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)

Between February and November 1983, 108 recipients of cadaveric renal transplants entered a randomized multicenter trial and were treated either with cyclosporine (CsA) and prednisone (n = 55) or with conventional treatment based on azathioprine (Aza) and glucocorticoids (n = 53). The graft survival probability at 3 years was 76% for CsA patients and 48% for Aza patients (P less than 0.001). The cumulative number of acute rejections was significantly lower in the CsA group (32 vs. 104, P less than 0.001). Incidence of early posttransplant anuria was similar in both groups and did not affect renal function after three years. Nephrotoxicity in CsA patients, when present, was handled by reducing the dose of CsA, but in 12/55 patients a change to conventional therapy was thought to be necessary. However, in this group of 12, one patient lost the allograft because of irreversible rejection and one patient died 14 months later because of an infection. Mean creatinine clearance after three years was significantly lower in the CsA patients (54.7 +/- 2.6 ml/min) than in Aza patients, (67.2 +/- 4.9 ml/min, P less than 0.05). Considering only patients with grafts functioning after three years and still on the original randomized therapy, the mean creatinine clearance was similarly and significantly decreased from 1 to 3 years in both groups. There were no significant differences in occurrence of severe infections. Side effects such as hypertension, hypertrichosis, tremor and gum hyperplasia were more frequent in CsA patients.
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PMID:The Milan clinical trial with cyclosporine in cadaveric renal transplantation. A three-year follow-up. 328 35

Nine renal transplant recipients were treated with Cyclosporin A (CyA). Seven of them were high risk patients (diabetics or above 55 years of age) receiving cadaveric grafts. Two were recipients of related grafts and azathioprine had been shown to give them severe GI symptoms. Secondary anuria developed presumably due to nephrotoxicity caused by CyA in 2 of the recipients of cadaveric kidneys. The patients were converted to conventional immunosuppressive drugs and after 2-3 weeks, renal function had recovered in both patients. Seven patients have been maintained on a combination of CyA and oral prednisolone. Four of these patients experienced one or more rejection episodes, all were reversible on treatment with methylprednisolone. Two patients had episodes of increased serum creatinine due to nephrotoxicity by CyA. Recovery occurred when the dose was reduced. Other side effects observed were: Hirsutism (3 patients), gingival hyperplasia (1), tremor (2) and leukopenia (1). Four patients had infectious complications and one died of cytomegalovirus pneumonia. Six patients are well having serum creatinine levels ranging from 89-181 mumol/1, 1 to 11 months after transplantation.
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PMID:Immunosuppression by Cyclosporin A in human renal transplant recipients. 675 83

We report on a 3-year-old girl with respiratory syncytial virus (RSV) encephalitis manifested by disturbance of consciousness, conjugate eye deviation, anuria, truncal ataxia and intention tremor. T2-weighted magnetic resonance imaging (MRI) showed hyperintense areas in the cerebellar cortex. No lesion was detected in the cerebral cortex, pons or spinal cord. The hyperintense areas in the cerebellar cortex diminished with recovery from the clinical manifestations and had resolved 2 months after onset. The MRI lesions in the cerebellum were considered to be due to oedema. SPECT and positron emission tomography (PET), performed 3 months after onset, disclosed areas of hypoperfusion and hypometabolism at the same sites. One year after onset, MRI showed mild atrophy of the cerebellum. Hypoperfusion on SPECT and hypometabolism on PET remained. Neuroimaging showed that ataxia and tremor in this case were the result of cerebellitis. The patient has no neurological deficit except for mild truncal ataxia. This patient is a rare example of RSV encephalitis.
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PMID:Sequential MRI, SPECT and PET in respiratory syncytial virus encephalitis. 1019 8

The authors submit the case-history of a 29-year-old man, followed up on account of liver steatosis with a toxic-nutritional etiology who developed, after previous increased physical exertion and alcohol abuse, fever associated with major muscular weakness. Gradually he developed an amental delirious state which was evaluated as suspect delirium tremens. Fever of 40-41 degrees C continued, the patient developed muscular rigidity, tremor and hypotension. After intubation during which succinylcholine was administered, the patient's condition deteriorated further with a rise of temperature and muscular rigidity. The patient developed acute renal failure with anuria and the necessity of repeated haemodialyses and severe acidosis of the mixed type on account of which he was intubated and switched to artificial ventilation. According to the case-history clinical and laboratory picture of the disease (extremely high creatine kinase activity, hyperkalaemia, acidosis, hepatorenal failure) malignant hyperthermia was suspected. After a single intravenous injection of sodium dantrolene, 2.5 mg/kg, the temperature dropped and within 24 hours the patient was afebrile. Gradually the acidosis improved, the blood pressure became stabilized and artificial ventilation was no longer used. The patient was discharged after 34 days in hospital in a state of cardiopulmonary compensation with mild polyuria but without signs of retention of nitrogenous substances with sideropenic anaemia and marginal creatine kinase and lactate dehydrogenase values. Within one month after discharge the laboratory values reached normal levels and only slight muscular weakness and greater fatiguability persisted.
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PMID:[An attack of malignant hyperthermia caused by a combination of the effects of succinylcholine, increased physical exertion and alcohol abuse]. 1095 47

Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. The efficacy of treatment with antidotes for cyanide poisoning has not been unequivocally determined for this kind of intoxication.
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PMID:[Sodium azide--clinical course of the poisoning and treatment]. 1772 2