Cases reported "Hypoparathyroidism"

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1/33. Idiopathic hypoparathyroidism and celiac disease in two patients with previous history of cataract.

    We report two patients with idiopathic hypoparathyroidism and celiac disease. Both had undergone surgery for cataract previously. The patients presented with tetany in the absence of gastrointestinal complaints. Investigations showed severe hypocalcemia, hypoparathyroidism, flattening of duodenal villi histologically, and diffuse cerebral and basal ganglia calcifications on CT scan. After a gluten-free diet with calcium supplementation, the clinical situation and biochemical values improved.
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2/33. digeorge syndrome with Graves' disease: A case report.

    digeorge syndrome (DGS) is characterized by aplasia or hypoplasia of the thymus and parathyroid glands, cardiac defects and anomaly face. This syndrome is usually associated with hypocalcemia resulting from hypoparathyroidism. In most cases the initial symptom is tetany caused by hypocalcemia within 24-48 hours after birth, with symptoms by immune abnormality appearing later. We report a woman who passed with no symptoms before age 18 and was diagnosed digeorge syndrome by tetany with developing auto-immune thyroid disease (Graves' disease). She had surgery for intraventricular septal defect at age 3, hypoparathyroidism, decrease of T cells in peripheral blood and the deletion of the 22nd chromosome long arm (22q11.2). It is supposed that abnormalities of immune function of this case are not complete as indicated by complicating of Graves' disease, and contributing to her long-term survival.
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3/33. Defective growth hormone secretion and hypogonadism in the new syndrome of congenital hypoparathyroidism, growth failure and dysmorphic features.

    A child with extreme growth failure, dysmorphic features, hypoparathyroidism, and abnormal skeletal survey was studied. He was a product of first degree consaguineous marriage who had intrauterine growth retardation and presented at 14 days of age with hypocalcemic tetany with normal cardiovascular system and immune function. Endocrine evaluation after infancy revealed defective growth hormone (GH) secretion in 2 provocation tests and lack of clinical and testosterone response to human chorionic gonadotrophin (HCG) therapy.
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4/33. 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.
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5/33. 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.
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6/33. 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.
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7/33. 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.
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8/33. Transverse leukonychia in severe hypocalcemia.

    We report the case of a 26-year-old man with acral tetany and muscular cramps of the upper limbs associated with hypocalcemia caused by hypoparathyroidism and celiac disease. physical examination revealed a transverse leukonychia which disappeared after treatment with calcium lactogluconate, calcium carbonate and calcitriol. hypocalcemia may induce nail alterations with a double mechanism represented by angiospasm and disorganization of the hard keratin and of the integrin subunits.
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9/33. Hypocalcemic myopathy without tetany due to idiopathic hypoparathyroidism: case report.

    Myopathy due to idiopathic hypoparathyroidism is very unusual. We report on a 30 years-old man referred with complaints of sporadic muscle pain and mild global weakness for 10 years. His physical examination showed normal strength in distal muscle and slightly weakness in the pelvic and scapular girdles with no atrophy. Deep muscle reflexes were slightly hypoactive. Trousseau's and Chvostek's signs were absent. He had bilateral cataract and complex partial seizures. His laboratory tests showed decreased ionised and total calcium and parathyroid hormone and increased muscle enzymes. EMG and muscle biopsy was compatible with metabolic myopathy. After treatment with calcium and vitamin d supplementation he showed clinical, neurophysiological and laboratorial improvement. In conclusion: patients with muscle symptoms, even when non-specific and with normal neurological examination, should have serum calcium checked, as myopathy due to idiopathic hypoparathyroidism, even being rare, is treatable and easy to diagnose.
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10/33. Hypocalcemic generalised seizures as a manifestation of iatrogenic hypoparathyroidism months to years after thyroid surgery.

    hypoparathyroidism is a relatively common side effect of a thyroidectomy and leads to hypocalcemia. Carpopedal spasm and tetany are typical manifestations and usually occur within weeks after surgery. The first signs can be less typical and include movement disorders such as chorea, as well as symptoms of increased intracranial pressure or epileptic seizures. We describe two cases with generalised tonic-clonic seizures as the first manifestation of postoperative hypoparathyroidism, appearing months and years after thyroidectomy. Iatrogenic hypoparathyroidism needs to be considered in the differential diagnosis of adult-onset, generalised, tonic-clonic seizures even if the thyroidectomy was performed years earlier.
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