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Naga P Chalasani

Publications and source records attributed to Naga P Chalasani.

6 recordsLinked to original sources
PubMed2025

A comprehensive evaluation of candidate genetic polymorphisms in a large histologically characterized MASLD cohort using a novel framework.

BACKGROUND: There is a substantial heritable component to metabolic dysfunction-associated steatotic liver disease (MASLD), and several genetic variants that promote MASLD development or associate with its severity have been reported. These associations vary in terms of their effect size and degree of replication. METHODS: We developed a framework to classify previously identified MASLD genetic polymorphisms into 4 tiers based on effect size and extent of replication in the literature. We tested the association between "tier 1" single-nucleotide polymorphisms (OR ≥1.5, replicated in >2 independent studies) and biopsy measures of MASLD severity in a large, well-characterized histologic cohort of MASLD patients (n=3094). RESULTS: Across 19 "tier 1" variants reflecting 11 genetic loci, only those in the PNPLA3-SAMM50-PARVB locus showed significant associations with biopsy-proven fibrosis severity and NAFLD activity score; the highest risk was for the rs738409 p.I148M variant in PNPLA3. A genetic risk score based on "tier 1" variants, as well as a previously developed genetic risk score based on variants in PNPLA3, TM6SF2, and HSD17B13, were both associated with fibrosis and NAFLD activity score, but these results were driven entirely by PNPLA3 rs738409. CONCLUSIONS: Our study provides a framework to prioritize evaluation of genetic polymorphisms for future replication efforts and demonstrates that in a large case-only cohort, histologic severity of MASLD is only robustly associated with the presence of variation in PNPLA3 among known candidate genes. These findings may have implications for patient risk stratification based on the presence of PNPLA3 rs738409.

Humans↗
PubMed2007

Complete reversal of glycogen hepatopathy with pancreas transplantation: two cases.

Glycogen hepatopathy is the pathological overloading of hepatocytes with glycogen that is associated with poorly controlled diabetes mellitus. Clinically, it presents with abdominal discomfort, tender hepatomegaly and elevated transaminases. In this report, we describe our experience with two cases of type I diabetes mellitus and glycogen hepatopathy. The patients underwent isolated pancreas transplantation, following which, we have been able to demonstrate complete histological resolution of glycogen hepatopathy associated with control of glucose metabolism.

Adolescent↗
PubMed2006

Severe liver injury after initiating therapy with atomoxetine in two children.

Two children presented with acute hepatitis after starting therapy with atomoxetine (Strattera). In one child, no competing diagnosis could be identified, and liver injury resolved completely on withdrawal of the medication. In the second child, the evaluation was suggestive of type 1 autoimmune hepatitis; she subsequently improved with removal of atomoxetine and concomitant immunosuppressive therapy. Atomoxetine may cause clinically significant hepatotoxicity either by metabolic idiosyncrasy or by inducing autoimmune hepatitis.

Adrenergic Uptake Inhibitors↗
PubMed2006

Autoimmune hepatitis triggered by statins.

Although the cause of autoimmune hepatitis (AIH) is unknown, drugs are believed to be potential triggers in some patients. In isolated case reports, statins have been considered such triggers. Here we describe 3 patients in whom it is probable that statins initiated the development of AIH. Two men (aged 47 and 51) and one woman (aged 57) developed AIH after the initiation of statin therapy. They developed positive titers of antinuclear antibodies, antismooth muscle antibodies (1/40 to 1/160), and hypergammaglobulinemia. Features of all 3 patients met the criteria for AIH according to the International Autoimmune Hepatitis Panel. Liver biopsies in all 3 showed varying stages of fibrosis and plasma cell infiltration, compatible with AIH. The woman developed hepatitis due to statins on 2 separate occasions: the first in 1999, due to simvastatin, and the second in 2001 to 2002, due to atorvastatin, which was severe and persisted even after discontinuing medication. Similarly, in the 2 other cases, exposure to statins preceded development of AIH, which persisted despite discontinuing medications. All 3 patients responded well to prednisone and azathioprine or mycophenolate therapy. 3 similar previously reported cases are reviewed. We conclude that the 3 cases reported here and 3 similar previously reported cases, indicate that severe, ongoing AIH on rare occasions can be triggered by statins.

Atorvastatin↗