Is vitamin D deficiency a risk factor for ischemic heart disease in patients with established cardiovascular disease? 10-year follow-up of the Nova Scotia Health Survey

Recent studies have reported that low serum vitamin D levels are associated with a variety of diseases, including cardiovascular disease and in particular ischemic heart disease (IHD). Possible mechanisms underlying this association include increased inflammation, reninangiotensin system upregulation, insulin resistance, altered lipid metabolism, and altered vascular smooth muscle growth and function that lead to hypertension, diabetes, dyslipidemia and atherosclerosis.[1][2] However, few longitudinal studies have explored the association between vitamin D levels and incident IHD. A nested case-control study of male health care professionals found an approximately doubled risk of incident myocardial infarction associated with lower vitamin D levels.[3] Other studies have identified trends between vitamin D levels and incident myocardial infarction but no statistically significant associations, [4][5][6] at least in part due to small sample sizes or short follow-up

Week 26 results from the PaTH Forward Open-Label Extension Trial Support TransCon PTH as a potential hormone replacement therapy for patients with hypoparathyroidism

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Bone Research / Assessment of bone turnover and bone quality in type 2 diabetic bone disease : current concepts and future directions

Substantial evidence exists that in addition to the well-known complications of diabetes, increased fracture risk is an important morbidity. This risk is probably due to altered bone properties in diabetes. Circulating biochemical markers of bone turnover have been found to be decreased in type 2 diabetes (T2D) and may be predictive of fractures independently of bone mineral density (BMD). Serum sclerostin levels have been found to be increased in T2D and appear to be predictive of fracture risk independent of BMD. Bone imaging technologies, including trabecular bone score (TBS) and quantitative CT testing have revealed differences in diabetic bone as compared to non-diabetic individuals. Specifically, high resolution peripheral quantitative CT (HRpQCT) imaging has demonstrated increased cortical porosity in diabetic postmenopausal women. Other factors such as bone marrow fat saturation and advanced glycation endproduct (AGE) accumulation might also relate to bone cell function and fracture risk in diabetes. These data have increased our understanding of how T2D adversely impacts both bone metabolism and fracture risk.(VLID)459018

Asymptomatic primary hyperparathyroidism: present management and future options

Primary hyperparathyroidism is a common disorder of mineral metabolism characterized by incompletely regulated, excessive secretion of parathyroid hormone from one or more of the parathyroid glands. In adults with the disease, a single, benign adenoma is seen approximately 80 percent of the time, with multiple gland involvement making up for most of the remaining patients. Very rarely, a parathyroid cancer is responsible but malignant parathyroid disease is rare, being seen in less than 0.5 percent of patients with primary hyperparathyroidism. Primary hyperparathyroidism is the most common cause of hypercalcemia and should always be considered in any individual with hypercalcemia. In this article, we will review important clinical and diagnostic features of primary hyperparathyroidism. We will review current recommendations by which the clinician is guided as to the choice between surgery and medical management, and focus then directly on non-surgical options in the management of asymptomatic primary hyperparathyroidism

Type 2 diabetes and bone

There is a growing body of research showing that diabetes is an independent risk factor for fracture. Type 2 diabetes (T2D), which predominates in older individuals and is increasing globally as a consequence of the obesity epidemic, is associated with normal or even increased dual-energy x-ray absorptiometry (DXA)-derived areal bone mineral density (BMD). Therefore, the paradoxical increase in fracture risk has led to the hypothesis that there are diabetes-associated alterations in material and structural properties. An overly glycated collagen matrix, confounded by a low turnover state, in the setting of subtle cortical abnormalities, may lead to compromised biomechanical competence. In current clinical practice, because BMD is central to fracture prediction, a consequence of this paradox is a lack of suitable methods, including FRAX, to predict fracture risk in older adults with T2D. The option of adding diabetes to the FRAX algorithm is appealing but requires additional data from large population-based cohorts. The need for improved methods for identification of fracture in older adults with T2D is an important priority for osteoporosis research

Hypoglycemia Secondary to Sulfonylurea Ingestion in a Patient with End Stage Renal Disease: Results from a 72-Hour Fast

Insulin, proinsulin, and C-peptide levels increase with sulfonylurea exposure but the acuity of increase has not been described in dialysis patients. We present a case of a dialysis patient who presented with hypoglycemia and was found to have accidental sulfonylurea ingestion. This is a 73-year-old man with ESRD on peritoneal dialysis, without history of diabetes, who presented with hypoglycemia. Past medical history includes multiple myeloma, congestive heart failure, and hypertension. At initial presentation, his blood glucose was 47 mg/dL, with concomitant elevations in the following: C-peptide 30.5 (nl: 0.8–3.5 ng/mL), insulin 76 (nl: 3–19 μIU/mL), and proinsulin 83.3 (nl: ≤8.0 pmol/L). During the 72-hour fast, which he completed without hypoglycemia, insulin declined to be within normal limits (to 12 μIU/mL); proinsulin (to 12.1 pmol/L) and C-peptide (to 7.2 ng/mL) levels decreased but remained elevated. The sulfonylurea screen ultimately returned positive for glipizide, clinching the diagnosis. This is the first reported case which characterizes the chronic elevation of proinsulin in a patient with ESRD, as well as its dramatic increase after a presumed solitary exposure to sulfonylurea. The 72-hour fast conducted gives insight into the clearance of insulin, proinsulin, and C-peptide after sulfonylurea ingestion in ESRD

Presentation of Asymptomatic Primary Hyperparathyroidism: Proceedings of the Third International Workshop

BACKGROUND: At the Third International Workshop on Asymptomatic Primary Hyperparathyroidism (PHPT) in May 2008, recent data on the disease were reviewed. We present the results of a literature review on issues arising from the clinical presentation and natural history of PHPT. METHODS: Questions were developed by the International Task Force on PHPT. A comprehensive literature search for relevant studies was reviewed, and the questions of the International Task Force were addressed by the Consensus Panel. CONCLUSIONS: 1) Data on the extent and nature of cardiovascular involvement in those with mild disease are too limited to provide a complete picture. 2) Patients with mild PHPT have neuropsychological complaints. Although some symptoms may improve with surgery, available data remain inconsistent on their precise nature and reversibility. 3) Surgery leads to long-term gains in spine, hip, and radius bone mineral density (BMD). Because some patients have early disease progression and others lose BMD after 8-10 yr, regular monitoring (serum calcium and three-site BMD) is essential in those followed without surgery. Patients may present with normocalcemic PHPT (normal serum calcium with elevated PTH concentrations; no secondary cause for hyperparathyroidism). Data on the incidence and natural history of this phenotype are limited. 4) In the absence of kidney stones, data do not support the use of marked hypercalciuria (>10 mmol/d or 400 mg/d) as an indication for surgery for patients. 5) Patients with bone density T-score -2.5 or less at the lumbar spine, hip, or distal one third radius should have surgery