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)

Liver involvement in systemic amyloidosis is frequent but is rarely of clinical importance. Five patients with severe cholestatic jaundice are described and an additional 20 from published reports are reviewed. The most frequent presenting symptoms were lethargy and abdominal pain, which were present for a median of 11 months before the onset of jaundice. Hepatomegaly, usually marked, was present in 92%, with ascites in 56% of the cases. The serum bilirubin concentration was noticeably high and the serum globulin low. Histology of the liver showed considerable perisinusoidal deposition with a slight predilection for the periportal area. Two patients presented with predominant centrilobular deposition. Congo red staining was not uniformly positive. A variety of treatment regimens was tried but median survival was only three months from the onset of jaundice.
Gut 1994 Sep
PMID:Primary amyloidosis and severe intrahepatic cholestatic jaundice. 795 46

To determine whether the aetiological agent of bovine spongiform encephalopathy (BSE) is pathogenic for mink, standard dark mink were inoculated with coded homogenates of bovine brain from the U.K. Two homogenates were from cows affected with BSE. The third was from a cow that came from a farm with no history of having had BSE or having been fed ruminant-derived, rendered by-products, the proposed vehicle for introduction of the BSE agent. Each homogenate was inoculated intracerebrally into separate groups of mink and a pool of the three was fed to a fourth group. Signs of neurological disease appeared in mink an average of 12 months after intracerebral inoculation and 15 months after feeding. Decreased appetite, lethargy and mild to moderate pelvic limb ataxia were the predominant clinical signs, quite unlike the classic clinical picture of transmissible mink encephalopathy (TME). Microscopic changes in brain sections of most affected mink were those of a scrapie-like spongiform encephalopathy. Vacuolar change in grey matter neuropil was accompanied by prominent astrocytosis. Varying greatly in severity from one mink to another, the degenerative changes occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe, corpus striatum, diencephalon and brainstem. Although resembling TME, the encephalopathy was distinguishable from it by less extensive changes in the cerebral cortex, by more severe changes in the caudal brainstem and by sparing of the hippocampus. The results of this study extend the experimental host range of the BSE agent and demonstrate for the first time the experimental oral infection of mink with a transmissible spongiform encephalopathy agent from a naturally infected ruminant species.
J Gen Virol 1994 Sep
PMID:Experimental infection of mink with bovine spongiform encephalopathy. 807 14

A retrospective examination of lethargic encephalitis finds many parallels with neuroleptic effects. The encephalitis, like the neuroleptics, produced an acute continuum of cognitive disorders from emotional indifference through apathy and onto a rousable stupor. It also produced similar acute dyskinesias, including akinesia, akathisia, dystonia, oculogyric crises, and tremors. The encephalitis also caused similar chronic effects, including dementia and psychosis, and somewhat different persistent dyskinesias. The chronic motor and cognitive disorders, like those associated with the neuroleptics, were often delayed in onset. An acute, severe episode of lethargic encephalitis also finds a parallel in the neuroleptic malignant syndrome. These parallels are probably due to a common site of action in the basal ganglia. They provide a model for understanding many neuroleptic effects and alert us to the probability of persistent cognitive deficits, including dementia, from neuroleptic treatment.
Brain Cogn 1993 Sep
PMID:Parallels between neuroleptic effects and lethargic encephalitis: the production of dyskinesias and cognitive disorders. 810 24

An AIDS patient with multiple opportunistic infections (Candida, Pneumocystis carinii and Isospora belli) was identified at the University Hospital, Kuala Lumpur. The patient presented with profuse diarrhoea associated with lethargy, anorexia and weight loss. Routine stool examination showed Isospora belli oocysts. The infection responded to treatment with trimethroprim-sulfamethoxazole but relapse occurred 8 weeks later. This represents the first documented case of isosporiasis to occur in an AIDS patient in Malaysia.
Med J Malaysia 1993 Sep
PMID:Human isosporiasis in an AIDS patient--report of first case in Malaysia. 818 53

A case of hypothalamic dysfunction in a girl with a twelve-year follow-up is reported. Onset occurred at the age of three with severe obesity, hypothermia, hypersomnia, and lethargy. Somatotropic, gonadotropic, and thyrotropic hormones were low, whereas prolactin was increased. Imaging techniques failed to disclose any lesion of the hypothalamus or pituitary. Clomipramine improved the vegetative disorders. The literature on clinical and hormonal disorders of hypothalamic dysfunction is reviewed.
Ann Pediatr (Paris) 1993 Sep
PMID:[Hypothalamic syndromes. Review of clinical and endocrinal semiology]. 823

The results of clinical and radiographic examinations of 15 dogs with confirmed malignant histiocytosis (MH) were reviewed. The most common clinical signs were anorexia (14 dogs), weight loss (13 dogs), lethargy (13 dogs), anaemia (11 dogs), and dyspnoea and/or coughing (8 dogs). Radiographs revealed abnormalities in all dogs, either intrathoracic (pulmonary nodules or consolidation [7 dogs], mediastinal masses [10 dogs], and incidentally pleural effusion [3 dogs]) or abdominal (hepatomegaly [6 dogs] and splenomegaly [2 dogs]), or both. MH occurs relatively frequently in Bernese Mountain dogs. Both clinical and radiographic signs are non-specific, but when they are present in a middle-aged Bernese Mountain dog, MH should be included in the differential diagnosis.
Vet Q 1993 Sep
PMID:Clinical and radiographic manifestations of canine malignant histiocytosis. 826 26

Ornithine transcarbamylase deficiency (OTCD) is caused by an alteration of urea synthesis, linked with partial modification of the X-chromosome, whose clinical manifestations are: lethargy, nausea, vomiting and cerebral edema. While in newborn males OTCD presents with hyperammoniemia leading to cerebral palsy with profound neurological impairment and eventually death, in women who are healthy carriers, it is possible to detect the disorder only through specific tests, since heterozygote women are rarely symptomatic. We describe the case of a young woman admitted to the hospital after an episode of mental confusion with vomiting and psychomotor restlessness, which had previously occurred several times during the premenstruum and lasted a few hours. A 2 day history of stupor made admission mandatory. Tests carried out during the hospital stay showed marked hyperammoniemia and unconjugated hyperbilirubinemia, marked cerebral edema documented by a CT scan. Liver biopsy and CSF test were normal. Screening of plasma and urinary aminoacids, level of orotic acid in the urine and OTC activity in the liver, confirmed the diagnosis of OTCD. The possibility of early diagnosis and therapy of a disease which otherwise leads to death, emphasizes the importance of precise evaluation of a possible organic cause of anorexia and behaviour disorders in young women.
Ital J Neurol Sci 1993 Sep
PMID:Hyperammoniemic coma in an adolescent girl: an unusual case of ornithine transcarbamylase deficiency. 828 23

A 19-year-old black man presented to the emergency room with superficial cuts on the anterior wrists, lethargy, tachycardia, and metabolic acidosis. Multiple containers of medication were found at the scene. Dysrhythmias developed and the patient died 7 h after admission. No anatomic cause of death was identifiable at autopsy. Toxicologic analysis identified the following drugs in the blood (mg/L): cyclobenzaprine (0.3), phenylpropanolamine (2.5), chlorpheniramine (0.2), lidocaine (6.6), phenytoin (19), and ibuprofen (130). Lidocaine and phenytoin had been administered therapeutically. The major symptoms displayed by the patient were tachycardia and metabolic acidosis, symptoms consistent with cyclobenzaprine and ibuprofen intoxication, respectively. Therefore, the medical examiner ruled that the cause of death was multiple drug intoxication and that the manner of death was suicide.
Am J Forensic Med Pathol 1993 Sep
PMID:A multiple drug intoxication involving cyclobenzaprine and ibuprofen. 831 Oct 59

Postlaparotomy patients who remain in the Surgical Intensive Care Unit (SICU) are frequently suspected of harboring an intra-abdominal abscess (IAA). Computed Tomography (CT) of the abdomen has been advanced as an accurate method to diagnose an IAA. To determine the clinical parameters predictive of CT scan results, and the survival of such patients, this study reviewed a consecutive series of 29 postlaparotomy patients who were evaluated by abdominal CT scan while in the SICU. An IAA was identified significantly more frequently by CT when patients were explored for a GI malignancy (70% vs 30%; P < 0.05) and when patients were operated upon electively (11.1% vs 20.0%; P < 0.05). Postoperatively, alert patients were significantly more likely to have a CT scan positive for an IAA than were patients who were lethargic or nonresponsive (90% vs 10%; P < 0.05). Laboratory data, including radiographic studies, were not predictive of the CT scan results. A negative CT scan modified therapy in only 10.5 per cent of patients, while a positive scan altered therapy in 70 per cent of patients (P < 0.05). The overall survival for this group was 48.1 per cent. The identification of an IAA by CT scan did not significantly improve survival (42% with an IAA vs 40% without an IAA). APACHY II scores were significantly increased in nonsurvivors (17.4 +/- 6.0 survivors vs 23.76 +/- 7.8 nonsurvivors; P < 0.05). Our data indicate that in critically ill postlaparotomy SICU patients who were evaluated by abdominal CT scanning, there are some clinical clues that tend to predict whether or not CT scanning will identify an IAA.(ABSTRACT TRUNCATED AT 250 WORDS)
Am Surg 1993 Sep
PMID:Predicting the results and outcome of patients who undergo abdominal CT scanning while in the surgical intensive care unit. 836 69

Rickets is a common and paradoxical feature of infantile malignant osteopetrosis and results from the inability of osteoclasts to maintain a normal calcium-phosphorus balance in the extracellular fluid. Despite a markedly positive total body calcium balance, rickets arises when the serum calcium x phosphorus product is insufficient to mineralize newly formed chondroid and osteoid. In five children with malignant infantile osteopetrosis, there were clinical, radiographic, biochemical, and histologic findings of rickets. Characteristic biochemical abnormalities included hypocalcemia, hypophosphatemia, and elevated levels of serum acid phosphatase, alkaline phosphatase, c-terminal parathyroid hormone, and 1,25-dihydroxyvitamin D. The urinary calcium/creatinine ratio was markedly depressed. The serum calcium x phosphorus product was below 30 in all children at the time the rickets was diagnosed, and above 40 by the time the rickets had resolved. Baseline bone density measurements were markedly elevated in all children (> 5 standard deviation above normal) and showed even significant increases (> 7 SD) when the rickets was treated with vitamin D and calcium. The children showed marked clinical improvement, decreased lethargy, increase in mobility and activity, and stimulation of appetite, without any additional adverse hematologic or neurologic effects. The rickets was reversible in all children: in one by HLA-identical sibling bone marrow transplantation and in four by physiologic doses of vitamin D and calcium. The parathyroid and renal responses to hypocalcemia were appropriate, but glucocorticoids, used in treating the hematologic complications of the disease, may have blunted the intestinal response to maximal vitamin D stimulation. This latter blockade can be overcome by increasing dietary calcium. By liberalizing rather than by restricting calcium and phosphorus intake, hypocalcemia can be minimized, phosphorus metabolism can be improved, and rickets can be cured.
Clin Orthop Relat Res 1993 Sep
PMID:Osteopetrorickets. The paradox of plenty. Pathophysiology and treatment. 839 71


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