Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Recognition of adrenal atrophy during a review of autopsy findings in two sisters who died at 8 months and 3 1/2 years prompted estimation of very long chain fatty acids, phytanic acid and pristanic acid on wet liver fixed in formalin for 12 years. These were shown to be markedly increased and defects in multiple peroxisomal functions and decrease in particulate catalase were shown in cultured fibroblasts, confirming an abnormality of peroxisomal biogenesis. The patients had presented with failure to thrive, recurrent diarrhoea and vomiting, poor mental development, retinal pigmentation, blindness and in the older patient deafness, with only mild dysmorphic features. Autopsy in the older patient showed adrenal atrophy, cirrhosis, and foamy histiocytes in multiple organs. The brain showed no demyelination, little cytoarchitectural abnormality, occasional perivascular histiocytes in the grey matter and meninges and prominent Purkinje cells in the molecular layer of the cerebellum. In the younger patient the changes were very subtle in spite of the marked clinical similarity. Despite the young age at death the clinicopathological features are most suggestive of infantile Refsum disease. In many situations anatomical pathology can be very useful in the recognition and study of peroxisomal disorders.
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PMID:Autopsy findings in two siblings with infantile Refsum disease. 137 19

Cutaneous histiocytosis may take two principal forms. It is either a benign proliferative process or a relentless, progressive process with a poor prognosis. In histiocytic medullary reticulosis, histiocytes demonstrate nuclear atypia and the outcome is uniformly fatal. Benign cephalic histiocytosis X causes lesions similar to those of histiocytosis X, but Langerhans' cells are absent. In congenital self-healing histiocytosis X, the Letterer-Siwe-like cutaneous infiltrate contains Langerhans' cells, but the lesions heal spontaneously without treatment. The nodular cutaneous lesions of juvenile xanthogranuloma appear in infancy and resolve without treatment; however, the higher percentage (10%) of associated ocular lesions may lead to glaucoma and blindness. In histiocytosis X, the cutaneous lesions show a marked proliferation of Langerhans' cells, with prognosis dependent on the patient's age and the extent of organ dysfunction. Patients who survive the acute form of the disease may develop diabetes insipidus, growth retardation, pulmonary fibrosis, and biliary cirrhosis. A subtle immunologic defect has been identified in patients with histiocytosis X, yet the pathogenesis of the disease is still speculative. Familial disease occurring in early infancy should be differentiated from complete or partial immunodeficiency syndromes. Guidelines for evaluating patients with cutaneous histiocytosis are reviewed.
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PMID:Cutaneous histiocytosis syndromes. 299 40

We report a case of recurrent hepatic encephalopathy accompanied by transient cortical blindness. The patient with cryptogenic liver cirrhosis had six attacks of hepatic encephalopathy of grades II to III during 1 yr after admission. In the beginning of each episode of encephalopathy, when the patient was conscious, a complete loss of vision occurred, but with a normal pupillary reflex to light. At the same time, the visual evoked potential recorded the second negative wave with a prolonged latency and a diminished amplitude. His sight completely returned, and the electroencephalogram tracing and the visual evoked potential response normalized after treatment for the encephalopathy. The loss of vision was thought to be cortical blindness accompanied by hepatic encephalopathy. Thus, in rare cases of hepatic encephalopathy, the visual cortex may be affected, and cortical blindness may occur before the loss of consciousness.
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PMID:Hepatic encephalopathy and reversible cortical blindness. 338 12

Trachomatous tarsitis is characterized by personal criteria the development of a fibrous and retractile scar tissue inducing cirrhosis with static and hemodynamic changes of the eye lid: lesions of the ciliary stratum, entropion and trichiasis which in their turn give a range of conjunctivocorneal complications, the ultimate stage being xerosis and blindness. To avoid this kind of evolution some easy surgical technics are available. The option between them is mainly oriented by personal criteria and the following pattern may be proposed: -- For upper lid, in regard to degree of tarsis hypertrophy, either Trabut's tarsotomy, or Streatfield-Snellen's tarsectomy, or a joint intervention of Cuenod and Nataf, might be selected. -- For lower lid and in children, the Trabut's transconjunctival tarsotomy is recommended. -- In relapsing cases and when trichiasis prevails over entropion, Van Millingen's marginoplasty will give satisfactory results.
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PMID:[Trachomatous tarsitis: its consequences and their surgical treatment (author's transl)]. 701 38

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

The rhino-orbito-cerebral mucormycosis is an acute rapidly progressive fungal infection. This disease is caused by a zygomycetes fungus, most often from the Rhizopus genus. This fungus is saprophitic of the nasal cavity and paranasal sinuses. It becomes pathogenic in some particular conditions, specially during diabetes mellitus. Histopathological study is the only method allowing the diagnosis, by revealing the tissue invasion by characteristic hyphae. Mycologic study allows a definitive identification of the fungus. The authors report a case of rhino-orbito-cerebral mucormycosis in a 44 year-old woman with cirrhosis. She presented an acute blindness and ophthalmoplegia. Despite of a rapid histologic diagnosis from the nasal and ethmoidal biopsies, the patient died 3 days after.
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PMID:[Rhino-orbito-cerebral mucormycosis caused by Rhizopus oryzae.A typical case in a cirrhotic patient]. 839 43

We report an autopsy case of 53-year-old male with poor controlled diabetes mellitus and hepatocellular carcinoma who developed rhino-orbito-cerebral mucormycosis. Initial complaints were epistaxis and headache followed by a sudden blindness, the 2nd through 7th cranial nerve palsy and diabetes inspidus. Laboratory data revealed that he had liver cirrhosis due to hepatitis C virus infection and diabetes mellitus. Head CT and MRI showed no significant findings. Eleven days after the onset, he died of subarachnoid hemorrhage. The postmortem examination revealed severe infiltration of numerous mucors in the sphenoid sinus, cavernous sinus and bilateral internal carotid arteries. Severe granulomatous vasculitis was seen in the cavernous portion of the bilateral internal carotid arteries. Thus, we considered that this case had been caused by the infiltration of mucors to the cavernous sinus, resulting in the obstruction of ophthalmic arteries. Rupture of the right internal carotid artery was seen at the branching portion of the ophthalmic artery, demonstrating the cause of his death. We would like to emphasize that rhino-orbito-cerebral mucormycosis should be ruled out if we examine a nondiagnostic case of diabetes mellitus or immunosuppressed disease associated with rapid multiple cranial nerve palsy following the orbital symptoms.
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PMID:[An autopsy case of rhino-orbito-cerebral mucormycosis associated with multiple cranial nerve palsy and subsequent subarachnoid hemorrhage]. 971 Nov 24

We report the case of a 66-year-old man with chronic hepatitis C and a slowly growing left chest wall mass. Two years after the patient first noticed the mass, it was resected. A diagnosis of hepatocellular carcinoma (HCC) was established. The liver was studied by ultrasound, computed tomography (CT), magnetic resonance imaging (MRI) and angiography, but no mass was found. Blind liver biopsy showed mild chronic hepatitis without cirrhosis or HCC. Three years after the discovery of the chest wall HCC, no liver mass had appeared at CT and MRI. We conclude that solitary extrahepatic HCC (i) may arise in ectopic liver tissue; (ii) should not be considered as a metastasis of an occult HCC; and (iii) can be amenable to cure through resection.
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PMID:Ectopic hepatocellular carcinoma arising in the left chest wall: a long-term follow-up. 1147 20

In a cattle herd problems were noticed during 1.5 years, characterised by emaciation and loss of milk production with lower fat- and protein%, tenesmus, central nervous symptoms (aggression, circling and blindness), diarrhoea, eczema solare and death. Clinical, laboratory and post mortem examinations did not reveal a specific cause at first. An intoxication was suspected based on the clinical symptoms, the course of the disease in sick animals and severe liver cirrhosis found in a sudden death cow: The animals were fed grassilage derived from an air force base on which an overwhelming amount of tansy ragwort (Senecio jacobaea) was present. On subsequent microscopic examination of the livers of 11 slaughtered clinically healthy animals all of these showed fibrosis in varying extension. Cirrhosis and fibrosis of the liver and the clinical symptoms are all features of chronic pyrrolyzidine alkaloidosis. Tansy ragwort poisoning has not been diagnosed in the Netherlands for years. The rise in cases is due to more extensive use of land.
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PMID:[Senecio jacobaea: deceiving beauty. Senecio jacobaea poisoning]. 1262 61


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