Cases reported "Alcoholism"

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1/7. Subacute endocarditis due to erysipelothrix rhusiopathiae.

    erysipelothrix rhusiopathiae is a rare cause of endocarditis. Most cases were observed in people working with animals. We report a case in a 45-year old man without any exposure to animals. He was admitted to our hospital because of dyspnoea. blood cultures were drawn following fever on day 8 of hospitalisation. erysipelothrix rhusiopathiae was cultured and echocardiography showed a vegetation on the mitral valve. Appropriate antibiotic therapy and surgical treatment led to a good outcome of the infection.
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keywords = animal
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2/7. Complete and prolonged suppression of symptoms and consequences of alcohol-dependence using high-dose baclofen: a self-case report of a physician.

    AIMS: To test whether the dose-dependent motivation-suppressing effect of baclofen in animals could be transposed to humans, and suppress craving and sustain abstinence. methods: Neurologists safely use up to 300 mg/day (10 times the dosage currently used for alcohol dependence) of high-dose oral baclofen, to control spasticity, in order to avoid invasive therapy. I am a physician with alcohol dependence and comorbid anxiety. I self-prescribed high-dose baclofen, starting at 30 mg/day, with 20 mg increments every third day and an (optional) additional 20-40 mg/day for cravings. RESULTS: Cravings became easier to combat. After reaching the craving-suppression dose of 270 mg/day (3.6 mg/kg) after 5 weeks, I became and have remained free of alcohol dependence symptoms effortlessly for the ninth consecutive month. anxiety is well controlled. Somnolence disappeared with a dosage reduction to 120 mg/day, now used for the eighth consecutive month. CONCLUSIONS: High-dose baclofen induced complete and prolonged suppression of symptoms and consequences of alcohol dependence, and relieved anxiety. This model, integrating cure and well-being, should be tested in randomized trials, under medical surveillance. It offers a new concept: medication-induced, dose-dependent, complete and prolonged suppression of substance-dependence symptoms with alleviation of comorbid anxiety.
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keywords = animal
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3/7. Severe monochlorobenzene-induced liver cell necrosis.

    benzene derivatives can induce severe liver cell necrosis in animals. A case of a 40-year-old man whose daily consumption of alcohol was 200 g and who had a severe monochlorobenzene-induced liver necrosis is described. liver biopsy specimen showed centrilobular and mediolobular necrosis, similar to that in mice after experimental bromobenzene administration. Monochlorobenzene serum concentration, assayed from day 3 to day 15 after poisoning, decreased monoexponentially with a half-life of 40.3 hours. Prostaglandin E1 was administered from day 3 to day 8. The patient ultimately recovered. The mechanism of monochlorobenzene-induced liver injury and the possible aggravating role of chronic alcohol consumption are discussed.
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keywords = animal
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4/7. Factitious elevation of thyrotropin in a new ultrasensitive assay: implications for the use of monoclonal antibodies in "sandwich" immunoassay.

    Three patients who had falsely elevated serum TSH concentrations (initial values, 30.5, 74, and greater than 50 mU/L) in a mouse monoclonal immunoradiometric assay are reported. Two patients were treated for hypothyroidism inappropriately, and one underwent unnecessary diagnostic testing. Immunoaffinity chromatography of serum from one patient indicated that the serum TSH level was truly low. Addition of mouse serum or immunoglobulin g (IgG) or absorption of patient serum with solid phase-bound mouse IgG-1 reduced the TSH content in the serum of the three patients to undetectable levels. Blocking studies revealed that all patients had antibodies directed at mouse IgG-1, the subclass of mouse antibody present in the assay kit. The serum of one patient who had autoimmune disease with elevated serum Igs had much broader species cross-reactivity than that of another patient who had known exposure to rats and mice. We hypothesize that such antimouse antibodies can arise either from endogenous autoimmunity or exogenous animal exposure. serum TSH elevations also were found when the serum samples were tested in other mouse monoclonal immunoassays, underscoring the fact that antibody interference can potentially affect many assays used in endocrinology and other areas of medicine to make major diagnostic and therapeutic decisions. Clinicians must be aware of such interactions; relatively simple laboratory maneuvers can differentiate true from false results in assays of this type.
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keywords = animal
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5/7. Steatosis of granular pneumocytes in alcoholics with acute alveolar injury.

    Accumulation of neutral lipid in the type II alveolar epithelial cells of the lung has been described in experiments involving animals with conditions such as hypoxia or on alcohol administration. In two cases involving human subjects, this change was observed at autopsy by histochemical stains and electron microscopy. In both instances, the patients had had severe alcoholic liver disease, as well as extreme hypoxia resulting from acute alveolar injury. The lungs of six alcoholic patients with liver disease but without acute alveolar injury showed no lipid vesicles on histochemical staining. These observations suggest that a metabolic insult or combination of insults, such as alcohol or hypoxia, might lead to accumulation of neutral lipid, especially in regenerating alveolar epithelial cells that may be more susceptible to such injury.
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keywords = animal
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6/7. Filamentous axonopathy in disulfiram neuropathy.

    A 52-year-old female developed a sensorimotor polyneuropathy while on treatment with disulfiram. Electron microscopic examination of a sural nerve biopsy disclosed occasional axons distended by intermediate filaments. Identical changes can be induced in animals by carbon disulfide (CS2), a metabolite of disulfiram. Our findings suggest that disulfiram neurotoxicity is mediated by CS2 and is exerted on the distal axon.
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keywords = animal
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7/7. hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome.

    Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
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keywords = animal
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