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)

We report on a series of three patients with an unusual syndrome of eosinophilia and myalgia associated with the oral ingestion of tryptophan that was recognized in New Mexico in October 1989. All three patients, who were women 37 to 44 years of age, had severe muscle pain, muscle weakness, mouth ulcers, and striking eosinophilia (more than 8 X 10(9) cells per liter). Other manifestations included fever, abdominal pain, dyspnea, skin rash, and elevated serum concentrations of aminotransferase and aldolase. The women had been taking tryptophan in doses of 1.2 to 2.4 g a day for three weeks to 2 1/2 years. The discontinuation of tryptophan and the initiation of glucocorticoid treatment resulted in improvement, but all three women were still symptomatic three to five months later. Tests for trichinosis and other parasites and for allergic and connective-tissues disorders were negative, and serum immunoglobulin concentrations and erythrocyte sedimentation rates were normal. A muscle biopsy in one patient and biopsies of the vagina, liver, and other abdominal organs in another revealed eosinophilic infiltration, as well as the extracellular deposition of eosinophil-granule major basic protein. All three patients had elevated serum and urinary levels of this protein and eosinophil-derived neurotoxin, indicative of eosinophil degranulation. The syndrome of eosinophilia and myalgia in association with the ingestion of tryptophan that was seen in these three patients is a newly recognized adverse effect of tryptophan ingestion. Our identification of this association in these patients led to the discovery of an epidemic of what is now called the eosinophilia-myalgia syndrome.
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PMID:Association of the eosinophilia-myalgia syndrome with the ingestion of tryptophan. 231 25

Overwork weakness has been reported in survivors of poliomyelitis with residual paralysis. Investigators have recently reported that approximately 25% of polio survivors experience functional declines with onset of symptoms of new weakness, fatigue, and muscle pain. The diagnosis of overwork weakness has remained a clinical diagnosis, as previous investigations have failed to uncover reliable, objective, diagnostic methods to confirm the diagnosis in symptomatic individuals. A case is presented in which markedly elevated levels of CPK were present with symptoms of weakness, fatigue, and muscle pain. These levels declined after clinical intervention, with resolution of symptoms. This case represents an overuse syndrome in which muscle fibers were being damaged through overuse. This case further suggests the possible role of serum CPK in the diagnosis of, and in monitoring clinical intervention in, some polio survivors who experience overwork weakness.
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PMID:Overwork weakness with evidence of muscle damage in a patient with residual paralysis from polio. 231 46

Myalgic Encephalomyelitis (ME) is a form of post viral fatigue syndrome resulting in myalgia and fluctuating fatiguability. Symptoms reflecting central nervous system dysfunction are common and include muscle weakness, headache, sensory disturbances, poor short term memory and impairment of concentration. In view of the fact that sensory and cognitive disturbances are experienced by many patients objective evidence was sought with multi-modality sensory evoked potentials and auditory event-related cognitive potentials in a group of ME patients both with and without the enteroviral antigen, VP1 test positive. The auditory brainstem, median nerve somatosensory and pattern reversal checkerboard visual potentials were normal for all 37 patients tested. In contrast to the sensory potentials significant differences in the mean latencies of the cognitive potential N2 and P3 were found. Reaction times were also significantly prolonged but the performance in terms of error was not significantly affected. No significant difference emerged in any of the parameters for the VP1 test. P3 was abnormal in latency or amplitude in 36% of the VP1 positive patients for the frequency discrimination task and 48% for the more difficult duration discrimination task. The abnormalities indicate attentional deficits in some patients and slower speed of information processing in others. The prolonged latencies observed in these patients have not been observed in patients with depression in many other studies.
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PMID:Sensory and cognitive event-related potentials in myalgic encephalomyelitis. 232 56

Rhabdomyolysis, secondary to chronic small bowel obstruction. The authors report the case of a 48-year old man, who developed rhabdomyolysis based only upon hypokalemia secondary to a chronic gastro-intestinal disorder (chronic obstruction of the small bowel). They would like to point out that despite the rare occurrence of rhabdomyolysis associated with hypokalemia, this pathological condition cannot be underestimated. Complaints of acute myalgia and general muscle weakness are characteristic. Early recognition of this syndrome is mandatory because myoglobinuria could provoke acute renal failure with eventual fatal outcome.
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PMID:[Hypokalemia with rhabdomyolysis secondary to chronic small bowel obstruction]. 233 25

Eighteen patients with old poliomyelitis were assessed in order to determine the incidence and severity of late complications. Sixty-one percent complained of new weakness, 83% fatigue and 17% muscle pain. After assessment 33% (six patients) were judged to have significant new weakness and muscle fatigue that could not be explained by other causes, and this group may have postpoliomyelitis progressive muscular atrophy or postpolio syndrome. Onset of symptoms was typically about 30 years after the acute illness; new weakness was relatively mild and progression was slow over many years. Clinically and pathologically this disorder is distinct from idiopathic motor neuron disease, and is not life threatening.
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PMID:Neuromuscular symptoms in patients with previous poliomyelitis: a New Zealand study. 252 9

A case of myasthenia gravis accompanied with polymyositis and malignant thymoma, detected immune complexes in the sera and around the muscle fibers, was described. A 37-year-old woman was admitted to Shinshu University Hospital in September, 1987 because of dyspnea, dysphagia and muscle weakness. She first noticed her right blepharoptosis 3 weeks before admission. Weakness of all four limbs and myalgia of lower extremities were noticed one week later. These symptoms got worse and nocturnal dyspnea, dysphagia and easy fatigability at mastication appeared. On admission, she looked ill and neurological examination revealed left blepharoptosis, bilateral facial weakness, weakness of all four limbs, more prominent in proximal muscles and tenderness of lower extremities. Edrophonium test was positive, improving her muscle weakness. Laboratory examination revealed the elevated serum levels of CK, the increased titre of circulating immune complexes and high titres of acetylcholine receptor antibodies and anti-skeletal muscle antibodies. Electromyographic study showed myogenic pattern and Harvey-Masland test revealed waning at low frequency stimulation. Muscle biopsy showed marked perivascular infiltration of lymphocytes, accompanied by phagocytosis and interstitial fibrosis. IgG deposits were shown around the muscle fibers exclusively around the infiltrates of mononuclear cells. Granular deposits of C3 were also shown specifically around the muscle fibers exclusively around the infiltrates of mononuclear cells. Thymectomy was performed on September 21, 1987. Invasion of thymoma, predominantly lymphocytic type, to right lung and pericardium was observed histologically. After thymectomy, she got better. Immunological data and immunohistochemical examination of the present case suggest that in the case of myasthenia gravis accompanied with polymyositis and malignant thymoma, immune complexes may play a primary role on the pathogenesis of myositis.
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PMID:[Detection of immune complexes in the sera and around the muscle fibers in a case of myasthenia gravis and polymyositis]. 253 18

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

There have been few cases of polymyositis in patients with AIDS, and polymyositis is rarely a cause of myoglobinuria. We studied a 20-year-old homosexual man with recurrent myoglobinuria. He was asymptomatic between episodes. Each episode was accompanied by muscle pain, limb weakness, high serum levels of creatine kinase, and pigmenturia. Muscle biopsy showed active necrosis without inflammation or abnormalities of glycolytic or other energy-generating enzymes. Antibodies to HIV were present in serum. Clinical evidence of AIDS has not developed in 2 years. Recurrent myoglobinuria may be another consequence of HIV infection.
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PMID:Recurrent myoglobinuria and HIV seropositivity: incidental or pathogenic association? 260 81

We report a family with an X-linked recessive disorder characterized by muscle cramps and myalgia. Nine affected male family members had high resting serum levels of creatine kinase, and well-developed musculature with calf hypertrophy but no evidence of muscular weakness. Symptoms began in childhood and did not progress. Electromyographic findings were consistent with myopathy while muscle biopsies showed nonspecific myopathic changes without evidence of storage of glycogen or lipid. Analysis of DNA revealed a deletion in the 1st third of the dystrophin gene. Western blot analysis revealed that dystrophin was smaller than that in normal samples, with no reduction in the amount of the protein present. This disorder represents a new clinical phenotype associated with a deletion in the dystrophin gene. This deletion affects a portion of the dystrophin molecule that clinically does not appear to significantly alter its function. Other patients with deletions in this region may have truncated dystrophin without clinical signs of progressive muscle disease.
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PMID:Familial X-linked myalgia and cramps: a nonprogressive myopathy associated with a deletion in the dystrophin gene. 267 30

Tubular aggregates (TA) are unusual intramuscular structures stained basophilic on hematoxilin and eosin (HE) staining and red on modified Gomori trichrome (GT) staining. The structures are said to be originated from sarcoplasmic reticulum and are collections of tubules with double membranes on electron microscopic studies. The TA are usually seen in biopsy muscles from patients with muscle pain and cramps but without muscle weakness, periodic paralysis or alcoholic myopathy. In addition, there are five reports on families with progressive myopathy and tubular aggregates in the literature. We presented here a 48-year-old postman without any family history, who had had progressive muscle weakness for 17 years. He had never noticed pain or cramps in his muscles, not taken any particular medicine, and not had regular alcoholic beverages. There was no ptosis, facial weakness, masticatory muscle weakness or dysphagia. Muscle wasting, started from the proximal part of four extremities had progressed to the distal part of them. He could not walk on heels or toes and walked with waddling gait. He stood up with Gowers' maneuver. Serum GOT, GPT and CK were elevated. EMG showed myogenic pattern and MCV was normal. The muscle biopsies were performed; the first one taken from quadriceps femoris muscle at 42 years old showed myopathic changes including marked variation in fiber sizes, with scattered necrotic fiber splitting and TA in type 2B fibers. The second biopsy from biceps brachii muscle at the age of 48 years, showed densely proliferated fibrous tissues, marked variation fiber sizes and scattered split fibers. The TA were rarely seen and type 2B fibers were decreased in number.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive myopathy with tubular aggregates]. 268 70


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