1/10. Disorders of maternal calcium metabolism implicated by abnormal calcium metabolism in the neonate.Normal fetal and neonatal calcium homeostasis is dependent upon an adequate supply of calcium from maternal sources. Both maternal hypercalcemia and hypocalcemia can cause metabolic bone disease or disorders of calcium homeostasis in neonates. Maternal hypercalcemia can suppress fetal parathyroid function and cause neonatal hypocalcemia. Conversely, maternal hypocalcemia can stimulate fetal parathyroid tissue causing bone demineralization. We report two asymptomatic women, one with previously unrecognized hypoparathyroidism and the other with unrecognized familial benign hypercalcemia, who were diagnosed when their newborn infants presented with abnormalities of calcium metabolism. J.B. was born at 34 weeks' gestation with transient hyperbilirubinemia and thrombocytopenia. At 1 month of age he had severe bone demineralization, cortical irregularities, widening and cupping of the metaphyses, and lucent bands in the scapulae. The total serum calcium and phosphorus were normal with an ionized calcium of 5.4 mg/dL (4.6-5.4). His alkaline phosphatase, parathyroid hormone, and 1,25-dihydroxyvitamin D levels were all increased. P.B., mother of J.B., had no symptoms of hypocalcemia either prior to, or during this pregnancy. She had severe hypocalcemia and hyperphosphatemia, laboratory values typical of hypoparathyroidism. J.N. presented at 6 weeks of age with new onset of seizures and tetany secondary to severe hypocalcemia. The serum phosphorus, creatinine, alkaline phosphatase, and parathyroid hormone levels were normal. At 15 weeks of age his calcium was slightly elevated with a low fractional excretion of calcium. P.N., mother of J.N., had no symptoms of hypercalcemia either prior to, or during this pregnancy. Her serum calcium was 12.7 mg/dL and urine calcium was 66.5 mg/24 hr, with a low fractional excretion of calcium ranging from 0.0064 to 0.0073. P.N. has a brother who previously had parathyroid surgery. Both J.N. and P.N. meet the diagnostic criteria for familial benign hypercalcemia. These cases illustrate the important relationships between maternal serum calcium levels and neonatal calcium homeostasis. They emphasize the need to assess maternal calcium levels when infants are born with abnormal serum calcium levels or metabolic bone disease.- - - - - - - - - - ranking = 1keywords = homeostasis (Clic here for more details about this article) |
2/10. Prolonged, symptomatic hypocalcemia with pamidronate administration and subclinical hypoparathyroidism.A 62-yr-old woman with thyroid carcinoma metastatic to bone, and a history of subclinical hypoparathyroidism was admitted to the hospital in hypocalcemic crisis 5 wk after receiving iv pamidronate. The patient had tetany and laryngospasm. An electrocardiogram showed junctional rhythm with QT segment prolongation. The patient had previously maintained a low-normal serum calcium on 500-750 mg of calcium carbonate and 600 IU of vitamin d daily. One week after pamidronate administration the patient's calcium and vitamin d supplementation were inadvertently discontinued. She continued to take daily intranasal calcitonin. At the time of her hospitalization for hypocalcemia, the patient's serum calcium was 4.3 mg/dL. The patient received aggressive calcium and vitamin D supplementation. However, her serum calcium remained below 6 mg/dL for a 2-wk period, and took another week to return to the normal range. In this article, we discuss the counterregulatory responses necessary to maintain calcium homeostasis following osteoclast inhibition by bisphosphonates. We also review the risk factors for hypocalcemia following bisphosphonate administration. Pamidronate and other bisphosphonates are becoming an integral part of the management of normocalcemic patients with malignant bone disease. Therefore, awareness of risk factors for hypocalcemia and familiarity with avenues available for protection from potentially catastrophic hypocalcemia are both crucial.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
3/10. Transient hypoparathyroidism due to amphotericin b-induced hypomagnesemia in a patient with beta-thalassemia.OBJECTIVE: To report a case of transient hypoparathyroidism that developed in a beta-thalassemic patient due to amphotericin b-induced hypomagnesemia. CASE SIJMMARY: A 21-year-old man with beta-thalassemia was treated with amphotericin b for candida albicans intravenous line sepsis. After five days of treatment (cumulative dose 160 mg), he developed hypomagnesemia, which caused hypoparathyroidism and hypocalcemia; all three abnormalities resolved after the drug was withdrawn. DISCUSSIoN: patients with beta-thalassemia may develop endocrinologic abnormalities due to excessive iron deposition. Some may have subclinical hypoparathyroidism that clinically emerges after even a mild homeostasis disturbance. amphotericin b is associated with variable adverse effects including renal tubular insult, which may induce hypomagnesemia following relatively short treatment. The resolution of hypomagnesemia, hypocalcemia, and hypoparathyroidism in our patient after discontinuation of amphotericin b treatment suggests that the endocrine dysfunction was due to a drug-related adverse effect and not to parathyroid dysfunction caused by iron deposition. CONCLUSIONS: This case demonstrates a known but rarely reported adverse effect of amphotericin b, namely hypomagnesemia, that may occur even at a low cumulative dose. It also emphasizes that patients with an underlying disease, such as thalassemia, may be more susceptible to hypoparathyroidism and hypocalcemia during treatment with amphotericin b.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
4/10. Reversible peripheral neuropathy in idiopathic hypoparathyroidism.We describe a 40-year-old male with idiopathic hypoparathyroidism presenting with tetany, proximal weakness, signs of hypocalcaemia including Chvostek and Trousseau's and diminished tendon reflexes in the upper and lower limbs. Electrophysiological studies revealed a sensory-motor neuropathy, predominantly axonal as evidenced by decreased CMAP amplitudes, with normal distal latencies-velocites, except for median nerve where a prolonged distal latency was observed. Serial nerve conduction studies were performed at repeated intervals for 2 years, while he received treatment for hypoparathyroidism (calcium and vitamin d supplementation). A progressive improvement in neuropathy both clinical and on electrophysiological studies was observed. Occurrence of peripheral neuropathy in hypocalcaemic states such as hypoparathyroidism and its reversibility after normalization of calcium homeostasis lend proof to the role of critical Ca2 ion concentration in the normal functioning of the peripheral axons.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
5/10. Cortisol-dihydrotachysterol antagonism in a patient with hypoparathyroidism and adrenal insufficiency: apparent inhibition of bone resorption.This report describes a case of chronic mucocutaneous candidiasis with associated hypoparathyroidism and acutely developed adrenocortical insufficiency. The latter was heralded by hypercalcemia. Upon the institution of cortisol therapy, while still under the effects of a vitamin d analog dihydrotachysterol (DHT), the patient exhibited severe hypocalcemia and tetany. Since calcium intake was minimal during this period of presumed corticosteroid-DHT antagonism, it is suggested that the cortisol disturbed calcium homeostasis by in inhibiting bone calcium resorption.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
6/10. The first successful parathyroid transplant from an identical twin for the cure of permanent postoperative hypoparathyroidism.Long-lasting hypoparathyroidism is a severe disease with poor response to unsatisfactory therapy. A successful parathyroid isograft in a patient with postoperative hypoparathyroidism from an identical twin was performed in December 1984. Function was proved by the increase of serum parathyroid hormone from undetectable to normal levels, the ability to discontinue all supportive medications, and the maintenance of normal calcium homeostasis to date. The combination of hypoparathyroidism and the availability of an identical twin will be rare, but if it occurs parathyroid isografting should be considered.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
7/10. Postpartum resolution of hypocalcemia in a lactating hypoparathyroid patient.A 24 year old woman with post-surgical hypoparathyroidism was studied during pregnancy and lactation. During pregnancy the patient required less vitamin d therapy for control of her hypoparathyroidism and, while lactating, maintained a normal serum calcium without any supplemental vitamin d. The serum parathyroid hormone concentration and plasma 1,25 (OH)2 vitamin d concentration were undetectable and low normal respectively at a time when the serum calcium concentration was normal and the patient was not on vitamin d therapy. Urinary calcium excretion was low during this period and may explain the normalization of the serum calcium. The mechanism by which the improvement in calcium metabolism occurred is unknown, but may be secondary to a direct effect of prolactin on calcium homeostasis.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
8/10. Addison's disease presenting as a hypercalcemic crisis in a patient with idiopathic hypoparathyroidism.A patient with idiopathic hypoparathyroidism complicated by Addison's disease is described. The development of adrenal insufficiency was accompanied by a hypercalcaemic crisis. The hypercalcaemia appeared to result from a reduction in the filtered load and enhanced renal tubular reabsorption of calcium. cortisone therapy was followed by the characteristic renal tubular leak of calcium associated with hypoparathyroidism and a return of the serum calcium to normal. The possible mechanisms for these changes in calcium homeostasis are discussed.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
9/10. thyrotoxicosis and hungry bone syndrome--a cause of posttreatment hypocalcemia.We report a case of a 54 year old woman with a history of recurrent Graves' disease, treated previously by thyroidectomy and later by radioiodine, who subsequently presented with tetany. Laboratory results revealed a profound hypocalcemia (total calcium 1.00 mmol/L; ionized calcium 0.53 mmol/L) and hyperphosphatemia (2.66 mmol/L) with low levels of parathyroid hormone. Although the patient's symptoms resolved after 5 days of treatment, hypocalcemia and elevated serum levels of bone-specific alkaline phosphatase (ALP, EC 3.1.3.1) activity and skeletal muscle isoenzyme (CK-MM) creatine kinase (EC 2.7.3.2) activity persisted to her discharge, 3 weeks later. attention is drawn to the recognition and management of recalcification tetany due to the "Hungry (for calcium) Bone syndrome," a biochemical and hormonal disturbance of calcium homeostasis and bone metabolism in the posttherapy thyrotoxic patient with hypoparathyroidism. This condition can be monitored by the use of calcium profile investigations, including bone-specific ALP, in addition to routine laboratory tests of thyroid function.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
10/10. Dental manifestations of autoimmune hypoparathyroidism.The histopathologic changes in three permanent molars from two siblings with autoimmune hypoparathyroidism as part of candida endocrinopathy syndrome are described. These teeth developed after the diagnosis of hypoparathyroidism and while each subject was receiving vitamin d and calcium supplementation. The pathogenesis of the dental changes is unknown, but it is possible that parathormone may directly influence tooth development independent of its role in calcium and phosphorous homeostasis.- - - - - - - - - - ranking = 0.33333333333333keywords = homeostasis (Clic here for more details about this article) |
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