Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 70-year-old man was admitted to our hospital because of fever and progressive dyspnea in December 1989. He was already diagnosed as having erythrocytosis secondary to pulmonary fibrosis 4 years previously and the values of his hematocrit (Ht) were maintained between 44.5 and 62.9% by repeated phlebotomy. Immediately after admission, severe diarrhea developed and the Ht value was 61.5%. Around 1:30 a.m. of the 3rd hospital day, he developed disturbance of consciousness. In addition, the serum levels of LDH, CPK, aldolase, and myoglobin of muscle origin increased markedly and the Ht value showed 78.5%. While the level of consciousness was gradually restored by 600 ml phlebotomy and 1,500 ml saline infusion, dysarthria and hemiplegia became evident. The Ht value early in the morning of the 3rd hospital day was reduced to 59.4%. Although cranial CT and MRI performed 74 days and 15 months, respectively, after the onset of the symptoms failed to reveal any abnormal shadow, he was clinically suspected to have cerebral infarction. These findings emphasize that abrupt increase in Ht or blood viscosity is a possible factor triggering cerebral infarction, and adequate control of Ht value is recommended for the prevention of such a condition in the aged.
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PMID:[Cerebral infarction and high serum levels of muscle-derived enzymes associated with abrupt increase in hematocrit in a patient with secondary erythrocytosis]. 175 34

A necropsy case of a primary rhabdomyosarcoma with chronic paragonimiasis in the cerebrum of a 68-year-old man is reported. The clinical data showed a right hemiplegia and dysarthria which became lethal in 6 months even though operation and radiation therapy were performed. Computed tomography revealed a large low-density area associated with the peripheral enhancement in the left basal ganglia, and multiple conglomerated calcified masses in the left temporal and occipital lobes. Biopsied and necropsied materials of the tumor in the basal ganglia was reddish brown in color and histologically was composed of purely mesenchymal derivatives with both embryonal and mature striated muscle cells but neither neuronal nor glial elements. Some of the tumor cells with extending slender cytoplasms showed obvious cross striations at the light and electron microscope levels and immunohistochemical reactivity for myoglobin. All tumor cells were also positive for vimentin, but not for glial fibrillary acidic protein. The clinical and necropsy findings revealed no primary lesion anywhere but in the brain. In addition, numerous dead oval eggs of Paragonimus westermani were found in many cystoid lesions encapsulated by thick connective tissues with calcification and/or ossification. Clinicopathological features of 24 cases of primary rhabdomyosarcoma of the central nervous system reported in the literature are reviewed briefly. The histogenesis of this tumor are discussed together with comments on cerebral paragonimiasis.
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PMID:Primary rhabdomyosarcoma combined with chronic paragonimiasis in the cerebrum: a necropsy case and review of the literature. 382 17

We reported two cases of acute alcoholic myopathy associated with rhabdomyolysis. The first case was 62 year-old man, who had been drinking every day for 40 years. Following diarrhea, he had psychic symptoms, and was admitted to our hospital. He was in a state of delirium. Tremor in extremities, dysarthria and weakness of lower extremities were observed. Neither swelling nor grasping pain were seen in any muscles. Laboratory data showed severe hypokalemia and high levels of serum muscle enzymes and myoglobin. An increase of lactate and pyruvate was not seen in ischemic exercise test performed at the acute or the recovery phase. It was suggested that glycolysis in muscles was suppressed in this case. The second case was 43 year-old man, who had been drinking every day for 27 years. Rapidly progressive weakness of both lower extremities was seen, and he was admitted to our hospital. Grasping pain of both legs and proximal muscle weakness of extremities were observed. Laboratory date showed normokalemia and high levels of serum muscle enzymes and myoglobin. Muscle biopsy showed no abnormal findings in histology and electron microscopy. Although the pathogenesis of acute alcoholic myopathy is unknown, suppression of muscle glycolysis enzyme caused by ethanol may play an important role in the first case.
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PMID:[Two cases of acute alcoholic myopathy associated with rhabdomyolysis]. 829 65

We here report on a 74-year-old man diagnosed with a pT3cN0 BRAF-mutated and mismatch repair-deficient adenocarcinoma in the colon ascendens and 3 liver metastases. After hemicolectomy, the patient received treatment with the PD-1 inhibitor pembrolizumab. Three weeks later (on day 22), laboratory tests showed leukocytosis and an increase in transaminases; immune checkpoint inhibitor (ICI)-induced hepatitis was suspected and prednisolone therapy was initiated. On day 29, the patient was acutely hospitalized due to dyspnea, somnolence and walking difficulties. Dysarthria, hoarseness, muscle pain and weakness had developed and the dose of prednisolone was increased. Serum levels of lactate dehydrogenase, creatine kinase and myoglobin were increased and ICI-induced myositis was suspected. Antibodies against acetylcholine receptor and titin were present, indicating myasthenia gravis. Eventually, bulbar myopathy developed, including dysarthria and dysphagia, and the patient could no longer attain saturation without oxygen. The patient was transferred to the intensive care unit, intubated and given methylprednisolone, intravenous immunoglobulins and infliximab. The patient developed carbon dioxide retention and died on day 39. Microscopical examination of the intercostal musculature, diaphragm, cervical musculature and tongue showed inflammatory infiltration and fibrosis consistent with a pronounced myositis. In the liver, microscopical examination did not show metastases from colorectal cancer but instead a hepatocellular cancer. The cause of death was determined as respiratory insufficiency due to polymyositis. In conclusion, ICIs may induce myositis combined with neurological immune-related adverse events. In patients developing muscle weakness and pain under ICI therapy, myositis should be suspected.
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PMID:Immune Checkpoint Inhibitor-Induced Polymyositis and Myasthenia Gravis with Fatal Outcome. 3325 Jul 39