Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoimmune inner ear disease is an uncommon but distinct clinical entity. Our ignorance of the immune mediating pathways, need of further animal model experimentation, variability of laboratory test results and of patient treatment responses illustrate how poorly we understand this disorder. The purpose of this review is to compare practical vs theoretical management of autoimmune inner ear disease, based upon our current knowledge of the disease process and upon a review of clinical experience at the Cleveland Clinic Foundation. Representative case histories are presented. The following preliminary conclusions are discussed: Autoimmune inner ear disease can present as a systemic or localized otologic immune disorder. Hearing loss can begin at any age, with unilateral or bilateral sudden onset, fluctuating or progressive symptoms, with or without associated dizziness. The pathogenesis of autoimmune inner ear disease is probably multifactorial (cellular and humoral). The sensitivity and specificity of different laboratory tests vary greatly, but even the most sensitive tests may be falsely normal when symptoms are not acute or when the patient is taking immunosuppressant medication. The mainstay of autoimmune inner ear treatment is steroids: however, cytotoxic drugs are recommended when there is no response to steroid treatment. Apheresis is reserved for selected cases. Hearing improvement can be dramatic even after 2 months of profound deafness. Flare-ups of autoimmune ear disease are best managed by increasing steroid dosage or adding cytotoxic medications. Unfortunately, some patients will develop progressive hearing loss despite vigorous treatment.
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PMID:Practical versus theoretical management of autoimmune inner ear disease. 637 41

The association between macroamylasaemia and coeliac disease in Down syndrome with multiple autoimmune abnormalities has never been reported. A 40-year-old woman with a 15-year history of immunoglobulin A and immunoglobulin M hypergammaglobulinaemia, chronic diarrhoea, persistent mild aspartate aminotransferase (AST) elevation and anaemic syndrome was admitted to hospital because in the previous 3 months she had developed amenorrhoea, dizziness, alopecia, constipation, pallor and asthenia. Biochemical and immunological analyses showed macroamylasaemia. The patient presented clinical and intestinal histopathological features of coeliac disease. Immunological abnormalities included the presence of antigliadin, antiendomysium, antitransglutaminase, antinuclear, antismooth muscle and anti-SSA/Ro antibodies. Macroamylase resulted in a complex of amylase and immunoglobulin A. Later clinical follow-up of a gluten-free diet showed a transitory decrease in seric immunoglobulin A and macroamylase with persistent autoantibodies and AST elevation. An intestinal mucosal immune disorder could lead to coeliac disease and macroamylasaemia in a patient with Down syndrome presenting other immune alterations.
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PMID:Macroamylasaemia, IgA hypergammaglobulinaemia and autoimmunity in a patient with Down syndrome and coeliac disease. 1273 20

Rhinosinusitis is an inflammation or infection of the nose and air pockets (sinuses) above, below and between the eyes which connect with the back of the nose through tiny openings (ostia). Rhinosinusitis can be caused by bacteria, viruses, fungi (molds) and possibly by allergies. Chronic rhinosinusitis (CRS) is an immune disorder caused by fungi. The immune response produced by eosinophils causes the fungi to be attacked, which leads to damage of the sinus membranes, resulting in full-blown rhinosinusitis symptoms. Gaseous nitric oxide (NO) is naturally released in the human respiratory tract. The major part of NO found in exhaled air originates in the nasal airways, although significant production of NO also takes place in the paranasal sinuses. Proper ventilation is essential for maintenance of sinus integrity, and blockage of the ostium is a central event in pathogenesis of sinusitis. Concentrations of NO in the healthy sinuses are high. Nasal NO is known to be increased 15- to 20-fold by humming compared with quiet exhalation. NO is known to be broadly antifungal, antiviral and antibacterial. This case report shows that a subject hummed strongly at a low pitch ( approximately 130 Hz) for 1h (18 hums per minute) at bedtime the first night, and hummed 60-120 times 4 times a day for the following 4 days as treatment for severe CRS. The humming technique was described as being one that maximally increased intranasal vibrations, but less than that required to produce dizziness. The morning after the first 1-h humming session, the subject awoke with a clear nose and found himself breathing easily through his nose for the first time in over 1 month. During the following 4 days, CRS symptoms slightly reoccurred, but with much less intensity each day. By humming 60-120 times four times per day (with a session at bedtime), CRS symptoms were essentially eliminated in 4 days. Coincidentally, the subject's cardiac arrhythmias (PACs) were greatly lessened. It is hypothesized that strong, prolonged humming increased endogenous nasal NO production, thus eliminating CRS by antifungal means.
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PMID:Strong humming for one hour daily to terminate chronic rhinosinusitis in four days: a case report and hypothesis for action by stimulation of endogenous nasal nitric oxide production. 1640 89