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)

Chronic hypertrophic gastritis in a 7-year-old Boxer dog is described. This gastritis resembles Menetrier's disease in man. The dog was emaciated, lethargic, vomiting and had a poor appetite over a 4-month period. There was anaemia, and the blood smear was characterized by hypochromasia, strong anisoplania and striking poikilocytosis. There was a protein loss and at a later stage of the disease, a hypoalbuminaemia. On gastroscopic examination the plicae gastricae were numerous and strongly marked; moreover, they were granulated with numerous small haemorrhages. Radiographically, the stomach had a marked folding, primarily at the greater curvature. The passage of contrast medium from the stomach into the duodenum was strongly retarded. The pathological findings included macroscopical folding caused by local gland cell hyperplasia in the body as well as the pylorus, foveolar hyperplasia and, in the fundus and in the corpus near the greater curvature, folding of the muscularis mucosae and the submucosa. A superficial gastritis was found particularly in the fundus and corpus, whereas the pyloric antrum showed a more diffuse inflammation.
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PMID:A boxer dog with chronic hypertrophic gastritis resembling Menetrier's disease in man. 93 24

Urea cycle disorders and other hyperammonemic syndromes should be considered in the differential diagnosis in newborns with a history of severe vomiting, lethargy, and seizures, and in infants with feeding problems, episodic vomiting, and altered consciousness. Although the acute neonatal forms of urea cycle disorders are almost always lethal, several of the subacute forms of hyperammonemic syndromes respond favorably to early treatment.
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PMID:Congenital hyperammonemic syndromes. 95 43

As a causative factor in spontaneous subarachnoid hemorrhage, vascular anomalies, especially aneurysm or arteriovenous malformation, have been generally recognized. On the other hand, subarachnoid hemorrhage from brain tumor and cryptic vascular malformation are rare. We experienced two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma as an initial symptom. Case 1: A 48-year-old woman, who complained of severe headache and vomiting on Feb. 10th, 1972, gradually became lethargic. Lumbar puncture revealed moderately hemorrhagic C.S.F.. On the fifth day after the onset, she was admitted to our hospital. On admission she showed disorientation and disturbance of resent memory. Aphasia and agnosia were slightly observed. On ophthalmologic examination right homonymous lower quadrant hemianopsia was observed. The carotid angiogram showed slight square shift of the anterior cerebral artery to the right side, elevation of the middle serebral artery and a homogeneous tumor stain in the occipital region in capillary phase. A walnut sized tumor invading the middle portion of the left lateral sinus and showing firm adhesion to the tentrium was found. There was an intracerebral hematoma behined the tumor. The tumor, the tentrium and the lateral sinus were extirpated en bloc and the intracerebral hematoma was aspirated. Histologically, the tumor was angioblastic meningioma. Case 2: A 7-year-old boy, who complained of severe abrupt headache, nuchal pain and vomiting on Sept. 17th, 1972, became gradually lethargic. Lumbar puncture revealed hemorrhagic C.S.F., On the tenth day after the onset, he was admitted to our hospital. He showed confusion and agitation. The carotid angiogram showed an unrolling of the pericallosal artery, but no findings of space taking lesions. An air study indicated a globular filling defect protruding into the anterior horn of the right lateral ventricle. The tumor located in the laterobasal wall of the anterior horn was removed picemiel by transventricular approach. Histologically, the tumor was vascular hamartoma. Furthermore, we discussed various brain tumors showing subarachnoid hemorrhage as an initial symptom, its frequency and bleeding mechanism on the literature.
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PMID:[Two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma (author's transl)]. 98 94

A case of lactic acidosis associated with phenformin therapy for diabetes mellitus is reported, and 34 previously reported cases of lactic acidosis associated with phenformin therapy are reviewed to determine if any predisposing factors to lactic acidosis were apparent. Observations of sex, age, duration of diabetes, pathologic conditions, dosage, duration of phenformin therapy and the onset of symptoms preceding lactic acidosis were made. Renal impairment, urinary tract infections, hepatic impairment, ethanol ingestion and poorly controlled congestive heart failure were found to be predisposing factors to lactic acidosis. The appearance of a syndrome of impending lactic acidosis consisted of anorexia, nausea, vomiting with abdominal pain or lethargy.
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PMID:Phenformin-associated lactic acidosis; a review. 114 21

This report, which describes an epidemic of St. Louis encephalitis in northwestern Mexico, was prompted by the apparent infrequency of previous Mexican outbreaks of this disease. The site of the epidemic was the Municipality of Hermosillo in the State of Sonora. This municipality, with a population of about 273,000, is situated in a hot flat area which is naturally dry but which is also well-irrigated. Here, over an eithy-week period, 51 persons became ill and were hospitalized with symptoms including fever, vomiting, stiff neck, lethargy, and increased cell/protein levels in their cerebrospinal fluid. Sera from 12 of these patients were tested for SLE antibodies by hemagglutination inhibition, complement fixation, and neutralization. The results of these tests were positive and showed a fairly high degree of correlation. In addition, paired serum samples showed a significant rise in SLE antibody titers. Over half of the cases occurred in the City of Hermosillo, the municipal seat; the remainder occurred in 13 outlying areas, most of them quite nearby. Virtually all of the city dwellers affected were residents of low-income districts. The rate of hospital cases was roughly 19 per 100,000 inhabitants, and the case-fatality rate among these cases was approximately 20 per cent. The ratio of male to female patients was 1.3 to 1; sixty-nine per cent of the patients were under 16 years of age.
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PMID:St. Louis encephalomyelitis in Hermosillo, Sonora, Mexico. 121 40

Intussusception is the most frequent cause of intestinal occlusion in children aged 3-5 years. Diagnosis is easy to perform in cases with typical clinical presentation. However diagnosis may be difficult in rare cases with atypical symptoms characterized by SNC involvement, that could delay a convenient treatment. We report 4 cases of intussusception presenting initially with consciousness abnormalities, hypotonia and vomiting. In these cases differential diagnosis with other conditions associated with comatose states has to be performed. Some hypothesis may be considered to explain these clinical pictures: 1. increased endorphins excretion during abdominal pain; 2. neurotoxins of bacterial origin released and absorbed by altered bowel; 3. intestinal hormones abnormally produced during the disease. As recommended by Rachmel, the condition should be suspected in all children presenting with the association of vomiting and lethargy and a radiological or tomographic study of abdomen should be performed also in cases without intussusception typical symptoms.
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PMID:[Changes in the consciousness state as a symptom of intestinal invagination onset]. 129 38

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

We reported a clinical course and autopsy results of an 8-year-old severely handicapped girl with marked periventricular leukomalacia. She was well until 3 days prior to first admission in local hospital. Two days prior to admission, she began to vomit. Twelve hours later, she was noted to be lethargic and developed malaise with frequent vomiting. At physical examination on admission, she had frequent fits and her posture was decerebrate rigidity. Consciousness disturbance continued for two weeks. Thereafter, she became severely handicapped with spastic quadriplegia, mental retardation and intractable epilepsy. She was transferred to our hospital one month later. We cared her totally and carefully with our rehabilitation staff, but during her course several rare happening occurred; she suffered from subdural hemorrhage due to hypocupremia and received an operation for the release of contracture of her hips. She died of acute cardio-respiratory failure at 8 years and 5 months of age. Her autopsy findings were characteristic of the damage to an immature brain during development; cactus formation of cerebellar cortex and periventricular leukomalacia.
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PMID:[A clinical course and autopsy results of an 8-year-old severely handicapped girl with marked periventricular leukomalacia]. 138 94

Medical records of 11 cats with lymphoma involving large granular lymphocytes were reviewed. All 9 cats tested were FeLV-negative. Ten cats had a history of anorexia, lethargy, vomiting, or diarrhea, and had lymphoma involving abdominal viscera. The most common site of tumor in these cats was the jejunum. One cat had cutaneous masses caused by dermal and epidermal infiltration with neoplastic large granular lymphocytes. The most common hematologic abnormality was leukocytosis, characterized by neutrophilia with a left shift (7 cats); 2 cats had a left shift without neutrophilia. None of the cats had lymphocytosis, but immature large granular lymphocytes were found in the blood of 4 cats. The most common serum biochemical abnormalities were hypoalbuminemia (10 cats), hypocalcemia (10 cats), hypoproteinemia (9 cats), high aspartate transaminase activity (9 cats), and hyperbilirubinemia (8 cats). Large granular lymphocytes were characterized by abundant cytoplasm containing distinct azurophilic granules that varied in size and number. The most common cytochemical staining pattern included detection of alpha-naphthyl butyrate esterase, acid phosphatase, and beta-glucuronidase activities. On examination of histologic sections, granules stained weakly eosinophilic with Giemsa and moderately with periodic acid-Schiff reaction. Ultrastructurally, the granules appeared membrane bound and contained an electron-dense matrix in 4 cats.
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PMID:Lymphoma involving large granular lymphocytes in cats: 11 cases (1982-1991). 142 72

Therapeutic use of the anticonvulsant valproate (VPA) has been associated with a rare, but severe and often fatal hepatotoxicity. Cases usually present with lethargy, anorexia, and vomiting with rapid progression to coma. Liver histopathology is characterized by steatosis with and without necrosis. In some instances only necrosis was present. Several hypotheses of pathogenesis have been postulated. These deal mainly with biochemical systems that are known to be affected by VPA, or with the possible idiosyncratic production of toxic VPA metabolites, especially delta 4-VPA. At present, no hypothesis entirely explains the diverse characteristics of the disorder.
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PMID:Valproate hepatotoxicity syndrome: hypotheses of pathogenesis. 150 10


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