Deficiency hypoparathyroidism

Hyperparathyroidism and aluminium hydroxide lead to aluminium-related bone disease however, total parathyroidectomy does not lead to failure of aluminium mobilization after renal transplantation. This man had satisfactory graft function, and the aluminium excretion that was achieved by deferoxamine suggests that the renal transplant was not the limiting factor for the mobihzation of aluminium. The most likely explanation was that he developed adynamic bone through a combination of vitamin D deficiency, hypoparathyroidism, and aluminium deposition. Vitamin D supplementation failed to prevent the osteodystrophy on its own. When aluminium chelation therapy was used, bone healing occurred and his symptoms improved. 

Hypoalbuminemia Chronic renal failure Magnesium deficiency Hypoparathyroidism Pseudohypoparathyroidism... 

Uses Calcium source, dietary supplement for pharmaceuticals, orals, injections, syrups, low-birth-wt. infants, treatment of hypocalcemia, calcium deficiency, hypoparathyroidism, osteoporosis, rickets Regulatory USP compliance Manuf./Distrib. Calcium Group Shan Par Ind. http //www.shanpar. com... 

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

Hepatic encephalopathy Hyperbilirubinemia Hypocalcemia Hypercalcemia Hyperparathyroidism Hypoparathyroidism Thiamine deficiency (Wernicke s) encephalopathy Diabetic ketoacidosis Nonketotic hyperosmolar coma Phosphate depletion Hypoglycemia Hypoxemia Hypercapnia... 

Hypocalcemia results from altered effects of parathyroid hormone and vitamin D on the bone, gut, and kidney. The primary causes are postoperative hypoparathyroidism and vitamin D deficiency. 

Oral calcium supplementation (e.g., 1 to 3 g/day of elemental calcium) is indicated for chronic hypocalcemia due to hypoparathyroidism and vitamin D deficiency. If serum calcium does not normalize, a vitamin D preparation should be added. 

Oral As a dietary supplement when calcium intake may be inadequate. Conditions that may be associated with calcium deficiency include the following Vitamin D deficiency, sprue, pregnancy and lactation, achlorhydria, chronic diarrhea, hypoparathyroidism, steatorrhea, menopause, renal failure, pancreatitis, hyperphosphatemia, and alkalosis. Some diuretics and anticonvulsants may precipitate hypocalcemia, which may validate calcium replacement therapy. Calcium salt therapy should not preclude the use of other corrective measures intended to treat the underlying cause of calcium depletion. 

Vitamin D preparations are also used to treat hypoparathyroidism, but they require even larger doses, often up to 2.5 mg (100,000 units) daily to increase the serum calcium back to normal. As in vitamin D deficiency, the dose must be carefully monitored. 

These hormones and drugs are used most commonly for disorders of calcium and bone metabolism rather than to correct specific hormone deficiencies. For example, the use of PTH replacement in hypoparathyroidism in the past was not practical because of the difficulty in ob-... 

The main features of hypocalcemia are neuromuscular—tetany, paresthesias, laryngospasm, muscle cramps, and convulsions. The major causes of hypocalcemia in the adult are hypoparathyroidism, vitamin D deficiency, chronic kidney disease, and malabsorption. Neonatal hypocalcemia is a common disorder that usually resolves without therapy. The roles of PTH, vitamin D, and calcitonin in the neonatal syndrome are under active investigation. Large infusions of citrated blood can produce hypocalcemia by the formation of citrate-calcium complexes. Calcium and vitamin D (or its metabolites) form the mainstay of treatment of hypocalcemia. 

As a brief introductory summary, vitamin D substances perform the following fundamental physiological functions (1) promote normal growth (via bone growth) (2) enhance calcium and phosphorus absorption from the intestine (3) serve to prevent rickets (4) increase tubular phosphorus reabsorpiion (5) increase citrate blood levels (6) maintain and activate alkaline phosphatase m bone (7) maintain serum calcium and phosphorus levels. A deficiency of D substances may be manifested in the form of rickets, osteomalacia, and hypoparathyroidism. Vitamin D substances are required by vertebrates, who synthesize these substances in the skin when under ultraviolet radiation, Animals requiring exogenous sources include infant vertebrates and deficient adult vertebrates, Included there are vitamin D (calciferol ergocalciferol) and vitamin D< (activated 7-dehydrocholesterol cholecalciferol). 

Such observations have led to the idea that depression may be a pseudomonoamine deficiency due to a deficiency in signal transduction from the monoamine neurotransmitter to its postsynaptic neuron in the presence of normal amounts of neurotransmitter and receptor. If there is a deficiency in the molecular events that cascade from receptor occupancy by neurotransmitter, it could lead to a deficient cellular response and thus be a form of pseudomonoamine deficiency (i.e., the receptor and the neurotransmitter are normal, but the transduction of the signal from neurotransmitter to its receptor is somehow flawed). Such a deficiency in molecular functioning has been described for certain endocrine diseases such as hypoparathyroidism (parathyroid hormone deficiency), pseudohypoparathyroidism (parathyroid receptors deficient but parathyroid hormone levels normal), and pseudo-pseudohypoparathyroidism (signal transduction deficiency leading to hypoparathyroid clinical state despite normal levels of hormone and receptor). 

The metabolism of phosphorus (P) is largely related to that of calcium (Ca). The Ca P ratio in the diet affects the absorption and excretion of these elements (Harper 1969). Any increase in serum phosphorus results in a decrease of serum calcium by mechanisms which are still unknown. For example, increased serum phosphorus levels and decreased serum calcium levels are seen in uremia (renal retention of phosphorus), hypoparathyroidism, hypocalcemia (decreased serum calcium levels), and hyperphosphatemia (increased serum phosphorus levels), and the reverse is seen in hypercalcemia (increased serum calcium levels) and hyperparathyroidism. Hypophosphatemia (low serum phosphorus levels) is seen in ricketts (vitamin D deficiency) (Harper 1969 Tietz 1970). 

Q10 Hypoparathyroidism is a rare condition which could develop following a decrease or deficiency of PTH secretion, or be due to reduction in the effectiveness of PTH on target cells. Deficiency of PTH may follow damage to the parathyroid glands during thyroid surgery. Deficiency of PTH decreases the concentration of plasma calcium and increases phosphate concentration. A metabolic crisis can occur when hypocalcaemia coincides with hypoparathyroidism. 

Q13 Magnesium is a major intracellular cation which acts as a co-factor in many intracellular enzyme reactions. Plasma concentration is normally 2 mg dl-1. This ion is abundant in the diet, and hypomagnesaemia is relatively uncommon, unless there is malabsorption or excessive loss via the kidney. However, when present, hypomagnesaemia can lead to hypoparathyroidism. Adjustment to the levels of magnesium can shift the function of the parathyroid glands back to normal. Chronic alcoholism, malnutrition, malabsorption, renal tubular dysfunction and excessive use of diuretics, such as loop and thiazide diuretics, may lead to hypomagnesaemia. Symptoms of magnesium deficiency include depression, confusion, muscle weakness and sometimes convulsions. 

Advantages of alfacalcidol and dihydrotachysterol include a fast onset and short duration of clinical effect (days) which renders them suitable for rapid adjustment of plasma calcium, e.g. in hypoparathyroidism. Such factors are not relevant to the slower adjustment of plasma calcium (weeks) with vitamins Dg and Dg in the ordinary management of vitamin D deficiency. 

Hypocalcemia can result from hypoparathyroidism, chronic renaJ failure, vila-niin D deficiency, and hypomagnesemia. Hypomagnesemia occurs mainly in those with alcoholism so severe as to requite hospitaiization. Magnesium deficiency results in a decline in the responsiveness of osteoclasts to FTH, resulting in interruption of the normal process of bone fumover. In this case, hypocalcemia cannot be effectively corrected unless magnesium therapy is used. 

The vitamin Ds are important in the therapeutics of hypoparathyroidism and of vitamin D deficiency. Ergocalciferol, cholecalciferol, and dihydrotachysterol are recognized by... 

The initial laboratory evaluation is directed toward the assessment of renal function and measurement of serum albumin and magnesium concentrations. Serum intact PTH concentrations are low or inappropriately normal in hypoparathyroidism and elevated in pseudohypoparathyroidism. Vitamin D deficiency is characterized by low serum 25(OH)D> high PTH (secondary hyperparathyroidism), and high serum alkaline phosphatase (ALP). 

In pseudohypoparathyroidism, hypocalcemia, and hyperphosphatemia are accompanied by normal or high concentrations of PTH in plasma. In some forms, resistance to PTH is due to deficiency of a G-protein that couples PTH-receptor binding to cAMP synthesis (Chapter 30). Pseudopseudohypoparathyroidism is a variant that occurs in some relatives of patients with pseudohypoparathyroidism. These individuals have developmental and skeletal defects without clinical or metabolic evidence of hypoparathyroidism. 

Hypocalcemia is the result of alterations in the effect of parathyroid hormone and vitamin D on the bone, gut, and kidney (see Fig. 49-9). The primary causes of hypocalcemia are postoperative hypoparathyroidism and vitamin D deficiency. Other causes include magnesium deficiency, thyroid surgery, medications, hypoalbuminemia, blood transfusions, peripheral blood progenitor cell harvesting, tumor lysis syndrome, and mutations in the calcium-sensing receptor. " Parathyroid hormone concentrations are elevated in conditions of hypocalcemia, with the exception of hypoparathyroidism and hypomagnesemia (Fig. 49-11). ... 

Lanthanum carbonate Decreased dietary phosphorus intake Glucocorticoids Vitamin D deficiency/resistance Hypoparathyroidism Chronic diarrhea Steatorrhea... 

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