Complicanze muscolari in donne in postmenopausa affette da Iperparatiroidismo Primitivo: principali meccanismi patogenetici

Impairment in muscle strength and its determinants in primary hyperparathyroidism: A study in postmenopausal women

Retinal micro-vascular and aortic macro-vascular changes in postmenopausal women with primary hyperparathyroidism

Aim of the study was to evaluate the micro and macro-vascular changes in patients with primary hyperparathyroidism (PHPT) compared to controls. 30 postmenopausal PHPT women (15 hypertensive and 15 normotensive) and 30 normotensive controls underwent biochemical evaluation of mineral metabolism and measurements of arterial stiffness by 24 hour ambulatory blood pressure monitoring. Retinal microcirculation was imaged by a Retinal Vessel Analyzer. PHPT patients also underwent bone mineral density measurements and kidney ultrasound. PHPT patients had higher mean calcium and parathyroid hormone values compared to controls. Evaluating macro-vascular compartment, we found higher values of 24 hours-systolic, diastolic blood pressure, aortic pulse wave velocity (aPWV) and aortic augmentation index (Aix) in hypertensive PHPT, but not in normotensive PHPT compared to controls. The eye examination showed narrowing arterial and venular diameters of retinal vessels in both hypertensive and normotensive PHPT compared to controls. In hypertensive PHPT, 24 hours systolic blood pressure was associated only with parathyroid hormone (PTH) levels (beta = 0.36, p = 0.04). aPWV was associated with retinal diameter (beta = −0.69, p = 0.003), but not with PTH. Retinal artery diameter was associated with PTH (beta = −0.6, p = 0.008). In the normotensive PHPT, only PTH was associated with retinal artery diameter (beta = −0.60, p = 0.01) and aortic AIx (beta = 0.65, p = 0.02). In conclusion, we found macro-vascular impairment in PHPT and that micro-vascular impairment is negatively associated with PTH, regardless of hypertension in PHPT

Valori di calcemia e shock distributivo refrattario

Abbiamo letto con interesse la recente review pubbli- cata su CHEST (agosto 2018) da Jentzer e collaboratori1 sul trattamento dello shock distributivo refrattario. Siamo inoltre compiaciuti nell’aver trovato menzionate numerose referenze bibliografiche in merito al possibile ruolo eziopatogenetico dell’ipocalcemia in tale ambito. Tuttavia, è solo parzialmente chiaro dal testo come la riduzione della calcemia possa determinare lo shock distributivo. Infatti, come dibattuto dagli autori, il rilievo della riduzione dei livelli di calcemia, potrebbe essere inquadrato come un epifenomeno, lasciando dubbi pertanto in merito al suo ruolo eziopatogenetico. In aggiunta, gli autori concludono che la sicurezza e l’efficacia di una terapia salvataggio, basata sull’infu- sione di calcio, sono ancora incerte

Understanding and managing secondary osteoporosis

Introduction: The term secondary osteoporosis (SO) identifies a reduction of bone mass related to a well-established disease or pharmacological agent. The identification of the underlying disease often represents a challenging situation in clinical practice. Areas covered: The prevalence of SO in the real world may vary, ranging from 17% to 80%; therefore, search for a form of SO represents a pillar when evaluating patients with osteoporosis. Guidelines for treatment of specific secondary forms of osteoporosis, such as glucocorticoid-induced osteoporosis, have been published even though often neglected in clinical practice. For the majority of SO, there are currently no specific guidelines concerning treatment with only few trials showing the effect of bone-active drugs on fracture risk reduction. Expert opinion: Healthcare professionals should be aware of the secondary forms of osteoporosis, in particular when the reason for reduced skeletal resistance is uncertain or when bone mineral density results are unsatisfactory in a patient compliant to therapy. In a few cases (such as, for example: no response to therapy, better classification of bone involvement in patients with kidney failure, suspicion of rare metabolic bone disease) bone biopsy is needed to investigate the patient. This review highlights recent advances in understanding and managing SO

Cardiovascular manifestations of primary hyperparathyroidism: A narrative review

Data on cardiovascular disease in primary hyperparathyroidism (PHPT) are controversial; indeed, at present, cardiovascular involvement is not included among the criteria needed for parathyroidectomy. Aim of this narrative review is to analyze the available literature in an effort to better characterize cardiovascular involvement in PHPT. Due to physiological effects of both parathyroid hormone (PTH) and calcium on cardiomyocyte, cardiac conduction system, smooth vascular, endothelial and pancreatic beta cells, a number of data have been published regarding associations between symptomatic and mild PHPT with hypertension, arrhythmias, endothelial dysfunction (an early marker of atherosclerosis), glucose metabolism impairment and metabolic syndrome. However, the results, mainly derived from observational studies, are inconsistent. Furthermore, parathyroidectomy resulted in conflicting outcomes, which may be linked to several potential biases. In particular, differences in the methods utilized for excluding confounding co-existing cardiovascular risk factors together with differences in patient characteristics, with varying degrees of hypercalcemia, may have contributed to these discrepancies. The only meta-analysis carried out in PHPT patients, revealed a positive effect of parathyroidectomy on left ventricular mass index (a predictor of cardiovascular mortality) and more importantly, that the highest pre-operative PTH levels were associated with the greatest improvements. In normocalcemic PHPT, it has been demonstrated that cardiovascular risk factors are almost similar compared to hypercalcemic PHPT, thus strengthening the role of PTH in the cardiovascular involvement. Long-term longitudinal randomized trials are needed to determine the impact of parathyroidectomy on cardiovascular diseases and mortality in PHPT

Multiple Vertebral Osteonecroses (Ká¹»mmellâ\u80\u99s Disease) After 10 Years on Denosumab: Is Osteocyte Apoptosis to Blame? More Evidence Needed

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