Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hypocalcemia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1975

Diminished prepartal plasma calcitonin concentration on cows developing parturient hypocalcemia.

Immunoreactive calcitonin and calcium concentrations were determined on 581 plasma samples collected during 23 studies on 20 cows. Sample collections in each study was begun approximately 1 month prior to parturition and continued for about 1 month after parturition. The cows were grouped according to the degree of hypocalcemia encountered at parturition. The parturient paresis group consisted of 10 cows which developed severe hypocalcemia (3.91 plus or minus 0.22 mg/100 ml, mean plus or minus se) accompanied by paresis; the nonparetic hypocalcemic group consisted of 5 cows which developed severe hypocalcemia (5.70 plus or minus 0.03 mg/100 ml) but not paresis; and the control group consisted of 8 cows which experienced only a mild hypocalcemia (8.50 plus or minus 0.27 mg/100 ml) at parturition. In the prepartal period prior to the onset of hypocalcemia, the respective mean plasma calcium concentrations (plus or minus se) of the 3 groups were 10.1 plus or minus 0.11, 9.95 plus or minus 0.20, and 10.2 plus or minus 0.17 mg/100 ml. The development of severe hypocalcemia in the parturient paresis and nonparetic hypocalcemic groups was not accompanied by an increase in plasma calcitonin concentration. Furthermore, plasma calcitonin concentraion of these 2 groups was less than that of control cows during the parturient period as well as during the month before and the month after parturition. The plasma calcium nadir at parturition was positively related to the mean prepartal (encompassing the period from 30 days until 60 h before parturition) plasma calcitonin concentration (r = 0.57, t= 3.14, p less than 0.005); i.e., the lower the prepartal plasma calcitonin concentration the more severe the hypocalcemia at parturtion. These observations suggest that the development of hypocalcemia at parturition is not due to an increased secretion of calcitonin, but instead they suggest that parturient hypocalcemia may be associated with a diminished prepartal secretion of calcitonin.

Animals↗
PubMed1979

Delayed hypocalcemia after thyroidectomy for Graves' disease is prevented by parathyroid autotransplantation.

Late hypocalcemia appears associated with thyroidectomy for Graves' disease more frequently than with thyroidectomy for other conditions. Of 62 total thyroidectomies done by a single surgeon, 28 were done for carcinoma, 18 for benign disease (primarily nontoxic nodules with a history of radiation therapy to the head and neck (RT)) and 16 for Graves' disease. Mean calcium concentrations measured two months or more after surgery were 9.38 +/- 0.07 (SEM)mg/% for patients with cancer, 8.79 +/- 0.31 mg/dl for patients with Graves' disease and 9.38 +/- 0.08 mg/dl for patients with other benign diseases. No patient without Graves' disease developed late hypocalcemia. In contrast, six of 16 patients with Graves' developed significant late hypocalcemia requiring calcium therapy. The incidence of hypocalcemia after total thyroidectomy for Graves' disease was significantly greater than that seen in other conditions (p < 0.01). Since no parathyroids were removed in the patients with Graves' disease, and since branches of the inferior thyroid artery were invariably ligated distal to the parathyroids, we hypothesized that the late hypocalcemia might be associated with a peculiarity in scar formation in the presence of this autoimmune disease. Accordingly, parathyroid autotransplantation was performed synchronously as a prophylactic measure in nine subsequent patients undergoing total thyroidectomy for Graves' disease; no instance of late hypocalcemia has occurred in this group. The decreased incidence of late hypocalcemia is highly significant (p < 0.01). Although the precise etiology of late hypocalcemia after thyroidectomy for Graves' disease remains undetermined, this experience indicates that synchronous parathyroid autotransplantation is beneficial in preventing this complication.

Calcium↗
PubMed1977

Hypocalcemia after thyroidectomy: mechanisms and management.

Hypocalcemia persists as a problem after thyroidectomy. We reviewed our experience with 245 thyroidectomies to define the spectrum of hypocalcemia, elucidate the mechanisms of hypocalcemia, and formulate a rational basis for its management. Postoperative hypocalcemia occurred in 8.6% of all patients undergoing thyroid surgery with incidence the highest in patients with total thyroidectomy for cancer (28%) and those with subtotal thyroidectomy for thyrotoxicosis (23%). Incidence was low in patients having subtotal thyroidectomy for other diseases (1.5%) and lobectomy (0%). The high incidence of hypocalcemia following subtotal thyroidectomy for thyrotoxicosis but not for other diseases suggests that a mechanism other than removal or damage of the parathyroids is responsible for the hypocalcemia. This may well be thyrotoxic osteodystrophy. This hypocalcemia usually occurs early, is of moderate degree, and is transient. Management includes calcium gluconate for acute symptoms and calcium lactate with vitamin D2 for chronic symptoms.

Calcium↗
PubMed1978

Etiologic factors in hypocalcemia secondary to operations for carcinoma of the pharynx and larynx.

Hypocalcemia, although a relatively uncommon sequela of operations for carcinoma of the larynx and pharynx, often presents as an acute medical emergency. In its chronic form, hypocalcemia may be a difficult disorder to control. Understanding the etiologic basis of hypocalcemia secondary to operations for carcinoma of the head and neck requires knowledge of the pathophysiology of the preoperative and postoperative factors affecting calcium homeostasis. These factors include thyroidectomy, hypoparathyroidism, hypomagnesemia, anticonvulsant therapy, estrogen replacement therapy, oral contraceptives, blood transfusions, hyperventilation alkalosis, hypoalbuminemia, corticosteroid therapy, depression, emotional stress and diet. Often the onset of symptoms and signs of hypocalcemia occurs within 24 to 48 hours after the operation. The symptoms may include mental depression, headache, tingling of the hands and perioral region and abdominal pain. Unrecognized chronic hypocalcemia may lead to the development of cataracts, convulsions and psychosis.

Alkalosis↗
PubMed1979

Hypocalcemia. Differential diagnosis and mechanisms.

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.

Calcium↗
PubMed1975

Hypocalcemia complicating acute leukemia.

Eighteen of 54 adults with acute leukemia developed severe hypocalcemia during a 20 month period. Hypocalcemia (mean lowest serum calcium 6.3 mg/100 ml with a range of 4.1 to 7.0 mg/100 ml) lasted 2-29 days and was symptomatic in all but one patient. Six patients were hypocalcemic at the time of death, 5 died within 1 week of hypocalcemia, and 2 had antibiotic-induced respiratory arrest. All patients had severe infections; 17 of 18 were with gram-negative organisms. No patient had severe azotemia, diarrhea, alkalosis, or hypoalbuminemia. Hypophosphatemia was seen in 14 patients, suggesting no hypoparathyroidism. The serum calcium of patients with acute leukemia should be measured frequently, especially when they have infection. Hypocalcemia is a sign of poor prognosis and should signal the need for careful observation of ventilation, caution in the use of aminoglycoside antibiotics, and vigorous attempts at calcium administration.

Adolescent↗
PubMed1975

Mechanisms of hypocalcemia in acute hemorrhagic pancreatitis.

Thyrocalcitonin release mediated by glucagon secreted from the acutely inflamed pancreas has been postulated as a possible mechanism for hypocalcemia in acute pancreatitis. To test this hypothesis, hemorrhagic pancreatitis was induced in a group of thyroidectomized pigs. No source of thyrocalcitonin other than the thyroid has been described in the pig. Their subsequent serum calcium concentrations were compared with those in a group of thyroid intact pigs also given hemorrhagic pancreatitis. The results indicate that the hypocalcemia observed during the first 24 hours following induction of pancreatitis is not related to the presence of an intact thyroid. Differences observed in the degree of hypocalcemia between the two groups 30 to 48 hours after pancreatitis developed may be of significance but could be explained by dilutional differences alone. Thyrocalcitonin apparently has little if any role in the hypocalcemia observed during the course of acute pancreatitis.

Acute Disease↗
PubMed1975

Ionized calcium: serum levels during symptomatic hypocalcemia.

The concentration (activity) of ionized calcium in serum [Ca-++] was measured in nine patients with symptomatic hypocalcemia of diverse etiology. In all nine patients the [Ca-++] was smaller than or equal to 2.50 mg/dl. No significant correlation was found between the [Ca-++] and serum levels of either total calcium or phosphate. Use of the McLean-Hastings nomogram failed to reveal any significant statistical correlation between the predicted [Ca-++] values and those actually measured. These data indicate that: (1) symptomatic hypocalcemia occurs when levels of ionized calcium in serum fall near or below a critical threshold concentration of 2.50 mg/dl and (2) the [Ca-++] must be measured directly to confirm the clinical impression of hypocalcemia.

Acid-Base Equilibrium↗
PubMed1976

1,25-Dihydroxycholecalciferol deficiency: the probable cause of hypocalcemia and metabolic bone disease in pseudohypoparathyroidism.

Pseudohypoparathyroidism (PsH) is a genetic disease characterized by hypocalcemia, hyperphosphatemia, and metabolic unresponsiveness to parathyroid hormone (PTH). The administration of PTH elicits neither a significant rise in serum calcium (calcemic response) nor a decrease in the renal tubule reabsorption of phosphorus (phosphaturic response). The diminished phosphaturic response is due to an inability of PTH to generate cyclic AMP in renal tubule cells. We investigated the question of whether hypocalcemia and deficient calcemic response to PTH are due to a similar cyclic AMP defect in bone or to an acquired vitamin D deficiency. Four patients were studied. The active form of vitamin D (1,25-dihydroxycholecalciferol) was measured in 3 and was low. Treatment with vitamin D2 restored the serum calcium and the calcemic response to PTH to normal without changing the impaired renal response. Bone biopsy was performed in 2 patients and showed morphologic evidence of increased osteoclastic activity and osteomalacia. The data indicate that the hypocalcemia and bone disease in PsH are due to active vitamin D deficiency, possibly resulting from the genetic renal lesion.

Adult↗
PubMedDate not supplied

Hypocalcemia, hypomagnesemia, and transient hypoparathyroidism during therapy with potassium phosphate in diabetic ketoacidosis.

The effects of intravenous administration of potassium phosphate in the treatment of diabetic ketoacidosis were studied in nine children, ages 9 9/12 to 17 10/12 yr. During phosphate infusion (20--40 meq/L of fluid), all children maintained normal serum concentrations of phosphorus. Transient hypocalcemia occurred in six and transient hypomagnesemia in five patients. One child developed carpopedal spasms refractory to intravenous infusion of calcium gluconate but responsive to intramuscular injection of magnesium sulfate. In three patients, serum levels of intact parathyroid hormone were low at the time of hypocalcemia, an observation that suggests transient hypoparathyroidism. This study indicates that the use of potassium phosphate as the sole source of potassium replacement might potentiate ketoacidosis-induced hypocalcemia through multiple mechanisms.

Adolescent↗
PubMed1975

Hypomagnesemic hypocalcemia secondary to renal magnesium wasting.

Two patients developed severe hypomagnesemia, hypocalcemia, and hypokalemia as a result of renal wasting of magnesium and potassium shortly after being treated with large doses of gentamicin. When therapy with gentamicin was discontinued renal loss of magnesium and potassium ceased, and serum calcium, magnesium, and potassium returned toward normal. Serum immunoreactive parathyroid hormone levels were inappropriately low during the episodes of hypocalcemia. Both patients represent examples of hypomagnesemic hypocalcemia induced by inappropriate magnesuria, possibly caused by gentamicin. These observations suggest that serum calcium, magnesium, and potassium should be monitored during gentamicin therapy.

Aged↗
PubMed1975

Increased parathyroid hormone secretion and hypocalcemia in experimental pancreatitis: necessity for an intact thyroid gland.

Elevated concentrations of serum parathyroid hormone and hypocalcemia occur following the induction of experimental pancreatitis in the pig, but only when the thyroid gland is present. Prior thyroidectomy completely eliminates these changes. Serum magnesium concentrations remained normal throughout the experiments despite the occurrence of hypocalcemia. These data support the hypothesis that calcitonin or another thyroid-related substance plays a role in the mechanism of the hypocalcemia which accompanies experimental pancreatitis in the pig.

Animals↗
PubMed1976

Experimental parturient hypocalcemia in cows following prepartal chemical inhibition of bone resportion.

Cows fed a balanced diet with the required amounts of calcium and phosphorus developed acute hypocalcemia and hypophosphatemia shortly after parturition, even in the presence of the a responsive parathyroid gland, when bone resorption was selectively inhibited by the prepartal administration of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP). When serum total and ionized calcium levels declined below 6.0 and 1.0 mg/100 ml, respectively, cows developed clinical signs similar to naturally occurring parturient paresis. The plasma immunoreactive parathroid hormone levels were similar prepartum, at parturition, and 1 day postpartum in cows administered EHDP as in control cows. Parathyroid chief cells were predominately in the actively synthesizing phase of the secretory cycle with a prominent Golgi apparatus and lamellar arrays of rough endoplasmic reticulum. Many chief cells were degranulated of mature secretory gransules. Calcitonin activity in thyroid extracts, determined by bioassay, and the numbers of secretory granules in thyroid C-cells were similar in both groups of cows. EDTA infusion after 60 days of the experiment demonstrated that the immediately available calcium reserves were reduced in EHDP-treated cows. The serum calcium remained significantly lower and did not return to preinfusion levels by 24 hours. Serum calcium in control cows returned to within the normal range by 6 hours after EDTA infusion. The urinary excretion of hydroxyproline was consistently reduced prepartum and following EDTA infusion in cows receiving EHDP. The experimental induction of parturient of parturient hypocalcemia by the prepartal administration of EHDP provides a valuable model for studies to investigate the mechanisms in bone responsible for the development of severe hypocalcemia that occurs in response to the increased calcium demand imposed by parturition and the initiation of lactation.

Animals↗
PubMed1977

The prevention and correction of hypocalcemia in the parathyroidectomized rat by portacaval shunt.

Adult rats underwent end-to-side portacaval shunt either 30 days prior to or 12 days following parathyroidectomy. When portacaval shunt was performed initially, the serum calcium failed to decrease following subsequent parathyroidectomy and remained within normal levels up to 110 days. When parathyroidectomy first was done, the significant hypocalcemia was corrected subsequently by portacaval shunt and serum calcium remained close to the normal level up to 75 days. The effect of portacaval shunt depended on the calcium content of the food and was obtained only when rats were fed by a regular diet. Rats on a calcium-deficient diet were hypocalcemic, similar to the parathyroidectomized rats without the portacaval shunt. Prolonged calcium-deficient diet alone, without parathyroidectomy, did not by itself result in hypocalcemia either in the intact rat or in the portacaval shunted rat. The data indicate that portacaval shunt prevents and corrects hypocalcemia in the parathyroidectomized Lewis rat as long as sufficient calcium is available in the diet.

Animals↗
PubMed1979

Ventricular pump performance during hypocalcemia: clinical and experimental studies.

We have compared indices of ventricular function during rapid transfusion of citrated (1.5 ml/kg/min) or heparinized (1.5 ml/kg/min) autologous blood in six patients following discontinuation of cardiopulmonary bypass. Infusion of citrated blood was associated with a lowering of plasma ionized calcium concentration ([Ca++], from 0.90 +/- 0.04 to 0.71 +/- 0.4 mM, p less than 0.001) and an increase in pulmonary artery balloon-occluded pressure (PA0, from 9.4 +/- 2.6 to 15.5 +/- 1.7 mm Hg, p less than 0.u1), without a change in left ventricular stroke work index, stroke index, or cardiac index. Transfusion of heparinized blood caused no change in plasma [Ca++]. A rise in PA0, which was similar in magnitude to that observed during citrated blood transfusion, was associated with increased left ventricular stroke work index, stroke index, cardiac index, and mean arterial pressure. Although data obtained during citrated blood transfusion suggest the presence of transient left ventricular dysfunction, its magnitude is not readily expressed in terms of ventricular function curves when accompanied by a simultaneous change in [Cized closed-chest dog by volume loading during hypocalcemia, when mean arterial pressure, heart rate, and [Ca++] were in a steady state, both prior to and following beta blockade with propranolol. Function curves obtained during severe hypocalcemia ([Ca++] = 0.43 +/- 0.02 mM) were shifted significantly to the right and downward, when compared to those obtained during normocalcemia ([Ca++] = 1.06 +/- 0.03 mM). Hypocalcemia combined with beta blockade resulted in severe left ventricular failure, as demonstrated by a flat ventricular function curve.

Aged↗
PubMedDate not supplied

Neonatal hypocalcemia mechanism of occurrence and management.

Early neonatal hypocalcemia occurs in premature infants, infants with birth asphyxia, and infants of diabetic mothers. Etiological considerations include decreased calcium (Ca) supply, increased endogenous phosphate load, hypomagnesemia, alkali therapy, functional hypoparathyroidism, defects in vitamin D metabolism, and possibly calcitonin excess. Late neonatal hypocalcemia occurs, with malabsorption of magnesium (Mg), increased exogenous phosphate loading, after alkali therapy of diarrheal acidosis, hypoparathyroidism, and vitamin D related disorders. The therapy of hypocalcemia includes oral or iv Ca salts and in the near future, possibly the newly discovered vitamin D metabolites.

Acidosis↗
PubMed1977

[A test for acute hypocalcemia using swine and salmon calcitonin].

The production of acute hypocalcemia was investigated using either 80 U. MRC of salmon calcitonin or 160 1. mrc of pork calcitonin in 117 subjects (58 patients with Paget's disease, 22 with osteoporosis, 22 with Sudeck-Leriche algodystrophy and 15 control subjects). The results obtained with the two types of calcitonin did not differ. Induced acute hypocalcemia was more pronounced in patients with Paget's disease than in the other subjects studied. In patients with Paget's disease there were statistically significant correlations between the hypocalcemia produced and the initial levels of alkaline phosphatase and total 24 hours urinary hydroxyproline.

Acute Disease↗
PubMed1975

The importance of the stomach in gastrin-induced hypocalcemia in the rat.

Hypocalcemia following gastrin administration occurs in thyroparathyroidectomized (TPTX) as well as thyroid intact rats. Hypophosphatemia does not accompany the hypocalcemia induced by gastrin. These data suggest that a mechanism other than release of calcitonin from the thyroid gland may be involved in this response in the rat. Neither adrenalectomy, nephrectomy, nor excision of the pancreas and small and large intestine altered the hypocalcemic response to gastrin. Gastrectomy, however, eliminated all hypocalcemia following administration of this polypeptide in both thyroid intact and TPTX rats. Removal of the antrum of the stomach did not influence the hypocalcemic response to gastrin. Resection of the proximal 75% of the stomach, however, inhibited the hypocalcemic response to gastrin as did total gastrectomy. Thus, in the rat, the proximal stomach appears to play an important role in mediating this response.

Adrenal Glands↗