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TM6SF2 E167K variant predicts severe liver fibrosis for human immunodeficiency/hepatitis C virus co-infected patients, and severe steatosis only for a non-3 hepatitis C virus genotype

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World Journal of Gastroenterology 2016年第38期22卷 8509-8518页

作者： Caterina Sagnelli Marco Merli Caterina Uberti-Foppa Hamid Hasson anna grandone Grazia Cirillo Stefania Salpietro Carmine Minichini Mario Starace Emanuela Messina Patrizia Morelli Emanuele Miraglia Del Giudice Adriano Lazzarin Nicola Coppola Evangelista Sagnelli Department of Clinical and Experimental Medicine and Surgery F. Magrassi e A. LanzaraSecond University of Naples 80131 Naples Italy Department of Infectious Diseases Vita-Salute University San Raffaele Scientific Institute 20127 Milan Italy Department of Pediatrics Second University of Naples 80131 Naples Italy Department of Mental Health and Public Medicine Section of Infectious Diseases Second University of Naples 80131 Naples Italy

AIM To evaluate the impact of the Glu167Lys(E167K) transmembrane 6 superfamily member 2(TM6SF2) variant on the biochemical and morphologic expression of liver lesions in human immunodeficiency virus(HIV)/hepatitis C virus(HCV) co-infected patients.METHODS The study comprised 167 consecutive patients with HIV/HCV coinfection and biopsy-proven chronic hepatitis. A pathologist graded liver fibrosis and necroinflammation using the Ishak scoring system, and steatosis using Kleiner's scoring system. Patients were genotyped for TM6SF2 E167K(rs58542926) by real-time Polymerase chain reaction. The 167 patients, 35 therapy-naive and 132 receiving ART, were prevalently males(73.6%), the median age was 40.7 years and the immunological condition good(median CD4+ cells/mm3 = 505.5).RESULTS The 17 patients with the TM6SF2 E167 K variant, compared with the 150 with TM6SF2-E/E, showed higher AST(P = 0.02) and alanine aminotransferase(P = 0.02) and higher fibrosis score(3.1 ± 2.0 vs 2.3 ± 1.5, P = 0.05). In a multivariate analysis, TM6SF2 E167 K was independently associated with severe fibrosis. The same analysis showed that HCV-genotype 3, present in 42.2% of patients was an independent predictor of severe steatosis. The association of TM6SF2 E167 K with severe steatosis, absent for the whole group of 167 patients, was re-evaluated separately for HCVgenotype 3 and non-3 patients: No factor was independently associated with severe steatosis in the HCV-genotype-3 subgroup, whereas an independent association was observed between severe steatosis and TM6SF2 E167 K in non-3 HCV genotypes. No association between the TM6SF2 E167 K variant and severe liver necroinflammation was observed.CONCLUSION In HIV/HCV coinfection the TM6SF2 E167 K variant is an independent predictor of severe fibrosis, but appears to be independently associated with severe steatosis only for patients with a non-3 HCV genotype.

关键词： Human immunodeficiency virus/hepatitis C virus co-infection TM6SF2 Liver histology Liver steatosis Liver biopsy

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Understanding the pathophysiological mechanisms in the pediatric non-alcoholic fatty liver disease: The role of genetics

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World Journal of Hepatology 2015年第11期7卷 1439-1443页

作者： Pierluigi Marzuillo anna grandone Laura Perrone Emanuele Miraglia del Giudice Department of Women and Children and General and Specialized Surgery Seconda Università degli Studi di Napoli

Classically, the non-alcoholic fatty liver disease(NAFLD) physiopathology and progression has been summarized in the two hits hypothesis. The first hit is represented by the action of hyperinsulinemia and insulin resistance, accompanying obesity, that leads to liver steatosis increasing the absolute non esterified fatty acids uptake in the liver and the esterification to form triacylglycerol. The oxidative stress is involved in the second hit leading to the progression to nonalcoholic steatohepatitis(NASH) because of its harmful action on steatosic hepatocytes. However, at the present time, the two hits hypothesis needs to be updated because of the discover of genetic polymorphisms involved both in the liver fat accumulation and progression to NASH that make more intriguing understanding the NAFLD pathophysiological mechanisms. In this editorial, we want to underline the role of PNPLA3 I148 M, GPR120 R270 H and TM6SF2 E167 K in the pediatric NAFLD development because they add new pieces to the comprehension of the NAFLD pathophysiological puzzle. The PNPLA3 I148 M polymorphism encodes for an abnormal protein which predisposes to intrahepatic triglycerides accumulation both for a loss-of-function of its triglyceride hydrolase activity and for a gain-of-function of its lipogenic activity.Therefore, it is involved in the first hit, such as TM6SF2 E167 K polymorphisms that lead to intrahepatic fat accumulation through a reduced very low density lipoprotein secretion. On the other hand, the GPR120 R270 H variant, reducing the anti-inflammatory action of the GPR120 receptor expressed by Kuppfer cells, is involved in the second hit leading to the liver injury.

关键词： Pediatric non-alcoholic fatty liver disease GPR120 PNPLA3 TM6SF2 Alanine transaminase

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Subclinical hypothyroidism in atopic South Italian children

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World Journal of Clinical Pediatrics 2016年第3期5卷 306-310页

作者： Marcella Pedullà Vincenzo Fierro Pierluigi Marzuillo Ester Del Tufo anna grandone Laura Perrone Emanuele Miraglia del Giudice Department of Woman Child and General and Specialized SurgerySeconda Università degli Studi di Napoli

AIM:To verify if subclinical hypothyroidism(SCH) could be associated to atopy in children.METHODS:Seven hundred and thirty-two Caucasian children from South Italy presenting symptoms of allergic disease were enrolled and submitted to atopy,obesity,chronic low grade inflammation,and SCH work up.RESULTS:Four hundred and forty-five out of 705(63.12%) children affected by allergic disease were diagnosed as atopic and 260(36.88%) as not atopic.The SCH prevalence was 6.3%.Significant higher prevalence of SCH among atopic children with average(group 2) and high(group 3) low grade chronic inflammation compared to atopic children with mild(group 1)low grade chronic inflammation was present.Moreover,group 1 and group 2 presented an OR to show SCH of2.57(95%CI:1.55-6.26) and 2.96(95%CI:1.01-8.65),respectively.Both in atopic and not atopic children we found C3 serum levels significantly higher in group 3respect to group 2 and group 1.Noteworthy,among atopic patients,also total immunoglobulin E(IgE) serum levels,were significantly higher in group 3 compared to group 2 and group 1 children.In atopic children,C3 and total IgE serum values increased in parallel with the increase of C-reactive protein values,while in not atopic children this phenomenon was not evident.CONCLUSION:The possibility exists that an increasing atopic inflammation contributes to SCH occurrence.So far this is the first report in literature showing an association between SCH and atopy but further studies are needed to confirm our data.

关键词： Thyroid derangement Atopy Children Low grade chronic inflammation Subclinical hypothyroidism

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