Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Wisconsin Division of Health (DOH) began surveillance for severe illnesses associated with group A beta-hemolytic streptococcus (GABS) infections in late 1989 to describe the current epidemiologic features and clinical spectrum of these infections in the state. Severe illness was defined by the isolation of GABS from the blood or by the development of one or more of the following in a patient infected with GABS: shock, extensive tissue injury, desquamating rash, disseminated intravascular coagulation, renal failure, adult respiratory distress syndrome, or death. Case reports involving 28 patients with severe GABS-related illnesses with onset from November 1989 through October 1990 were received by the DOH. The majority of the case-patients had sepsis (57%), cellulitis (50%) or both. Nine (32%) cases were fatal. Those who died were older than those who survived (median age 74 years v 43 years, p = 0.002) and were more likely to have clinical diagnoses that included pneumonia (relative risk [RR] 3.0, 95% confidence interval [CI] 1.2, 7.3) or necrotizing fasciitis/myositis (RR 3.7, 95% CI 1.5, 9.0). The median interval from illness onset to hospitalization was similar for fatal cases (1 day) and non-fatal cases (2 days), suggesting that early intervention after the appearance of clinical illness may not improve the outcome.
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PMID:Severe illness associated with group A-hemolytic streptococcal infections. 194 73

Two infants with fatal echovirus type 11 infections are described. Disseminated intravascular coagulation developed in both patients, and at postmortem examination, diffuse hemorrhagic necrosis of multiple organ systems was evident, most strikingly in the liver. A 3-month-old child is described, in whom lethargy, vomiting, pitting edema of the occipital scalp and neck, and subsequent diffuse echovirus disease developed. The clinical manifestation in this infant of focal myositis with histologic documentation at postmortem examination is unique to echovirus 11 disease. To our knowledge, this child represents the first described patient with nonparalytic, fatal echovirus type 11 infection occurring beyond the immediate neonatal period.
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PMID:Fatal echovirus type 11 infections. 729 6

Over the period 1985 through 1994, observations are conducted on forty-eight patients, 35 men and 13 women, with age ranging from 11 to 56 years, presenting anaerobic non-spore-forming infection of the soft tissues (necrotizing fasciitis (3), postinjection nonclostridial myositis (7), crepitant cellulitis in diabetic gangrene (21), neck phlegmon (5), perineal phlegmon (9), and progressive bacterial synergistic gangrene against the background of chronic osteomyelitis (3). Infection development is characterized by local necrotic processes, intoxication, crepitations, fetor, fever, and in part of the patients--septic shock and DIC syndrome. The microbiological study shows presence of anaerobes, as mono- and polyinfection, aerobic-anaerobic associations, and gram-negative aerobes--in one patient alone. Invariably, the general condition is rather serious. Lethality amounting to 12.5 percent is ascribed to the late detection and unspecified and inadequate treatment protocol in the initial period of observation. The treatment is complex: incisions with successive many-staged necrectomies, antibiotics, metronidazole, hyperbaric oxygenation and hemadsorption. If several (2-3) of the aforementioned symptoms are present, evidence of anaerobic flora should be mandatory and purposefully seeked.
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PMID:[Anaerobic nonclostridial soft-tissue infection]. 864 57

Twenty-eight patients with Japanese spotted fever were clinically investigated. The diagnosis was determined by confirming an increase of specific antibody. All patients were treated with minocycline, and all recovered, excluding one patient with a fulminant course. Fever and exanthema were observed in all patients, and an eschar was pointed out in 20 (71%) patients. The platelet count was 10 x 10(4)/microl or lower in 8 (28%) patients. The fibrin degradation product (FDP)-level was abnormally high, 10 microg/ml or more, in 16 (57%) patients. The creatine kinase (CK) value was high in 14 of 22 patients, suggesting the presence of myositis. The leukocyte count, FDP, C-reactive protein, and soluble interleukin 2 receptor (sIL2-R) levels were significantly higher in severe cases. In the group without concomitant steroid therapy, mean times of 54.7 h and 101.4 h were required to reduce the temperature to 38 degrees C and 37 degrees C or lower, respectively, after the initiation of tetracycline treatment. There were 6 severe cases: 1 with disseminated intravascular coagulation, 2 with multiorgan failure, 1 with acute respiratory distress syndrome, and 2 with meningoencephalitis. These severe cases formed a group that required 6 or more days to initiate therapy after the onset (P < 0.005 vs non-severe group), showing that delay in diagnosis and therapy is the major cause of aggravation. In the 2 patients complicated by multiorgan failure, the sIL2-R level, produced by activated lymphocytes, was 10,000 U/ml or higher, suggesting that an sIL2-R level of more than 10,000 U/ml can be used as a marker of poor prognosis. It may be better that moderate to severe cases are treated with minocycline plus short-term steroid therapy.
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PMID:Clinical study of Japanese spotted fever and its aggravating factors. 1267 13

Statins are considered to be safe, well tolerated and the most efficient drugs for the treatment of hypercholesterolemia, one of the main risk factor for atherosclerosis, and therefore they are frequently prescribed medications. The most severe adverse effect of statins is myotoxicity, in the form of myopathy, myalgia, myositis or rhabdomyolysis. Clinical trials commonly define statin toxicity as myalgia or muscle weakness with creatine kinase (CK) levels greater than 10 times the normal upper limit. Rhabdomyolysis is the most severe adverse effect of statins, which may result in acute renal failure, disseminated intravascular coagulation and death. The exact pathophysiology of statin-induced myopathy is not fully known. Multiple pathophysiological mechanisms may contribute to statin myotoxicity. This review focuses on a number of them. The prevention of statin-related myopathy involves using the lowest statin dose required to achieve therapeutic goals and avoiding polytherapy with drugs known to increase systemic exposure and myopathy risk. Currently, the only effective treatment of statin-induced myopathy is the discontinuation of statin use in patients affected by muscle aches, pains and elevated CK levels.
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PMID:Statin-induced myopathies. 2200 73

A 14-year-old child with acute lymphoblastic leukemia who had completed induction chemotherapy presented with fever and diffuse musculoskeletal pains which was thought to be a constellation of myositis, arthralgias and arthritis. Investigations revealed initially showed normal peripheral blood counts but had pancytopenia and pre-terminally blasts were seen in the peripheral blood smear. He had bone marrow necrosis. Disseminated intravascular coagulation was suspected with a positive fungal serology. At autopsy, he had evidence of disease relapsed in lymph nodes, liver, spleen, testes and kidneys. There was extensive pseudomembranous colitis and appendicitis with changes of toxic megacolon.
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PMID:A young leukemic patient with unusual catastrophic intestinal complication. 2567 92