[Hemochromatosis--a rare cause of hypogonadism]. / Hemokromatose--en sjelden årsak til hypogonadisme.

A 28-year-old man presented in 1992 with decreased libido and erectile dysfunction. He was found to have central hypogonadism with low serum levels of testosterone, LH and FSH. Computer tomography of the cella turcica was normal. Apart from hypogonadism, the pituitary function was normal. He was successfully treated with testosterone injections. In June 1995, elevated levels of serum ferritin (4,094 micrograms/l) and transferrin saturation (94%) raised suspicion of hemochromatosis. The diagnosis was confirmed by a percutaneous liver biopsy, and treatment started with regular phlebotomies. After three years of treatment the serum levels of LH and testosterone were normalized. Hypogonadism is, except for diabetes mellitus, the most frequent endocrine disturbance in hemochromatosis. It is found almost exclusively in male patients. It is important to exclude hypogonadism in male patients with hemochromatosis, but it is also important to exclude hemochromatosis in male patients with hypogonadism.

NIDDM: a rapid progressive disease. Results from a long-term, randomised, comparative study of insulin or sulphonylurea treatment.

The objective of the present study was to assess the relative efficacy of insulin or glibenclamide treatment for non-insulin-dependent diabetes mellitus (NIDDM) over 42 months. We performed a randomised, controlled trial allocating patients treated with diet and oral antihyperglycaemic agents to treatment with glibenclamide or insulin to achieve HbAlc levels under 7.5%. We included 36 subjects with established NIDDM of more than 2 years' duration. Mean HbAlc levels were significantly reduced in patients allocated to insulin treatment from 9.1 +/- 1.4% before the start to 7.8 +/- 1.3% (p < 0.05) after 1 year, and did not change significantly thereafter throughout the study period. Mean HbAlc levels increased during the study in the patients allocated to glibenclamide treatment, and 11 of 18 patients had to be switched to insulin treatment due to increasing hyperglycaemia (HbAlc > 10%). Mean body weight increased in the subjects allocated to insulin by 7.2 +/- 4.1 kg during the study period. In conclusion, insulin was more effective than glibenclamide treatment in obtaining control over hyperglycaemia in these patients, and once improved, glycaemic control did not deteriorate over 42 months in the insulin-treated group. Two thirds of the patients allocated to glibenclamide treatment had to be given insulin due to inadequate glycaemic control.

Bone mass in non-insulin-dependent diabetes mellitus.

In view of the contradictory results of earlier reports regarding bone mass in patients with non-insulin-dependent diabetes, we measured bone mass using dual X-ray absorptiometry and ultrasound measurements of the right calcaneus in 36 type 2 diabetic subjects, i.e. 21 men and 15 postmenopausal women aged 40-65 years, and compared their bone mass to a sex- and age-matched control group. We also measured several metabolic parameters in the diabetic population and studied the relationship between these metabolic parameters and the bone parameters using correlation analysis. We found a tendency to higher bone mass in the diabetic subjects compared to the normal controls. In the Type 2 diabetic postmenopausal women, fat mass and lean body mass correlated positively with total body bone mineral density (BMD) (r = 0.53 and 0.68), and with total body bone mineral content (BMC) (r = 0.58 and 0.77). Insulin sensitivity (GDR/I) correlated negatively with total body BMC and BMD (r = -0.68 and -0.61). Serum insulin correlated positively with the same bone parameters. When controlling for fat mass or lean body mass using a multiple regression analysis, the correlation between insulin sensitivity and BMD became non-significant. This suggests that body mass is a more important determinant of BMD than hyperinsulinaemia or insulin resistance in diabetic women. Among the diabetic men there was a significant positive correlation between lean body mass and BMC (r = 0.66), between serum oestrone and BMD (r = 0.49) and between serum insulin and femoral neck BMD (r = 0.53).(ABSTRACT TRUNCATED AT 250 WORDS)