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)

Three operated cases of congenital deficiency of factor XIII (fibrin-stabilizing factor) associated with intracranial hematomas were described and the diagnosis, replacement therapy of the factor were discussed. Congenital deficiency of factor XIII is quite rare coagulation disorder and only 100 patients were reported in the literatures in which we could find only one case who had craniotomy for associated intracranial hemorrhage. Case 1: A 41-year-old female with the history of unknown hemorrhagic diathesis complained of headache and right hemiparesis on August 2, 1980. CT scan showed left parietal intracerebral hematoma caused by unknown hemorrhagic diathesis and operated on under fresh blood transfusion. Postoperative state was uneventful but bleeding from the operated wound and rebleeding in the operated hematoma cavity were found on 5th postoperative day. The screening test for factor XIII was abnormal but replacement therapy with fresh plasma and factor XIII failed to control hemorrhagic diathesis. The patients died of GI bleeding and recurrent intracerebral hematoma on 21st postoperative day. Case 2: A 1.4-year-old boy with the history of umbilical bleeding on delivery and diagnosed as congenital deficiency of factor XIII in the other hospital fall down and struck his occiput on September 20, 1980. He vomited and became stuporous two days after injury, and was transferred to Ryukyu University Hospital. CT can revealed epidural hematoma at the left posterior fossa which extended to the supratentorium. The hematoma was successfully evacuated under infusion of fresh plasma and he showed uneventful recovery without rebleeding by postoperative appropriate replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
No Shinkei Geka 1984 Sep
PMID:[3 operated cases of congenital deficiency of Factor XIII associated with intracranial hematomas]. 650 54

The authors report spongy degeneration in experimental scrapie (second passage) in mice. The scrapie agent was originally isolated from Suffolk sheep imported from Canada and diagnosed histopathologically to be infected with scrapie by intracerebral inoculation into JCL/ICR mice. Ten female SIc/ICR mice, 4 weeks of age, were injected intracerebrally in the right frontal lobus with 20 microliter of 10(-1) or 10(-4) dilution of JCR/ICR mice brain homogenate involving scrapie agent. All animals showed signs of the advanced stages of the disease, clinically manifested by lassitude, arched backs, lethargy and paresis of hind quarters. They were sacrificed five to six months post inoculation, and sections of the brain and spinal cord were examined by light and electron microscopy. Focal symmetrical spongiform lesions were seen light microscopically in the cerebral mantle, thalamus, hypothalamus, midbrain, medulla oblongata, cerebellum and cervical mark. There was evidence that these lesions tended to be more intense in the mice inoculated a higher concentration of scrapie agent. Astrocytic proliferation was present in the deep layer of cerebral gray matter, white matter, corpus callosum, dorsal part of hippocampus and thalamus. No leukocytic infiltration was observed. Electron microscopically, the spongiform lesions were shown to be caused by vacuolation or swelling within the neuropil, and vacuolation and focal swelling in the neuronal perikaryon. The changes in the neuronal perikaryon were caused by enlargement of endoplasmic reticulum and cisterns of the Golgi apparatus, accompanied by spherical swelling of a part of the cytoplasm. The vacuolation near or within the neuron produced deformation of the cell contours and displacement of the nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
No To Shinkei 1984 Sep
PMID:[Spongiform encephalopathy in mice inoculated with scrapie material of sheep origin]. 650 58

Zinc is essential for many metabolic and enzymatic functions in man. Deficiency of zinc in man has now been recognized to occur not only as a result of nutritional factors, but also in various disease states, including malabsorption syndromes, acrodermatitis enteropathica, Crohn's disease, alcoholism and cirrhosis of the liver. The deficiency state in human subjects exists as a spectrum extending from mild to severe degree. The clinical manifestations of mild zinc deficiency include oligospermia, weight loss and hyperammonaemia. Moderate zinc deficiency is characterized clinically by growth retardation, hypogonadism in males, skin changes, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In severe zinc deficiency states, bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorders, weight loss, intercurrent infections, hypogonadism in males and, if unrecognized, death have been observed. Zinc is needed for the functions of over 100 enzymes. It is essential for DNA, RNA and protein synthesis and, as such, is important for cell division. Zinc is an inducer of mRNA of metallothionein, a protein which may have an important role in the regulation of intestinal zinc absorption. Zinc has a specific effect on testes in animals and man. Recent reports indicate that in human subjects thymopoietin may be zinc dependent and in animal studies somatomedin may be affected adversely due to dietary zinc restriction. Zinc plays an important role in the protection of cell membrane integrity and may be protective against free radical injury. Zinc is known to compete with cadmium, lead, copper, iron and calcium for similar binding sites. In the future, a potential use of zinc may be to alleviate toxic effects of cadmium and lead in human subjects. Recent evidence suggests that thymic-dependent lymphocytes (T cells are zinc dependent. T-helper and suppressor cells, T-effector cells and T-natural killer cells appear to be zinc dependent. Zinc is also essential for some of the neutrophil functions. Thus, it appears that zinc may play an important role in immunity. One may suggest that some of the clinical features of cirrhosis of the liver, such as testicular atrophy, loss of body hair, night blindness, poor wound healing, poor appetite, susceptibility to infections and enhanced sensitivity to drugs, may be related to conditioned deficiency of zinc, future studies are required to determine whether or not zinc supplementation is beneficial to these patients.
Clin Gastroenterol 1983 Sep
PMID:The role of zinc in gastrointestinal and liver disease. 661 39

Chronic renal failure was diagnosed in 6 young Standard Poodles from 2 related litters. Clinically, the disease was characterized by polydipsia, polyuria, anorexia, lethargy, vomiting, and bony deformities suggestive of fibrous osteodystrophy. Laboratory evaluation revealed azotemia and hypercholesterolemia in all 6 dogs and nonregenerative anemia in 3 dogs. Two dogs had hyperphosphatemia and another 2 were hypercalcemic. Isosthenuria and proteinuria were found in both dogs for which urinalyses were available. The kidneys were characterized pathologically by interstitial fibrosis, variable interstitial infiltrates of lymphocytes and plasma cells, tubular atrophy, tubular dilatation, tubular basement membrane mineralization, cystic glomerular atrophy, and immaturity of glomeruli, with inconspicuous capillary lumens.
J Am Vet Med Assoc 1983 Sep 15
PMID:Juvenile renal disease in related Standard Poodles. 662 80

Episodic hyperhidrosis and hypothermia are the primary symptoms of a rare central nervous system disorder of thermoregulation which is often associated with agenesis of the corpus callosum and can present in childhood or adult years. During attacks, patients may exhibit confused, withdrawn, and lethargic behavior and ataxia or other neurologic symptoms. A 21-year-old man with temperature chronically between 30 and 32 degrees C transiently responded to phenobarbital and to cyproheptadine therapy. A 34-year-old woman with frequent, brief episodes of hypothermia and hyperhidrosis improved with chlorpromazine treatment. Episodic thermoregulatory disturbance has been attributed to "vagal attacks" or "diencephalic epilepsy," but the pathophysiology remains undefined.
Neurology 1983 Sep
PMID:Episodic hyperhidrosis, hypothermia, and agenesis of corpus callosum. 668 46

Chronic depletion of body chloride developed in a group of infants ingesting a diet consisting almost exclusively of chloride deficient Neo-Mull-Soy. Ten of the 12 infants were on this diet three to five months before loss of appetite, failure to thrive, muscle weakness, and lethargy led to a diagnostic evaluation. The outstanding laboratory features were severe hypokalemic metabolic alkalosis, low urinary chloride concentrations (< 10 mEq/liter), and erythrocyturia. There was marked decrease in weight for age in all 12 infants. Head circumference for age had decreased in five of six and length for age in five of ten infants for whom earlier measurements were available. The biochemical abnormalities reverted to normal following dietary supplementation with either sodium or potassium chloride. Appetite, affect, and muscle strength improved, and weight gain resumed. Head circumference for age has moved toward the percentile level present prior to starting Neo-Mull-Soy in all instances. With one exception, length measurements show a similar pattern. The erythrocyturia has decreased or vanished. Chloride deficiency led to contraction of the extracellular volume and the substitution of poorly reabsorbable anions for readily reabsorbable chloride. These alterations caused development of the negative hydrogen ion and potassium balances which led to the hypokalemic metabolic alkalosis.
Pediatrics 1980 Sep
PMID:The dietary chloride deficiency syndrome. 693 41

A Phase I trial of acivicin [L-(alpha S,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid] has been performed on an escalating-dosage 24-hr continuous i.v. infusion schedule. Thirty-one patients received 77 courses of treatment, and all but one were evaluable for toxicity. Pharmacological monitoring in selected patients demonstrated that peak plasma levels correlated with dose. Postinfusion t1/2 beta was 6 to 9 hr, and urinary recovery of the administered dose was 14 to 19% as unchanged drug during the 24-hr infusion. Hematological and gastrointestinal toxicities were variable and not dose related. In contrast, neurotoxicity characterized by lethargy, fatigue, confusion, disorientation, hallucinations, nightmares, and truncal ataxia was dose limiting and related to plasma drug levels. A minimal antitumor response was observed in a patient with colorectal carcinoma, and a partial response occurred in a patient with liver metastases from gastric carcinoma. The recommended dose for Phase II trial by 24-hr infusion is 160 mg/sq m.
Cancer Res 1982 Sep
PMID:Phase I and pharmacological study of acivicin by 24-hour continuous infusion. 710 49

The clinical signs and gross and microscopic lesions of Lassa virus infection in the rhesus monkey are described. Of 17 monkeys infected with Lassa virus, nine died or were killed when moribund. The clinical signs were lethargy, aphagia, constipation, fever, conjunctivitis, and skin rash. Pulmonary congestion, pleural effusion, pericardial edema, hydropericardium, and a few visceral hemorrhages were present grossly. Major microscopic lesions were necrotizing hepatitis and interstitial pneumonia. Other microscopic changes were present in the heart, small intestine, spleen, lymph nodes, kidney, urinary bladder, adrenal glands, and central nervous system; however, most of these lesions were mild. In fact, death could not always be attributed to the morphologic changes; therefore, function alterations must be examined.
Am J Trop Med Hyg 1982 Sep
PMID:Pathology of Lassa virus infection in the rhesus monkey. 712 56

Computed tomography in a 3 1/2-year-old boy with ataxia, lethargy, fever, vomiting, and increasing irritability revealed moderate hydrocephalus and a blood density mass lesion lying superior and posterior to the 3rd ventricle. On several of the sections, the blood density was greater in the dependent than in the superior portion of the mass. The average attenuation number within the mass was 40 EMI units. The infusion of contrast agent demonstrated capsular enhancement (a target sign), which was also demonstrated by angiography. The diagnosis, which was confirmed at operation, was thrombosis of an aneurysm of the vein of Galen. The massive thrombus was resected, but the aneurysm was not excised. The patient's recovery was uneventful.
Neurosurgery 1980 Sep
PMID:Thrombosed aneurysm of the vein of Galen. 720 47

Maytansine, a new ansa macrolide antitumor antibiotic, was administered to a total of 107 patients in a Phase I-II study. Dose-limiting toxic reactions which occurred at 0.75-1.0 mg/M2 in both Phase I and II were neurologic and consisted primarily of lethargy/weakness (a debilitation syndrome) and paresthesias. Gastrointestinal and neurologic toxic reactions increased in frequency and severity as a function of dose. Myelosuppression, while infrequent, occurred only in previously treated patients. Changes in liver function tests were subclinical. Two partial remissions were observed at a dose-level of 0.5 mg/M2 in Phase I:1 patient with squamous cell carcinoma of the lung responded for five weeks, while the other patient with adenocarcinoma of the lung responded for four weeks. One partial remission, lasting 14 weeks was seen in Phase II in a patient with malignant melanoma treated at dose-level of 1.0 mg/M2. All responses were in heavily pretreated patients. pairs of small bowel biopsy specimen used to define the mitotic index demonstrated peak mitotic arrest at 24 hours in contrast to vinca alkaloids which appear to have a peak mitotic arrest at 12-24 hours.
Cancer 1980 Sep 01
PMID:A phase I-II study of maytansine utilizing a weekly schedule. 721 95


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