Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 55-year-old man with addiction of alcohol was admitted to our hospital with hematoemesis. After admission, the rupture of esophageal varices was observed and it was treated with endoscopic injection sclerotherapy. On the 3rd hospital day, the patient showed alcohol withdrawal syndrome and therefore haloperidol was administered intramuscularly and intravenously. After a half day of this treatment, high fever, diaphoresis, hypotension, tachycardia, muscular rigidity and tremor developed. With the laboratory data including high serum levels of CK, LDH, GOT and GPT, neuroleptic malignant syndrome (NMS) was suspected. Regardless of intensive care, hepatic failure, DIC and acute renal failure promptly developed, and he died on the 11th hospital day. Neuroleptics may cause serious side effects, such as NMS, when the physical status of patients was deteriorated. Especially in exhausted patient such as our case, even the small dose of neuroleptics caused NMS within short term. Thus, it seemed to be important for clinicians to pay attention to choice of neuroleptics.
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PMID:[A case of neuroleptic malignant syndrome developed in liver cirrhosis patient addicted to alcohol]. 177 76

We have recently experienced a case of Vibrio vulnificus septicemia which occurred in a patient with hepatic cirrhosis, and as we were able to give early antibiotic treatment, the patient survived. We would like to report this case here together with another case experienced 2 years ago. Case 1 was a 58-year-old male who was attending our hospital as an outpatient for hepatic cirrhosis. At 5:30 pm on August 8, 1987, he consumed abalone and giant clam and at 9 pm complained of high fever with shaking chills. He was admitted to our department as an emergency case. Cefoperazone was administered resulting in a decline of fever on the following day. During the course of treatment he fell transiently into pre-DIC, but due mainly to the administration of antibiotics his condition was subsided. Case 2 was a 53-year-old male who was under medical care in our hospital for grave hepatic cirrhosis. On October 11, 1985, he consumed sushi and two days later suffered chills and pyrexia. A blood culture revealed Vibrio vulnificus. His condition improved transiently with administration of Cefazolin, but oliguria, hypotension and ascites occurred subsequently, and finally the patient died on the 22nd day.
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PMID:[Two case reports of septic shock due to Vibrio vulnificus with liver cirrhosis]. 250 32

A case of toxic leucoencephalopathy induced by 5 FU derivatives is reported. A 46-year-old woman was diagnosed as having breast cancer, and radical mastectomy was performed on May, 1982. After operation, she was given irradiation and 5FU derivative (tegafur or carmofur) 600 mg and Nolvadex 20 mg (tamoxifen citrate) were administered every day. After taking the medication for a month, she began to stagger and developed a tremor in both arms. She was admitted to our hospital on August 16, because she showed evidence of dysarthria and memory disturbance in addition to her initial complaints. Soon after admission, she developed akinetic mutism, and metastasis in the brain stem was suspected. In spite of her severe condition, she was given radiation over the posterior fossa and continued the medication. On September 22, CT disclosed low density area in the centrum semiovale bilaterally. She died of DIC on November 30. An autopsy was performed. The brain weight was 1110 g and the outer surface of the brain was normal. In frontal cut surfaces stained with K.B., bilateral degeneration of the centrum semiovale was apparent. Microscopically, the degree of myelin degeneration was stronger than that of axon, and numerous fatty granular cells were found in the degenerated area. There were no bizarre shaped astrocytes, inclusion body or cellular infiltration. Fibrillary gliosis was scanty. No metastasis was found in the central nervous system or other organs. Based on these pathological findings and clinical history, toxic leucoencephalopathy induced by 5 FU derivatives was suggested.
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PMID:[A case of toxic leucoencephalopathy induced by 5FU derivatives]. 393 66

We report a 85-year-old woman who had an onset of gait disturbance at 80 years of the age. She had a dizzy spell when she was 80-year-old. She was evaluated at another hospital where paroxysmal tachycardia and sinus arrest lasting as long as 5.8 seconds were found. She was diagnosed as having sick sinus syndrome and a pace maker was inserted. She had a gradual onset of disturbance of gait shortly after the above dizzy spell. She became unable to walk fast and her steps became small. Neurologic examination at age 83 revealed small step gait with freezing episodes. Retropulsion was present. No motor weakness or origidity was noted. She had no tremor. Mentally she was alert and sound. Cranial nerves were essentially normal. Cranial CT scan revealed slight diffuse low density change in the bilateral cerebral white matter. She was treated with amantadine HCI and levodopa with carbidopa. Her gait and balance showed some improvement. She developed pneumonia and worsening of her gait when she was 85 years of the age, and she was admitted again to our hospital. She was mentally alert and sound but she showed marked freezing of gait with loss of postural reflex; she would have fallen down unless supported upon standing. Cranial nerves were again essentially normal. Her hospital course was complicated by pneumonia, DIC, and renal failure. She expired suddenly on the 10th day of her last admission. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had vascular parkinsonism due to lacunar state. However, paucity of vascular changes in her CT scan remained as a question. Other participants thought that she had nigral cell loss secondary to her aging and circulatory disturbance which would have been caused by her sick sinus syndrome. Post-mortem examination revealed marked loss of nigral pigmented cells; the cell loss was diffusely seen in the substantia nigra. Neurofibrillary tangles were seen in the remaining neurons. In addition, gliosis was noted in the globus pallidus and the subthalamic nucleus, however, neuronal loss was very mild in those nuclei. In the superior colliculus, neuronal loss was mild, however, gliosis was seen. No clear neuronal loss was observed in the locus coeruleus, however, Lewy bodies were seen in the remaining neurons. Furthermore, Lewy bodies were also found in the substantia sigra. It was thought that she had progressive supranuclear play (PSP). Question was whether or not she was complicated by Parkinson's disease. Clinically, she had no rigidity or tremor. Pathologically, locus coeruleus did not show neuronal loss. Therefore, incidental Lewy body disease was raised as a possibility. Finally, it should be pointed out that she had no oculomotor disturbance or dementia, yet she had PSP. Her clinical features were those of pure akinesia. Pathologic changes were also relatively mild except for those in the substantia nigra. Possibility of post-encephalitic parkinsonism without encephalitis was also discussed, however, over all distribution of her pathologic changes was more consistent with PSP.
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PMID:[A 85-year-old woman with the onset of progressive gait disturbance at 80 years of the age]. 912 48

A 55-year-old man with prostate cancer received a total prostatectomy. Two days after the operation, he suffered from high fever and shaking chilliness, followed by skin eruption, hypotension, diarrhea and chest pain. The results of blood bacterial culture and endotoxin were negative. Toxic shock syndrome was suspected, and the administration of vancomycin (VCM) and continuous hemodialysis-filtration (CHDF) were performed. The steroid pulse therapy for adult respiratory distress syndrome (ARDS) and the treatments for DIC were also done, and they were effective. The desquamation of the extremity was observed on 10 days after the operation. MRSA was finally identified from pus discharge of the operation wound 13 days after the operation. The prevention and treatments for toxic shock syndrome were discussed.
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PMID:[Toxic shock syndrome due to methicillin resistant staphylococcus aureus (MRSA) after total prostatectomy]. 1184 39