Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231528 (myalgia)
 6,565 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four cases of dengue haemorrhagic fever/dengue shock syndrome were studied in Delhi in the months of September and October, 1988. The majority of these cases were boys aged 6-10 years. Classical symptoms of dengue (fever, headache, aesthesia, myalgia) occurred in all the patients. Digestive symptoms (nausea, vomiting, anorexia, abdominal pain and hepatomegaly) were also common. Haemorrhagic manifestations were present in 41.7% of the cases. Of these, 90% had gastrointestinal haemorrhages. Shock occurred in 17 cases (70.8%). Thrombocytopenia and prolongation of coagulation profile were found in 62.5% of cases. Three patients (12.5%) who presented with encephalopathy died. The other 21 patients recovered after an average period of 2-8 days.
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PMID:An epidemic of dengue haemorrhagic fever and dengue shock syndrome in Delhi: a clinical study. 170 58

The case of a young woman with a rare syndrome of acute encephalopathy followed by deafness and retinopathy developing over 1 year is reported. Unlike previously described similar cases, she had considerable systemic symptoms and signs including polyarthralgia-arthritis, diffuse myalgia, malar rash, livedo reticularis, night sweats, and fatigue suggestive of systemic lupus erythematosus. However, results of most immunological investigations were repeatedly normal, including antinuclear antibodies. Anticardiolipin antibodies were elevated on one occasion. Cyclophosphamide has been the most effective treatment for exacerbations of the disease, which have continued to occur over 6 years. This microangiopathic syndrome more likely relates to an immunologically mediated vasculitis of small blood vessels than to a thromboembolic etiology.
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PMID:Microangiopathy with retinopathy, encephalopathy, and deafness (RED-M) and systemic features. 178 49

A case of fulminant hepatitis in a patient taking lisinopril for 5 weeks for arterial hypertension is reported. Jaundice, fever, myalgia, and marked increase in serum aminotransferase activities occurred after 2 weeks of treatment. Continuation of lisinopril administration for 3 weeks after the onset of jaundice was associated with the development of grade III encephalopathy and a marked decrease in prothrombin and proaccelerin levels. This case strongly suggests that lisinopril may induce acute hepatitis and that continuation of the treatment after the onset of jaundice can lead to life-threatening hepatic failure.
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PMID:Fulminant hepatitis after lisinopril administration. 217 73

We describe the clinical spectrum of the L-tryptophan-associated eosinophilia-myalgia syndrome in 20 patients. In all but one case, patients met the Centers for Disease Control (CDC) case definition for the syndrome: peripheral blood eosinophilia (eosinophil count greater than 1.0 x 10(9)/L) and generalized, disabling myalgias without other recognized causes. Three patients with eosinophilia and myalgia developed eosinophilic fasciitis, and 4 other patients developed, respectively, pneumonitis and myocarditis, neuropathy culminating in respiratory failure, encephalopathy, and fibrosis about the common bile duct. No relation was apparent between dose or duration of L-tryptophan exposure and the eosinophilia-myalgia syndrome. No organic contaminants were identified in L-tryptophan preparations taken by patients or asymptomatic users when these preparations were examined by chromatography or mass spectroscopy. Biopsy specimens in 12 patients showed a mononuclear exudate with a variable admixture of eosinophils in affected tissues, including skin, fascia, muscle, and some viscera. Eosinophil toxic granule proteins, major basic protein, and eosinophil-derived neurotoxin were elevated in the serum and urine of patients compared with normal control subjects (P less than 0.01 and P less than 0.02, respectively). Immunofluorescence showed major basic protein deposited outside of eosinophils in affected tissues, indicating that toxic granule proteins are released in diseased organs. Treatment included withdrawal of L-tryptophan in all cases. Corticosteroids were prescribed for 16 patients and diuretics alone for 1 patient; no drugs were prescribed for 3 patients. Four patients have recovered fully, others are stable or slowly recovering, and 1 is gravely ill despite prolonged treatment.
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PMID:The clinical spectrum of the eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. Clinical features in 20 patients and aspects of pathophysiology. 222 57

We report a case of a female patient with chronic myelogenous leukemia who presented, 8 yr after initial diagnosis, with pancytopenia, encephalopathy, and myalgia. The tentative diagnosis was accelerated phase of chronic myelogenous leukemia. However, because the patient had been treated with cimetidine for 7 months we first omitted this drug. When cimetidine was stopped, bone marrow recovered, and myalgia and encephalopathy subsided. Immunological studies showed stimulation of the patient's lymphocyte blastogenesis by cimetidine and a marked increase in the proportion of cytotoxic/suppressor T lymphocytes after incubation of peripheral blood lymphocytes with cimetidine for 6 days. These findings indicate a role for cell-mediated immunity in the pathogenesis of cimetidine-induced pancytopenia in this patient.
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PMID:Immune basis for cimetidine-induced pancytopenia. 347 Oct 83

Three patients with skin or muscle biopsy evidence of small vessel vasculitis presented with neurological symptoms: (1) frequent transient ischaemic attacks, (2) myalgia with encephalopathy, and (3) myalgia with marked weakness. The diagnosis of small vessel vasculitis needs consideration especially if presentation with polyneuropathy or cutaneous involvement is associated with elevation of ESR or serum immunoglobulins. Neurological illness may be a more common presentation of small vessel vasculitis than previously recognised.
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PMID:Small vessel vasculitis presenting as neurological disorder. 623 85

The medical records of 31 immunocompromised patients who experienced varicella infections from 1975 to 1982 were reviewed. Fifteen of these patients had visceral involvement. In these 15 patients, two clinical patterns of progression were noted: (1) Eleven patients with life-threatening involvement experienced hepatitis (n = 11), pneumonitis (n = 11), abdominal pain (n = 11), encephalopathy (n = 10), coagulopathy (n = 10), inappropriate antidiuretic hormone (ADH) syndrome (n = 10), back pain or myalgia (n = 5), and myocarditis (n = 1). Seven of these patients survived, all without sequelae. (2) Four patients with a milder course experienced subclinical hepatitis (n = 4), mild pneumonitis (n = 4), postinfectious encephalitis (n = 1), and septic arthritis associated with disseminated intravascular coagulopathy (n = 1). All four of these patients recovered completely. In patients with severe involvement, intense abdominal pain was frequently the first sign of dissemination. Abdominal pain and inappropriate ADH syndrome were unexplained and have not been previously described in progressive varicella. A predictable pattern of organ involvement enabled starting therapy early and resulted in the survival of 11 of 15 patients.
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PMID:Varicella in immunocompromised children. Incidence of abdominal pain and organ involvement. 661 54

We reviewed retrospectively the clinical records of 30 cases of sporadic Legionella pneumophila infection that occurred in Iowa between FY 1972 and 1978. Cases occurred throughout the year, most between May and December. Twenty-one male patients and 9 female patients ranging in age from 5-80 years were infected. Half the patients smoked or had an underlying illness; five were receiving corticosteroids or immunosuppressive therapy. Occupations and exposures related to hospitals, construction and travel were common; four patients had been exposed to birds. In addition to L. pneumophila infection, six patients had evidence of infection with a viral, mycoplasmal, bacterial, mycobacterial or fungal pathogen; three had had preceding dental infections. Twenty-seven cases were pneumonias visible on radiographs. Fever, cough, chills, myalgia and rales occurred inover half the cases. Headache, gastrointestinal symptoms and encephalopathy also were seen. Upper respiratory symptoms were uncommon. Urinalysis and blood studies often suggested renal and hepatic involvement, but other routine laboratory diagnostic tests were not helpful. All but two patients were hospitalized; seven required intensive care. The median duration of hospitalization was 12 days. Two patients who did not receive erythromycin or tetracycline therapy died.
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PMID:Legionnaires' disease among pneumonias in Iowa (FY 1972-1978) II. Epidemiologic and clinical features of 30 sporadic cases of L. pneumophila infection. 746 37

The eosinophilia-myalgia syndrome (EMS), a multisystem disorder associated with ingestion of L-tryptophan-containing products, causes sclerodermatous skin changes, cardiopulmonary disease, and a range of peripheral neurologic complications. Many EMS patients also report cognitive difficulty in association with the disease. To determine the frequency of objective neurocognitive impairment in EMS patients with subjective complaints of cognitive difficulty and to assess the relationship of neurocognitive loss with demographic features, degree of peripheral eosinophilia, and psychiatric diagnosis, we compared 24 EMS patients with 32 age- and education-matched healthy controls, using a comprehensive neuropsychological test battery. EMS patients additionally underwent a psychiatric interview and rheumatologic evaluation. Sixty-two percent (15 of 24) of the EMS patients demonstrated neurocognitive deficits. Compared with healthy controls, EMS patients demonstrated significant impairment on tests of verbal memory, visual memory, conceptual reasoning, and motor speed. Cognitively impaired EMS patients did not differ from those without cognitive impairment on demographic markers, degree of peripheral eosinophilia, presence of peripheral neuropathy, or frequency of concurrent psychiatric disorder, including major depression. These data support the hypothesis that EMS is associated with an encephalopathy in addition to its previously recognized peripheral neuropathy and other rheumatologic manifestations.
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PMID:Neurocognitive dysfunction in the eosinophilia-myalgia syndrome. 849 48

Eight genotypes of Borrelia burgdorferi are known currently. In Slovakia (Carpathian Euroregion) the most frequent genotypes are B. garini, B. afzelii, as well as B. valaisiana and B. lusitaniae. Infestation of the vector Ixodes ricinus is 3-30%. The most frequent early skin manifestation is erythema migrans (60-70%). Borrelia burgdorferi is suggested to be the causative agent in sclerodermia circumscripta, lichen sclerosus et atrophicus, maybe also in urticaria chronica, granuloma anulare, erythema anulare, erythema nodosum. It can be the causative agent also in neurological diagnoses as e.g. chronic oligosymptomatic encephalopathy, "sclerosis multiplex-like" syndrome and fatigue syndrome, arthralgia, myalgia, seronegative indifferentiated oligoarthritis and fibromyalgies. The serological diagnosis has to be coincide with clinical findings. Used serological examinations are ELISA, Immunoblot, indirect immunofluorescence examination. PCR is an important contribution in examination of synovial fluid (85% detection) and cerebrospinal liquor (24-100%). The importance of PCR is stressed in cases with mixed infections by several borrrelia genotypes. The first line treatment includes doxyciclin, amoxicilin, and erythromycin. The second line includes macrolides, cephalosporines. New perspectives are ascribed to active immunisation with recombined antigen OsA (LYMErix, ImuLyme).
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PMID:[Skin manifestations of Lyme borreliosis--occurrence, diagnosis, therapy]. 1121 59


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