Hypoparathyroidism

A form of hypoparathyroidism (hypofimction of the parathyroid glands) caused by the presence of activating mutations in the CaR, usually in the heterozygous state. 

Some patients with reduced or absent parathyroid function, e.g., primary hypoparathyroidism, harbor anti-CaR antibodies (Fig. 2) [4]. In two patients, the antibodies were shown to activate the CaR as assessed by stimulation of MAPK and PLC. Tims, analogous to activating mutations of the CaR, anti-CaR antibodies can increase the sensitivity of the receptor to CaQ+, thereby resetting parathyroid and kidney to maintain hypocalcemia. 

One of the major problems In the treatment of patients with vitamin D compounds (l.e., patients with hypoparathyroidism) has been the unpredictable development of hypercalcemia and the syndrome of vitamin D Intoxication. Although this problem may become less serious when some of the faster-acting metabolites and analogues of metabolites of vitamin D become available for clinical use. It Is likely that monitoring of serum levels of... 

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... 

Reduction in the serum 1,25-dihydroxyvitamin D concentration has been reported as an indicator of increased lead absorption or lead levels in the blood (Rosen et al. 1980). Lead inhibits the formation of this active metabolite of vitamin D, which occurs in bone mineral metabolism (EPA 1986a Landrigan 1989). Children with PbB concentrations of 12-120 pg/dL lead showed decreased serum 1,25-dihydroxyvitamin D concentrations comparable to those found in patients with hypoparathyroidism, uremia, and metabolic bone disease (Mahaffey et al. 1982 Rosen et al. 1980). This biomarker is clearly not specific for lead exposure and several diseases can influence this measurement. 

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

Cholestyramine, colestipol, orlistat, or mineral oil decrease vitamin D absorption Might induce hypercalcemia with thiazide diuretics in hypoparathyroid patients... 

Complications of surgery include persistent or recurrent hyperthyroidism (0.6% to 18%), hypothyroidism (up to about 49%), hypoparathyroidism (up to 4%), and vocal cord abnormalities (up to 5%). The frequent occurrence of hypothyroidism requires periodic follow-up for identification and treatment. 

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. 

Hypoeutectoid steels, 23 275 Hypohalous acid, 73 100 Hypomagnesia, 75 414 Hypomanganate, 75 592 Hypoparathyroidism, 25 791 Hypophosphites, 19 55 Hypophosphorous acid, 79 20, 54 Hypotension, antianginal agents for,... 

Decreased AP-levels could be seen in patients suffering from hypoparathyroidism and pernicious anaemia (i.e., an anaemia tending to be a fatal issue). 

Families affected by ADH, autosomal dominant hypoparathyroidism, and hypocal-cemic hypercalcinria have each been defined by gain-of-function mutations in the CASR gene (44). ADH is associated with the expression of constitutively activated CASR, which serves to suppress PTH secretion from the parathyroid gland. In the kidney it induces hypercalciuria, which further contributes to the hypocalcemia. 

Further work on ADH may identify the molecular mechanisms underlying the brain calcification and tonic-clonic seizures associated with the CASR-activating mutations. This information may refine therapy for ADH patients as well as hypoparathyroidism patients who harbor CASR mutations. Further details about ADH can be found in the CASR locus-specific database at http //www.casrdb. mcgill.ca/f4/). 

McLeod, D. R., Hanley, D. A., McArthur, R. G. 1989. Autosomal dominant hypoparathyroidism with intracranial calcification outside the basal ganglia. Am. J. Med. Genet. 32 32-5. 

In addition, for social policy reasons, since July 1975 prescriptions for oral contraceptives have also been exempt from charges. The medical grounds for exemption from prescription charge are diabetes mellitus, diabetes insipidus, hypopituitarism, hypothyroidism, hypoparathyroidism, hypoadrenalism, myaesthenia gravis, epilepsy and permanent fistula, for example colostomy, ileostomy. In addition, police personnel can claim back from their employing authority any prescription charge they incur. 

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. 

Calcitriol (Rocaltrol, Calcnex) [Antihypocalcemic/Vitamin D Analog] Uses Reduction of i PTH levels, -iTca on dialysis Action 1,25-Dihydroxycholecalcifool (vit D analog) Dose Adul. Renal failure 0.25 mcg/d PO, t 0.25 mcg/d q4-6wk PRN 0.5 meg 3 x/wk IV, t PRN Hypoparathyroidism ... 

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-... 

Calcium acetate Decreased renal function, hypoparathyroidism... 

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

Hypoparathyroidism PO 625 mcg-5 mg/day (with calcium supplements). Nutritional rickets, osteomalacia PO 25-125 meg/day for 8-12 wk. Those with malabsorption syndrome. 250-7,500 meg/day. 

Hypoparathyroidism IV 0.04-0.1 mcg/kg (2.8-7 meg) given as a bolus dose no more frequently than every other day at anytime during dialysis dose as high as 0.24 mcg/kg (16.8 meg) has been administered safely. Usually start with 0.04 mcg/kg 3 times/week as a bolus, increased by 0.04 mcg/kg every 2 weeks. Adjust dose based on serum PTH levels. Same or increasing serum PTH level. Increase dose. Serum PTH level decreased by <30% Increasedose. SerumPTHleveldecreasedby >30%and <60% Maintaindose. Serum PTH level decreased by >60% Decrease dose. Serum PTH level 1.5-3 times upper limit of normal Maintain dose. 

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