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)

We carried out a phase I trial with chlorambucil. Thirty patients with advanced cancer were entered in six dose levels: 36, 48, 60, 84, 108, and 144 mg/m2. The drug was given in six divided oral doses every 6 hours and the regimen was repeated every 3 weeks. The median age was 62 years (31-84), median Karnofsky performance status (KPS) 60 (40-90). All patients but one had received prior radiation therapy, chemotherapy, or both. Central nervous system toxicity was dose limiting, occurring in 5 of 6 patients at 144 mg/m2. It was characterized by transient seizures, hallucinations, lethargy, stupor, and coma. Metoclopramide was successful in controlling nausea and vomiting, which was severe if the antiemetic was not used. Leukopenia (3 patients) and thrombocytopenia (2 patients) were mild. One patient with colorectal carcinoma had a minor response, and two patients with non-small cell lung cancer had stable disease. A safe dose for phase II trials is 108 mg/m2 in six 6-hourly oral doses.
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PMID:A phase I trial of chlorambucil administered in short pulses in patients with advanced malignancies. 317 70

A retrospective study of nine sick premature infants with chronic lung disease who received captopril for control of systemic hypertension (systolic blood pressure (BP) greater than 113 mm Hg) was carried out to determine efficacy of therapy and associated complications. All nine infants had markedly elevated peripheral renin values, 134.3 +/- 128.1 ng/mL/hr (mean +/- SD). Five infants had abnormal renal sonographic and perfusion scans with evidence of renal artery thrombosis, parenchymal disease, or both. Captopril therapy (0.3 mg/kg) was instituted at a postnatal age of 123 +/- 108 days. After the initial dose, the systolic BP decreased significantly in all infants, the decrease ranging from 21% to 58% of the pretreatment value. Dosage was subsequently halved in all infants. Seventeen episodes of unpredictable decreases in BP more than 40% from baseline occurred during the reduced maintenance therapy. Four infants had a total of seven episodes during which the BP decreased by 57 +/- 10% from baseline; this decrease persisted for 17 +/- 6 hours and was unresponsive to volume reexpansion and inotropic therapy. All seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/hr) that persisted for 18 +/- 12 hours. These episodes were accompanied by neurologic signs (subtle seizures, lethargy, and/or apnea) within 18 +/- 6 hours after the onset of oliguria. The remaining five infants had a total of 13 episodes of decreased BP of 50 +/- 8% of baseline, which were of significantly shorter duration and responded to volume reexpanders, inotropic therapy, or both and were unaccompanied by oliguria. These data suggest the need for close observation of BP in infants receiving maintenance captopril therapy.
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PMID:Renal failure in sick hypertensive premature infants receiving captopril therapy. 328 14

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.
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PMID:Polydipsia and hyponatremia in psychiatric patients. 328 1

Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
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PMID:Chronic enteroviral meningoencephalitis in agammaglobulinemic patients. 329

The clinical and laboratory features of moderate to severe organophosphate and carbamate toxicity in 37 infants and children are presented. Ingestion of an improperly stored liquid pesticide was the most common route of intoxication (76% of patients); five (14%) children became intoxicated after playing on carpets and floors of homes that had been sprayed or fogged by unlicensed exterminators. The transfer diagnoses were incorrect for 16 or 20 patients who were transferred to our center from another institution. Miosis (73%), excessive salivation (70%), muscle weakness (68%), and lethargy (54%) were the most common abnormal signs; 49% and 22% of patients had tachycardia and seizures, respectively, and 38% of children had respiratory insufficiency that required endotracheal intubation and mechanical ventilation. The results of erythrocyte and serum cholinesterase activity assays were concordant in 83% of patients. Thirty-four (92%) patients were treated with atropine and/or pralidoxime; three patients required only supportive care. Most patients had a prompt response to therapy; however, two patients with organophosphate toxicity required multiple doses of atropine during a 24-hour period; in both instances, the doses of atropine were subtherapeutic. There were no deaths. Pneumonitis and/or atelectasis developed in ten patients, including six who had ingested a petroleum distillate-containing insecticide.
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PMID:Organophosphate and carbamate poisoning in infants and children. 333 78

Overall, acyclovir is a remarkably safe drug considering its potent antiviral effect. The most frequent reactions with short-term use of oral acyclovir are nausea and vomiting and with 6 months' use headache, diarrhea, nausea, and vomiting. These symptoms are also seen frequently with placebos. The most frequent adverse reaction to intravenous use has been inflammation and phlebitis at the injection site. The two most important serious adverse effects are (1) encephalopathic changes with abnormal electroencephalograms and lethargy, tremors, confusion, and seizures and (2) renal precipitation of the drug because of a rapid bolus of drug administered parenterally. Safety of acyclovir for use during pregnancy and in neonates and young children has not been established.
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PMID:Adverse reactions to acyclovir: topical, oral, and intravenous. 333 41

Two dogs were examined because of anorexia, lethargy, muscle tremors, weakness, and seizures that were associated with an acute onset of hypocalcemia. Both dogs had histories of chronic hypercalcemia. Examination of the parathyroid glands revealed infarction of focal parathyroid adenomas, with atrophy of the remaining parathyroid glands. It was concluded that the acute onset of hypocalcemia was caused by infarction of functional parathyroid adenomas that were previously responsible for the cause of persistent hypercalcemia. Infarction of a parathyroid adenoma should be included in a list of differential diagnoses of acute hypocalcemia in the dog, especially if hypercalcemia has been diagnosed previously.
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PMID:Acute hypocalcemia associated with infarction of parathyroid gland adenomas in two dogs. 335 Jul 46

Forty-one infants with neonatal seizures frequent enough to be captured by randomly recorded routine EEG examinations were studied to determine how often their electrographic seizures were occult (subclinical) and to examine the effects of seizure duration and mental status on their clinical visibility. Seizures were the result of diverse etiologies and most infants had received one or more antiepileptic drug prior to the EEG recordings. The majority of electrographic seizures were occult: only 84 of 393 (21%) were accompanied by distinctive clinical seizure activity; the remaining 79% were occult. There was no significant difference between the duration of EEG seizures with distinctive clinical signs and those without. There was no significant difference in the proportion of occult seizures in neonates with preserved consciousness compared with lethargic or comatose infants. We conclude that unaided visual inspection of infants seriously underestimates true seizure frequency. Long-term EEG monitoring may be necessary in many infants to determine their real seizure frequency and to judge the adequacy of antiepileptic drug treatment.
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PMID:Occult neonatal seizures. 337 Dec 82

The therapeutic responses of seven children with Wilson's disease who presented with neurological disease were evaluated. Neurological abnormalities comprised intellectual deterioration in 7, conduct disorder in five, dystonia in three, choreoathetosis in three, seizures in one and hemiparesis in one. Lethargy and weight loss were present for several months in 6 children. Four children had clinically demonstrable liver disease which was fatal in two. Electroencephalography performed in two children was normal. Computed tomography (CT) of the brain in three children showed cerebral atrophy in all and areas of low attenuation in the basal ganglia which resolved on treatment in one. All patients were treated with penicillamine but, in four, triethylene tetramine (TETA) was substituted because of adverse effects. Neurological abnormalities in these patients were reversible.
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PMID:Neurological abnormalities in Wilson's disease are reversible. 356 99

Two siblings with hyperornithinemia, hyperammonemia, and homocitrullinuria are reported. The clinical picture included protein intolerance, mental retardation, seizures, and stuporous episodes. One patient had cerebellar ataxia, myoclonus, convulsive seizure, and muscular weakness in both legs. Isolated liver mitochondria in the patient revealed that ornithine transport and citrulline synthesis were decreased, but urea cycle enzymes and ornithine aminotransferase were normal. Ornithine metabolism was decreased in cultured skin fibroblasts.
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PMID:Hyperornithinemia, hyperammonemia, and homocitrullinuria: case report and biochemical study. 367 Jun 19


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