1/101. Premalignant lesions and hepatocellular carcinoma in a non-cirrhotic alcoholic patient with iron overload and normal transferrin saturation.A 66-year-old white man had a hepatic resection for a 6-cm well-differentiated hepatocellular carcinoma which had developed in a non-cirrhotic liver. The only risk factors found were heavy drinking, smoking and heterozygosity for the C282Y mutation of the HFE gene. The liver was mildly fibrotic and overloaded with iron. It also contained numerous iron-free hepatocellular lesions from <1 to 10 mm, suggesting a premalignant change. These lesions were of three types: (i) iron-free foci, (ii) hyperplastic nodules and (iii) dysplastic nodules with severe dysplasia or even foci of well-differentiated grade I hepatocellular carcinoma. This observation suggests the possibility of malignant transformation of the liver in the newly-described syndrome of iron overload and normal transferrin saturation. It also illustrates the multistep process of carcinogenesis in the non-cirrhotic liver.- - - - - - - - - - ranking = 1keywords = hepatic (Clic here for more details about this article) |
2/101. hypothermia--a sign of hypoglycemia.hypothermia may occur in association with hypoglycemia, and indeed may be the only sign. Two cases are presented. In one, the patient presented with hypoglycemic encephalopathy. In the insulin dependent diabetic, the condition is life-threatening. Subnormal temperature is a clue to hypoglycemia in the alcoholic. The mechanism of hypothermia has been extensively studied, but remains unclear.- - - - - - - - - - ranking = 32.026634176516keywords = encephalopathy (Clic here for more details about this article) |
3/101. wernicke encephalopathy-like symptoms as an early manifestation of Creutzfeldt-Jakob disease in a chronic alcoholic.A case of Creutzfeldt-Jakob disease (CJD) with presenting wernicke encephalopathy (WE)-like symptoms and severe insomnia is presented. An 80-year-old alcoholic man with a 6 month history of tremors, ataxia, memory loss and confabulation, developed profound insomnia, confusion, and delirium with vivid hallucinations. polysomnography revealed a marked reduction of sleep time, with central-type sleep apnea. Neither myoclonus nor periodic synchronous discharge (PSD) was observed. An autopsy revealed diffuse spongiform changes and astrocytosis throughout the cerebral gray matter, with severe involvement of the mammillary bodies and thalamus. Prion protein (PrP) immunostaining was positive in kuru plaques in the cerebellum, PrP polymorphism at codon 129 was heterozygous Met/Val, and proteinase K resistant PrP (PrP(res)) was demonstrated by Western blotting. The lack of necrotizing lesions in the mammillary bodies, thalamus, and periaqueductal gray matter could rule out WE. The data suggest that the present case of CJD is consistent with PrP(res) type 2 (CJD M/V 2), but was unique in the lack of some typical CJD signs and the presence of signs of WE and sleep abnormalities.- - - - - - - - - - ranking = 160.13317088258keywords = encephalopathy (Clic here for more details about this article) |
4/101. survival from profound alcohol-related lactic acidosis.We present the case of a patient with profound alcohol-related lactic acidosis (lactate = 16.1 mmol/L; pH = 6.67) associated with a multitude of metabolic derangements who made a remarkable recovery following aggressive management. The patient was in extremis upon arrival in the emergency department (ED), and resuscitation was begun immediately. While in the ED, the problem list generated included: acute alcohol intoxication, severe lactic acidosis, dehydration, hypothermia, hypoglycemia, acute renal insufficiency, and hepatic failure. resuscitation continued in the intensive care unit with remarkable improvement and satisfactory outcome. In this patient, the severe lactic acidosis and associated abnormalities were all attributed to acute and chronic effects of ethanol. A brief summary of the proposed mechanism by which these metabolic derangements developed and an outline of her management follows.- - - - - - - - - - ranking = 1keywords = hepatic (Clic here for more details about this article) |
5/101. cyanamide-induced liver dysfunction after abstinence in alcoholics: a long-term follow-up study on four cases.BACKGROUND: cyanamide, an aversive agent widely used in japan, is known to induce various degrees of hepatic lesion with ground-glass inclusion bodies. When cyanamide-treated alcoholics relapse into drinking, more severe inflammation develops in the liver. However, it is controversial whether progressive hepatic lesions develop in complete abstainers as a result of long-term cyanamide treatment. case reports: Case 1: A 53-year-old male alcoholic received cyanamide treatment for 4.5 months and completely abstained without cyanamide treatment for 6 years. A liver biopsy shortly after abstinence showed extensive pericellular fibrosis, but a biopsy after 6 years showed very mild fibrosis. Case 2: A 43-year-old male alcoholic remained completely abstinent with cyanamide treatment for 5 years and complained of general fatigue. His serum transaminases were slightly elevated and hepatic hyperechogenicity was observed on ultrasonography. Only mild pericellular fibrosis was present in the liver biopsy specimen obtained shortly after abstinence, but after 5 years the second liver biopsy showed that thin septum-like fibrosis that formed portal-to-portal and portal-to-central linkage had developed and ground-glass hepatocytes had emerged extensively. Case 3: A 29-year-old female alcoholic complained of general fatigue and a slight fever after 1.5 years of abstinence with cyanamide treatment. Slight elevation of serum transaminases and hepatic hyperechogenicity were observed. The liver biopsy showed extensive ground-glass hepatocytes and thin septum-like fibrosis that formed portal-to-portal linkage. Case 4: A 61-year-old male alcoholic who remained completely abstinent while taking cyanamide for 3 years showed slight elevation of serum transaminases. liver biopsy showed extensive ground-glass hepatocytes and extension of thin septum-like fibers from portal tract to the lobule. ultrasonography revealed hepatic hyperechogenicity. CONCLUSION: In some abstainers who take cyanamide for several years, thin septum-like liver fibrosis progresses along with the emergence of ground-glass hepatocytes. Hepatic hyperechogenicity on ultrasonography and slight elevation of serum transaminases might erroneously lead to a diagnosis of hepatic steatosis without liver histology.- - - - - - - - - - ranking = 6keywords = hepatic (Clic here for more details about this article) |
6/101. Alpha-1-antitrypsin deficiency and liver in adults.Thirteen adult patients (aged 16 to 73 years) form 12 families are described with liver disease and alpha- 1- antitrypsin deficiency. Long-term observation of several of these patients suggests that the liver disease may be only slowly progressive, but review of possible factors aggravating this has failed to reveal any obvious clues. Progression to death from hepatic failure was the commonest outcome, but one patient developed a malignant hepatoma and two others died because of intraperitoneal haemorrhage due to ruptured cirrhotic nodules--a complication not hitherto described in association with this condtion. diagnosis of alpha-1-antitrypsin deficiency was based on serological, histological, immunopathological and genetic studies. The most useful screening test in liver disease was found to be the demonstration of PAS positive globules in liver biopsy material which is diagn by immunofluoresence or immunoperoxidase, the latter being a superior technique. serum estimation of alpha-1 -antitrypsin deficiency was performed by immunoelectropharetic and immunodiffusion techniques, the former being preferred because it gave more consistent results. Both methods, however, were of limited value since wide variations in the serum values are commonly found in normal and abnormal states. Genotyping was carried out using starch gel electrophoresis and although of value in family studies, its value as a diagnositc aid is limited because of technical difficulties and also because alpha-1-antitrypsin accumulation in the liver may be found in both homozygous and heterozygous states. It is suggested that adult liver disease associated with abnormalities in alpha-1-antitrypsin may be more common than has hitherto been reported. This condition should be systematically sought in all cases of liver disease of uncertain aetiology.- - - - - - - - - - ranking = 1keywords = hepatic (Clic here for more details about this article) |
7/101. marchiafava-bignami disease: two cases with favourable outcome.marchiafava-bignami disease (MBD) is a rare disorder of an unknown aetiology but strongly associated with alcoholism. MBD primarily affects the corpus callosum leading to confusion, dysarthria, seizures and frequently to death. Over 250 cases from all races and from almost all nationalities have been reported, most cases being alcoholics. We report two cases with a favourable outcome. magnetic resonance imaging (MRI) demonstrated a typical lesion of the corpus callosum, in both patients. The patients, a 44-year-old male and a 40-year-old female, presented with depressed consciousness and a variety of other symptoms, but finally made a reasonably good recovery leading to home discharge. To the best of our knowledge, only one additional case of MBD from scandinavia has been published. As alcoholism is a major public health problem in scandinavia, we assume that MBD is underdiagnosed and/or under-reported. Non-specific general symptoms and encephalopathy in an alcoholic may harbour undiagnosed MBD. We suggest that the incidence of MBD may be higher and its prognosis may be milder than generally believed.- - - - - - - - - - ranking = 32.026634176516keywords = encephalopathy (Clic here for more details about this article) |
8/101. Wernicke's encephalopathy in a non-alcoholic man: case report and brief review.Wernicke's encephalopathy, a serious neurological disorder caused by thiamine deficiency, is most commonly found in chronic alcoholics. We present a typical case of Wernicke's encephalopathy in a non-alcoholic man. Our patient presented with altered mental status, slurred speech, fever, vomiting and headache of one-week duration. An infectious etiology of the symptoms was ruled out by spinal fluid cultures. The patient improved dramatically within 24 hours of administration of thiamine.- - - - - - - - - - ranking = 192.1598050591keywords = encephalopathy (Clic here for more details about this article) |
9/101. Subacute encephalopathy with epileptic seizures in alcoholism (SESA): case report.The case of a 66-year-old patient is reported in view of the rarity of his condition: a case of subacute encephalopathy with seizures in alcoholics (SESA syndrome), described first in 1981 by Niedermeyer, et al. Wernicke-type aphasia, epileptic seizures (generalized tonic-clonic) and PLEDs EEG pattern dominated the neurological picture, in addition to hepatomegaly and rhabdomyolysis. This condition differs from all other known CNS complications in chronic alcoholism and is withdrawal-independent. It is prognostically favorable as far as the syndrome as such is concerned.- - - - - - - - - - ranking = 160.13317088258keywords = encephalopathy (Clic here for more details about this article) |
10/101. Subacute encephalopathy with seizures in chronic alcoholism (SESA syndrome).Report of a case of SESA syndrome: a rare CNS complication of chronic alcoholism, known since 1981 and characterized by epileptic seizures, multiple and reversible neurological deficits, as well as PLEDs in the EEG. The MRI showed enhanced occipital signals in the T2-weighted sequence, which resolved together with the clinical findings.- - - - - - - - - - ranking = 128.10653670606keywords = encephalopathy (Clic here for more details about this article) |
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