Primary hyperparathyroidism is the most common cause of hypercalcaemia in the ambulatory setting. 1 2 Although this condition can occur at any age, it commonly affects people over the age of 50 years and postmenopausal women. 2 3 Over the past few decades it has changed from being a condition usually defined by its symptoms to one that is often discovered on routine screening tests while the patient is still largely asymptomatic. In light of advances in research, new guidelines on the diagnosis and management of asymptomatic primary hyperparathyroidism have recently been developed. We review the presentation, diagnosis, and management of primary hyperparathyroidism for the generalist doctor, with evidence drawn from randomised controlled trials, cohort studies, and the most recent consensus guidelines.The four parathyroid glands are situated behind the thyroid gland. Parathyroid hormone (PTH) secreted by the chief cells regulates calcium homeostasis. Decreases in serum ionised calcium are sensed by the calcium sensing receptor on the chief cells, which increase the production and secretion of PTH, thereby enhancing renal tubular calcium reabsorption and osteoclast mediated bone resorption. PTH also enhances the conversion of 25-hydroxyvitamin D 3 into 1,25-hydroxyvitamin D 3 , which in turn increases the efficiency of calcium absorption from the bowel. 1 Rising calcium concentrations decrease the release of of PTH, normalising serum calcium values. What causes primary hyperparathyroidism? Tumours and hyperplasiaAbout 85% of cases are caused by a sporadic PTH secreting solitary adenoma of parathyroid chief cells. 1 Multiglandular parathyroid hyperplasia occurs in 1-15% of patients with primary hyperparathyroidism. 1 Parathyroid carcinoma is rare and occurs in less than 1% of cases. Adenomas may be found in ectopic locations in about 16% of cases-commonly the thymus, trachea-oesophageal groove, mediastinum, and the thyroid. 4 Familial disordersPrimary hyperparathyroidism may also be associated with uncommon familial disorders, including multiple endocrine neoplasia type 1 and type 2A syndromes, familial hyperparathyroidism-jaw tumour syndrome, neonatal severe hyperparathyroidism, and familial isolated hyperparathyroidism. In addition, familial hypocalciuric hypercalcaemia is a benign cause of hypercalcaemia, and it is inherited as an autosomal dominant condition that mimics primary hyperparathyroidism. It is caused by an inactivating mutation of the calcium sensing receptor gene that makes the receptor less sensitive to calcium in the parathyroid glands and the kidneys. Normally, activation of the calcium sensing receptor in the kidney enhances renal calcium clearance. An inactivating mutation leads to decreased sensing of calcium in the kidney and decreased renal calcium clearance, with relative hypocalciuria. 5 6 Drugs and radiation exposureDrugs such as thiazide diuretics and lithium may also alter calcium homeostasis. Thiazides may unmask underlying primary hyperparathyroidism because they reduce urinary calciu...

Background:Low serum vitamin (vit) D levels are common even in sunny countries. We assessed the prevalence and relationship of low vit D with cardiovascular risk factors in Qatar.Methods:Data were collected retrospectively from January 2008 and November 2009. In patients who had low vi t D (< 30 ng/ml ) , demographic and clinical profiles were analyzed and compared in males and females.Results:The overall mean level of vit D among 547 patients was 14.4±11 ng/mL. Among the low vitamin D group, 56% were females (mean age 48±12) and 44% males (mean age 49.6±13). Severely low vit D levels (<10 ng/mL) were found in 231 (46%) patients with mean age of 46±12 years. Compared with females, males with low vitamin D were more likely to have diabetes mellitus (38 vs 22%, p=0.001), dyslipidemia (41 vs 29%, p=0.007), myocardial infarction (5.5 vs 1.5%, p=0.001) and angiographically documented coronary artery disease (CAD) (53 vs 17%, p=0.001). Multivariate logistic regression analysis showed that in the presence of low vit D, age and hypertension were independent predictors of CAD (OR 1.07;95% CI: 1.02-1.11) and OR 8.0; 95% CI: 1.67-39.82), respectively.Conclusions:Our study supports the widespread prevalence of low vit D in sunny regions. Low vit D is associated with 3 times increase in the rate of MI among males. Hypertension increases the risk of CAD 8 times in the presence of low vit D regardless of gender.

BackgroundMetabolic abnormalities are common in patients maintained on antipsychotics. These abnormalities increase the risk of cardiovascular diseases and mortality in this population. The aim of this study is to assess the prevalence of metabolic syndrome (MetS) in subjects maintained on antipsychotics relative to controls in Qatar, and to assess the factors contributing to the development of MetS.MethodsA cross sectional design was used to collect data and fasting blood samples from subjects maintained on antipsychotics for at least six months (n = 112) and from a control group (n = 114). The groups were compared in regard to prevalence of MetS, and multiple regression analysis was used to determine the risk factors in each group.ResultsThe two groups (antipsychotics vs. control) were similar in regard to age (35.73 ± 10.28 vs. 35.73 ± 8.16 years) and gender ratio. The MetS was higher among the subjects on antipsychotics, but this difference did not reach statistical significance. Blood pressure (BP) was significantly higher in the antipsychotics group and BMI was the major risk factor to develop MetS in this group.ConclusionsThe prevalence of MetS in both groups is high and mostly attributed to obesity and high BP. Public health interventions are needed to address this major health problem overall. Larger studies are needed to further assess the impact of antipsychotics and mental illness on the development of MetS.

The role of cardiac biomarkers in risk stratification of syncope is unclear. We undertook a systematic review to assess their predictive value for short-term major adverse cardiovascular events (MACE). We conducted a systematic review using MEDLINE, EMBASE, DARE and Cochrane databases from inception to July 2014. We included studies involving adult syncope patients that evaluated cardiac biomarker levels for risk stratification during acute management and excluded case reports, reviews and studies involving children. Primary outcome (MACE) included death, cardiopulmonary resuscitation, myocardial infarction (MI), structural heart disease, pulmonary embolism, significant hemorrhage or cardiac procedural interventions. Secondary outcome analysis assessed for prediction of MI, cardiac syncope and death. Two reviewers extracted patient-level data based on the cut-off reported. Pooled sensitivities and specificities were calculated using patient-level data. A total of 1862 articles were identified, and 11 studies with 4246 patients were included. Studies evaluated 3 biomarkers: contemporary troponin (2693 patients), natriuretic peptides (1353 patients) and high-sensitive troponin (819 patients). The pooled sensitivities and specificities for MACE were: contemporary troponin 0.29 (95 % CI 0.24, 0.34) and 0.88 (95 % CI 0.86, 0.89); natriuretic peptides 0.77 (95 % CI 0.69, 0.85) and 0.73 (95 % CI 0.70, 0.76); high-sensitive troponin 0.74 (95 % CI 0.65, 0.83) and 0.65 (95 % CI 0.62, 0.69), respectively. Natriuretic peptides and high-sensitive troponin showed good diagnostic characteristics for both primary and secondary outcomes. Natriuretic peptides and high-sensitive troponin might be useful in risk stratification.