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There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

A 17-year-old woman manifested fever, abdominal pain, headache, and hypertension caused by a solitary, benign pheochromocytoma. She also had hypercalcemia and elevated plasma immunoreactive calcitonin levels. After removal of the pheochromocytoma, calcium and calcitonin levels returned to normal. Studies of peripheral and tumor venous blood showed no excess or ectopic parathyroid hormone secretion, but the tumor contained and secreted calcitonin. Sporadic pheochromocytoma may secrete calcitonin and cause hypercalcemia by non-parathyroid hormone-mediated mechanisms. The potential is clearly present for confusion with multiple endocrine neoplasia, type 2 (medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism).
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PMID:Pheochromocytoma associated with hypercalcemia and ectopic secretion of calcitonin. 46 64

Many recent studies, only a few of which are reviewed here (see Habener & Potts, 1976, for a detailed summary) have led to considerable clarification concerning critical features of the chemistry, biosynthesis, secretion and mode of action of parathyroid hormone. Certain of the confusion recently experienced in measurements of parathyroid hormone in blood is clearly explained by the heterogeneity arising from various forms of parathyroid hormone arising during biosynthesis and metabolism. Ultimately, as critical features of biosynthesis and metabolism of PTH as well as chemical definition of various molecular forms are achieved, considerable refinement in immunoassays should result. These advances in turn should provide better insights into the role of parathyroid dysfunction in various disorders of calcium and skeletal metabolism. From the physiological viewpoint, a clearer appreciation of the homeostatic role of parathyroid hormone in calcium metabolism is emerging as the essential features of biosynthesis, release, metabolism and action of the hormone are uncovered.
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PMID:Chemistry and physiology of parathyroid hormone. 80 86

A 26-year-old woman, gravida 1, para 0, having episodes of confusion, slurred speech, and blurred vision in pregnancy was documented to have severe hypoglycemia with elevated serum insulin and C-peptide levels. Emergency treatment for hypoglycemia was necessary several times during pregnancy. A healthy female infant was delivered after oxytocin induction of labor. Post partum the patient had numerous episodes of severe hypoglycemia in spite of constant intravenous glucose. Computerized tomographic scan of the pancreas failed to show a lesion, whereas pancreatic arteriography revealed a 2 cm mass in the tail of the pancreas. Partial pancreatectomy was performed 6 days after delivery. Microscopic examination of the tissue confirmed the presence of an insulinoma. Hypercalcemia developed together with elevated parathyroid hormone levels. The presence of an insulinoma, hypercalcemia, and a history of hyperparathyroidism in two relatives indicates that this is a case of multiple endocrine adenomatosis type I first diagnosed during pregnancy.
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PMID:Multiple endocrine adenomatosis type I in pregnancy. 197 95

Lithium is widely used in the management of patients with manic depressive illnesses. It is a valuable drug with a good safety record but occasionally causes severe disorders. A 71-year-old woman is described who previously had a good response to lithium carbonate treatment of a manic depressive illness. Because the patient appeared depressed and withdrawn, lithium carbonate dosage was increased. The development of confusion and choreiform movements precipitated hospital admission. The symptoms were relieved when lithium was stopped but recurred with the reinstitution of lithium. Spontaneous choreiform movements were again relieved on lithium withdrawal. Associated with the abnormal movements were alterations in the serum calcium concentrations, a rise in the parathyroid hormone concentration and a rise in the serum amylase concentration without features of acute pancreatitis.
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PMID:Acute lithium toxicity--chorea, hypercalcemia and hyperamylasemia. 248 12

Following a brief discussion of the diagnosis and classification of hypoparathyroidism, this review will focus on current concepts of pseudohypoparathyroidism. Topics to be covered will include differing resistance of kidney and bone to parathyroid hormone, relationship of estrogen and pregnancy to Ca homeostasis, normocalcemic pseudohypoparathyroidism, and current understanding of pathogenesis based on various defects in the hormone receptor-adenylate cyclase system. Evidence for physiologic derangements beyond the impaired generation of cyclic AMP will be reviewed, as well as involvement of nonendocrine systems by the deficiency of the stimulatory guanine nucleotide connecting protein. Finally, semantic confusion resulting from the faulty term "pseudopseudohypoparathyroidism" will be addressed.
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PMID:Pseudohypoparathyroidism: current concepts. 266 77

Hyperparathyroid crisis is a rare disease but should be suspected in acutely ill patients complaining of weakness, lethargy, nausea, vomiting, confusion and abdominal pain. Despite the variety of clinical manifestations, the syndrome forms a distinctive pattern which, in the presence of a serum calcium level greater than 16 mg/100 ml, should be recognized. The most difficult problem in diagnosis is the differentiation of hyperparathyroid crisis from ectopic parathyroid hormone-producing tumors. The disease is an endocrine emergency which requires prompt surgery after rapid correction of dehydration and hypercalcemia. The best results are achieved by removing offending parathyroid tissue within 72 hours after the onset of symptoms.
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PMID:Primary hyperparathyroidism: hyperparathyroid crisis. 730 6

Primary hyperparathyroidism causes excessive bone resorption with a decrease in bone mineral density. Fractures of the vertebras and appendicular bones, however, seem uncommon, even in the long term. We report three patients who presented with bone insufficiency fractures as the inaugural symptom of primary hyperparathyroidism. The three patients were women, aged 62, 65 and 86 years, respectively, who presented with fractures of the medial tibial plateau, femoral neck of femoral neck and tarsus. Laboratory tests showed hypercalcemia, hypophosphatemia and elevated parathyroid hormone levels. Apart from confusion in the 86-year-old patient, there were no clinical manifestations. A bone biopsy obtained in one patient showed increased resorption parameters with no loss of bone trabecular volume; the two other patients underwent absorptiometry, which disclosed a marked decrease in bone mineral density at the spine and femoral neck. There were no risk factors for osteopenia apart from advanced age and female gender. A parathyroid adenoma was removed surgically in all three cases. Vitamin D deficiency was a concomitant abnormality that probably exacerbated the adverse effects of hyperparathyroidism on the skeleton.
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PMID:Bone insufficiency fractures as an inaugural manifestation of primary hyperparathyroidism. 889 60

Hypercalcemia is a rare complication of chronic lymphocytic leukemia (CLL), mostly seen in the context of advanced disease, for which different pathogenetic mechanisms have been postulated. A CLL patient who developed hypercalcemia in the setting of Richter's syndrome is reported. She was a 69-year old woman with stage B (II) CLL of 28-month duration, who presented with mental confusion, anorexia, vomiting, and diffuse bone pain, with hypercalcemia being subsequently found. A lymph node biopsy demonstrated evolution of CLL into Richter's syndrome. Serum levels of parathyroid hormone (PTH), PTH-related peptide and several cytokines were normal. The hypercalcemia initially responded to conventional treatment and chemotherapy, but it reappeared coincidentally with disease progression and the development of osteolytic lesions. Richter's syndrome should be kept in mind in CLL patients with hypercalcemia.
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PMID:Hypercalcemia in a patient with chronic lymphocytic leukemia evolving into Richter's syndrome. 917 22

What we formerly called osteoporosis includes four conditions with an osteopenia: A) osteopenias usually due to mechanical disuse, where injuries cause fractures, and in limb bones more than the spine; B) osteopenias with such fragile bone that normal activities instead of injuries can cause fractures and/or bone pain, and in the spine more than limb bones; C) a group that combines features of (A) and (B); D) temporary osteopenias while major fractures, burns or other injures heal. If belatedly, we now realize our past failure to view those conditions as separate entities compromised many past studies of the prevalence, diagnosis and ways to prevent and cure each of them. That failure also compromised many past explanations of the nature, pathogenesis and natural course of "osteoporosis", and much of the related research. This caused some confusion as well as controversies about illusory instead of genuine issues. Controlling existing osteoblasts and osteoclasts with drugs has not prevented or cured those conditions. That will require controlling the modeling drifts and remodeling BMUs that create those cells. Modeling can increase bone mass and strength, remodeling can conserve or reduce them, and neither can provide the other's functions. During normal mechanical usage modeling is OFF and remodeling works in its "conservation mode" to keep existing bone. In disuse, modeling stays OFF while remodeling works in its "disuse mode" to remove bone and cause an osteopenia. Most natural nonmechanical agents (Table 1) can help or hinder those mechanical responses, but cannot duplicate or override them. Wrist and hip fractures from falls cause the most serious problems associated with these conditions. Those fractures begin in the cortex of epiphyseal-metaphyseal regions of limb bones. They never begin in trabecular bone and rarely in the shafts of long bones. They never begin in the trabecular bone and rarely in the shafts of long bones. Since a bone's strength depends on its shape and size (architecture) as well as on the amount of bone in it (bone mineral "density" and content), treatments intended to prevent or cure these conditions should strengthen the above cortex, and absorptiometric studies should begin to account for both bone architecture and bone tissue content. "Bone anabolic" agents (parathyroid hormone and some prostaglandins) can make modeling add bone to normal and osteopenic skeletons, but when the treatment stops remodeling begins removing that bone. "Antiremodeling agents" (including estrogen and many bisphosphonates) can make remodeling tend to keep existing bone, but when such treatments stop remodeling usually resumes removing bone. Combining anabolic agents with antiremodeling agents offers an exceptionally promising prospect of effective prevention and cure of the above osteopenias. Practical problems make this approach not yet ready for human use, but it soon could be.
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PMID:Osteoporosis treatment: quo vadis? (A brief overview). 956 65


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