Purpose. Fragility fractures in men constitute a major worldwide public health problem with a life-time risk of 13%. It cannot be directly inferred that antiosteoporotic drugs effective in women have the same effect in men. Our aim was to appraise the existing evidence for efficacy of osteoporosis treatment in men. Methods. This study was a systematic review of the published literature on the clinical efficacy of medical osteoporosis therapy in the reduction of fracture risk in men (age > 50 years). Studies included were randomised, placebo-controlled trials of men. Results. Five BMD studies of antiresorptive treatment were included. All studies showed an increase in BMD, but there was only a nonsignificant trend in the reduction of clinical fractures. Three BMD studies of anabolic treatment with teriparatide were also included. These showed a significant mean increase in spine BMD and for vertebral fractures a non-significant trend towards a reduction was seen. Conclusion. The evidence of medical osteoporosis treatment in men is scant and inconclusive due to the lack of prospective RCT studies with fracture prevention as primary end point. So far, all evidence is based on BMD increases in small RCT studies showing BMD increases comparable to those reported in postmenopausal women.
Aim: To study fracture risk in patients with hyperthyroidism and hypothyroidism. Subjects and methods: All patients with hyperthyroidism or autoimmune hypothyroidism diagnosed for the first time between 1983 and 1996 in Denmark were identified through the National Patient Discharge Register. Each patient was compared with three age- and gender-matched controls randomly selected from the general population. Fracture occurrence before and after diagnosis was compared between patients and controls. Results: 11,776 patients with hyperthyroidism (6301 patients with diffuse toxic goiter, mean age, 52.1 ± 18.6 years, and 5475 with nodular toxic goiter, mean age, 60.4 ± 15.9 years), and 4473 patients with hypothyroidism (mean age, 66.1 ± 17.3) were identified. In patients with hyperthyroidism, fracture risk was only significantly increased around the time of diagnosis (incidence rate ratio [IRR] between 1.26 and 2.29), but decreased to normal levels after diagnosis. Surgical treatment of hyperthyroidism was associated with a decreased fracture risk after diagnosis (RR = 0.66, 95% confidence interval [CI]: 0.55-0.78). In hypothyroidism, fracture risk was significantly increased both before and after diagnosis with a peak around the time of diagnosis (IRR between 2.17 and 2.35). Conclusions: Fracture risk is increased in hyperthyroidism and hypothyroidism. Thyroid surgery seems associated with a decreased fracture risk in hyperthyroid patients.
INTRODUCTION: The purpose of this study was to investigate the risk of metabolic sequelae and all-cause mortality in a population-based cohort of chronic pancreatitis (CP) patients with and without prior acute pancreatitis (AP). METHODS: We used nationwide health registries to identify all Danish residents (18 years and older) with incident CP from 2000 to 2018. Information on AP/CP diagnoses, metabolic sequelae (post-pancreatitis diabetes mellitus [PPDM], exocrine pancreatic dysfunction, and osteoporosis), and all-cause mortality were obtained from Danish national health registries. CP cases were stratified based on the presence of AP before CP diagnosis. The risk of metabolic sequelae and all-cause mortality was expressed as hazard ratios (HRs) with 95% confidence intervals (CIs), calculated using multivariate Cox proportional hazards models. RESULTS: A total of 9,655 patients with CP were included. Among patients with CP, 3,913 (40.5%) had a prior AP diagnosis. Compared with patients without a history of AP, patients with prior AP had a decreased risk of death (HR 0.79, 95% CI 0.74–0.84), which was largely confined to the initial period after CP diagnosis. Patients with prior AP had an increased risk of PPDM (HR 1.53, 95% CI 1.38–1.69), which persisted for up to a decade after CP diagnosis. No overall differences in risk were observed for exocrine pancreatic dysfunction (HR 0.97, 95% CI 0.87–1.07) and osteoporosis (HR 0.87, 95% CI 0.74–1.02). DISCUSSION: This nationwide study revealed that most of the patients with CP have no prior episode(s) of AP, indicating that an attack of AP sensitizing the pancreas is not essential for CP development. CP patients with and without prior AP have different risk profiles of PPDM and all-cause mortality.
Sex steroids are important physiologic regu- lators of bone mass, and genes regulating sex steroid production and metabolism are obvious as candidate genes for osteoporosis susceptibility. We present data from a study of 1795 recent postmenopausal women, assigned to either hormone replacement therapy (HRT) or no treatment and followed for 5 years. The associa- tion between bone mass measurements and two single nucleotide polymorphisms, a T (A1 )t o C( A2) transition in the 5¢-UTR of the cytochrome P450c17a (CYP17) gene and a G (Val )t o A( Met) transition in exon 4 of the catechol-O-methyltransferase (COMT) gene, was eval- uated. Association with CYP17 genotype was modified by body mass index (BMI). In lean women, individuals homozygous for the CYP17 A2 allele were 1 cm shorter and had lower baseline BMD (bone mineral density), BMC, and CSA (cross sectional area) in the spine and femoral neck than did other women (BMD spine A2A2: 0.975 g/cm 2 versus 1.011 g/cm 2 in A1A1 + A1A2, P = 0.002). Conversely, an adverse association with A2A2 and bone loss over 5 years seemed present only in overweight women, but differences were small. Response to HRT was not dependent on CYP17 genotype. COMT genotype was not associated with bone mass at baseline, bone loss in untreated women, or response to HRT. In conclusion, the A2 allele of the CYP17 T 27 -C poly- morphism is associated with reduced bone mass and bone size in lean perimenopausal women, whereas high BMI protects against this negative association. The COMT G 1947 -A polymorphism is not associated with bone parameters in this study.
Type 2 diabetes is associated with an increased risk of bone fractures. Bone mineral density (BMD) is increased and bone turnover is low in type 2 diabetes and the increased BMD does not explain the increased fracture risk. However, the low bone turnover may lead to insufficient bone renewal with unrepaired micro-cracks and thus increase fracture risk. Ingestion of food acutely decreases bone resorption markers and the macronutrient composition of meals and meal frequency may influence bone metabolism adversely in subjects with unhealthy eating patterns, e.g., patients with type 2 diabetes.The treatment strategy of bone disease in type 2 diabetics is covered in this review. The current management of diabetic bone disease consists of anti-osteoporotic treatment. However, anti-resorptives may further reduce an already low bone turnover with uncertain effects. Furthermore, the acute and long-term effects of meal ingestion, weight loss alone and in combination with exercise as well as the possible underlying mechanisms are covered in this systematic review.Current management of diabetic bone disease is based on principles of anti-osteoporotic treatment in non-diabetic subjects. However, studies are urged to investigate whether anti-resorptives are equally beneficial in type 2 diabetes as in non-diabetic individuals.
