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Pernicious anemia (also known as Biermer's anemia, Addison's anemia, or Addison–Biermer anemia) is one of many types of the larger family of megaloblastic anemias. It is caused by loss of gastric parietal cells which are responsible, in part, for the secretion of intrinsic factor, a protein essential for subsequent absorption of vitamin B12 in the ileum.
Usually seated in an atrophic gastritis, the autoimmune destruction of gastric parietal cells (and autoantibody inactivation of intrinsic factor) leads to a lack of intrinsic factor. Since the absorption from the gut of normal dietary amounts of vitamin B12 is dependent on intrinsic factor, the loss of intrinsic factor leads to vitamin B12 deficiency. While the term 'pernicious anemia' is sometimes also incorrectly used to indicate megaloblastic anemia due to 'any' cause of vitamin B12 deficiency, its proper usage refers to that caused by atrophic gastritis, parietal cell loss, and lack of intrinsic factor only.
The loss of ability to absorb vitamin B12 (B12) is the most common cause of adult B12 deficiency. Such a loss may be due to pernicious anemia (with loss of intrinsic factor) or to a number of other conditions that decrease
Myasthenia gravis (from Greek μύς "muscle", ἀσθένεια "weakness", and Latin: gravis "serious"; abbreviated MG) is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors throughout neuromuscular junctions. Myasthenia is treated medically with acetylcholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. The disease incidence is 3–30 cases per million per year and rising as a result of increased awareness. MG must be distinguished from congenital myasthenic syndromes that can present similar symptoms but offer no response to immunosuppressive treatments.
The most widely accepted classification of myasthenia gravis is the Myasthenia Gravis Foundation of America Clinical Classification:
The hallmark of myasthenia gravis is fatigability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and
Systemic lupus erythematosus (/sɪˈstɛmɪk ˈluːpəs ˌɛrɪθiːməˈtoʊsəs/), often abbreviated to SLE or lupus, is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body. As occurs in other autoimmune diseases, the immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage. It is a Type III hypersensitivity reaction caused by antibody-immune complex formation.
SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. The disease occurs nine times more often in women than in men, especially in women in child-bearing years ages 15 to 35, and is also more common in those of non-European descent.
SLE is treatable using immunosuppression, mainly with cyclophosphamide, corticosteroids and other immunosuppressants; there is currently no cure. SLE can be fatal, although with recent medical advances, fatalities are becoming increasingly rare. Survival for people with SLE in the United States, Canada, and Europe has risen to approximately 95% at five
Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks flexible (synovial) joints. The process involves an inflammatory response of the capsule around the joints (synovium) secondary to swelling (hyperplasia) of synovial cells, excess synovial fluid, and the development of fibrous tissue (pannus) in the synovium. The pathology of the disease process often leads to the destruction of articular cartilage and ankylosis (fusion) of the joints. Rheumatoid arthritis can also produce diffuse inflammation in the lungs, membrane around the heart (pericardium), the membranes of the lung (pleura), and white of the eye (sclera), and also nodular lesions, most common in subcutaneous tissue. Although the cause of rheumatoid arthritis is unknown, autoimmunity plays a pivotal role in both its chronicity and progression, and RA is considered a systemic autoimmune disease.
About 1% of the world's population is afflicted by rheumatoid arthritis, women three times more often than men. Onset is most frequent between the ages of 40 and 50, but people of any age can be affected. In addition, individuals with the HLA-DR1 or
Autoimmune Hepatitis is a disease of the liver that occurs when the body's immune system attacks cells of the liver. Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes, possibly due to genetic predisposition or acute liver infection, causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis. This abnormal immune response results in inflammation of the liver, which can lead to further complications, including cirrhosis.
Autoimmune hepatitis has an incidence of 1-2 per 100,000 per year, and a prevalence of 10-20/100,000. As with most other autoimmune diseases, it affects women much more often than men (70%). Liver enzymes are elevated, as may be bilirubin.
The patient is classically a young female. They may present with signs of chronic liver disease (cirrhosis, low albumin, spider nivae etc.) or acute hepatitis (25% present with fever, jaundice, painful hepatomegaly etc.). Commonly, the patient will have amenorrhoea - this may be the presenting complaint.
Four subtypes are recognised, but the clinical utility of distinguishing subtypes is limited.
The diagnosis of autoimmune hepatitis is best
Graves' disease is an autoimmune disease where the thyroid is overactive, producing an excessive amount of thyroid hormones (a serious metabolic imbalance known as hyperthyroidism and thyrotoxicosis). This is caused by thyroid autoantibodies that activate the TSH-receptor, thereby stimulating thyroid hormone synthesis and secretion, and thyroid growth (causing a diffusely enlarged goiter). The resulting state of hyperthyroidism can cause a dramatic constellation of neuropsychological and physical signs and symptoms.
Graves' disease is the most common cause of hyperthyroidism (60-90% of all cases), and usually presents itself during midlife, but also appears in children, adolescents, and the elderly. It has a powerful hereditary component, affects up to 2% of the female population, and is between five and ten times as common in females as in males. Graves’ disease is also the most common cause of severe hyperthyroidism, which is accompanied by more clinical signs and symptoms and laboratory abnormalities as compared with milder forms of hyperthyroidism. About 30-50% of people with Graves' disease will also suffer from Graves' ophthalmopathy (a protrusion of one or both eyes),
Multiple sclerosis (MS), also known as "disseminated sclerosis" or "encephalomyelitis disseminata", is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms. Disease onset usually occurs in young adults, and it is more common in women. It has a prevalence that ranges between 2 and 150 per 100,000. MS was first described in 1868 by Jean-Martin Charcot.
MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other effectively. Nerve cells communicate by sending electrical signals called action potentials down long fibers called axons, which are contained within an insulating substance called myelin. In MS, the body's own immune system attacks and damages the myelin. When myelin is lost, the axons can no longer effectively conduct signals. The name multiple sclerosis refers to scars (scleroses—better known as plaques or lesions) particularly in the white matter of the brain and spinal cord, which is mainly composed of myelin. Although much is known about the mechanisms involved in the disease process,
Goodpasture’s syndrome (also known as Goodpasture’s disease and anti-glomerular basement antibody disease) is a rare autoimmune disease in which antibodies attack the lungs and kidneys, leading to bleeding from the lungs and to kidney failure. It may quickly result in permanent lung and kidney damage, often leading to death. It is treated with immunosuppressant drugs such as corticosteroids and cyclophosphamide, and with plasmapheresis, in which the antibodies are removed from the blood.
The specific target of the immune attack is the GBM antigen, which is found in the lungs and kidneys. The antigen is a component of the non-collagenous 1 (NC1) domain of the alpha-3 chain of type IV collagen in the glomerular basement membrane.
Goodpasture's syndrome is a type II hypersensitivity reaction.
The disease was first reported by the American pathologist Ernest Goodpasture of Vanderbilt University, in 1919.
Goodpasture’s syndrome can cause people to cough up blood or feel a burning sensation when urinating. But its first signs may be vague, such as fatigue, nausea, difficulty breathing, or skin pallor. These signs are followed by kidney involvement, represented first by small amounts of
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the occurrence of chronic bronchitis or emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD.
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung.
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.
Worldwide, COPD ranked as the
Cholera is an infection in the small intestine caused by the bacterium Vibrio cholerae. The main symptoms are profuse, watery diarrhea and vomiting. Transmission occurs primarily by drinking water or eating food that has been contaminated by the feces of an infected person, including one with no apparent symptoms. The severity of the diarrhea and vomiting can lead to rapid dehydration and electrolyte imbalance, and death in some cases. The primary treatment is oral rehydration therapy, typically with oral rehydration solution (ORS), to replace water and electrolytes. If this is not tolerated or does not provide improvement fast enough, intravenous fluids can also be used. Antibacterial drugs are beneficial in those with severe disease to shorten its duration and severity. Worldwide, it affects 3–5 million people and causes 100,000–130,000 deaths a year as of 2010. Cholera was one of the earliest infections to be studied by epidemiological methods.
The primary symptoms of cholera are profuse, painless diarrhea and vomiting of clear fluid. These symptoms usually start suddenly, one to five days after ingestion of the bacteria. The diarrhea is frequently described as "rice water" in
Acute disseminated encephalomyelitis (ADEM) is an immune mediated disease of the brain. It usually occurs following a viral infection but may appear following vaccination (although there is no causal evidence linking vaccination to ADEM), bacterial or parasitic infection, or even appear spontaneously. As it involves autoimmune demyelination, it is similar to multiple sclerosis, and is considered part of the Multiple sclerosis borderline diseases. The incidence rate is about 8 per 1,000,000 people per year. Although it occurs in all ages, most reported cases are in children and adolescents, with the average age around 5 to 8 years old. The mortality rate may be as high as 5%, full recovery is seen in 50 to 75% of cases, while up to 70 to 90% recover with some minor residual disability. The average time to recover is one to six months.
ADEM produces multiple inflammatory lesions in the brain and spinal cord, particularly in the white matter. Usually these are found in the subcortical and central white matter and cortical gray-white junction of both cerebral hemispheres, cerebellum, brainstem, and spinal cord, but periventricular white matter and gray matter of the cortex, thalami and
Idiopathic thrombocytopenic purpura (ITP) is the condition of having an abnormally low platelet count (thrombocytopenia) of unknown cause (idiopathic). As most incidents of ITP appear to be related to the production of antibodies against platelets, immune thrombocytopenic purpura or immune thrombocytopenia are terms also used to describe this condition. Often ITP is asymptomatic (devoid of obvious symptoms) and can be discovered incidentally, but a very low platelet count can lead to an increased risk of bleeding and purpura.
ITP is diagnosed with a complete blood count (a common blood test). In some situations, additional investigations (such as a bone marrow biopsy) may be necessary to ensure that the platelet count is not decreased due to other reasons. Treatment may not be necessary in mild cases, but very low counts or significant bleeding might prompt treatment with steroids, intravenous immunoglobulin, anti-D immunoglobulin, or stronger immunosuppressive drugs. Refractory ITP (ITP not responsive to conventional treatment) may require splenectomy, the surgical removal of the spleen. Platelet transfusions may be used in severe bleeding together with a very low count. Sometimes
Chagas disease ( /ˈʃɑːɡəs/; Portuguese: doença de Chagas, [duˈẽsɐ dʒi ˈʃagɐʃ], Spanish: enfermedad de Chagas-Mazza, [ẽ̞ɱfe̞rme̞ˈð̞að̞ːe̞ ˈtʃaɣ̞az ˈmatsa], mal de Chagas in both languages; also called American trypanosomiasis) is a tropical parasitic disease caused by the flagellate protozoan Trypanosoma cruzi. T. cruzi is commonly transmitted to humans and other mammals by an insect vector, the blood-sucking "kissing bugs" of the subfamily Triatominae (family Reduviidae) most commonly species belonging to the Triatoma, Rhodnius, and Panstrongylus genera.
The disease may also be spread through blood transfusion and organ transplantation, ingestion of food contaminated with parasites, and from a mother to her fetus.
The symptoms of Chagas disease vary over the course of an infection. In the early, acute stage, symptoms are mild and usually produce no more than local swelling at the site of infection. The initial acute phase is responsive to antiparasitic treatments, with 60–90% cure rates. After 4–8 weeks, individuals with active infections enter the chronic phase of Chagas disease that is asymptomatic for 60–80% of chronically infected individuals through their lifetime.
Sjögren's syndrome (pronounced /ˈʃoʊɡrɨnz/ SHOH-grinz in English), also known as "Sicca syndrome", is a systemic autoimmune disease in which immune cells attack and destroy the exocrine glands that produce tears and saliva.
It is named after Swedish ophthalmologist Henrik Sjögren (1899–1986), who first described it.
Nine out of ten Sjögren's patients are women and the average age of onset is after menopause in women, although Sjögren's occurs in all age groups in both women and men. It is estimated to affect as many as 4 million people in the United States alone, making it the second most common autoimmune rheumatic disease.
Sjögren's syndrome can exist as a disorder in its own right (primary Sjögren's syndrome) or may develop years after the onset of an associated rheumatic disorder, such as rheumatoid arthritis, systemic lupus erythematosus, scleroderma, primary biliary cirrhosis etc. (secondary Sjögren's syndrome).
The disorder should not be confused with the Sjögren–Larsson syndrome, which was also denoted T. Sjögren syndrome in early studies. It shares clinical features with, and is sometimes concurrent with benign lymphoepithelial lesion or Mikulicz disease. They are,
Primary biliary cirrhosis, often abbreviated PBC, is an autoimmune disease of the liver marked by the slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. When these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the tissue. This can lead to scarring, fibrosis and cirrhosis. It was previously thought to be a rare disease, but more recent studies have shown that it may affect up to 1 in 3–4,000 people; the sex ratio is at least 9:1 (female to male).
Individuals with PBC may present with the following:
To diagnose PBC, distinctions should be established from other conditions with similar symptoms, such as autoimmune hepatitis or primary sclerosing cholangitis (PSC).
Diagnostic blood tests include:
Abdominal ultrasound or a CT scan is usually performed to rule out blockage to the bile ducts. Previously most suspected sufferers underwent a liver biopsy, and — if uncertainty remained — endoscopic retrograde cholangiopancreatography (ERCP, an endoscopic investigation of the bile duct). Now most patients are diagnosed without invasive investigation since the combination of anti-mitochondrial antibodies (see below) and
Pemphigus ( /ˈpɛmfɪɡəs/ or /pɛmˈfaɪɡəs/) is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes.
In pemphigus, autoantibodies form against desmoglein. Desmoglein forms the "glue" that attaches adjacent epidermal cells via attachment points called desmosomes. When autoantibodies attack desmogleins, the cells become separated from each other and the epidermis becomes "unglued", a phenomenon called acantholysis. This causes blisters that slough off and turn into sores. In some cases, these blisters can cover a significant area of the skin.
Originally, the cause of this disease was unknown, and "pemphigus" was used to refer to any blistering disease of the skin and mucosa. In 1964, a historic paper that changed the understanding of pemphigus was published. In 1971, an article investigating the autoimmune nature of this disease was published.
There are three types of pemphigus which vary in severity: pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus.
Note that Hailey-Hailey disease, also called familial benign pemphigus, is an inherited (genetic) skin disease, not an autoimmune disease. It is therefore not considered part of the
Vasculitis (plural: vasculitides) refers to a heterogeneous group of disorders that are characterized by inflammatory destruction of blood vessels. Both arteries and veins are affected. Lymphangitis is sometimes considered a type of vasculitis. Vasculitis is primarily due to leukocyte migration and resultant damage.
Although both occur in vasculitis, inflammation of veins (phlebitis) or arteries (arteritis) on their own are separate entities.
There are many ways to classify vasculitis.
According to the size of the vessel affected, vasculitis can be classified into:
Some disorders have vasculitis as their main feature. The major types are given in the table below:
Takayasu's arteritis, polyarteritis nodosa and giant cell arteritis mainly involve arteries and are thus sometimes classed specifically under arteritis.
Furthermore, there are many conditions that have vasculitis as an accompanying or atypical symptom, including:
Possible symptoms include:
Treatments are generally directed toward stopping the inflammation and suppressing the immune system. Typically, cortisone-related medications, such as prednisone, are used. Additionally, other immune suppression drugs, such as
Ankylosing spondylitis (AS, from Greek ankylos, stiff; spondylos, vertebrae), previously known as Bekhterev's disease, Bekhterev syndrome, and Marie-Strümpell disease, is a chronic inflammatory disease of the axial skeleton with variable involvement of peripheral joints and nonarticular structures. AS is a form of spondyloarthritis, a chronic, inflammatory arthritis where immune mechanisms are thought to have a key role. It mainly affects joints in the spine and the sacroiliac joint in the pelvis, and can cause eventual fusion of the spine.
It is a member of the group of the spondyloarthropathies with a strong genetic predisposition. Complete fusion results in a complete rigidity of the spine, a condition known as "bamboo spine". As of 2012, no cure is known for AS, although treatments and medications are available to reduce symptoms and pain.
AS has been suggested as the first recognized disease, having been distinguished from rheumatoid arthritis by Galen as early as the second century A.D.; however, skeletal evidence of the disease (ossification of joints and entheses primarily of the axial skeleton, known as "bamboo spine") was first discovered in an archaeological dig that
Antiphospholipid syndrome or antiphospholipid antibody syndrome (APS or APLS or), often also Hughes syndrome, is an autoimmune, hypercoagulable state caused by antibodies against cell-membrane phospholipids that provokes blood clots (thrombosis) in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, or severe preeclampsia. The syndrome occurs due to the autoimmune production of antibodies against phospholipid (aPL), a cell membrane substance. In particular, the disease is characterised by antibodies against cardiolipin (anti-cardiolipin antibodies) and β2 glycoprotein I. The term "primary antiphospholipid syndrome" is used when APS occurs in the absence of any other related disease. APS however also occurs in the context of other autoimmune diseases, such as systemic lupus erythematosus (SLE), in which case the term "secondary antiphospholipid syndrome" is used. In rare cases, APS leads to rapid organ failure due to generalised thrombosis; this is termed "catastrophic antiphospholipid syndrome" (CAPS) and is associated with a high risk of death.
Antiphospholipid syndrome is diagnosed with blood tests. It often
In medicine, mixed connective tissue disease (also known as Sharp's syndrome), commonly abbreviated as MCTD, is an autoimmune disease, in which the body's defense system attacks itself. It was characterized in 1972.
It is sometimes equated with the term "Undifferentiated connective tissue disease",) but some sources specifically reject such assertions of equivalence. The term was introduced by Leroy in 1980.
MCTD combines features of scleroderma, myositis, systemic lupus erythematosus, and rheumatoid arthritis (with some sources adding polymyositis, dermatomyositis, and inclusion body myositis) and is thus considered an overlap syndrome.
MCTD commonly causes:
Distinguishing laboratory characteristics are a positive, speckled anti-nuclear antibody and an anti-U1-RNP antibody.
It has been associated with HLA-DR4.
The prognosis for MCTD tends to be better than other autoimmune diseases due to lack of renal disease and response to corticosteroids.
Addison’s disease (also chronic adrenal insufficiency, hypocortisolism, and hypoadrenalism) is a rare, chronic endocrine disorder in which the adrenal glands do not produce sufficient steroid hormones (glucocorticoids and often mineralocorticoids). It is characterised by a number of relatively nonspecific symptoms, such as abdominal pain and weakness, but under certain circumstances, these may progress to Addisonian crisis, a severe illness which may include very low blood pressure and coma.
The condition arises from problems with the adrenal gland itself, a state referred to as "primary adrenal insufficiency," and can be caused by damage by the body's own immune system, certain infections or various rarer causes. Addison's disease is also known as chronic primary adrenocortical insufficiency, to distinguish it from acute primary adrenocortical insufficiency, most often caused by Waterhouse-Friderichsen syndrome. Addison's disease should also be distinguished from secondary and tertiary adrenal insufficiency, which are caused by deficiency of ACTH (produced by the pituitary gland) and CRH (produced by the hypothalamus), respectively. Despite this distinction, Addisonian crises can
Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes. It was the first disease to be recognized as an autoimmune disease. It was first described by the Japanese specialist Hakaru Hashimoto in Germany in 1912.
Hashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism. Symptoms of Hashimoto's thyroiditis include Myxedematous psychosis, weight gain, depression, mania, sensitivity to heat and cold, paresthesia, fatigue, panic attacks, bradycardia, tachycardia, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, cramps, memory loss, infertility and hair loss.
The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by
Autoimmune inner ear disease is a suspected autoimmune disease characterized by rapidly progressive bilateral sensorineural hearing loss. It occurs when the body's immune system attacks cells in the inner ear that are mistaken for a virus or bacteria. Autoimmune inner ear disease was first described by Dr. Brian McCabe of the University of Iowa in 1979.
AIED is generally caused by either antibodies or immune cells that cause damage to the inner ear. There are several autoimmune disorders to which AIED is related:
Research has found that long term abuse of opiate-based painkillers (such as OxyContin and Hydrocodone) can lead to profound hearing loss caused by damage to the inner ear, according to Dr. Gail Ishiyama, an assistant professor at the UCLA department of neurology.
AIED treatment is a rapidly changing field. Steroids are often used in the treatment of AIED, as well as cytotoxic agents such as Cyclophosphamide and Methotrexate.
More recently, in order to avoid many of the side effects of steroids, alternative medications and surgical procedures are used. Since these change quite frequently, it is a good idea to check many sources in locating the most cutting-edge procedure
Bullous pemphigoid is an acute or chronic autoimmune skin disease, involving the formation of blisters, more appropriately known as bullae, at the space between the skin layers epidermis and dermis. It is classified as a type II hypersensitivity reaction.
Clinically, the earliest lesions may appear urticarial (like hives). Tense bullae eventually erupt, most commonly at the inner thighs and upper arms, but the trunk and extremities are frequently both involved. Any part of the skin surface can be involved. Oral lesions are present in a minority of cases. The disease may be acute, but typically will wax and wane. Several other skin diseases may have similar symptoms. However, milia are more common with epidermolysis bullosa acquisita, because of the deeper antigenic targets. A more ring-like configuration, with a central depression or centrally collapsed bullae may indicate linear IgA disease.
Very rarely seen in children, bullous pemphigoid most comonly occurs in people 70 years of age and older. Estimated frequency is seven to 14 cases per million per year, but has been reported to be as high as 472 cases per million per year in Scottish men older than 85. At least one study
Diabetes mellitus type 1 (type 1 diabetes, T1DM, formerly insulin dependent or juvenile diabetes) is a form of diabetes mellitus that results from autoimmune destruction of insulin-producing beta cells of the pancreas. The subsequent lack of insulin leads to increased blood and urine glucose. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.
Incidence varies from 8 to 17 per 100,000 in Northern Europe and the U.S., with a high of about 35 per 100,000 in Scandinavia, to a low of 1 per 100,000 in Japan and China.
Eventually, type 1 diabetes is fatal unless treated with insulin. Injection is the most common method of administering insulin; other methods are insulin pumps and inhaled insulin. Pancreatic transplants have been used. Pancreatic islet cell transplantation is experimental, though growing.
Most people who develop type 1 are otherwise healthy. Although the cause of type 1 diabetes is still not fully understood, it is believed to be of immunological origin.
Type 1 can be distinguished from type 2 diabetes via a C-peptide assay, which measures endogenous insulin production.
Type 1 treatment
Cancer /ˈkænsər/, known medically as a malignant neoplasm, is a broad group of various diseases, all involving unregulated cell growth. In cancer, cells divide and grow uncontrollably, forming malignant tumors, and invade nearby parts of the body. The cancer may also spread to more distant parts of the body through the lymphatic system or bloodstream. Not all tumors are cancerous. Benign tumors do not grow uncontrollably, do not invade neighboring tissues, and do not spread throughout the body. There are over 200 different known cancers that afflict humans.
Determining what causes cancer is complex. Many things are known to increase the risk of cancer, including tobacco use, certain infections, radiation, lack of physical activity, obesity, and environmental pollutants. These can directly damage genes or combine with existing genetic faults within cells to cause the disease. Approximately five to ten percent of cancers are entirely hereditary.
Cancer can be detected in a number of ways, including the presence of certain signs and symptoms, screening tests, or medical imaging. Once a possible cancer is detected it is diagnosed by microscopic examination of a tissue sample. Cancer is
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration. The lifetime of the RBCs is reduced from the normal 100–120 days to just a few days in serious cases. The intracellular components of the RBCs are released into the circulating blood and into tissues, leading to some of the characteristic symptoms of this condition. The antibodies are usually directed against high-incidence antigens, therefore they also commonly act on allogenic RBCs (RBCs originating from outside the person themselves, e.g. in the case of a blood transfusion) AIHA is a relatively rare condition, affecting one to three people per 100,000 per year.
The terminology used in this disease is somewhat ambiguous. Although MeSH uses the term "autoimmune hemolytic anemia", some sources prefer the term "immunohemolytic anemia" so drug reactions can be included in this category. The National Cancer Institute considers "immunohemolytic anemia", "autoimmune hemolytic anemia", and "immune complex hemolytic anemia" to all be synonyms.
AIHA is classified as
Coeliac disease ( /ˈsiːli.æk/; spelled celiac disease in North America and often celiac sprue) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy onward. Symptoms include chronic diarrhoea, failure to thrive (in children), and fatigue, but these may be absent, and symptoms in other organ systems have been described.
Increasingly, diagnoses are being made in asymptomatic persons as a result of increased screening; the condition is thought to affect between 1 in 1,750 and 1 in 105 people in the United States. Coeliac disease is caused by a reaction to gliadin, a prolamin (gluten protein) found in wheat, and similar proteins found in the crops of the tribe Triticeae (which includes other common grains such as barley and rye).
Upon exposure to gliadin, and specifically to three peptides found in prolamins, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the small-bowel tissue, causing an inflammatory reaction. That leads to a truncating of the villi lining the small intestine (called villous atrophy). This interferes with the absorption of nutrients, because the
Guillain–Barré syndrome (GBS) (French pronunciation: [ɡiˈlɛ̃ baˈʁe], English pronunciation: /ˈɡiːlænˈbɑreɪ/), sometimes Landry's paralysis or Guillain–Barré–Strohl syndrome, is an acute polyneuropathy, a disorder affecting the peripheral nervous system. Ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk, is the most typical symptom, and some subtypes cause change in sensation or pain as well as dysfunction of the autonomic nervous system. It can cause life-threatening complications, in particular if the respiratory muscles are affected or if there is autonomic nervous system involvement. The disease is usually triggered by an infection.
The diagnosis is usually made by nerve conduction studies and with studies of the cerebrospinal fluid. With prompt treatment by intravenous immunoglobulins or plasmapheresis, together with supportive care, the majority will recover completely. Guillain–Barré syndrome is rare, at 1–2 cases per 100,000 people annually, but is the most common cause of acute non-trauma-related paralysis in the world. The syndrome is named after the French physicians Georges Guillain and Jean Alexandre Barré, who described it in
Polymyositis (PM)("inflammation of many muscles") is a type of chronic inflammation of the muscles (inflammatory myopathy) related to dermatomyositis and inclusion body myositis.
Symptoms include pain, with marked weakness and/or loss of muscle mass in the proximal musculature, particularly in the shoulder and pelvic girdle. The hip extensors are often severely affected, leading to particular difficulty in ascending stairs and rising from a seated position. Thickening of the skin on the fingers and hands (sclerodactyly) is a frequent feature, although this is non-specific and occurs in other autoimmune connective tissue disorders. Dysphagia (difficulty swallowing) and/or other aspects of oesophageal dysmotility occur in as many as 1/3 of patients. Low grade fever and peripheral adenopathy may be present. Foot drop in one or both feet can be a symptom of advanced polymyositis and inclusion body myositis. Polymyositis is also associated with interstitial lung diseases.
Polymyositis is linked to an increase in the occurrence of certain cancers (particularly Non-Hodgkin lymphoma, lung and bladder cancers), but the overall association is weaker than in the related condition
Wegener's granulomatosis (WG), more recently granulomatosis with polyangiitis (Wegener's) (GPA), is an incurable form of vasculitis (inflammation of blood vessels) that affects the nose, lungs, kidneys, and other organs. Due to its end-organ damage, it is life-threatening and requires long-term immunosuppression. Five-year survival is up to 87%, with some of the mortality due to toxicity of treatment. It is named after Dr. Friedrich Wegener, who described the disease in 1936. In 2011, three professional bodies proposed a more descriptive name.
Wegener's granulomatosis is part of a larger group of vasculitic syndromes, all of which feature an autoimmune attack by an abnormal type of circulating antibody termed ANCAs (antineutrophil cytoplasmic antibodies) against small and medium-size blood vessels. Apart from Wegener's, this category includes Churg–Strauss syndrome and microscopic polyangiitis. Although Wegener's granulomatosis affects small and medium-sized vessels, it is formally classified as one of the small vessel vasculitides in the Chapel Hill system.
Initial signs are extremely variable, and diagnosis can be severely delayed due to the nonspecific nature of the symptoms.