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. 2019 Aug 22;2(4):e00090.
doi: 10.1002/edm2.90. eCollection 2019 Oct.

Hepatic steatosis in patients with acromegaly

Andreani Koutsou-Tassopoulou  1 , Ifigeneia Papapostoli-Sklavounou  1 , Marcin Krawczyk  1   2 , Bettina Friesenhahn-Ochs  1 , Susanne N Weber  1 , Frank Lammert  1 , Caroline S Stokes  1
Affiliations

Hepatic steatosis in patients with acromegaly

Andreani Koutsou-Tassopoulou et al. Endocrinol Diabetes Metab. .

Abstract

Objective: Comorbid NAFLD is increasingly being diagnosed in patients with diabetes and nondiabetic endocrinopathies. The aim of this study was to assess hepatic steatosis noninvasively by transient elastography in patients with acromegaly.

Design: A cross-sectional study including 22 patients with acromegaly.

Methods: Hepatic steatosis was quantified using controlled attenuation parameter (CAP) during elastography. Anthropometric measurements were obtained, serum liver function tests and lipid and hormone profiles were measured, and prosteatogenic gene variants were genotyped using standard assays.

Results: In total, 41% of patients were women (mean age 60 ± 14.7 years, mean BMI 31.2 ± 4.6 kg/m2). Hepatic steatosis, as defined by CAP > 248 dB/m, was present in 66% of patients. Five (45%) of the patients with hepatic steatosis also had fibrosis, and one presented with cirrhosis. Nine patients were carriers of the PNPLA3 p.I148M prosteatogenic [M] risk allele, eight of whom were heterozygotes. CAP values were significantly (P = .045) higher in these patients and corresponded to advanced steatosis, as compared to patients with the wild-type genotype, who demonstrated CAP values consistent with mild steatosis (311 ± 33 dB/m. vs 254 ± 62 dB/m). CAP values did not differ significantly in carriers of distinct TM6SF2 and MBOAT7 genotypes; however, carriers of the risk alleles displayed higher CAP as compared to wild-type patients.

Conclusions: This study shows that in patients with acromegaly, carriers of the PNPLA3 susceptibility allele are at risk of developing hepatic steatosis, as assessed by CAP. Comorbid NAFLD might compound prognosis in such patients; thus, further research into the pathomechanisms and treatment of NAFLD in acromegaly is warranted.

Keywords: MBOAT7; TM6SF2; adiponutrin; controlled attenuation parameter; nonalcoholic fatty liver disease; transient elastography.

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Conflict of interest statement

The authors of this study explicitly declare that there are no conflicts of interest in connection with this article.

Figures

Figure 1
Figure 1
A, Boxplots depicting noninvasive transient elastography results for controlled attenuation parameter (CAP) and liver stiffness measurements (LSMs) in the entire study group. B, Boxplots comparing CAP values for the four different groups of patients with acromegaly: patients without fatty liver compared to patients with fatty liver, and with fibrosis and cirrhosis. The CAP cut‐off for fatty liver was 248 dB/m. Liver fibrosis was defined by LSM > 6.0 kPa, and LSM > 12.0 kPa indicated cirrhosis
Figure 2
Figure 2
Individual patient CAP scores (as well as mean ± SD) based on genotype for the following single nucleotide polymorphisms: patatin‐like phospholipase domain–containing 3 (PNPLA3) p.I48M; membrane‐bound O‐acyltransferase domain–containing 7 (MBOAT7) p.G17E; and transmembrane 6 superfamily member 2 (TM6SF2) p.E167K. CAP values differed significantly (P = .045) between patients who were heterozygous carriers of the PNPLA3 risk allele (IM) as compared to the wild‐type patients (II). No significant differences in CAP were demonstrated between the three MBOAT7 genotypes, where the lowest mean CAP value was observed in carriers of the wild‐type genotype (GG) and the highest in patients homozygous for the risk allele (EE). No difference in CAP was observed between the TM6SF2 genotypes
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