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Non-alcoholic steatohepatitis and hepatic steatosis in patients with adult onset growth hormone deficiency
  1. T Ichikawa1,
  2. K Hamasaki1,
  3. H Ishikawa1,
  4. E Ejima1,
  5. K Eguchi1,
  6. K Nakao2
  1. 1First Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan
  2. 2Health Research Center, Nagasaki University, Nagasaki, Japan
  1. Correspondence to:
    T Ichikawa, First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852–8501, Japan;
    ichikawa{at}net.nagasaki-u.ac.jp

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Adult onset growth hormone (GH) deficiency closely resembles syndrome X.1 Patients with syndrome X often suffer from obesity, dyslipidaemia, insulin resistance, and hypertension, and hepatic steatosis and non-alcoholic steatohepatitis (NASH) have also been characterised as symptoms of syndrome X.2,3 However, the relationship of GH deficiency to hepatic steatosis and NASH remains unclear.

We looked for the presence of hepatic steatosis using computer tomography (CT) in a study of 18 patients with adult onset anterior lobe pituitary hormone deficiency, with or without GH deficiency. We also performed a liver biopsy in one patient with adult onset GH deficiency. None of the patients was positive for hepatitis B surface antigen, hepatitis C virus antibody, antinuclear antibody, or antimitochondrial antibody. The criterion used for diagnosing hepatic steatosis was a ratio for the liver/spleen CT value of less than 0.9.4 In 13 patients with GH deficiency, seven showed hepatic steatosis (53.8%) while in five patients without GH deficiency no hepatic steatosis was present (p=0.035). Body mass index (BMI kg/m2), serum triglyceride level (TG mg/dl), and serum total cholesterol (T-ch mg/dl) were similar in patients with or without GH deficiency (table 1). The significance of the per cent hepatic steatosis was evaluated by χ2 test. BMI, TG, and T-ch were analysed using an unpaired Student’s t test.

The male patient on whom we performed a liver biopsy was diagnosed with GH deficiency at 58 years old. He showed hepatic steatosis, measured by CT, at 64 years. Serum aspartate aminotransferase level fluctuated from 20 to 80 U/l. The patient did not have a history of alcohol abuse but was slightly obese (BMI 30 kg/m2). Liver biopsy was performed when the patient was 72 years old, and this showed the presence of NASH (fig 1).

We have demonstrated that hepatic steatosis is more frequently observed in patients with GH deficiency than in those without GH deficiency. Furthermore, by liver biopsy, we have shown that a patient with GH deficiency also had NASH. These results indicate that adult onset GH deficiency is a possible risk factor for hepatic steatosis and NASH.

Table 1
Figure 1

Histology of the liver biopsy. Macrovesicular steatosis, pericellular and centrilobular fibrosis, and ballooned hepatocytes are all observed in this section. (Method: needle biopsy; haematoxylin-eosin staining.)

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