Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-one patients developed acute renal failure in association with nontraumatic rhabdomyolysis and myoglobinuria. The illness followed an overdose of ethanol, heroin, or other depressant drug in 18 patients. Lethargy or coma was present in 17 patients and muscle swelling in 11. Evidence of rhabdomyolysis included markedly elevated creatine phosphokinase, myoglobinuria, and aldolase in blood. Initial biochemical findings were similar to those of acute renal failure due to other causes, but the abnormalities were exaggerated. There was a disproportionate rise in serum creatinine concentration in relation to serum urea nitrogen concentration. Profound hyperuricemia was present in most patients. Transient hypercalcemia developed during the diuretic phase in 5 patients. One patient died. We conclude that nontraumatic myoglobinuria with acute renal failure is not infrequent and may occur after an overdose of ethanol or heroin. The disease has good prognosis despite severe hypercatbolism and untreated profound hyperuricemia.
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PMID:Acute renal failure due to nontraumatic rhabdomyolysis. 93 19

The incidence and significance of elevated serum levels of creatine phosphokinase (CPK) in febrile diseases were studied prospectively in all patients admitted with fever to a department of medicine during 1 year. High serum CPK levels were detected in 70 (28%) of 247 febrile patients but in only six (6%) of 105 afebrile control patients (P = .0001). Elevated CPK levels were not related to any specific diagnosis. Logistic regression analysis identified five factors that correlated both significantly and independently with elevation of CPK values: increased blood urea nitrogen level, low serum phosphate level, a stuporous or comatose state, tremor, and muscle tenderness. Myoglobinuria, detected in 14 patients, was predictive of a fatal outcome, but a high CPK level by itself was not an independent correlate of mortality. In summary, CPK elevation is not uncommon in febrile diseases, but because it does not reflect a specific etiology it does not necessarily indicate that an extensive diagnostic work-up is required.
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PMID:Significance of elevated levels of serum creatine phosphokinase in febrile diseases: a prospective study. 204 54

Lethargy, hyperpyrexia, tremor, and rigidity associated with leukocytosis and elevation of the creatine kinase level occurred in a patient with a closed head injury who was being treated with haloperidol for control of agitation. This constellation of symptoms, known as the neuroleptic malignant syndrome (NMS), partially improved when the neuroleptic medication was stopped, but complete resolution of the syndrome did not occur until the patient was treated with bromocriptine. Because haloperidol is the most widely used medication for the agitation that develops in patients with significant closed head injuries, neurosurgeons should be aware of the NMS. The NMS is caused by neuroleptic medications and may initially present with unexplained hyperpyrexia, leukocytosis, and elevated creatine kinase levels. Halting the neuroleptic, supportive care, and the use of dantrolene sodium and bromocriptine are the treatment modalities of choice for this syndrome, which has a mortality rate of 20 to 30% and may be linked to malignant hyperthermia.
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PMID:Neuroleptic malignant syndrome complicating closed head injury. 396 Feb 97

A Phase I trial of 2-beta-D-ribofuranosylthiazole-4-carboxamide (NSC 286193, tiazofurin) was conducted using a 5-day continuous infusion schedule. Twenty-four patients with advanced cancer were entered on this trial. Dose levels ranged from 360 to 2350 mg/sq m/day for 5 days. Neurotoxicity was dose limiting and occurred in six patients. Neurotoxicity was expressed as confusion, lethargy, or obtundation and was associated with focal neurological deficits in four of six patients: hemiparesis, three; cortical blindness and bilateral upper extremity weakness, one. Neurotoxicity was not clearly dose related, occurring at 900 mg/sq m/day for 5 days (two patients), 1100 mg/sq m/day for 5 days (two patients), 1850 mg/sq m/day for 5 days, and 2350 mg/sq m/day for 5 days (one patient each). Other toxicities seen were myelosuppression, desquamation of palms and soles, malar erythema, and hyperpigmentation, stomatitis, chest pain, drug fever, and increased serum creatine phosphokinase. Administered drug [71.5 +/- 11.2% (SE)] was recovered intact in the urine within 24 h of administration. Terminal-phase mean harmonic half-life was 8.0 h. The unpredictable neurotoxicity seen following continuous infusion therapy with tiazofurin suggests that Phase II trials of this schedule are not indicated until better understanding of the biochemical effects of tiazofurin is achieved.
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PMID:Phase I clinical study with pharmacokinetic analysis of 2-beta-D-ribofuranosylthiazole-4-carboxamide (NSC 286193) administered as a five-day infusion. 398 12

Lethargy, marked muscle weakness and rigidity, a maximal temperature of 40 degrees C, and a maximal creatine kinase value of 17,240 IU/liter developed in a 36-year-old woman following treatment with several neuroleptics. Initial treatment with dantrolene was unsuccessful. The patient's condition improved gradually over a 10-day period with no specific therapy. Muscle biopsy revealed a contracture pattern diagnostic of malignant hyperthermia susceptibility, as well as abnormal sensitivity to fluphenazine. This report may be the first description of a patient with neuroleptic malignant syndrome in whom muscle biopsy response similar to that seen in malignant hyperthermia occurred and documents that dantrolene is not uniformly successful therapy for this syndrome.
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PMID:Neuroleptic malignant syndrome. Patient with unique clinical and physiologic features. 614 89

Four patients with rhabdomyolysis due to drug intoxication were found to have peripheral nerve damage. Three patients were comatose and one was lethargic. The diagnosis of rhabdomyolysis was made by marked elevation in blood levels of creatine phosphokinase and strongly positive orthotoluidine test without RBCs in the urine. Acute renal failure developed in three patients and one had mild renal insufficiency. Electromyography showed damage to the brachial plexus in three of the patients and there was involvement of the musculocutaneous, radial, ulnar, and peroneal nerves in the fourth patient. The neurologic abnormalities disappeared completely within six weeks in two patients and considerably improved within four weeks in another patient after discharge from the hospital.
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PMID:Peripheral nerve damage in patients with nontraumatic rhabdomyolysis. 630 96

Possibilities of recognizing cerebral function disturbances in newborns as early as the acute phase of the condition, and of prognosticating permanent brain damage are described. Clinical findings such as lethargy or spasms in the second and third weeks of life following hypoxia indicate severe function disturbances with poor prognosis. In contrast, the same symptoms in the first week after a hypoxia or following a cerebral hemorrhage are only of relatively slight prognostic significance. Metabolic parameters such as lactate, hypoxanthine, CK-BB, and ammoniemia are elevated in the first few hours and days after a perinatal hypoxia and correlate with the current disturbances in the central nervous system. However, they are not indicative of a possible occurrence of later brain damage. Cerebral sonography furnishes excellent information concerning gross structural changes and cerebral hemorrhages. The extent of the hemorrhages, classified in 4 stages, correlates well with the later development. Less severe functional disturbances can also be identified by electroencephalography together with observation of behavior (polygraphy). Here also, findings correlate well with the children's subsequent development. The combination of sonographic findings and neurophysiological diagnosis is at present the best source of information concerning the later occurrence of brain damage.
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PMID:[Diagnosis of cerebral function disorders and subsequent brain damage in newborn infants under intensive care]. 639 20

Twenty beef calves weighing approximately 180 kg were allotted to 3 groups. In group A, 6 calves were given 25 mg of mycelial monensin/kg of body weight orally and were evaluated at 1, 2, and 4 days for clinical, ECG, clinicopathologic, and pathologic alterations. In group B, 7 calves were given a single dose of monensin (40 mg/kg) and 5 were given a 2nd 40 mg/kg dose on day 7; calves were evaluated at days 1, 2, 4, 7, 8, 9, and 11. In group C, 2 calves served as controls. Monensin-treated calves developed anorexia, diarrhea, and lethargy after day 1. One group B calf died on day 7 with lesions of congestive heart failure. Electrocardiographic abnormalities were not observed in group A calves; in group B, prolongation of Q-T and QRS intervals occurred from days 2 to 11 and first degree heart block was seen from days 7 to 11. Clinicopathologic alterations included: increased serum activities of aspartate aminotransferase and creatine kinase in group B calves after day 2; decreased serum K+, Na+, and Ca2+ concentrations in both groups, and postdosing occurrence of leukocytosis. Calves were euthanatized sequentially and the lesions of monensin toxicosis were present in the heart, skeletal muscles, and rumen in groups A and B. Disseminated pale yellowish-brown areas of necrosis were present in the ventricular myocardium of 6 of 12 group B calves. Gross lesions were not present in the skeletal muscles or rumen. Microscopically, the myocardial and skeletal muscular lesions were characterized by sarcoplasmic vacuolation from mitochondrial swelling and lipid accumulation in calves killed after day 1 in groups A and B, and by myocardial necrosis with contraction bands, but without calcification, in group B calves killed by day 4. Acute rumenitis was present in groups A and B calves. Myotoxic effects of monensin may be related to its action as an ionophore producing altered intracellular ion concentrations and initiating degeneration and necrosis in striated muscle fibers.
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PMID:Clinical, clinicopathologic, and pathologic alterations in acute monensin toxicosis in cattle. 665 Sep 60

Hypothyroidism is commonly thought to cause decreased gastric emptying and secretion, but these may be related to associated autoimmune disease or chronic changes. Therefore, we measured gastric emptying and secretion in 11 healthy controls and in nine patients (19-54 years old; five females and 4 males) rendered athyreotic by surgery and/or 131I for thyroid cancer. Replacement T4 was stopped 47-65 days and subsequent replacement T3 was stopped 33-40 days before the study. All patients were symptomatic with complaints including weight gain, lethargy, and constipation. Deep tendon reflexes had delayed relaxation phase. Serum cholesterol and creatine phosphokinase levels were elevated. Thyroid hormone levels were markedly decreased (means +/- SE; T4: 0.7 +/- 0.3 micrograms/dl; free T4: 0.2 +/- 0.1 ng/dl; T3: 28 +/- 6 ng/dl) and TSH was markedly increased (88 +/- 16 microU/ml). Gastric fractional emptying rate (%/min) and hydrogen ion (H+) output (meq/hr) were determined before and following two sequential stimulations: a 250-ml water load and an intravenous infusion of pentagastrin (6 micrograms/kg/hr). There were no significant differences between controls and athyreotic patients. Our data demonstrated that short-term, profound, thyroid hormone deficiency does not modify gastric emptying or acid output.
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PMID:Gastric secretion and emptying in hypothyroidism. 671 56

Two brothers had intermittent episodes of muscle weakness, lethargy, hyperammonemia, rhabdomyolysis, and elevated activities of creatine phosphokinase (CPK), lactic dehydrogenase, and SGOT in serum associated with low muscle carnitine but normal serum carnitine concentrations. These siblings represent a "mixed" form of carnitine deficiency with the elements of both systemic and myopathic carnitine deficiency. The older sibling died suddenly after a 24-hour fast. The younger boy has received carnitine for three years. During this period, serum CPK activity has remained elevated and increased further during illnesses, but no clinical symptoms of encephalopathy or myopathy have appeared.
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PMID:Encephalopathy and fatal myopathy in two siblings. Their association with partial deficiency of muscle carnitine. 709 Oct 87


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