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)

Interferon (IFN) related neurotoxicity includes somnolence and confusion, fatigue, lethargy, psychiatric symptoms, conceptual disorganization, neurological deficits, cortical blindness, coma and, rarely, death. The neurologic syndromes seem to be more common in elderly patients, following intramuscular or intravenous administration, at higher doses of frequent injections of IFN-alpha and in primary renal cell carcinoma. The duration of the treatment was not strongly related to neurotoxicity. Computed tomography findings were non-specific and included atrophy or periventricular lucencies. Electroencephalograph studies demonstrated a generalized increase in slow wave activity which returned to normal after cessation of treatment. Behavioral and mental changes in patients treated with IFN are warning signs, and indicate the need to withdraw treatment.
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PMID:Neurotoxicity of interferon-alpha. 128 26

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

In September 1991 cataracts occurred in two year-classes of triploid Atlantic salmon. The fish showed varying degrees of blindness, were lethargic and became emaciated owing to their inability to feed. The lesions in the lens were mainly in the anterior and posterior cortex and perinuclear areas, the capsule and embryonic nucleus remaining unaffected. Diploid fish of the same year-class did not have cataracts. The origin of the triploid fish, the method of triploidisation, their diet and disease status were investigated, but no predisposing factors could be found to account for the high incidence of cataracts.
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PMID:Occurrence of cataracts in triploid Atlantic salmon (Salmo salar) on four farms in Scotland. 148 45

Rostral and middle cranial fossa tumors affecting the optic chiasm and resulting in acute visual deficits were diagnosed in 7 dogs and 1 cat. Blindness and dilated nonresponsive pupils were the primary signs in all animals. Other concurrent neurologic deficits were either absent or were equivocal. Behavioral changes, including signs of depression and lethargy, were noticed in 1 dog and the cat subsequent to the onset of blindness. Retinal function was assessed as normal by electroretinography in all animals. The histologic necropsy diagnosis was pituitary carcinoma in 1 dog and the cat and paranasal sinus carcinoma with intracranial extension in 1 dog. A cytologic diagnosis of polycentric lymphosarcoma affecting the optic chiasm was diagnosed in 1 dog. In the remaining 4 dogs, results of computed tomographic imaging or endocrine function testing suggested pituitary gland neoplasia. Four dogs were treated with cobalt-60 radiation or chemotherapy. There was partial return of visual function in only 1 of the dogs treated with radiation.
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PMID:Acute blindness associated with intracranial tumors in dogs and cats: eight cases (1984-1989). 195 68

School performance testing was completed at 8 years of age on 145 children who had had neonatal encephalopathy associated with birth asphyxia as term infants and on a comparison peer group of 155 children. The prospectively identified clinical categories of encephalopathy for the neonates were 56 mild (hyperalertness, hyperexcitability), 84 moderate (lethargy, hypotonia, suppressed primitive reflexes), and 5 severe (stupor, flaccidity, absent primitive reflexes). The mortality rate to 8 years of age was 13%. The incidence of impairment, which included cerebral palsy, blindness, cognitive delay, convulsive disorder, and severe hearing loss, was 16% among those assessed at 8 years (75% of survivors). Intellectual, visual-motor integration, and receptive vocabulary scores, as well as reading, spelling, and arithmetic grade levels for those with moderate or severe encephalopathy, were significantly below (p less than 0.01) those in the mild encephalopathy or peer comparison groups. Predictors of reading performance for the study group included category of encephalopathy, birth weight for gestational age, native language, and mother's educational level (multiple R = 0.58). Nonimpaired survivors of moderate encephalopathy were more likely to be more than one grade level delayed than were children from the peer group (reading 35% vs 15%, spelling 18% vs 8%, arithmetic 20% vs 12%, p less than 0.01). Thus children who had moderate and severe neonatal encephalopathy are at risk for physical and mental impairment and reduced school performance. Children with mild encephalopathy had school performance scores similar to those of their peers.
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PMID:School performance of survivors of neonatal encephalopathy associated with birth asphyxia at term. 246 89

A case of malignant choroid plexus papilloma (choroid plexus carcinoma) originated in the third ventricle is reported. A 14-month old girl was admitted to our department with two-month history of impaired vision and gait disturbance. Neurological examination on admission disclosed a lethargy, blindness, and left hemiparesis. Computed tomographic (CT) scan and magnetic resonance imaging (MRI) demonstrated a large contrast-enhancing mass, approximately 5 cm in diameter, in the region of third ventricle, extending to the bilateral lateral ventricles. The patient had gross total removal of the tumor via lateral ventricle route, and received 40 Gy of postoperative radiation therapy. Light microscopically, the tumor was composed of epithelial cells showing both papillary and poorly differentiated pattern. There were considerable cellular pleomorphism, frequent mitoses, and occasional necroses. Immunohistochemically, anti-keratin antibody was detected within majority of neoplastic cells. Both neoplastic epithelial cells and stroma showed negative reaction to anti-GFAP antibody. Ultrastructurally, the shape of the nuclei varied from ovale to irregular with many indentations. The chromatin was clumped around the periphery of the nuclei. The neoplastic cells contained numerous free ribosomes, glycogen granules, and rough endoplasmic reticulum. The apical cell surfaces showed various size of club-like or roundish microvilli filled with glycogen granules, and rarely 9 + 2 cilia. Elongated junctional complexes were occasionally seen near the apical ends. The basal portions of the cells had a continuous basement membrane. These immunohistochemical and ultrastructural findings were comparable to the choroid plexus papilloma with malignant features.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of large malignant choroid plexus papilloma in the third ventricle--immunohistochemical and ultrastructural studies]. 248 83

Sarcoidosis is a multisystem disease of unknown etiology that is rarely diagnosed in children. When mass screening is performed, the incidence of the disease in children approaches that of adults with similar demographics. Most childhood cases occur around ages 9 to 15 years, with small clusters of cases occurring in children under age 4 years. The disease in these two age groups has very different clinical features. Children under age 4 have a clinical triad of rash, arthritis, and uveitis. The classic syndrome in older children involves primarily lungs, lymph nodes, and eyes. In older children, constitutional symptoms (fatigue, lethargy, malaise) and pulmonary symptoms (cough, dyspnea) predominate. Mortality in childhood sarcoidosis is about 5%, with long-term sequelae in 10% to 20%. Early recognition may prevent complications such as blindness, pulmonary insufficiency, and renal impairment.
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PMID:Sarcoidosis in children. 332 85

Portosystemic shunt was diagnosed in a 6-month-old Quarter Horse filly with acute onset of apparent blindness and a 3-month history of depression, lethargy, and ataxia. Clinicopathologic test results indicated slightly high gamma-glutamyl transpeptidase activity and serum total bilirubin concentration. Sulfobromophthalein half time was prolonged, and plasma ammonia and serum bile acid concentrations were high as well. Histopathologic findings of percutaneous liver biopsy included widespread hepatocyte atrophy and numerous prominent small arterioles in the area of the portal triad. On the basis of history, clinical findings, and clinicopathologic abnormalities, a presumptive diagnosis of portosystemic vascular anomaly was made. To confirm the tentative diagnosis, nuclear hepatic scintigraphy and operative mesenteric portography were performed. Medical treatment was unsuccessful, and the foal was euthanatized. Portosystemic shunts have been described in dogs and cats, but few cases have been reported in large animal species. Other, more common causes of neurologic abnormalities in foals, such as trauma, vertebral body abscesses, brain abscesses, and meningitis, must be ruled out before portosystemic shunt is considered.
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PMID:Clinical and diagnostic features of portosystemic shunt in a foal. 335 82

Intracarotid BCNU (100 mg/m2) and cisplatin (60 mg/m2) were administered to 36 patients with malignant brain tumors recurrent or progressive after cranial irradiation. Courses of therapy were repeated at 4-6 week intervals. Of 23 evaluable patients with recurrent glioma, 9 (39%) had tumor regression by CT scan and 3 had stable disease. The median time to tumor progression for responding patients was 37 weeks. For all patients with primary tumors it was 14 weeks. Six of 9 patients with no prior chemotherapy had a response and 1 had stable disease. Of 14 patients who had received prior chemotherapy, 3 had a response and 2 had stable disease. Survival ranged from 9 weeks to 95+ weeks (median 34 weeks) from start of therapy. Six of 23 patients with primary tumors are alive 1 year or more following therapy. Four of 11 patients with brain metastases had a response and 2 had stable disease. Major neurologic toxicity of intracarotid BCNU and cisplatin appeared cumulative and consisted of reversible hemiparesis in 3% of 118 courses, TIA in 1%, expressive aphasia in 9%, lethargy in 3%, seizures in 12%, and reversible confusion in 1%. Retinal toxicity consisted of mild blurring of vision in 4 patients and ipsilateral blindness in 5 patients. Three of 22 patients who had received supraophthalmic infusion later developed evidence of leukoencephalopathy. Intracarotid BCNU and cisplatin appears to have modest increase in activity over intracarotid cisplatin alone (Cancer 54:794, 1984), however, neurologic and retinal toxicity may also be increased.
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PMID:Phase II trial of intracarotid BCNU and cisplatin in primary malignant brain tumors. 370 37

A Phase I trial of 2-beta-D-ribofuranosylthiazole-4-carboxamide (NSC 286193, tiazofurin) was conducted using a 5-day continuous infusion schedule. Twenty-four patients with advanced cancer were entered on this trial. Dose levels ranged from 360 to 2350 mg/sq m/day for 5 days. Neurotoxicity was dose limiting and occurred in six patients. Neurotoxicity was expressed as confusion, lethargy, or obtundation and was associated with focal neurological deficits in four of six patients: hemiparesis, three; cortical blindness and bilateral upper extremity weakness, one. Neurotoxicity was not clearly dose related, occurring at 900 mg/sq m/day for 5 days (two patients), 1100 mg/sq m/day for 5 days (two patients), 1850 mg/sq m/day for 5 days, and 2350 mg/sq m/day for 5 days (one patient each). Other toxicities seen were myelosuppression, desquamation of palms and soles, malar erythema, and hyperpigmentation, stomatitis, chest pain, drug fever, and increased serum creatine phosphokinase. Administered drug [71.5 +/- 11.2% (SE)] was recovered intact in the urine within 24 h of administration. Terminal-phase mean harmonic half-life was 8.0 h. The unpredictable neurotoxicity seen following continuous infusion therapy with tiazofurin suggests that Phase II trials of this schedule are not indicated until better understanding of the biochemical effects of tiazofurin is achieved.
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PMID:Phase I clinical study with pharmacokinetic analysis of 2-beta-D-ribofuranosylthiazole-4-carboxamide (NSC 286193) administered as a five-day infusion. 398 12


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