Growth Hormone Reverses Nonalcoholic Steatohepatitis in a Patient With Adult Growth Hormone Deficiency

Context: It is assumed that hepatic steatosis plays a role in the development and progression of the metabolic syndrome and its cardiovascular sequelae. Low serum IGF1 levels might mediate these associations. Objectives: The aims of this study were i) to investigate the associations of hepatic steatosis with serum IGF1 and IGF binding protein-3 (IGFBP-3) levels using ultrasound and serum alanine aminotransaminase (ALT) data to define hepatic steatosis, and ii) to analyze the specific role of alcohol consumption in this context. Design: We analyzed data from the population-based Study of Health in Pomerania. Methods: We used data from 3863 subjects (1971 women) aged 20-79 years who had no history of viral hepatitis, liver cirrhosis, or malignant diseases. Liver hyperechogenicity was diagnosed using ultrasound. Serum IGF1 and IGFBP-3 levels were determined by automated two-site chemiluminescence immunoassays. Results: Hyperechogenic liver pattern was associated with low serum IGF1 levels and low serum IGF1/IGFBP-3 ratios. The lowest serum IGF1 and IGF1/IGFBP-3 values and highest IGFBP-3 levels were present in subjects who had a hyperechogenic liver pattern and increased serum ALT levels. All of these associations were independent of alcohol consumption. Conclusions: Our data show that hepatic steatosis is associated with low serum IGF1 levels. This association is independent of alcohol consumption.

Section: Discussionmentioning

confidence: 97%

Association between hepatic steatosis and serum IGF1 and IGFBP-3 levels in a population-based sample

Völzke

Nauck²,

Rettig³

et al. 2009

“…The introduction of GH replacement reduced liver enzyme concentrations and in the five patients who underwent paired biopsies before and after GH replacement, 6-12 months of treatment improved histological findings (11). A further case report has also identified histological improvement in NAFLD following GH replacement therapy (62). Conversely, in a separate study in patients with GHD, GH replacement decreased subcutaneous and visceral but not hepatic fat (63).…”

Section: Oestrogensmentioning

confidence: 93%

Mechanisms in endocrinology: Non-alcoholic fatty liver disease in common endocrine disorders

Hazlehurst

Tomlinson

2013

Non-alcoholic fatty liver disease (NAFLD) is a spectrum of disease spanning from simple benign steatosis to steatohepatitis with fibrosis and scarring that can eventually lead to cirrhosis. Its prevalence is rising rapidly and is developing into the leading indication for liver transplantation worldwide. Abnormalities in endocrine axes have been associated with NALFD, including hypogonadism, hypothyroidism, GH deficiency and hypercortisolaemia. In some instances, correction of the endocrine defects has been shown to have a beneficial impact. While in patients with type 2 diabetes the association with NAFLD is well established and recognised, there is a more limited appreciation of the condition among common endocrine diseases presenting with hormonal excess or deficiency. In this review, we examine the published data that have suggested a mechanistic link between endocrine abnormalities and NAFLD and summarise the clinical data endorsing these observations.

“…Ichikawa et al (5) showed that hepatic steatosis was more frequently observed in hypopituitary patients with GHD than in patients without GHD, with hepatic steatosis present in 54% of the patients with GHD. In another case of adult hypopituitary patients with GHD accompanied by nonalcoholic steatohepatitis (NASH) and hyperlipidemia, we reported that GH replacement therapy drastically reversed NASH (6). Moreover, the severity of fatty liver was shown to be related to hypopituitary patients' GH levels (7).…”

Section: Introductionmentioning

confidence: 94%

Nonalcoholic fatty liver disease in adult hypopituitary patients with GH deficiency and the impact of GH replacement therapy

Nishizawa

Iguchi

Murawaki

et al. 2012

142

132

Background: Liver dysfunction in adult hypopituitary patients with GH deficiency (GHD) has been reported and an increased prevalence of nonalcoholic fatty liver disease (NAFLD) has been suggested. Objective: The objective of the present study was to elucidate the pathophysiology of the liver in adult hypopituitary patients with GHD. Patients and methods: We recruited 69 consecutive Japanese adult hypopituitary patients with GHD and examined the prevalence of NAFLD by ultrasonography and nonalcoholic steatohepatitis (NASH) by liver biopsy. Patients had been given routine replacement therapy except for GH. We compared these patients with healthy age-, gender-, and BMI-matched controls. We further analyzed the effect of GH replacement therapy on liver function, inflammation and fibrotic markers, and histological changes. Results: The prevalence of NAFLD in hypopituitary patients with GHD was significantly higher than in controls (77 vs 12%, P!0.001). Of 16 patients assessed by liver biopsy, 14 (21%) patients were diagnosed with NASH. GH replacement therapy significantly reduced serum liver enzyme concentrations in the patients and improved the histological changes in the liver concomitant with reduction in fibrotic marker concentrations in patients with NASH. Conclusions: Adult hypopituitary patients with GHD demonstrated a high NAFLD prevalence. The effect of GH replacement therapy suggests that the NAFLD is predominantly attributable to GHD.