Nonalcoholic fatty liver disease (NAFLD) is a liver condition that is being recognized with increasing frequency, and it may progress to end-stage liver disease (1). NAFLD can affect any age-group and has been described in most racial groups. In most series, the typical picture is a middle-aged woman (1). Obesity has the strongest association with NAFLD, but regardless of BMI, the presence of type 2 diabetes significantly increases the risk and severity of NAFLD. The prevalence of NAFLD in the general population ranges from 13 to 15% (2). The prevalence increases in subjects with diabetes and with severe obesity and has been reported to range from 25 to 75% or even higher (3). In Saudi Arabia, a prevalence of 7–10% has been reported in the general population (4,5). The aim of our work is to determine the prevalence and characteristics of NAFLD in Saudi type 2 diabetic subjects attending King Abdulaziz University Hospital. A sample of 116 patients was randomly selected over 1 year. All participants provided informed consent before participation. The entire sample had an abdominal ultrasound examination (using an ATL HDI 5000 abdominal probe at 2.5–3 MHz) and liver enzyme measurement performed. The sonographic findings used to diagnose NAFLD were diffuse increase in echogenicity of the liver parynchyma, which is assessed by absence of hyperechoic walls of the portal vein radicals, and absence of interface between diaphragm and liver. All radiological examinations were done by the same radiologist. The upper limit of normal liver size was 16 cm in the longitudinal plane; any measurement above this was considered hepatomegaly. Mild hepatomegaly was defined as liver size >16–18 cm in the longitudinal plane. Secondary causes of liver disease were excluded, in particular ethanol abuse (the sample studied did not drink alcohol) and use of drugs known to promote hepatic steatosis. In patients with elevated liver enzymes, those who used hepatotoxic drugs were excluded.
The mean age of the study group was 54 ± 12.8 years with a male-to-female ratio of 1:2.6. The mean duration of diabetes was 8.85 ± 6.18 years, mean BMI was 30 ± 5.5 kg/m2, and HbA1c was 7.9 ± 1.1%. NAFLD was diagnosed in 64 (55%) subjects. Right upper quadrant discomfort was reported in 11 of 64 (17%) subjects and elevated liver enzymes were found in 12 of 64 (19%). Mean aspartate aminotransferase level was 23.75 ± 10.3 units/l (normal range 5–65 units/l), alanine aminotransferase 71 ± 22.04 units/l (normal range 5–38 units/l), and alkaline phosphatase 112.62 ± 58.13 units/l (normal range 35–136 units/l). Fifty-six (88%) subjects had hepatomegaly as assessed by ultrasound, which was mild in two-thirds of them. None of the patients without NAFLD had hepatomegaly. The average liver size was 17.2 ± 3.1 cm in patients with fatty infiltration and 13 ± 2.4 cm in non-NAFLD patients. A significant relationship was found between the presence of NAFLD and female sex (P = 0.05). No significant relationship was found between the presence of NAFLD and age, duration of diabetes, or degree of glycemic control. Multiple regression analysis after adjustment for all factors and sex identified obesity as an independent factor associated with the development of NAFLD (P = 0.06).
Our results agree with those reported in the literature. The natural history of NAFLD has not been well defined, but it seems to be determined by the severity of histological damage (2). Hepatomegaly with mild to moderate elevation in serum levels of transaminases has been reported; however, this doesn’t correlate with liver histology (1,6). Future prospective studies need to clarify whether diabetic subjects have the same natural history, i.e., whether they are affected by the same histological changes or have other additional factors that may play a role, such as insulin resistance or type of treatment.
We can conclude that NAFLD, as determined by ultrasound, is common in Saudi type 2 diabetic subjects. As in reports from other ethnic groups, female sex and obesity were the two predominant features of patients with NAFLD in Saudi Arabia. In this small cohort of patients, neither glycemic control nor duration of diabetes had any relationship with fatty liver infiltration. This suggests that factors other than hyperglycemia operate to cause hepatic steatosis.
