The prevalence of radiographic osteoarthritis in hand and knee joints was studied in elderly patients with acromegaly and growth hormone deficiency, respectively, and compared with a normal population of elderly people. There were no major differences in the prevalence of osteoarthritis between the acromegalics and the normal population, but the patients with growth hormone deficiency had significantly (p<0.001) less osteoarthritis than the normal population. The lack of differences between the acromegalics and the normal population could be an effect of the age interval studied in which the prevalence of osteoarthritis is high. The low prevalence of osteoarthritis in patients with growth hormone deficiency suggests that growth hormone is an important factor in the development of osteoarthritis.
Eva Bagge, Staffan Edén, Thord Rosén and Bengt-Åke Bengtsson
Axel Tjörnstrand, Kerstin Gunnarsson, Max Evert, Erik Holmberg, Oskar Ragnarsson, Thord Rosén and Helena Filipsson Nyström
The number of studies on the incidence of pituitary adenomas (PAs) is limited. The aim of this study was to evaluate the standardised incidence rate (SIR) of PAs in western Sweden.
Design, subjects and methods
Data from adult patients diagnosed with PAs in 2001–2011, living in the Västra Götaland County, were collected from the Swedish Pituitary Registry (SPR). In addition, medical records on all patients diagnosed with PAs at the six hospitals in the region were reviewed. In total, 592 patients were included in the study.
Age-SIR, given as rate/100 000 inhabitants (95% CI), was calculated using the WHO 2000 standard population as a reference.
The total SIR for PAs was 3.9/100 000 (3.6–4.3); 3.3/100 000 (2.9–3.7) for men and 4.7/100 000 (4.1–5.3) for women. In men, SIR increased with age, while in women SIR peaked at 25–34 years, mainly due to prolactinomas. Non-functioning PA (NFPA) was the most common PA (54%, 1.8/100 000 (1.6–2.0)) followed by prolactinomas (32%, 1.6/100 000 (1.3–1.9)), acromegaly (9%, 0.35/100 000 (0.25–0.45)), Cushing's disease (4%, 0.18/100 000 (0.11–0.25)) and TSH-producing PA (0.7%, 0.03/100 000 (0.00–0.05)). The proportion of macroadenomas for NFPA was 82%, prolactinomas 37%, GH-producing PA 77%, ACTH-producing PA 28% and TSH-producing PA 100%. The lifetime risk for PAs was 0.27% (0.24–0.31) in men and 0.29% (0.26–0.33) in women.
This study provides a reliable estimate on the overall incidence of PAs and confirms an increased incidence of PAs compared with studies conducted in the pre-magnetic resonance imaging era. The lower proportion of prolactinomas compared with previous studies is probably explained by the different criteria used.
Thord Rosén, Tommy Hansson, Hans Granhed, Janos Szucs and Bengt-Åke Bengtsson
Bone mineral content was measured in a follow-up study of adult patients with hypopituitarism and growth hormone deficiency. There were 95 patients (59 males, mean age 54.0 years, range 21–74 years; 36 females, mean age 53.5 years, range 31–73 years). Routine replacement therapy with cortisone acetate and l-thyroxine was given. All males that were gonadal deficient were on proper testosterone therapy, except in four patients who were treated separately. Bone mineral content (g/cm) was measured using dual-photon absorptiometry in the third lumbar vertebra. Bone mineral content in the patients was compared with a control population (N=413, 25–74 years of age). Bone mineral content was significantly lower in males (N= 55, p<0.05) compared with controls. In females, bone mineral content was significantly lower both among the subjects with untreated gonadal deficiency (p<0.001) and among those with treated gonadal deficiency and normal premenopausal gonadal function (p<0.005) compared with controls. To summarize, patients with hypopituitarism on routine replacement therapy but not growth hormone have a lower bone mineral content than the controls. The reduced bone mineral content might be a result of untreated growth hormone deficiency.
Thord Rosén, Staffan Edén, Göran Larson, Lars Wilhelmsen and Bengt-Åke Bengtsson
Patients with adult onset growth hormone deficiency have a decreased life expectancy owing to an increased mortality from cardiovascular disease. In the present study, 104 subjects (66 men and 38 women, aged 22–74 years) with growth hormone deficiency and with adequate replacement therapy with glucocorticoids, thyroid hormones and gonadal steroids were studied with respect to known risk factors for cardiovascular disease. For comparison, data from a population study, "the MONICA study", were obtained. The patients had a significantly higher body mass index compared to controls (p<0.001). Serum triglyceride concentration was higher (p<0.001) but there was no difference in serum total cholesterol concentration. Serum high-density lipoprotein cholesterol concentration was lower (p<0.001) in the patients. There was no difference in the prevalence of diabetes mellitus. The prevalence of treated hypertension was higher (p<0.05) in the patients but the prevalence of smoking was lower (p <0.001). Even after taking the increased body mass index into consideration, the changes in the prevalence of treated hypertension (p<0.05) and in the serum concentrations of triglycerides (p<0.05) and high-density lipoprotein concentrations (p<0.001) remained. These results indicate that growth hormone deficiency alters lipoprotein metabolism and increases the risk for development of hypertension, which in turn might contribute to the increased risk for cardiovascular disease.
Marie Degerblad, Bengt-Åke Bengtsson, Margareta Bramnert, Olof Johnell, Per Manhem, Thord Rosén and Marja Thorén
Degerblad M, Bengtsson B-Å, Bramnert M, Johnell O, Manhem P, Rosén T, Thorén M. Reduced bone mineral density in adults with growth hormone (GH) deficiency: increased bone turnover during 12 months of GH substitution therapy. Eur J Endocrinol 1995;133:180–8. ISSN 0804–4643
To evaluate the consequences of growth hormone (GH) deficiency on bone mineral density and to evaluate the effects of GH substitution therapy, 68 adults (25 females and 43 males) aged 22–61 (mean 44.2 ± 1.2) years with GH deficiency (GHD) were studied. Fifty-eight patients had panhypopituitarism, three had isolated GHD and in seven patients at least one additional pituitary function was affected. Twenty-one patients had childhood onset GHD. The patients were randomized to receive either GH in daily injections (0.125 IU · kg−1 · week−1 for the first 4 weeks and subsequently 0.25 IU · kg−1 · week−1) or placebo for 6 months. The trial continued as an open study with GH treatment for 6 or 12 months, with data presented as compiled data of 12 months of GH treatment in 64 patients. Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry and bone turnover was assessed by serum markers of bone metabolism (osteocalcin, procollagen I peptide, crosslinked telopeptide of type I collagen and alkaline phosphatase activity). In women with adult onset GHD (N = 19) and in men with childhood onset GHD (N = 15), total body, spine and hip BMD was significantly reduced at baseline compared to Swedish age- and sex-matched control material. In men with adult onset of GHD (N = 28), BMD did not differ from male controls. During the placebocontrolled period, GH induced decreased total body and spine BMD, probably due to an expansion of the remodelling space, whereas all serum markers of bone turnover increased. Compiled GH data showed similar results after 6 months of treatment. After 12 months of GH treatment, BMD did not differ from basal values except for total body BMD, which was lower, whereas the serum markers of bone metabolism were still increased as compared to basal values. Two-thirds of the patients experienced fluid retention with peripheral oedema and arthralgias on the higher GH dosage. One obese patient developed non-insulin-dependent diabetes mellitus and was withdrawn from the study. These results demonstrate that GHD has negative effects on BMD and that GH substitution induces increased bone turnover. Continued long-term observations will reveal if there is a positive effect of GH substitution on bone mass in the adult GHD patient.
Marie Degerblad, Department of Endocrinology and Diabetology, Karolinska Hospital, S-17176 Stockholm, Sweden