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Gluten-Free hepatomiracle in "celiac hepatitis": A case highlighting the rare occurrence of nutrition-induced near total reversal of advanced steatohepatitis and cirrhosis.
Gaur, K, Sakhuja, P, Puri, AS, Majumdar, K
Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association. 2016;(6):461-464
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Abstract
Regression of hepatic fibrosis is increasingly becoming a reality, both in clinical as well as experimental models. Reversal or near-total regression of marked liver steatohepatitis and fibrosis, however, remains a rare event. We report the case of a 20-year-old female presenting with diarrhea due to celiac disease and biopsy proven cirrhosis with portal hypertension who had a remarkable clinical improvement in response to a gluten free diet (GFD). A follow-up liver biopsy 9 months after the initiation of GFD revealed a remarkable regression of both fibrosis as well as steatosis. Villous atrophy, as seen in patients with celiac disease, could lead to a deprivation of trophic factors leading to liver injury and subsequent cirrhosis. A gluten-free dietary regimen can produce a reversal of fibrosis leading to the amelioration of symptoms associated even with advanced liver disease.
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Acute kidney injury in patients with cirrhosis: perils and promise.
Belcher, JM, Parikh, CR, Garcia-Tsao, G
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2013;(12):1550-8
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Abstract
A 62-year-old man with cirrhosis secondary to hepatitis C and chronic alcohol abuse was admitted to the intensive care unit with hematemesis and mental status changes. Physical examination showed ascites and stigmata of chronic liver disease. Blood pressure was noted as 87/42 mm Hg and laboratory studies showed a serum creatinine level of 0.8 mg/dL, an estimated glomerular filtration rate of 84 mL/min/1.73 m(2) calculated using the Modification of Diet in Renal Disease Study equation, a serum sodium level of 123 mEq/L, a total serum bilirubin level of 4.3 mg/dL, and an international normalization ratio of 1.6. The patient was resuscitated with packed red blood cells and fresh-frozen plasma and bleeding was controlled. However, on the third day of admission, creatinine level increased to 1.5 mg/dL. Examination of urine sediment showed 1 to 5 bilirubin-stained granular casts per high-powered field and a few renal tubular epithelial cells. The urine sodium level was 21 mEq/L and the fractional excretion of sodium was 0.43%.
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Can the tyrosine kinase inhibitors trigger metabolic encephalopathy in cirrhotic patients?
Brandi, G, de Rosa, F, Calzà, L, Girolamo, SD, Tufoni, M, Ricci, CS, Cirignotta, F, Caraceni, P, Biasco, G
Liver international : official journal of the International Association for the Study of the Liver. 2013;(3):488-93
Abstract
BACKGROUND Sorafenib is the standard treatment of advanced hepatocarcinoma (HCC) in cirrhotic patients with preserved liver function. It shares many adverse effects with other tyrosine-kinase (TK) inhibitors and antiangiogenic drugs. TK inhibitors could have a direct toxicity on CNS, both by interfering with TK-related pathways and by inhibiting angiogenesis. AIMS The aim of this study was to investigate whether sorafenib administration can be associated to metabolic encephalopathy in patients with cirrhosis. METHODS We retrospectively reviewed medical records of all cirrhotic patients treated with sorafenib for HCC afferent at our Department from January 2009 to December 2011. RESULTS Among 62 patients, we identified 10 patients with clinically significant cognitive impairment. Seven of these were clearly diagnosed with overt hepatic encephalopathy (HE), one with brain metastases and two with drug-related toxic-metabolic encephalopathy. These last two cases were characterized by severe cognitive impairment, mood alteration and memory deficit. Clinical exam, blood tests and brain CT excluded organic causes of encephalopathy and precipitating factors of HE. Sorafenib discontinuation was associated with complete reversal of the syndrome, which recurred on drug re-administration in one case. CONCLUSIONS Our study suggests that sorafenib may be a precipitating factor of metabolic encephalopathy in cirrhotic patients with advanced HCC. This neurological syndrome appears to be not responsive to the conventional treatment for HE, but it is fully reversible by drug discontinuation. It can be speculated that the potential direct neuronal action of sorafenib may represent a trigger for the onset of metabolic encephalopathy in a subset of cirrhotic patients.
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Wernicke encephalopathy presented in the form of postoperative delirium in a patient with hepatocellular carcinoma and liver cirrhosis: a case report and review of the literature.
Onishi, H, Sugimasa, Y, Kawanishi, C, Onose, M
Palliative & supportive care. 2005;(4):337-40
Abstract
OBJECTIVE Although Wernicke encephalopathy has been reported in the oncological literature, it has not previously been reported in postoperative cancer patients. METHODS In this communication, we report a patient of hepatocellular carcinoma with liver cirrhosis who developed Wernicke encephalopathy in the form of postoperative delirium. Preoperatively, the patient had a very good appetite and had eaten all the food of an 1800 cal/day diet until 1 day before operation. The operation was done without any complications. The patient developed delirium 2 days after the lobectomy of the liver. The level of delirium remained unchanged until administration of thiamine starting on day 7 postoperatively, which resulted in palliation of delirium without brain damage. Laboratory data demonstrated that the serum thiamine level at day 6 postoperatively was below the lower limit of normal. As the mechanism of Wernicke encephalopathy, we thought that decreased ability to store thiamine due to liver cirrhosis led to depletion of thiamine faster than had been expected. RESULTS AND SIGNIFICANCE OF THE RESEARCH In cancer patients, clinicians must always remain aware of the possibility of Wernicke encephalopathy, especially in patients with liver dysfunction, which decreases the ability to store thiamine in the liver. Early detection and intervention may alleviate the symptoms of delirium and prevent irreversible brain damage.