ascorbic-acid and Hypoparathyroidism

This review provides an update on hypoparathyroidism (HPT), focusing on the major aspects of diagnosis, clinical manifestations and management of patients with hypocalcaemia due to HPT.. Recent advances in the understanding of the physiologic actions of parathormone (PTH) and vitamin D, and the application of molecular genetics, have clarified certain aspects of the pathogenesis, classification, diagnosis and management of HPT.. PTH promotes bone resorption, decreases urinary calcium excretion, enhances the conversion of 25-hydroxyvitamin D to 1, 25-dihydroxyvitamin D and increases intestinal calcium absorption and phosphate renal excretion. Understanding the molecular cause of the disease in patients and their families has the potential for proper tailoring of genetic counselling, family screening and treatment. Signs and symptoms may be associated not only with the severity, chronicity and therapeutic endpoints in HPT but also with the different causes of the disease. Hypocalcaemia may be an asymptomatic laboratory finding or a life-threatening metabolic disturbance. Although the therapy of acute hypocalcaemia is usually readily accomplished, chronic hypocalcaemia remains a very difficult treatment problem. Replacement therapy with PTH could be a therapeutic option for refractory HPT.

Topics: Adolescent; Adult; Ascorbic Acid; Bone Resorption; Child; Female; Homeostasis; Humans; Hypocalcemia; Hypoparathyroidism; Male; Parathyroid Hormone; Vitamin D

In hypoparathyroidism, plasma parathyroid hormone (PTH) levels are inadequate to maintain plasma calcium concentration within the reference range. On conventional treatment with calcium supplements and active vitamin D analogues, bone turnover is abnormally low, and BMD is markedly increased. We aimed to study the effects of PTH-replacement therapy (PTH-RT) on calcium-phosphate homeostasis and BMD. In a double-blind design, we randomized 62 patients with hypoparathyroidism to daily treatment with PTH(1-84) 100 µg or similar placebo for 24 weeks as add-on therapy to conventional treatment. Compared with placebo, patients on PTH(1-84) reduced their daily dose of calcium and active vitamin D significantly by 75% and 73%, respectively, without developing hypocalcemia. However, hypercalcemia occurred frequently during the downtitration of calcium and active vitamin D. Plasma phosphate and renal calcium and phosphate excretion did not change. Compared with placebo, PTH(1-84) treatment significantly increased plasma levels of bone-specific alkaline phosphatase (+226% ± 36%), osteocalcin (+807% ± 186%), N-terminal propeptide of procollagen 1 (P1NP; +1315% ± 330%), cross-linked C-telopeptide of type 1 collagen (CTX; +1209% ± 459%), and urinary cross-linked N-telopeptide of type 1 collagen (NTX; (+830% ± 165%), whereas BMD decreased at the hip (-1.59% ± 0.57%), lumbar spine (-1.76% ± 1.03%), and whole body (-1.26% ± 0.49%) but not at the forearm. In conclusion, the need for calcium and active vitamin D is reduced significantly during PTH-RT, whereas plasma calcium and phosphate levels are maintained within the physiologic range. In contrast to the effect of PTH(1-84) treatment in patients with osteoporosis, PTH-RT in hypoparathyroidism causes a decrease in BMD. This is most likely due to the marked increased bone turnover. Accordingly, PTH-RT counteracts the state of overmineralized bone and, during long-term treatment, may cause a more physiologic bone metabolism.

Topics: Adult; Aged; Ascorbic Acid; Bone Density; Calcium; Female; Homeostasis; Humans; Hypoparathyroidism; Male; Middle Aged; Parathyroid Hormone; Phosphorus; Placebos

Topics: Ascorbic Acid; Disease; Humans; Hypoparathyroidism; Parathyroid Diseases; Parathyroid Glands; Vitamin D; Vitamins

Topics: Ascorbic Acid; Disease; Humans; Hypoparathyroidism; Parathyroid Diseases; Parathyroid Glands; Vitamin D; Vitamins