children under the age of 16, causing inflammation in the joints and potentially leading to long-term complications.
7. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dryness in the eyes and mouth.
8. Fibromyalgia: A condition characterized by widespread pain, fatigue, and sleep disturbances.
9. Gout: A type of inflammatory arthritis caused by excessive levels of uric acid in the blood, leading to sudden and severe attacks of joint pain.
10. Osteoporosis: A condition characterized by brittle bones and an increased risk of fractures, often occurring in older adults.
Rheumatic diseases can be challenging to diagnose and treat, as they often involve complex symptoms and a range of possible causes. However, with the help of rheumatology specialists and advanced diagnostic tools, it is possible to manage these conditions effectively and improve quality of life for patients.
The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:
* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure
Glomerulonephritis can be caused by a variety of factors, including:
* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia
The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.
Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:
* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases
The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.
The primary symptom of PAP is shortness of breath (dyspnea), which can range from mild to severe and may be accompanied by coughing, wheezing, and chest tightness. PAP can also lead to respiratory failure, which can be life-threatening if left untreated.
The diagnosis of PAP is based on a combination of clinical symptoms, physical examination findings, and diagnostic tests such as chest radiographs (X-rays), computed tomography (CT) scans, and lung biopsy. A lung biopsy is the most definitive test for PAP, allowing for the identification of characteristic pathological features such as the accumulation of lipoproteinaceous material within the air spaces of the lungs.
Treatment options for PAP include surgical lung biopsy to obtain a definitive diagnosis and monitor disease progression, chest radiation therapy to reduce symptoms and slow disease progression, and medications such as corticosteroids to modulate the immune system and reduce inflammation. In severe cases, lung transplantation may be necessary.
The prognosis for PAP varies depending on the severity of the disease and response to treatment. With appropriate therapy, many patients with PAP can achieve stabilization of their symptoms and improved lung function. However, some patients may experience recurrent episodes of disease exacerbation and may require long-term management and monitoring.
The symptoms of myasthenia gravis can vary in severity and may include:
* Weakness in the arms and legs
* Fatigue and muscle tiredness
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Drooping eyelids (ptosis)
* Double vision (diplopia)
* Weakness in the muscles of the face, arms, and legs
The exact cause of myasthenia gravis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can also be caused by other medical conditions such as thyroid disease, vitamin deficiencies, or infections.
There is no cure for myasthenia gravis, but there are various treatments available to manage the symptoms and improve quality of life. These include:
* Medications such as corticosteroids, immunosuppressants, and cholinesterase inhibitors
* Plasmapheresis, a procedure that removes harmful antibodies from the blood
* Intravenous immunoglobulin (IVIG), which contains antibodies that can help block the immune system's attack on the nerve-muscle junction
* Surgery to remove the thymus gland, which is believed to play a role in the development of myasthenia gravis
It is important for individuals with myasthenia gravis to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with myasthenia gravis are able to lead active and fulfilling lives.
Acantholysis is caused by a variety of factors, including genetic mutations, autoimmune disorders, and exposure to certain medications or chemicals. It can affect any area of the body, but it most commonly occurs on the skin of the face, neck, and hands.
The symptoms of acantholysis can vary depending on the underlying cause of the condition. Common symptoms include:
* Thin, fragile skin that is prone to tearing or breaking
* Formation of small, flat scars or lesions on the skin
* Skin that is sensitive to touch or pressure
* Redness and inflammation around the affected area
Acantholysis can be diagnosed through a combination of physical examination, medical history, and laboratory tests. Treatment for acantholysis depends on the underlying cause of the condition and may include topical medications, oral medications, or injectable treatments. In severe cases, surgery may be necessary to repair damaged skin tissue.
Preventing acantholysis can be challenging, but there are some steps that can help reduce the risk of developing the condition. These include:
* Avoiding exposure to harsh chemicals or medications
* Protecting the skin from excessive sun exposure and using sunscreen when necessary
* Using gentle skincare products and avoiding scrubbing or rubbing the skin excessively
* Managing underlying medical conditions, such as autoimmune disorders or hormonal imbalances, that can contribute to acantholysis.
Overall, acantholysis is a rare and complex condition that requires careful diagnosis and management to prevent complications and improve quality of life for individuals affected by the condition.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
The exact cause of NMO is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy cells in the body. Genetic and environmental factors may contribute to the development of NMO. The disease is more common in women than men, and typically affects people between the ages of 20 and 50.
The symptoms of NMO can vary widely depending on the location and severity of the inflammation. Common symptoms include:
* Vision loss or blurred vision
* Pain or numbness in the eyes, face, or neck
* Weakness or paralysis of the limbs
* Difficulty walking or maintaining balance
* Bladder or bowel dysfunction
* Fatigue and fever
NMO can be difficult to diagnose, as the symptoms are similar to those of other conditions such as multiple sclerosis. A diagnosis of NMO is typically made based on a combination of clinical findings, laboratory tests, and imaging studies such as MRI or CT scans.
Treatment for NMO typically involves immunosuppressive medications to reduce inflammation and prevent future attacks. In some cases, corticosteroids may be prescribed to reduce swelling in the central nervous system. Plasmapheresis, a process that removes harmful antibodies from the blood, may also be used in some cases. Physical therapy and other supportive measures can help manage the symptoms of NMO and improve quality of life.
Prognosis for NMO varies depending on the severity of the inflammation and the promptness of treatment. In general, early diagnosis and aggressive treatment can lead to a better outcome. However, some individuals with NMO may experience long-term or permanent damage to their optic nerves or other parts of the central nervous system.
There is currently no cure for NMO, but ongoing research is exploring new treatments and therapies that may help improve outcomes for individuals with this condition. With proper treatment and supportive care, many people with NMO are able to manage their symptoms and lead active lives.
The syndrome is typically diagnosed based on the presence of anticardiolipin antibodies (aCL) or lupus anticoagulant in the blood. Treatment for antiphospholipid syndrome may involve medications to prevent blood clots, such as heparin or warfarin, and aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation. In some cases, intravenous immunoglobulin (IVIG) may be given to reduce the levels of antibodies in the blood. Plasmapheresis, a process that removes antibodies from the blood, may also be used in some cases.
Antiphospholipid syndrome is associated with other autoimmune disorders, such as systemic lupus erythematosus (SLE), and may be triggered by certain medications or infections. It is important for individuals with antiphospholipid syndrome to work closely with their healthcare provider to manage their condition and reduce the risk of complications.
The main symptoms of PTI include:
* Purple spots or bruises (purpura) on the skin, which may be caused by minor trauma or injury.
* Thrombocytopenia (low platelet count), typically less than 50,000 platelets/mm3.
* Mild anemia and reticulocytosis (increased immature red blood cells).
* Elevated levels of autoantibodies against platelet membrane glycoproteins (GP) and other platelet proteins.
* No evidence of other causes of thrombocytopenia, such as bone marrow disorders or infections.
The exact cause of PTI is unknown, but it is believed to involve an immune-mediated response triggered by a genetic predisposition. Treatment options for PTI include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy in severe cases. The prognosis for PTI is generally good, with most patients experiencing resolution of symptoms and normalization of platelet counts within a few months to a year after treatment. However, some individuals may experience recurrent episodes of thrombocytopenia and purpura throughout their lives.
The hallmark of Wegener Granulomatosis is the formation of granulomas, which are clusters of immune cells that form in response to infection or inflammation. In this condition, however, the granulomas are not caused by an infectious agent but rather by the body's own immune system attacking its own tissues.
The symptoms of Wegener Granulomatosis can vary depending on the organs affected and can include:
* Joint pain
* Weight loss
* Shortness of breath
* Chest pain
* Coughing up blood
* Abdominal pain
* Blood in urine or stool
The exact cause of Wegener Granulomatosis is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment typically involves the use of corticosteroids and other immunosuppressive medications to reduce inflammation and prevent further damage to the body. In some cases, plasmapheresis (plasma exchange) may also be used to remove harmful antibodies from the blood.
Wegener Granulomatosis is a relatively rare condition, affecting approximately 2-4 people per million each year. It can occur at any age but is most commonly diagnosed in adults between the ages of 40 and 60. With early diagnosis and proper treatment, many people with Wegener Granulomatosis can experience a good outcome and improved quality of life. However, if left untreated, the condition can be fatal.
Symptoms of CNS lupus vasculitis can include headaches, seizures, confusion, weakness or paralysis, vision problems, and changes in personality or behavior. The condition can be difficult to diagnose, as it may mimic other conditions such as stroke, infection, or tumors.
Treatment of CNS lupus vasculitis typically involves high doses of corticosteroids to reduce inflammation and prevent further damage. In severe cases, intravenous immunoglobulin (IVIG) or plasmapheresis may be used to remove harmful antibodies from the blood. Anticoagulation therapy may also be prescribed to prevent blood clots.
While CNS lupus vasculitis can be a life-threatening condition, early diagnosis and aggressive treatment can improve outcomes. However, long-term follow-up is essential to monitor for recurrences of the disease and manage any ongoing neurological symptoms.
The primary symptoms of celiac disease include diarrhea, abdominal pain, fatigue, weight loss, and bloating. However, some people may not experience any symptoms at all, but can still develop complications if the disease is left untreated. These complications can include malnutrition, anemia, osteoporosis, and increased risk of other autoimmune disorders.
The exact cause of celiac disease is unknown, but it is believed to be triggered by a combination of genetic and environmental factors. The disease is more common in people with a family history of celiac disease or other autoimmune disorders. Diagnosis is typically made through a combination of blood tests and intestinal biopsy, and treatment involves a strict gluten-free diet.
Dietary management of celiac disease involves avoiding all sources of gluten, including wheat, barley, rye, and some processed foods that may contain hidden sources of these grains. In some cases, nutritional supplements may be necessary to ensure adequate intake of certain vitamins and minerals.
While there is no known cure for celiac disease, adherence to a strict gluten-free diet can effectively manage the condition and prevent long-term complications. With proper management, people with celiac disease can lead normal, healthy lives.
Adrenergic receptor autoantibodies
Anti-glutamate receptor antibodies
Anti-smooth muscle antibody
Chronic inflammatory demyelinating polyneuropathy
Inflammatory demyelinating diseases of the central nervous system
RAS-associated autoimmune leukoproliferative disorder
Reference ranges for blood tests
Anti-citrullinated protein antibody
Eric John Holborow
Thomas P. Stossel
Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
Researchers Identify the Origin of Subset of Autoantibodies That Worsen Lupus
SSc Autoantibody Identified with Link to GI Dysfunction
Clinical and serological features of patients with autoantibodies to GW/P bodies
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- Rheumatoid arthritis is a systemic, polygenic, and multifactorial syndrome characterized by erosive polyarthritis, damage to joint architecture, and presence of autoantibodies against several self-structures in the serum and synovial fluid. (hindawi.com)
- In this study, Luciferase Immunoprecipitation Systems (LIPS), a fluid phase immunoassay, was used to analyze SS serum autoantibody responses to 12 recombinant autoantigens in a cohort of 17 healthy volunteers and 72 patients with primary SS. (nih.gov)
- High prevalence of serum folate receptor autoantibodies in children with autism spectrum disorders. (blogspot.com)
- Our high-density protein microarray assays and advanced bioinformatics enable highly specific and reproducible detection of disease-relevant autoantibodies directly from patient serum. (sengenics.com)
- IgG autoantibody testing of a subsample of stored serum from phase 1 (1988-91) NHANES III participants was conducted to estimate the prevalence and specificities of selected autoantibodies in the US population. (cdc.gov)
- To compare the participation of desmogleins 1, 2 and 3 through the production of serum autoantibodies, and protein and gene expression in the skin/mucosa of patients with pemphigus foliaceus and pemphigus vulgaris. (anaisdedermatologia.org.br)
- In vitro qualitative detection of autoantibodies against diabetes in human serum provides a reference for the classification, prediction and prevention of diabetes. (szblot.com)
Systemic lupus erythem4
- In an effort to understand the origin of systemic lupus erythematosus and why some patients present with more severe disease than others, Johns Hopkins Medicine researchers say they have identified a type of autoantibody that may worsen the condition and have also found how these autoantibodies originate. (hopkinsmedicine.org)
- Additional testing revealed that certain SS patients were also seropositive for autoantibodies classically associated with other autoimmune conditions, including gastric ATPB (autoimmune gastritis), PDCE2 (primary biliary cirrhosis), RNP-A (systemic lupus erythematosus) and CENP-A (systemic sclerosis) and GAD65 (autoimmune encephalitis). (nih.gov)
- Systemic lupus erythematosus (SLE) is a systemic autoimmune disease which is classically characterised by a variety of autoantibodies to deoxyribonucleic acid (DNA), ribonucleic acid (RNA), other nuclear and cytoplasmic antigens. (openrheumatologyjournal.com)
- Systemic lupus erythematosus, autoantibodies, nucleoporin p62. (openrheumatologyjournal.com)
- McMahan and colleagues then investigated the prevalence of the autoantibody by screening the sera of 188 patients with SSc who presented consecutively to the Johns Hopkins Scleroderma Center between April 2016 and August 2017, as well as 40 controls, and compared GI symptom severity between antibody-positive and antibody-negative patients with SSc. (medscape.com)
- To compare the prevalence of positive autoantibodies in patients with thyroid disorders and healthy subjects in an iodine-replete area of the Islamic Republic of Iran, we studied 930 women in a clinic-based study: 698 patients (286 hypothyroid, 140 hyperthyroid, 272 with simple goitre) and 232 healthy women. (who.int)
- These autoantibodies (anticitrullinated protein/peptide antibodies (ACPAs), rheumatoid factors (RF), anticollagen type II antibodies, antiglucose-6 phosphate isomerase antibodies, anticarbamylated protein antibodies, and antiacetylated protein antibodies) have different characteristics, diagnostic/prognostic value, and pathological significance in RA patients. (hindawi.com)
- Our findings provide a simple explanation for the differences of anti-DNA antibodies in SLE by demonstrating that some of these autoantibodies have multiple functions," says corresponding author Felipe Andrade, M.D., Ph.D. , an associate professor of medicine in the Division of Rheumatology at the Johns Hopkins University School of Medicine. (hopkinsmedicine.org)
- SLE is serologically defined by a variety of autoantibodies including anti-DNA, anti-phospholipid, anti-Sm and other antinuclear antibodies. (openrheumatologyjournal.com)
- Problem: Antiphospholipid autoantibodies (aPL), antithyroid antibodies and anti-extractable nuclear antigens (anti-ENA) have all been reported to be associated with recurrent miscarriages (RM) and infertility. (biu.ac.il)
- Materials and Methods: Fifty-eight women with impaired fertility (38 women with RM and 20 women with infertility, but no miscarriages) and 28 control parous women were screened for seven autoantibodies [antithyroglobulin (aTG), antithyroid peroxidase (aTPO), anticardiolipin (aCL), antiphosphatidyl-serine (aPS), antiprothrombin antibodies (aPT), anti-beta 2 glycoprotein 1 (aβ 2 GP1), and anti-ENA]. (biu.ac.il)
- We hypothesized that autoantibodies against ACE2 may develop after SARS-CoV-2 infection, as anti-idiotypic antibodies to anti-spike protein antibodies . (bvsalud.org)
- Incorporation of these additional serological targets increased the sensitivity of autoantibody testing for SS to ~80% without decreasing specificity. (nih.gov)
- Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in the preclinical phase of type 1 diabetes (T1D). (bris.ac.uk)
- Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, which affects approximately 1% of the world population, and is characterized by autoantibody production, synovial inflammation, cartilage destruction, and bone erosion [ 1 ]. (hindawi.com)
- Specificities of anti-neutrophil autoantibodies in patients with rheumatoid arthritis (RA). (ox.ac.uk)
- Testing of IgG autoantibodies to human cellular antigens was performed by the HEp-2 cell immunofluorescence assay using slides from INOVA Diagnostics, San Diego, CA (Cat # 508100) following the manufacturer's instructions and evaluated primarily using their NOVA View system. (cdc.gov)
- The objective of this study was to characterize antigens recognized by neutrophil-specific autoantibodies from patients with RA. (ox.ac.uk)
- In conclusion, anti-neutrophil autoantibodies from RA patients recognize different antigens in the cytoplasm and in the nucleus. (ox.ac.uk)
- In this review, the diagnostic value of autoantibodies, their synthesis and function as a mediator of joint inflammation, and the significance of IgG-Fc glycosylation are discussed. (hindawi.com)
- We are currently expanding the autoimmune screening panel to include additional autoantigen targets and are determining the clinical significance of autoantibodies to these targets in individual SS cases. (nih.gov)
- The remarkable heterogeneity of autoantibodies observed in SS may represent a personalized diagnostic for SS patients and provides insight into the complex nature of this autoimmune disease. (nih.gov)
- Little is known about the factors that influence autoantibody profiles and the continuation of the autoimmune response post-diagnosis. (bris.ac.uk)
- Background: Autoimmune chronic spontaneous urticaria (aiCSU) is an important sub‐ type of chronic spontaneous urticaria (CSU) in which functional IgG autoantibodies to IgE or its high‐affinity receptor (FcεRI) induces mast cell degranulation and subsequent symptom. (marcus-maurer.com)
- Dr. Mammen and his colleagues at Hopkins discovered a novel form of autoimmune myopathy associated with statin use and autoantibodies recognizing HMG-CoA reductase, the pharmacologic target of statins. (nih.gov)
- Suffice to say these are autoantibodies - where the body mounts an immune response against 'self' - that target a particular protein called folate receptor protein alpha which plays an important role in transporting something called 5-methyltetrahydrofolate (5-MTHF) into the brain. (blogspot.com)
- A new autoantibody marker called neuromyelitis optica immunoglobulin G (NMO-IgG), which targets the water channel protein aquaporin-4, is highly specific for NMO. (elsevier.com)
- Questioning Answers: Folate receptor autoantibodies and autism. (blogspot.com)
- Not only that, they represent scientific replication covering an increasingly important issue in relation to [some] autism: a possible role for folate receptor autoantibodies (FRAA) . (blogspot.com)
- In short, folate receptor autoantibodies are probably important to at least some autism. (blogspot.com)
- Folate receptor autoantibodies are prevalent in children diagnosed with autism spectrum disorder, their normal siblings and parents. (blogspot.com)
- High milk consumers have an increased risk of folate receptor blocking autoantibody production but this does not affect folate status in Spanish men and women. (blogspot.com)
- Ultimately, the detection of IFN-γ autoantibodies in high levels explained these abnormalities. (cdc.gov)
- In addition, autoantibodies are proven to be useful disease markers for RA, and different diagnostic tools are being developed for early diagnosis of the clinical disease. (hindawi.com)
- Background: The anti-DFS70 autoantibodies are one of the most commonly and widely described agent of unknown clinical significance, frequently detected in healthy individuals. (ljmu.ac.uk)
- Our solutions enable the discovery and validation of autoantibody biomarker signatures for patient stratification, therapeutic response prediction and development of companion diagnostics. (sengenics.com)
- The interferon- γ (IFN-γ)/interleukin-12 (IL-12) axis is a critical pathway for intracellular killing of mycobacteria ( Technical Appendix Figure) ( 1 ).We report a case of disseminated NTM infection in a woman from Laos who showed IFN-γ autoantibodies. (cdc.gov)
- Specific treatment for IFN-γ autoantibodies-associated NTM infection is not codified and required prolonged, multiple-drug regimens. (cdc.gov)
- Development of ACE2 autoantibodies after SARS-CoV-2 infection. (bvsalud.org)
- 2) elucidating the role of myositis autoantibodies in the pathogenesis of myositis. (nih.gov)
- Graphs showing difference between normalized RFUs in 8 autoantibodies that were significantly elevated in cases (H. pylori seropositive PD patients, n=30) versus controls (H. pylori sero-negative PD patients, n=30). (sengenics.com)
- It is not known whether the DFS70 autoantibodies are protective or pathogenic. (ljmu.ac.uk)
- A large number of studies have found that abnormally increased immune cells (T cells, B cells, macrophages, and neutrophils) and immune molecules (cytokines, autoantibodies, and heat shock proteins) are present in the synovial tissue and fluid of RA patients, which suggest that the release or activation of them may be involved in the initiation and perpetuation of RA. (hindawi.com)
- Anti-gephyrin autoantibodies have been tied to lower gastrointestinal (GI) dysfunction, such as severe constipation and distention, in patients with systemic sclerosis (SSc), new research suggests. (medscape.com)
- Afin de comparer la prévalence des autoanticorps positifs chez les patients atteints de troubles thyroïdiens et chez des sujets en bonne santé dans une région riche en iode de la République islamique d'Iran, nous avons effectué une étude clinique sur 930 femmes : 698 patientes (286 hypothyroïdiennes, 140 hyperthyroïdiennes et 272 présentant un goitre simple) et 232 femmes en bonne santé. (who.int)
- 2016) Augmentation of Autoantibodies by Helicobacter pylori in Parkinson's Disease Patients May Be Linked to Greater Severity. (sengenics.com)
- The autoantibodies were titrated by ELISA in 202 samples of pemphigus foliaceus, 131 pemphigus vulgaris, 50 and 57 relatives of patients with pemphigus foliaceus and pemphigus vulgaris, respectively, and 114 controls. (anaisdedermatologia.org.br)
- The phenotype of myositis patients with anti-Ku autoantibodies. (nih.gov)
- Among those elevated were autoantibodies that recognize Nuclear factor I subtype A (NFIA), Platelet-derived growth factor B (PDGFB) and Eukaryotic translation initiation factor 4A3 (eIFA3) - all proteins involved in normal neurological function. (sengenics.com)
- Recently several novel autoantibodies against a variety of specific nuclear pore proteins have been described, including the nucleoporin p62. (openrheumatologyjournal.com)
- The determination of autoantibody titers from 1:80 to 1:1280 was performed by serial dilution on samples that showed a 3+ or greater nuclear and/or cytoplasmic immunofluorescence pattern. (cdc.gov)
- Various genetic and environmental factors are associated with autoantibody production against different autoantigenic targets. (hindawi.com)
- Only C3 NeF type II were found to be associated with circulating autoantibodies to the collagenous region of C1q (aC1qCLR). (avhandlingar.se)
- A significant association was found between RM, and autoantibodies in the 'aTG + aTPO + anti-ENA' or 'aTG + aTPO' panels. (biu.ac.il)
- Autoantibodies were found. (medlineplus.gov)
- She tested negative for hepatitis markers and for autoantibodies. (nih.gov)
- I and II) Autoantibodies to the C3 cleaving enzyme complex of the alternative pathway, C3 nephritic factors (C3 NeF), cause partial C3 deficiency and are associated with increased susceptibility to bacterial infections. (avhandlingar.se)
- Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish TEDDY Children at Increased Risk for Type 1 Diabetes. (arctichealth.org)
- AVHANDLINGAR.SE: Complement aberrations and autoantibodies to complement proteins in relation to disease mechanisms. (avhandlingar.se)
- This acquired autoantibodies-mediated immunodeficiency is more frequent among women, in whom the disease typically manifests in the second half of adult life (median 48 [IQR 44.8-60.0] years of age). (cdc.gov)
- Anti-mitochondrial autoantibodies are associated with cardiomyopathy, dysphagia, and features of more severe disease in adult-onset myositis. (nih.gov)
- Conclusions: RM was associated with autoantibodies to aTPO and the combined panel of aTPO, aTG and anti-ENA, but not with aPL. (biu.ac.il)
- IFN-γ autoantibodies remained positive at the time of this report, 2 years after azithromycin initiation. (cdc.gov)
- That patient had GI dysfunction but no defined SSc-associated autoantibodies. (medscape.com)