Tissue iron quantification in chronic liver diseases using MRI shows a relationship between iron accumulation in liver, spleen, and bone marrow.

AIM: To investigate iron loading within the liver, pancreas, spleen, and bone marrow using magnetic resonance imaging (MRI) transverse relaxation rate (R2*), in patients with diffuse liver diseases; to evaluate the relationships between iron accumulation in these tissue compartments; and to assess the association between tissue iron overload and the pattern of hepatic cellular iron distribution (hepatocytes versus Kupffer cells). MATERIAL AND METHODS: Fifty-six patients with diffuse liver diseases had MRI-derived R2* values, using a multi-echo chemical-shift encoded MRI sequence, of the liver, pancreas, spleen, and vertebral bone marrow. All patients had liver biopsy samples scored for hepatic iron grading (0-4) and iron cellular distribution (within hepatocytes only or within both hepatocytes and Kupffer cells). RESULTS: Liver R2* increased with histological iron grade (RS=0.58, p<0.001) and correlated with spleen (RS=0.71, p<0.001) and bone marrow R2* (RS=0.66, p<0.001), but not with pancreatic R2* (RS=0.22, p=0.096). Splenic and bone marrow R2* values were also correlated (RS=0.72, p<0.001). Patients with iron inside Kupffer cells had the highest R2* in liver, spleen and bone marrow. CONCLUSIONS: Patients with chronic diffuse liver diseases have concomitant hepatic, splenic, and bone marrow iron loading. The highest hepatic iron scores and iron inside Kupffer cells were associated with the highest splenic and bone marrow deposits, suggesting systemic iron accumulation in the mononuclear phagocytic system.

Liver transplant recipients have a higher prevalence of anal squamous intraepithelial lesions.

BACKGROUND: Anal squamous intraepithelial lesions (ASIL) are precancerous lesions of anal squamous cell carcinoma, with a higher prevalence in immunosuppressed patients. There are some studies in kidney transplant recipients, but there is no information regarding prevalence in liver transplantation. Our aim was to evaluate the prevalence of ASIL in this setting. METHODS: Prospective case-control study involving liver transplant recipients without any other known risk factor for ASIL (n=59), which were compared with a healthy control group (n=57). All were submitted to anal cytology and high-resolution anoscopy was performed in those with abnormal results. RESULTS: Ten (17%) of liver transplant recipients had abnormal cytological results, seven patients had atypical squamous cells of undetermined significance (ASC-US), one patient had atypical squamous cells that cannot exclude high-grade (ASC-H) and two patients had high-grade squamous intraepithelial lesions (HSIL). In the control group, one patient (2%) had an ASC-US result (P=0.005). Anal squamous intraepithelial lesions were confirmed in 7 out of 10 of liver transplant patients and 0 out of 1 in the controls (P=0.013) by high-resolution anoscopy with biopsies. Current smoking was the only risk factor for abnormal cytology (odds ratio=5.87, 95% confidence intervals=1.22-28.12, P=0.027). CONCLUSIONS: Liver transplant patients have a higher risk of ASIL. Screening should be considered, especially in smokers.

Hepatic sarcoidosis with portal hypertension. A report of seven cases with a review of the literature.

We have reviewed the clinical, histological and hemodynamic features of sarcoidosis complicated by portal hypertension in seven patients and in 40 previously reported cases. Young black patients of either sex and white females over 40 years were selectively affected. In 12 of these 47 patients, portal hypertension appeared to be a consequence of cirrhosis due to longstanding intrahepatic cholestasis; in white patients, this condition was clinically, histologically, and serologically indistinguishable from primary biliary cirrhosis. In most of the other patients, portal hypertension was the predominant and often the presenting symptom of hepatic sarcoidosis; in these patients portal hypertension was due to a presinusoidal block probably determined by portal granulomas, with or without superimposed sinusoidal block determined by fibrosis. Corticosteroids did not prevent the development of portal hypertension.