Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abrupt or gradual discontinuation of tricyclic antidepressants may precipitate withdrawal symptoms. The most common of these are general somatic or gastrointestinal distress, anxiety and agitation, sleep disturbance, akathisia, parkinsonism, paradoxical behavioral activation and mania. There are very few reports of withdrawal reactions following discontinuation of clomipramine since it has not been in use in the US until recently. 2 patients with withdrawal symptoms following discontinuation of clomipramine are presented. A 45-year-old man had general somatic symptoms, including headache, myalgia, weakness, fatigue (flu-like syndrome) and nervousness and insomnia after clomipramine, 75 mg/d, had been discontinued abruptly. All symptoms disappeared without treatment after 3 days. A 47-year-old woman presented mainly with severe insomnia, anxiety, agitation, jitteriness and tension after discontinuing a low dose of 25 mg/d of clomipramine. Symptoms disappeared after she started self-treatment with 50 mg/d of the drug. It is important to differentiate withdrawal symptoms from relapse of the primary psychiatric disorder.
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PMID:[Withdrawal reactions after clomipramine]. 145 99

A severe foodborne outbreak of group A streptococcal disease (T28) affected 122/169 people (72%) who attended a church party or ate leftovers from the party. The median incubation time was 42 h. Muscular pain or weakness and fatigue usually preceded pharyngeal symptoms. Complications included otitis media with perforation, peritonsillitis requiring tonsillectomy, arthritis and pericarditis. A 45-year-old man died 36 h after he developed an influenza-like illness, and at necropsy there were histological signs of early streptococcal septicaemia. The strain produced erythrogenic exotoxins B and C. Streptococci were probably transmitted by sliced eggs on sandwiches. Laboratory experiments showed that there was an increment in viable count of streptococci with 6 logs after incubation in egg yolk for 24 h at room temperature. The unusually warm climate and flaws in food handling routines contributed to this large foodborne epidemic.
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PMID:A foodborne outbreak of group A streptococcal disease at a birthday party. 146 75

We conducted a retrospective review examining lipid profiles, creatine phosphokinase (CK) levels, and alanine aminotransferase levels (ALT) in patients receiving the combination of gemfibrozil and lovastatin. Serum lipid levels were significantly improved with therapy over those before therapy. Of the 70 patients receiving the combination, 5 experienced mild elevations in CK, 1 a mild elevation in ALT, and 1 mild elevations in both. No patient reported muscle weakness or muscle pain. The combination of these two medications appeared to be at least additive, highly effective, and well tolerated. The mean total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels decreased from 278, 306, and 180 mg% to 200, 151, and 129 mg%, respectively, and the mean high-density lipoprotein cholesterol levels increased from 34 to 40 mg%. This retrospective data analysis suggests that the combination of gemfibrozil and lovastatin may be safe in patients with normal renal function when the dosage of lovastatin is limited and when CK and ALT levels are monitored carefully.
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PMID:A retrospective review of the use of lipid-lowering agents in combination, specifically, gemfibrozil and lovastatin. 149 8

A 24-year-old woman with familial Mediterranean fever (FMF) had for one year been treated with colchicine, 1 mg daily, for repeated bouts of fever, abdominal pain and arthritis. She was also known to have renal amyloidosis. Lately she had developed gastrointestinal symptoms, muscle pain and obvious, predominantly proximal muscular weakness in both legs. The cause of the symptoms was rhabdomyolysis with an increased creatinine activity of 1000 U/l and marked myoglobinuria (1600 micrograms/l), as well as renal failure with normal uric acid and a creatinine clearance of 3 ml/min per 1.73 m2. Serum creatinine concentration was 970 mumol/l, urea 34 mmol/l. Muscle biopsy corresponded to a subacute necrotizing myopathy with vacuole formation, signs typical of toxic damage. Renal biopsy confirmed advanced amyloidosis. The colchicine dose was reduced to 0.5 mg/d. The renal failure responded to conservative treatment. The myopathy symptoms receded within 4 weeks, creatinine clearance rising to 25 ml/min per 1.73 m2. 12 months after reduction of the colchicine dose the patient was without any FMF-related symptoms.
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PMID:[Toxic myopathy with kidney failure as a colchicine side effect ifn familial Mediterranean fever]. 149 22

We report here the long-term sequelae in 22 patients with L-tryptophan-induced eosinophilia-myalgia syndrome (EMS). The mean follow-up was 23 months (range, 5 to 40 months). Myalgia, rash, pruritus, edema, and respiratory symptoms often improved with the use of corticosteroids, but fatigue and weakness persisted in most cases. Other abnormalities that commonly persisted were arthralgia, muscle-cramping, peripheral neuropathy, and thickened skin. One patient had chronic pulmonary hypertension. These findings indicate that for most patients, EMS is a chronic disorder.
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PMID:Eosinophilia-myalgia syndrome: the aftermath. 152 46

Eosinophilia-myalgia syndrome (EMS) is a newly described syndrome associated with use of L-tryptophan. A neuropathy with features of axonal degeneration has also been described in conjunction with EMS. Demyelinating polyneuropathy is not a well recognised association of the syndrome. The two patients with EMS reported presented with profound weakness and sensory loss and were found to have clinical, electrophysiological and pathological evidence of a chronic demyelinating polyneuropathy. The concurrence of this neuropathy with EMS, as well as several other features of their illness, is suggestive of an immune mediated mechanism in the pathophysiology of EMS.
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PMID:Chronic demyelinating polyneuropathy associated with eosinophilia-myalgia syndrome. 153 36

A 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
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PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

We describe the histopathologic changes of skin, muscle, vessels, and fascia in 11 patients with eosinophilia myalgia syndrome, a newly described entity that has been linked to the ingestion of L-tryptophan. This syndrome is defined clinically by severe incapacitating myalgias and a peripheral eosinophilia. Arthralgias, edema of the extremities, morbilliform rashes, skin induration, weakness, fatigue, and respiratory weakness may be present as well. The earliest apparent histologic changes were observed at the septa between subcutaneous fat lobules and in the deep dermis or fascia. The septa and fascia were infiltrated with a sparse mixture of lymphocytes and histiocytes. In the deep fascia, in addition to inflammatory cells, there were distinctive, reactive mesenchymal cells that showed features of both histiocytes and fibrocytes. Minimal tissue eosinophilia was seen despite the extent of blood eosinophilia. Dermal thickening and homogenization of collagen bundles occurred with replacement of fat and adnexa (changes indistinguishable from scleroderma or morphea). Vessel walls in the dermis and fascia showed thickening and endothelial swelling, but no overt vasculitis was noted. Skeletal muscle biopsies showed a perimysial, epimysial, and/or fascial inflammatory infiltrate of lymphocytes and distinctive reactive mesenchymal cells with some eosinophils. Minimal myofiber atrophy, regeneration, or necrosis was seen despite the clinical history of severe myalgias in almost all patients. This syndrome should help gain insight into the mechanisms of fibrosis in environmental-induced, scleroderma-like syndromes and in idiopathic, scleroderma-like disorders as well.
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PMID:Pathologic manifestations of the eosinophilia myalgia syndrome: analysis of 11 cases. 156 45

We reviewed the pulmonary history, dyspnea ratings, and pulmonary function test results in 16 patients with L-tryptophan-induced eosinophilia myalgia syndrome to determine the correlation between reported pulmonary complaints and pulmonary function abnormalities. All patients reported pulmonary symptoms. Dyspnea, seen in 14 of 16 (87 percent) patients, was the most common symptom. The severity of dyspnea was graded by the baseline dyspnea index and the oxygen cost diagram. Pulmonary function testing including maximal static inspiratory and expiratory pressures were measured. The DCO was diminished in 12 of 16 (75 percent) patients. The MSIP was decreased in seven out of ten (70 percent) and the MSEP was decreased in nine out of ten (90 percent) of those patients tested. There was a statistically significant correlation between the severity of dyspnea as graded by the BDI and OCD, and the decrease in DCO. These results and a review of the literature of the pulmonary manifestations of EMS lead us to conclude that patients with EMS have a high prevalence of dyspnea, and it appears to be caused by both lung parenchymal involvement, as well as respiratory muscle weakness.
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PMID:Dyspnea and pulmonary function in the L-tryptophan-associated eosinophilia-myalgia syndrome. 158 85

The occurrence of clinical and biochemical side effects of bezafibrate (400 mg daily) or simvastatin (20 mg daily) alone or combined was appraised in 13 healthy male normolipidemic subjects according to a single blind design. Each period of 2 weeks of treatment with bezafibrate or simvastatin or bezafibrate plus simvastatin was followed by a period of placebo (1 week). No subjects experienced myalgia or muscle weakness. Plasma creatine kinase (CK) elevations, particularly skeletal muscle CK (CK-MM), were observed in 6 subjects: 11 times during different placebo periods, 5 times on bezafibrate, 4 times on simvastatin, and 4 times on combined bezafibrate-simvastatin, but never reached 1,600 IU/L. Only a trend to an increase of CK mean values on combined bezafibrate-simvastatin was shown. The hepatic transaminase and gamma-glutamyltransferase activities remained unmodified throughout the trial, unlike alkaline phosphatase activity, which fell on bezafibrate and on bezafibrate plus simvastatin. The low-density lipoprotein cholesterol level was more reduced with simvastatin than with bezafibrate. The addition of bezafibrate to simvastatin did not decrease it further. Lecithin:cholesterol acyltransferase activity expressed as fractional esterification rate was enhanced only on simvastatin and bezafibrate-simvastatin.
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PMID:Effects of combined bezafibrate-simvastatin appraised in healthy subjects. 158 59


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