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)

Primary hypothyroidism was diagnosed in a 26-yr-old female western lowland gorilla (Gorilla gorilla gorilla) on the basis of serum levels of thyroxine (T4), free T4, and thyroid-stimulating hormone (TSH) measured by human immunoassays. Compared with clinically normal gorillas, the TSH level (107 mlIU/L) was markedly elevated, and T4 (<14.0 nmol/L) and free T4 (5.0 pmol/L) levels were decreased. Thyroid hypofunction could explain the weight gain, unsettled appetite, anxious behavior, lethargy, and poor intraspecies interactions shown by this gorilla. The antibodies in the commercial immunoassay used in this study apparently cross-reacted with gorilla TSH. Supplementation with levothyroxine sodium was initiated and was followed by a marked decrease in circulating TSH and a noticeable improvement in the animal's physiologic status and activity level.
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PMID:Diagnosis of hypothyroidism in a western lowland gorilla (Gorilla gorilla gorilla) using human thyroid-stimulating hormone assay. 1074 41

Signs of mild colic, intermittent lethargy, and weight loss of 6 weeks' duration in a 2-year-old Quarter Horse gelding were attributed to persimmon (Diospyros virginiana) phytobezoar formation. Diagnosis of the phytobezoar was facilitated by gastric endoscopy. Signs of gastrointestinal tract obstruction were associated with a large phytobezoar in the lumen of the stomach, gastric ulceration, and obstruction of the small intestine (as a consequence of fragmentation of the primary bezoar). Conservative treatment, using mineral oil and dioctyl sodium sulfosuccinate, was unsuccessful. A celiotomy was performed, and gastric impaction and partial obstruction of the small intestine associated with phytobezoar formation and fragmentation were identified. The horse made a complete recovery following removal of all phytobezoars. Persimmon phytobezoar should be considered in the fall and winter as a possible cause of lethargy, colic, and weight loss in horses allowed access to persimmon fruit.
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PMID:Gastric impaction and obstruction of the small intestine associated with persimmon phytobezoar in a horse. 1076 70

A 7-month-old infant presented to the emergency department with diarrhea, vomiting, and decreased activity. The infant was febrile, tachycardic, tachypneic, lethargic, and had a prolonged capillary refill. Initial serum sodium was 197 mmol/L. Ultimately, the infant was diagnosed with central diabetes insipidus complicated by severe dehydration secondary to rotavirus infection. A brief review of infant hypernatremia and its evaluation and treatment in the emergency department follows.
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PMID:Infant hypernatremia: a case report. 1090 64

Three artemisinin antimalarials, arteether (AE), artesunate (AS), and artelinate (AL) were evaluated in rats using an auditory discrimination task (ADT) and neurohistology. After rats were trained on the ADT, equimolar doses of AE (25 mg/kg, in sesame oil, n=6), AS (31 mg/kg, in sodium carbonate, n=6), and AL (36 mg/kg, in saline, n=6), or vehicle (sodium carbonate, n=6) were administered (IM) for 7 consecutive days. Behavioral performance was evaluated, during daily sessions, before, during, and after administration. Histological evaluation of the brains was performed using thionine staining, and damaged cells were counted in specific brainstem nuclei of all rats. Behavioral performance was not significantly affected in any rats treated with AS, AL, or vehicle. Furthermore, histological examination of the brains of rats treated with AS, AL, and vehicle did not show damage. In stark contrast, all rats treated with AE showed a progressive and severe decline in performance on the ADT. The deficit was characterized by decreases in accuracy, increases in response time and, eventually, response suppression. When performance on the ADT was suppressed, rats also showed gross behavioral signs of toxicity that included tremor, gait disturbances, and lethargy. Subsequent histological assessment of AE-treated rats revealed marked damage in the brainstem nuclei, ruber, superior olive, trapezoideus, and inferior vestibular. The damage included chromatolysis, necrosis, and gliosis. These results demonstrate distinct differences in the ability of artemisinins to produce neurotoxicity. Further research is needed to uncover pharmacokinetic and metabolic differences in artemisinins that may predict neurotoxic potential.
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PMID:Behavioral and neural toxicity of the artemisinin antimalarial, arteether, but not artesunate and artelinate, in rats. 1111 82

A report from England has suggested that Chronic Fatigue Syndrome exists in equines and constitutes an emerging veterinary problem. Preliminary epidemiological studies seem to confirm the zoonotic implications of CFS. An arsenical drug, sodium thiacetarsamide, was administered to four horses with a diagnosis of Chronic Fatigue Syndrome (CFS), already treated unsuccessfully with different medications. The CFS-like lethargy, with accompanying symptoms and signs, of the four animals obtained a complete remission after intravenous treatment with this drug at low dosage (0.1 mg/kg/day). No adverse side effects were ever noticed. This clinical response was associated with recovery from anaemia and decrease of muscular enzyme values in two of the four horses. In all patients, micrococci-like bacteria found before treatment adhering to the outer surface of many red blood cells, disappeared at post-treatment controls. Considerations are made on the possible action of an arsenical drug, used in isolation, in the treatment of CFS.
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PMID:Chronic fatigue syndrome in horses: diagnosis and treatment of 4 cases. 1113 Oct 41

Many important aspects of our life are regulated by the free cytosolic Ca2+ concentration. The intracellular Ca2+ signal is regulated both in space, frequency and amplitude. Each cell chooses a unique set of Ca2+ signals to control its function. Ca2+ signal transduction is based on rises in free cytosolic Ca2+ concentration. Ca2+ can come from the extracellular space or be released from intracellular stores. Extracellular Ca2+ enters the cell through various types of plasma-membrane Ca2+ channels and leaves the cell using Ca2+ pumps and Na+/Ca(2+)-exchangers. Ca2+ is accumulated in intracellular stores by means of Ca2+ pumps and is released via inositol 1,4,5-trisphosphate (IP3) and ryanodine receptors. Mutations or abnormalities in one of the above mentioned Ca(2+)-transporting proteins can lead to disease. Skeletal-muscle pathology can be caused by abnormal ryanodine receptors (malignant hyperthermia, porcine stress syndrome, central core disease), plasma-membrane Ca2+ channels (hypokalemic periodic paralysis, muscular dysgenesis mice, paraneoplastic Lambert-Eaton myasthenia syndrome) or Ca2+ pumps (Brody disease). Neurologic disorders can be related to altered function of plasma-membrane Ca2+ channels (episodic ataxia type 2, spinocerebellar ataxia type 6, familial hemiplegic migraine, glutamate excitotoxicity, tottering, leaner, lethargic and stargazer mice), IP3 receptors (Lowe's oculocerebrorenal syndrome, manic depression, Alzheimer's disease, opisthotonos mice) and Ca2+ pumps (deafwaddler mouse and wriggle mouse sagami). Two skin diseases are caused by Ca(2+)-pump mutations (Darier disease and Hailey-Hailey disease). Incomplete X-linked congenital stationary night blindness is caused by a mutation in the plasma-membrane Ca2+ channels in rods and cones.
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PMID:[Intracellular calcium: physiology and physiopathology]. 1119 78

There is a controversy whether central pontine myelinolysis can complicate either hyponatremia or its rapid correction. We report a 69 years old woman with a history of one month of vertigo, nausea, vomiting and diarrhea. She was admitted dehydrated ad stuporous, and initial laboratory values showed a serum sodium of 96 mEq/L. She was treated with dextrose 5% and 3% NaCl. Serum sodium raised to 120 mEq/L at the next day and the level of consciousness improved. At the 4th day of admission, the patient was again stuporous and with spastic quadriplegia. A magnetic resonance imaging showed a central and symmetrical pontine lesion on T1 and T2 weighed images. Thereafter, the patient experienced a progressive improvement of her neurological condition and was discharged three months later, moving her lower limbs. Nine month later she was able to walk.
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PMID:[Central pontine myelinolysis and hyponatremia. Clinical case]. 1141 96

Pregnancies in women with epilepsy are high risk and need careful management by both the medical and obstetric teams due to the increased incidence of complications and adverse outcomes of pregnancy. By the time a pregnant woman with epilepsy presents, the foetus is virtually fully formed and the opportunity for altering drug treatment has passed. Women need to be counselled and told to seek advice about their anticonvulsant therapy should they wish to become pregnant. All major anticonvulsant drugs are teratogenic but the main risk to the developing foetus appears to be when the mother is on polytherapy especially if sodium valproate forms part of the combination. Folate supplements (5 mg) before conception are advisable. There appears to be a minor but significant increased risk of maternal complications in women with epilepsy such as hyperemesis gravidarum, pre-eclampsia and eclampsia, vaginal bleeding and premature labour. In the majority of women seizure control will not alter during pregnancy. Oral vitamin K should be given to the mother receiving enzyme-inducing antiepileptic drugs. Post-natal infant development: there is an increased risk of prematurity (9-11%), stillbirth, neonatal and perinatal death, haemorrhagic disease of the newborn, low Apgar scores and low birth weight (7-10%). Breast feeding: virtually all the anticonvulsant drugs are excreted in breast milk in low concentrations. Feeding difficulties, irritability and lethargy can occur. However, the benefits of breast feeding usually far outweigh any minor risks to the baby.
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PMID:CPD-Education and self-assessment: Epilepsy and pregnancy. 1143 22

Twenty patients of either sex, with refractory partial epilepsy with or without secondary generalisation were entered in an open label study to evaluate the efficacy and safety of topiramate in them. Topiramate was used as an adjunctive therapy with an initial starting dose of 50 mg/day. The dose was then titrated upwards with increments of 50 mg per week, till a time the most effective and the best tolerated dose was reached. This most effective/tolerated dose was then continued for 6 months. Of the 17 patients entering the maintenance phase, 4 patients (24%) became seizure free, while a total of 14 patients (83%) out of 17 cases responded with a reduction in monthly seizures rate by 50% or more. Mean reduction of 68.9% was observed in monthly seizure rate during the maintenance phase. The median effective dose of topiramate was 600 mg per day. Five patients dropped out of the study due to adverse events such as anxiety, aggressiveness, rash, lethargy, etc. The central nervous system (CNS) related side effects such as dizziness, headache, and tremor were reported, which are commonly seen with other presently available antiepileptics like carbamazepine, phenytoin sodium, sodium valproate, etc, as well. Most adverse events, however, were mild and transient and did not interfere with the day to day activity of the patients. Topiramate was not associated with any abnormality in laboratory or neurological examination findings. The excellent response with topiramate therapy in Indian patients, uncontrolled with the available antiepileptics, as well as its good safety profile endorse the international efficacious and safe image of topiramate.
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PMID:Topiramate: a new safe and effective antiepileptic. 1188 61

We used exchange transfusion as an alternative to hemodialysis in an infant with severe salicylism. A 4-mo old, 5 kg male was presented to a local hospital with acute vomiting, tachypnea, hyperpnea and intermittent agitation and lethargy. Shortly after a generalized tonic-clonic seizure he passed several tablets in his stool. Salicylate (ASA) level was 85 mg/dL. He was transferred to our institution for further management: i.v. fluids, activated charcoal, whole bowel irrigation and supplementation with sodium bicarbonate, potassium and calcium. The patient's mental status and gas exchange deteriorated and he was intubated. Despite large amounts of sodium bicarbonate and potassium, severe hypokalemia, anion gap metabolic acidosis and aciduria persisted for 10 h. The small size of the infant precluded use of hemodialysis. An exchange transfusion using 180 mL/kg packed red blood cells reconstituted in fresh frozen plasma was performed. The pre-exchange transfusion ASA level was 70.1 mg/dL; the post-exchange transfusion ASA level was 34.4 mg/dL. There was rebound elevation of ASA to 35.2 mg/dL at 6 h post-exchange transfusion. The 18, 36 and 48 h post-exchange transfusion ASA levels were 20.2, 6.8 and < 2 mg/dL respectively. The ASA level dropped 17.6% before, 41.9% in 8.5 h during, and 40.5% by 48 h after the exchange transfusion. There were no complications. The patient recovered completely to his pre-morbid state. Double volume exchange transfusion was used safely as an effective alternative to hemodialysis in this case of severe infant salicylate poisoning.
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PMID:Exchange transfusion in severe infant salicylism. 1213 72


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