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-five CAPD patients were given gemfibrozil in increasing doses for a total of 14 weeks. Parameters of lipid metabolism including serum total cholesterol, LDL cholesterol, HDL cholesterol, HDL2 cholesterol, HDL3 cholesterol triglyceride, apolipoprotein A-1, apolipoprotein B, postheparin lipoprotein lipase, and hepatic lipase activities were measured before the commencement, at every increment in the dose of gemfibrozil and 4 weeks after discontinuation of therapy. Gemfibrozil normalized the deranged parameters of lipid metabolism. Thus, with treatment, serum triglyceride, and total cholesterol, LDL cholesterol and apo B decreased, whereas serum HDL cholesterol, HDL2, and HDL3 (predominantly the latter subfraction), hepatic lipoprotein lipase activities increased. Apo A-1 did not change significantly. Even in normotriglyceridemic patients serum HDL cholesterol increased. The side effects consisted of muscle aches and a significant rise in serum CPK. Gemfibrozil produced a significant decrease in gamma-GT activities. A possible mechanism for the interconversion between HDL2 and HDL3 that resulted in a preferential increase in the latter was discussed. It was concluded that gemfibrozil, in a dose not exceeding 300 mg twice a day favorably improved the risk factor for ischemic heart disease in CAPD patients.
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PMID:Gemfibrozil improves abnormalities of lipid metabolism in patients on continuous ambulatory peritoneal dialysis: the role of postheparin lipases in the metabolism of high-density lipoprotein subfractions. 250 77

A 55-year-old Japanese male who developed acute polymyositis and chorioretinitis due to toxoplasmosis is described. The patients was well until one month prior to the present admission, when he had an onset of painful swelling of lymphnodes in the posterior cervical region, proximal muscle weakness, myalgia and a partial defect in the visual field of the right eye. He admitted that he had had a chance to eat half-cooked mutton while he had visited Saudi Arabia 40 days before. He was unable to go up and down the stairs at the peak of the illness. Serum CPK was 2050 u/l (N = 5-50) on January 11, 1989. These symptoms improved spontaneously except for the visual field defect. He was admitted to our hospital on January 31, 1989. On admission, neurological examination was unremarkable except for retinal exudate in the right eye which appeared consistent with the clinical diagnosis of toxoplasma chorioretinitis. Serum CPK was 103 u/l, and EMG showed myogenic changes. The IgM-immunofluorescent (IFA) anti-Toxoplasma gondii antibody titer was elevated to 640, and IgG-immunofluorescent antibody to 20480 after IgM-IFA. These clinical and serological findings indicate acute and recent Toxoplasma gondii infection. It appeared likely that Toxoplasma gondii directly caused acute myositis and chorioretinitis. Clinical manifestations of toxoplasma myositis may mimic those of idiopathic polymyositis, however, the clinical course of the former is usually self-limited probably because of generation of antibodies which will inhibit the growth of the organism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute acquired toxoplasmosis presenting as polymyositis and chorioretinitis in a Japanese male]. 260 34

A 63-year-old man with polymyalgia rheumatica (PMR) with cytoplasmic bodies (CB) in biopsied muscle was reported. He was referred to our hospital in June 1988 because of myalgia of four extremities. The ESR was 114 mm/hr and the serum CPK level was normal. Needle EMG and nerve conduction velocities showed normal findings. On light microscopic examination in biopsied muscle, the inclusion bodies which appeared on HE stained sections as deep reddish masses were present in 10% of all fibers. By electron microscopy the core of the bodies consisted of a dense tangle of thin filaments which were intermixed with granular material. Around the core a network of irregularly or radially oriented filaments was observed. These bodies were identified with cytoplasmic bodies. Since there has been no previous report of PMR with CB, our case is important to discuss the relationship between the pathogenesis of PMR and CB.
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PMID:[A case of polymyalgia rheumatica with cytoplasmic bodies]. 260 38

A 66-year-old woman, who had had bronchial asthma, was admitted to our hospital because she suffered from fever, productive cough, wheezing, dyspnea, and chest pressure sensation. Her chest X-ray showed migrating infiltration and marked cardiomegaly. Her ECG at the admission revealed abnormal Q wave and T wave inversion, though that of 3 years before had been almost normal. Hematology showed leukocytosis and eosinophilia of 8,000/mm3 without abnormal cells. All immunological tests were negative and the specific cause of the eosinophilia was unknown. 2 weeks after admission, she complained of severe chest pain suddenly and her ECG showed ST elevation on V1-4 and serum CPK level was elevated to 290 IU/l. By the thrombolytic agent and anticoagulant therapy, her symptom was lightened immediately. 2 months later, we made her cardiac catheterization and myocardial biopsy. Her LVG showed a small aneurysm of the apex, though her CAG was normal finding. The biopsy revealed moderate fibrosis and cellular infiltration including a few eosinophils. We thought that eosinophilic endocarditis had existed first, and secondary embolism continued led to the small infarction. The hypereosinophilia was spontaneously normalized 2 months after admission, but the patient complained of myalgia and sensory disturbance of extremities. The biopsy of quadriceps muscle could prove neither infiltration of eosinophils nor vasculitis. But we diagnosed mononeuritis multiplex due to hypereosinophilia. Judging from various symptoms and laboratory findings, this case was included to the hypereosinophilic syndrome. We also thought allergic granulomatosis and angitis as one of the differential diagnoses, but histologically vasculitis was not proved. In this case, eosinophilia was disappeared without using corticosteroids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of hypereosinophilic syndrome associated with eosinophilic endocarditis]. 261 22

A chronically hemodialyzed patient experienced recurrent episodes of myalgia while on cimetidine treatment (400 mg/day). After two uneventful courses of cimetidine, the pain appeared at the end of a third fourteen-weeks long course. Severe myalgia occurred at the sixth week of a fourth exposure to cimetidine. Pain was predominant in the hip area, disappeared within a few days after withdrawal and recurred three weeks after resuming therapy. There was no sign of neurological involvement and CPK remained consistently normal. Ranitidine was subsequently administered for four months whereby the patient showed no symptoms of myalgia. This observation suggests that, in susceptible individuals, a progressive decrease in tolerance to cimetidine might occur with repeated courses.
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PMID:Recurrent myalgias associated with cimetidine. 373 85

Adenoviral pneumonia, while most common in infancy and young childhood, is rare in school childhood. Here, we report one case, a 13 years old otherwise healthy girl, suffered from fulminating pneumonia caused by adenovirus infection. She had dry cough, pharyngitis, lethargy, myalgia and fever in the beginning. Four days later, the patient became tachypneic, dyspneic and drowsy, and developed hypoxemia and diffuse bilateral infiltrates on chest radiographs. The laboratory data revealed elevated SGOT, CPK and LDH. Adenovirus was isolated from patient's endotracheal suction tube tips. Fortunately, weaning from mechanical ventilation was accomplished on the fifth day of hospitalization, despite of the high fatality rate of adenoviral pneumonia in this age group. The clinical characteristics and therapeutic management of our case are discussed and literatures reviewed.
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PMID:[Fulminating adenovirus pneumonia: report of one case]. 794 37

Some patients of dermatomyositis (DM) with interstitial pneumonia (IP) have common clinical features. Clinical features of these patients are acute onset, very poor prognosis and that patients have fever, arthritis, typical skin rash, mild myositis and show low ratio of CPK/LDH, low incidence of antinuclear antibody (ANA) appearance, low inflammatory signs. We experienced two cases of this category of DM with IP and examined immunological aspects. Case 1. A 52-year-old woman was admitted in June 1, 1990 with a one-month history of arthralgia and a ten-days history of fever, skin rash, myalgia and dyspnea on exertion. On examination she had Gottron's papules on her fingers, erythema on back, bilateral elbows and legs, proximal muscle weakness and arthritis. Fine crackles were audible in the lower lung fields. Laboratory data included CPK 200 IU/l, ALD 3.2 IU/l, LDH 805 IU/l. Analysis of bronchoalveolar lavage fluid (BALF) revealed increased cellularity with lymphocytosis. She was treated with oral corticosteroid (CS), pulse CS, cyclosporin A. Inspite of these therapies, she died of progressive respiratory insufficiency in July 10, 1990. Case 2. A 23-year-old woman was admitted in April 1, 1991, with a two-month history of arthralgia and a one-month history of fever, skin rash, stomatitis, alopecia. On examination she had Gottron's papules on her fingers, erythema on malar, bilateral elbows and legs, arthritis and stomatitis. Laboratory data included CPK 97 IU/l, ALD 8.5 IU/l, LDH 779 IU/l. She began experiencing dry cough and dyspnea on exertion in May 1991. Analysis of BALF revealed increased cellularity with lymphocytosis. She was treated with oral corticosteroid(CS), pulse CS, pulse cyclophosphamide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of acute progressive interstitial pneumonia associated with dermatomyositis--clinical features and immunological disorders]. 823 10

Dengue is known to produce a syndrome involving muscles, tendons and joints. The hallmark of this syndrome is severe myalgia but includes fever, cutaneous rash, and headache. The neuromuscular aspects of this infection are outlined only in isolated reports, and the muscle histopathological features during myalgia have not been described. In order to ascertain the actual neuromuscular involvement in dengue and better comprehend the histological nature of myalgia, we performed a clinical and neurological evaluation, a serum CPK level and a muscle biopsy (with histochemistry) in 15 patients (4 males), median age 23 years (range 14-47) with classic dengue fever, serologically confirmed, during the brazilian dengue epidemics from September 1986 to March 1987. All patients had a history of fever, headache and severe myalgia. Upon examination 4 had a cutaneous rash, 3 had fever, and 3 a small hepatomegaly. The neurological examination was unremarkable in all and included a manual muscle test. CPK was mildly elevated in only 3 patients. Muscle biopsy revealed a light to moderate perivascular mononuclear infiltrate in 12 patients and lipid accumulation in 11. Mild mitochondrial proliferation was seen in 3, few central nuclei in 3, rare foci of myonecrosis in 3, and 2 patients had type grouping. Dengue in our patients, produced myalgia but no detectable muscle weakness or other neuromuscular involvement. The main histopathological correlation with myalgia seems to be a perivascular mononuclear infiltrate and lipid accumulation.
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PMID:Dengue. Muscle biopsy findings in 15 patients. 827 73

A 73 year old male who had been prescribed fenofibrate for years developed a slightly asymmetric paraparesis of both lower extremities. CPK values rose to 9800 U/l, EMG of the quadriceps femoris muscle was myopathic. Muscle biopsy revealed a necrotic myopathy. Discontinuation of fenofibrate induced a rapid decline of CPK values, followed by a slower remission of muscular symptoms and persisting pseudo-myotonic discharges in EMG. The spectrum of neuromuscular side effects of cholesterol lowering agents, consisting of myalgia, cramps and reversible CPK elevation, is discussed. Only rarely necrotic myopathies have been described.
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PMID:[Necrotizing myopathy with antilipemic agents. Case report and review of the literature]. 841 53

We report a case of dermatomyositis (DM) in a 15-year-old female with toxoplasmosis after ingestion of raw bovine liver. Facial erythema and cervical lymphadenopathy preceded myalgia and muscle weakness of the extremities. The diagnostic criteria of DM was fulfilled because of symmetrical and proximal dominant muscle weakness, elevation of myogenic enzyme (CPK, GOT, LDH, myoglobin, aldorase), myogenic pattern of electromyogram, skeletal muscle biopsy showing interstitial myositis with mild destruction of muscle fiber, and facial erythema. Immunological findings showed IgG anti-toxoplasma antibody to be 1340 IU/ml and IgM to be 7.0 (Cut off index 0.7), suggesting acute toxoplasmosis. Treatment with prednisolone for DM and acetylspiramycin for toxoplasmosis was successful. Toxoplasmosis should be considered as a possibility in patients with myositis.
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PMID:[A case of toxoplasmosis with dermatomyositis]. 870 14


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