Most cases of type 1 diabetes (T1DM) are due to an immune‐mediated destruction of the pancreatic beta cells, a process that is conditioned by multiple genes and environmental factors. The main susceptibility genes are represented by the class II HLA‐DRB1 and DQB1 alleles. The aim of our study was to reconfirm the contribution of HLA‐DQB1 polymorphisms to T1DM genetic susceptibility for the Romanian population. For this, 219 Romanian T1DM families were genotyped at high resolution for HLA DQB1 using the PCR‐SSOP method (Polymerase Chain Reaction ‐ Sequence Specific Oligonucleotide Probes). Allele transmission to diabetics and unaffected siblings was studied using the Transmission Disequilibrium Test (TDT). We found an increased transmission of DQB1 *02 (77.94% transmission, PTDT= 7.18 × 10−11) and DQB1*0302 (80.95% transmission, PTDT= 2.25 × 10−10) alleles to diabetics, indicating the diabetogenic effect of these alleles. Conversely, DQB1*0301, DQB1*0603, DQB1*0602, DQB1*0601 and DQB1*05 alleles are protective, being significantly less transmitted to diabetics. In conclusion, our results confirmed the strong effect of HLA‐DQB1 alleles on diabetes risk In Romania, with some characteristics which can contribute to the low incidence of T1DM in this country.

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Type 2 diabetes, one of the most frequent chronic diseases, has an important effect on bone metabolism, with most studies reporting an increased prevalence of fractures in these patients despite an apparently increased bone mineral density. Most probable explanation is an alteration of bone structure/ quality with increased fragility but the different diabetes medications influence the risk of fracture. While metformin and incretin-based therapies are safe, thiazolidinediones and canagliflozin (sodium-glucose cotransporter-2 inhibitor) negatively impact bone metabolism and should be avoided in subjects at increased risk of fractures. Insulin and sulphonylureas are generally safe but can increase the risk of hypoglycemia and falls with subsequent traumatic fractures. Their combination should be avoided, especially in elderly subjects.

Patients with type-2 diabetes mellitus (T2DM) have normal or increased bone mineral density (BMD) but despite that, they are characterized by an increased hip and vertebral fracture risk that involves the alteration of bone quality and not the reduction in bone mass. BMD is utilized for the diagnosis and evaluation of osteoporosis, but BMD itself cannot provide an accurate diagnosis of the individuals at increased risk of fracture and, therefore, studies have focused on identifying other risk factors that are partially or fully independent of BMD. The fracture risk score tool-FRAX® models provide information about a 10-year probability of osteoporotic fractures, but do not include risk factors specific to illness such as diabetes duration, diabetes drug therapy, glycemic control, or the presence of micro-vascular complications. Multiple markers have been investigated to provide information on the risk of fractures in patients with T2DM such as: advanced glycation end products (AGEs), insulin-like growth factor-I (IGF-I), osteocalcin (OC), adiponectin, and sclerostin, but epidemiological studies did not provide homogeneous information regarding the link between these markers and bone fragility in T2DM subjects. Markers that increase the accuracy of fracture risk estimation in patients with T2DM need to be identified and employed in current medical practice. Keywords  diabetes mellitus, bone fragility, markers of fracture risks Highlights  Patients with type 2 diabetes mellitus have significantly higher scores in over-vigilance and inhibition schematic domains.  Epidemiological studies do not provide unitary information on the association between markers of bone fragility and fracture risk in T2DM.

Introduction. Acute or recurrent pancreatitis may be a complication of primary hyperparathyroidism and patients with previous episodes of pancreatitis may develop secondary diabetes mellitus. Case report. We describe the clinical case of a 52-year old Caucasian man diagnosed with chronic recurrent pancreatitis in 2007. The first episode of acute pancreatitis occurred in 2002, followed by another 4 episodes in 2004 and 2007. In 2004, papilosfincterectomy was implemented with a stent mount that was removed one month later. In 2005, the patient underwent a surgical intervention for the diagnosis of chronic lithiasis, and cholecystectomy was performed. Additional investigations on the etiology of recurrent chronic pancreatitis, initially diagnosed as idiopathic, revealed elevated values of total serum calcium, serum parathormone, and the presence of a parathyroid adenoma in the right lower pole of the thyroid. In September 2007, parathyroidectomy was performed with a favorable evolution and the remission of the acute pancreatitis episodes. The patient had not had any family history of diabetes; in 2017 he was diagnosed with diabetes. Conclusion. In cases of recurrent pancreatitis, screening for hyperparathyroidism is recommended. Metabolic evaluation is required, because the risk of developing diabetes in patients with recurrent pancreatitis is high.