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At least 19 recordsLinked to original sources
PubMed1996

Hysteresis of the PTH-calcium curve during hypocalcemia in the dog: effect of the rate and linearity of calcium decrease and sequential episodes of hypocalcemia.

Several studies have shown the presence of hysteresis of the parathyroid hormone (PTH)-calcium relationship in both normal humans and hemodialysis patients; for hypocalcemia, hysteresis is defined as a lower PTH level for the same serum calcium during the recovery from than the induction of hypocalcemia. However, some have questioned whether hysteresis is only a function of the rate and/or direction of change in calcium, and others have proposed that hysteresis is due to depletion of PTH stores. To address these issues, two groups of dogs were studied. To induce hypocalcemia, sodium EDTA (50 mg/kg) was infused either over 60 (termed slow) or 30 (termed fast) minutes; immediately after the cessation of the ethylenediamine tetracetate (EDTA) infusion, calcium chloride (0.75 mEq/kg) was infused over 60 or 30 minutes, respectively, to correct the hypocalcemia. The EDTA infusion produced a linear decrease in serum calcium by progressively increasing the infusion rate at regular intervals. A second cycle of hypocalcemia and recovery using the same protocol was started immediately after the completion of the first cycle. To determine whether a nonlinear decrease in the serum calcium affected the PTH response to hypocalcemia, a third group of dogs, termed superfast, was studied; in this group, EDTA was infused for 30 minutes at a constant rate of 50 mg/kg. The hysteretic loops of PTH produced by the two sequential slow and fast cycles and the superfast cycle during the induction of and recovery from hypocalcemia were similar. Moreover, the maximal PTH level for the two sequential slow and fast cycles and the superfast cycle was not different even though the rates of calcium decrease varied and the calcium decrease was nonlinear in the superfast cycle. In conclusion, (1) since hysteresis was reproducible and the maximal PTH was not different during two sequential cycles of hypocalcemia, hysteresis is not due to PTH depletion; (2) the PTH-calcium curve is not affected by the rate at which hypocalcemia is induced; and (3) the maximal PTH level is not influenced by either the rate or linearity of the reduction in serum calcium.

Analysis of Variance↗
PubMed1990

Intraperitoneal free fatty acids induce severe hypocalcemia in rats: a model for the hypocalcemia of pancreatitis.

Indirect evidence suggests a causative role for intraperitoneal free fatty acids (FFA) in hypocalcemia associated with pancreatitis. We examined the effects of intraperitoneal injection of four naturally occurring FFAs on serum calcium in rats. Two saturated FFAs, stearate and palmitate, induced little or no hypocalcemia. Two unsaturated FFAs, oleate and linoleate, caused dramatic hypocalcemia in treated versus control rats (6.3 +/- 1.4 and 5.3 +/- 0.7 mg/dl, respectively, versus 10.1 +/- 0.6). Dose-response studies demonstrated that minute quantities of oleate (100 microliters per 250 g rat) caused marked hypocalcemia (7.2 +/- 0.3 mg/dl). Treated versus control rats also revealed a decrease in ionized calcium (3.15 +/- 0.2 versus 5.6 +/- 0.05 mg/dl) and magnesium (1.4 +/- 0.15 versus 2.0 +/- 0.10), an appropriate increase in PTH levels (1670 +/- 451 versus 396 +/- 235 pg/ml), and a fall in calcitonin levels (70.4 +/- 21.3 versus 47.5 +/- 16.4 pg/ml) but no change in albumin or phosphate levels. In vitro, the Ksp of calcium dioleate was shown to be 5.3 x 10(-8) m3/liter3; thus under physiologic conditions 100 microliters oleate binds 7.2 mg calcium, or approximately twice the total ECF ionized calcium in the rat. The amounts of intraperitoneal FFA that can easily be achieved in pancreatitis complex pathophysiologically significant amounts of calcium and may lead to severe hypocalcemia.

Animals↗
PubMed1992

Relationship between cardiovascular functions and ionic hypocalcemia induced by citrate infusion in anhepatic swines: CaCl2 therapy in severe ionic hypocalcemia.

Baseline and serial values of serum [Ca++], [K+], [Na+], arterial blood gas tensions, acid-base status, temperature and hemodynamic functions were measured during infusion of citrate-phosphate-dextrose (CPD) solution (0.35 ml.kg-1 x min-1) in anhepatic pigs of three randomized groups. Thirteen pigs (group I) continued to receive intravenous infusion of CPD solution until cardiac arrest. When mean arterial pressure (MAP) decreased to about 50 mmHg (group II, n = 7), or 40 mmHg (group III, n = 7) infusion of CPD solution was discontinued, and pigs received CaCl2 (20 mg/kg) intravenously. Serial (1, 4, 8, and 12 min after CaCl2 administration) values of all the above variables and serum citrate at baseline and lowest [Ca++] were measured. After hepatectomy and venovenous bypass, cardiac output (CO) decreased 30%. When ionic hypocalcemia was above 0.7 mM, there was no significant change of cardiovascular functions. When [Ca++] was between 0.34-0.7 mM, there were linear relationships between [Ca++] and CO, systemic vascular resistance (SVR) and MAP, respectively. When [Ca++] was below 0.34 mM, cardiovascular functions decreased abruptly, and the pigs died at [Ca++] of 0.26 +/- 0.06 mM. When [Ca++] decreased to 0.36 +/- 0.06 mM and MAP to 50 +/- 4 mmHg, most hemodynamic functions could be reversed by calcium therapy. However, when [Ca++] decreased to 0.33 +/- 0.05 mM and MAP to 40 +/- 2 mmHg, hemodynamic functions could not be reversed by calcium therapy alone.

Animals↗
PubMed2000

ECG changes in a 25-year-old woman with hypocalcemia due to hypoparathyroidism. Hypocalcemia mimicking acute myocardial infarction.

The case of a 25-year-old woman presenting with chest pain, ECG changes, and laboratory findings suggestive of myocardial infarction is reported. Cardiac catheterization showed impaired left ventricular performance but otherwise normal coronary arteries. Laboratory analyses revealed primary hypoparathyroidism, and supplementation with calcium and vitamin D(3) was initiated. There was subsequent improvement in laboratory findings as well as echocardiographically determined left ventricular performance. Thereafter, the patient remained asymptomatic. Apart from some persisting ECG repolarization disturbances, there was complete normalization of the initial changes. This case demonstrates a combination of clinical, blood biochemical, and ECG findings mimicking acute myocardial infarction.

Adult↗
PubMed1992

Prediction of the outcome of postoperative hypocalcemia in Graves' disease.

Symptomatic hypocalcemia sometimes follows subtotal thyroidectomy for Graves' disease. Irreversible damage to the parathyroids contributes to permanent hypocalcemia and the mechanism for a transient hypocalcemia is thought to be different from that of a permanent one. However, sensitive assays for parathyroid hormones (PTH), which had recently become available, revealed that levels of PTH decrease in patients with transient hypocalcemia. In order to differentiate a prolonged hypocalcemia from a transient one, calcium and inorganic phosphate concentrations in serum as well as in urine, and whole molecule-PTH levels were determined in 18 Graves' disease patients with postoperative hypocalcemia just after the initial symptoms for hypocalcemia appeared. In 13 patients, medication was withdrawn within one month since serum calcium levels had returned to normal (transient hypocalcemia). In five other patients, medication was required for six months or more to maintain normocalcemia (prolonged hypocalcemia). The same parameters were determined after surgery in eight Graves' disease patients without hypocalcemia. Urinary inorganic phosphate concentrations in patients with prolonged hypocalcemia (0.02 +/- 0.01 mmol/mmol Cr) were significantly lower (P less than 0.01) than those in patients with transient hypocalcemia (1.59 +/- 1.59 mmol/mmol Cr) or those in control patients (1.27 +/- 0.70 mmol/mmol Cr). Preoperative concentrations of calcium and inorganic phosphate in serum and urine, and serum alkaline-phosphatase activities were also determined. However, there were no significant differences in these parameters between patients with prolonged and those with transient hypocalcemia. It is concluded that prolonged hypocalcemia is discriminated from the transient type by determining the urinary inorganic phosphate at the time of appearance of the initial symptoms for hypocalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2002

[Prospective study of early predictive factors of permanent hypocalcemia after bilateral thyroidectomy].

AIM OF THE STUDY: The aim of this prospective cohort study was to identify the early criteria potentially predictive for outcome of permanent hypocalcemia after thyroidectomy. PATIENTS AND METHODS: Serum calcium (Ca) et phosphorus (Ph) were measured daily until discharge in 2035 consecutive patients undergoing bilateral thyroidectomy. In all patients experiencing postoperative hypocalcemia, defined as a Ca < 8.0 mg/dl on two consecutive days, parathyroid hormone was measured prior initiation of calcium therapy et discharge (early PTH), et blood sample was also obtained 7 to 14 days after discharge for Ca et Ph measurements (delayed Ca et Ph). These patients were then followed up until complete resolution of hypocalcemia or at least one year. Those still needing substitutive therapy to maintain normocalcemia one year after surgery were considered to have permanent hypocalcemia. Correlation of outcome with clinical characteristics, postoperative Ca et Ph levels, early PTH, et delayed Ca et Ph were examined with univariate analysis et multivariate logistic regression. RESULTS: Postoperative hypocalcemia occurred in 153 patients (7.5%) and spontaneously recovered in all but 7 patients (0.3%). Delayed Ca, and delayed Ph were found to be predictive for outcome of hypocalcemia by univariate analysis (p < 0.01). Relative risk to develop permanent hypocalcemia was 15 for patients with early PTH < 12 pg/ml, 52 when delayed Ph was > 4.0 mg/dl, and 121 when delayed Ca was < 8.0 mg/dl. None of the 113 patients with delayed Ca > or = 8.0 mg/dl and delayed Ph < or = 4.0 mg/dl developed permanent hypocalcemia, in contrast to 1 out of 31 patients (3%) with delayed Ca > 8.0 mg/dl or delayed Ph > 4.0 mg/dl, and 6 out of 9 patients (66%) with delayed Ca < 8.0 mg/dl and delayed Ph > 4.0 mg/dl. Both delayed Ca and delayed Ph appeared as independent factors predicting outcome of hypocalcemia at one year with multivariate logistic regression analysis. CONCLUSION: Delayed serum calcium and phosphorus levels, when measured one week after starting calcium therapy but prior to administration of any vitamin D analogs, accurately predict outcome of hypocalcemia after thyroidectomy. Patients with delayed Ca under 8.0 mg/dl and/or delayed Ph above 4.0 mg/dl are at high risk to develop permanent hypocalcemia.

Adult↗
PubMed2000

Risk factors for postoperative hypocalcemia after surgery for primary hyperparathyroidism.

HYPOTHESIS: A variety of clinical and biochemical variables may be associated with hypocalcemia after surgery for parathyroid adenoma. DESIGN: A prospective study of patients who underwent surgery for solitary parathyroid adenoma. SETTING: A university hospital department of surgery. PATIENTS: Eighty-six consecutive patients who underwent surgery for solitary parathyroid adenoma. INTERVENTION: Parathyroidectomy according to the principles of unilateral neck exploration. MAIN OUTCOME MEASURES: Clinical and biochemical risk factors for early (< or =4 days after surgery) and late (1 year after surgery) postoperative symptomatic and biochemical hypocalcemia. RESULTS: Twenty-two patients developed early symptomatic hypocalcemia. The difference in total serum calcium levels between patients, with and without early symptomatic hypocalcemia, was evident on the third and fourth postoperative days. Serum level of osteocalcin greater than 6.0 microg/L, bilateral neck exploration, and history of cardiovascular disease were risk factors for symptomatic hypocalcemia (odds ratios [95% confidence intervals]: 4.4 [1.4-14.1], 3.8 [1.3-11.6], and 0.1 [0.02-0.60], respectively). Patients with up to 1 risk factor had a possibility of only 7% to develop early symptomatic hypocalcemia. One year after surgery, 16 patients had low levels of total serum calcium (late biochemical hypocalcemia) and were asymptomatic. Preoperative intermittent hypercalcemia was associated with an increased risk for late biochemical hypocalcemia (odds ratio, 3.9; 95% confidence interval, 1.0-16.3). CONCLUSIONS: Clinical and biochemical risk factors for early and late postoperative hypocalcemia in patients who underwent surgery for solitary parathyroid adenoma were found. A clinically useful prognostic index for early symptomatic hypocalcemia was constructed using these risk factors.

Adenoma↗
PubMed2003

Both duration and degree of hypercalcemia influence the reduced parathyroid hormone response to hypocalcemia after hypercalcemia.

The stimulation of parathyroid hormone (PTH) secretion by hypocalcemia is reduced when hypocalcemia is preceded by hypercalcemia. The present study investigates whether the duration and degree of hypercalcemia influence the reduced PTH response to hypocalcemia after hypercalcemia. In addition, the implication of the arachidonic acid (AA) signaling pathway in this effect is evaluated. The PTH response to hypocalcemia has been studied in a control group and in four groups of rabbits subjected to hypercalcemia for different periods of time (between 30 and 120 min) and at two levels of hypercalcemia (1 x 9 and 2 x 1 mM). AA levels have been measured in parathyroid glands from rabbits subjected to hyper- and hypocalcemia. When compared with controls, rabbits that had been hypercalcemic (2 x 1 mM) for 2 h showed a markedly attenuated PTH response to hypocalcemia (50% of normal PTHmax), rabbits that had been in hypercalcemia (2 x 1 mM) for 75 min had an intermediate PTH response to hypocalcemia (70% of normal PTHmax) and rabbits that had been subjected to either 30 min hypercalcemia of 2 x 1 mM or 120 min hypercalcemia of 1 x 9 mM had a normal PTH response to hypocalcemia. AA levels increased in hypercalcemia and decreased in hypocalcemia; however, no differences were observed at either calcium level in short-time (30 min) versus long-time (120 min) hypercalcemia. In conclusion, the attenuated PTH response to hypocalcemia after hypercalcemia is dependent on both the period of time that the parathyroid glands have been exposed to hypercalcemia and the degree of hypercalcemia. In addition, this reduced PTH response does not seem to be related to changes in the AA signaling pathway.

Animals↗
PubMed2003

Intraoperative parathyroid hormone assay: an accurate predictor of symptomatic hypocalcemia following thyroidectomy.

HYPOTHESIS: Intraoperative parathyroid hormone (IOPTH) assay is useful for predicting symptomatic hypocalcemia following total thyroidectomy. DESIGN: A prospective study of 30 patients undergoing total thyroidectomy with IOPTH levels obtained following skin closure and ionized calcium (Ca2+) levels obtained 6 hours postoperatively and on postoperative day 1. All patients were evaluated for symptoms of hypocalcemia. SETTING: University teaching hospital. MAIN OUTCOME MEASURES: Patients who developed symptomatic hypocalcemia were compared with asymptomatic patients in regard to age, diagnosis, thyroid weight, thyrotropin level, Ca2+ level, parathyroid status, and IOPTH level. RESULTS: The onset of symptomatic hypocalcemia ranged from 8 to 48 hours postoperatively (n = 10). One patient required readmission. Of 10 patients with symptoms, 5 developed tetany. There were no significant differences in age, diagnosis, thyroid weight, thyrotropin level, or the number of parathyroid glands preserved in patients with or without symptomatic hypocalcemia. All patients with an IOPTH level of less than 10 pg/mL (1.1 pmol/L) had symptoms (n = 8). The mean +/- SD IOPTH level (7.6 +/- 12.0 pg/mL [0.8 +/- 1.3 pmol/L]) in patients who developed symptomatic hypocalcemia was significantly lower than the mean IOPTH level (55.7 +/- 31.8 pg/mL [5.9 +/- 3.3 pmol/L]) in patients without symptoms (P =.001). The 6-hour and postoperative day 1 Ca2+ levels were significantly lower in patients with symptomatic hypocalcemia (P =.19 and P =.13, respectively). An IOPTH level of less than 10 pg/mL is 80% sensitive and 100% specific for the development of symptomatic hypocalcemia. CONCLUSION: The incorporation of the IOPTH assay in the management of thyroid disease is recommended to prevent and prospectively treat symptomatic hypocalcemia, thereby reducing readmissions following thyroidectomy.

Adult↗
PubMed1989

Hypocalcemia in critically ill children.

To determine the prevalence and clinical consequences of hypocalcemia in pediatric intensive care unit patients, we prospectively studied calcium homeostasis in 145 of these patients. The total serum calcium concentration was measured in all patients. The serum ionized calcium concentration was measured in blood samples collected from those 71 (49%) patients who had low total serum calcium values (less than 8.5 mg/dl (2.12 mmol/L). Of the 71 patients, 26 (36.6%) had ionized hypocalcemia. Therefore the prevalence of ionized hypocalcemia was at least 17.9% (26/145). Death occurred in 8 (31%) of 26 patients with ionized hypocalcemia versus 3 (2.5%) of 119 patients with normocalcemia (p less than 0.0001). However, the severity of illness score was higher (p less than 0.05) in the children with ionized hypocalcemia than in normocalcemic children (mean Therapeutic Intervention Scoring System score 33 +/- 17 vs 22 +/- 11, respectively). More of the children with ionized hypocalcemia had sepsis (p = 0.0299) and they required the administration of vasopressor agents more often (p = 0.0002) than their normocalcemic counterparts. Of the 26 patients with ionized hypocalcemia, 17 (65.4%) had biochemical evidence of either absolute or relative hypoparathyroidism, determined by means of an immunoradiometric assay that measures only biologically active parathyroid hormone. We conclude the following: (1) ionized hypocalcemia is common in severely ill children. (2) Patients with ionized hypocalcemia have a higher mortality rate than those with normocalcemia; however, because the former are more severely ill, no causality is apparent or suggested. (3) Functional hypoparathyroidism may occur in critically ill children.

Adolescent↗
PubMed2001

Hypocalcemia: a pervasive metabolic abnormality in the critically ill.

Hypocalcemia has been reported in critically ill patients, most commonly in association with sepsis syndrome. However, the severity and incidence of hypocalcemia in nonseptic but critically ill patients has not been well defined. Therefore, the goal of this study was to identify and compare the frequency and degree of hypocalcemia in critically ill patients with differing underlying illnesses (those admitted to medical, surgical, trauma, neurosurgical, burn, respiratory, and coronary intensive care units [ICUs]; group A; n = 99). Results were compared with the frequency and degree of hypocalcemia in non-critically ill ICU patients (initially admitted to an ICU but discharged within 48 hours; group B; n = 50) or hospitalized non-ICU patients (group C; n = 50). Incidences of hypocalcemia (ionized calcium [Ca] < 1.16 mmol/L [less than normal]) were 88%, 66%, and 26% for groups A, B, and C, respectively (P: < 0.001). In group A, the frequency of hypocalcemia did not depend on the ICU setting or presence of sepsis. However, the occurrence of hypocalcemia correlated with both Acute Physiology and Chronic Health Evaluation II score (r = -0.39; P: < 0.001) and patient mortality (eg, hazard ratio for death, 1.65 for Ca decrements of 0.1 mmol/L; P: < 0.002). Hypomagnesemia, number of blood transfusions, and presence of acute renal failure were each associated with depressed Ca levels. A weak association (r = -0.12; P: = 0.09) was noted between serum Ca level and QT interval. Clinical concern stemming from hypocalcemia was underscored by the substantial use of intravenous (IV) Ca therapy ( approximately 2 to 3 g IV). We conclude that hypocalcemia is extremely common in hospitalized patients (up to 88%) and correlates with severity of illness, but not with a specific illness per se. Whether it directly impacts patient survival remains unknown. Resolution of this issue appears to be critical because of the frequency with which it leads to high-dose IV Ca therapy.

APACHE↗
PubMed1999

Effect of calcitriol and age on recovery from hypocalcemia in hemodialysis patients.

Calcitriol is used to treat hyperparathyroidism in hemodialysis patients. Calcitriol treatment, either through a reduction in parathyroid hormone (PTH) levels or direct effect on bone, decreases the osteoblast and osteoclast surface and bone formation rate. Our study of 13 hemodialysis patients was designed to evaluate whether calcitriol treatment changed the rate of spontaneous recovery from hypocalcemia induced by a low-calcium dialysis. Calcitriol treatment decreased basal PTH levels from 614 +/- 84 to 327 +/- 102 pg/mL (P < 0.001) and maximal PTH levels from 1,282 +/- 157 to 789 +/- 161 pg/mL (P < 0.001), but the rate of serum ionized calcium recovery from hypocalcemia did not change. When the 13 patients were separated based on the median age of 64 years, the predialysis serum ionized calcium level was less in the younger (group I, 44 +/- 6 years; n = 6) than older (group II, 68 +/- 1 years; n = 7) patients (1.05 +/- 0.03 v 1.22 +/- 0.03 mmol/L, respectively; P < 0.01) despite similar basal (group I, 595 +/- 122 pg/mL v group II, 629 +/- 96 pg/mL) and maximal (group I, 1,114 +/- 299 pg/mL v group II, 1,425 +/- 141 pg/mL) PTH levels. Before calcitriol treatment, the rate of serum ionized calcium recovery from induced hypocalcemia was greater (P < 0.05) for similar PTH levels in the older than younger patients. After calcitriol treatment, despite a similar reduction in PTH levels, the rate of calcium recovery increased (P < 0.05) in the younger patients but did not change in the older patients. We also observed that toward the end of the low-calcium hemodialysis, PTH values decreased even though serum ionized calcium level continued to decline when the rate of calcium reduction slowed. In addition, hysteresis, defined as a lower PTH value during the recovery from hypocalcemia than during the induction of hypocalcemia for the same serum calcium concentration, was present during the spontaneous recovery from hypocalcemia. In conclusion, in the hemodialysis patient: (1) age appeared to affect the bone response to PTH and calcitriol treatment, (2) the PTH response to hypocalcemia was affected by a deceleration in the rate of calcium decrease, and (3) hysteresis of the PTH response to hypocalcemia occurred during the spontaneous recovery from hypocalcemia.

Adult↗
PubMed1989

Pulmonary vascular responses to hypercalcemia and hypocalcemia in the dog.

The pulmonary artery responses in the isolated whole-blood perfused canine lung to ionized calcium ([Ca++]) were quantified over a range of hypercalcemia and hypocalcemia values ([Ca++] = 0.23-1.88 mM) under conditions of controlled pulmonary blood flow and constant mean aortic and left atrial pressures. Calcium chloride, administered as bolus doses in the clinical range (5-15 mg.kg-1) at initial normocalcemia and without interventions producing vasoconstriction did not influence mean pulmonary artery pressure at constant pulmonary blood flow. Stable hypercalcemia ([Ca++] = 1.88 +/- 0.05 mM) did not influence the slope of the pulmonary artery pressure-flow plot. Because normal pulmonary vasomotor tone is low and cannot readily be lowered further, the possible vasodilator action of hypocalcemia was assessed by its ability to decrease the slope of the mean pulmonary artery pressure-flow plot, which had been first increased by alveolar hypoxia (AHX) or infusion of the prostaglandin endoperoxide analog U46619 (PG). During AHX (n = 5), a graded reduction from normocalcemia ([Ca++] = 1.08 +/- 0.02 mM) to moderate hypocalcemia ([Ca++] = 0.8 and 0.5 mM) did not alter the pulmonary artery pressure-flow plot, but severe hypocalcemia ([Ca++] = 0.26 +/- 0.01 mM) decreased the slope by 13 +/- 0.9 mmHg.l-1.min-1. The comparison of severe hypocalcemia ([Ca++] = 0.23-0.27 mM) versus a high dose of nifedipine (bolus of 10 micrograms/kg followed by continuous infusion at 40 micrograms.kg-1.h-1) on pulmonary vascular tone increased by either AHX or PG infusion indicated that both hypocalcemia and nifedipine decreased the slope of the relationship between mean pulmonary artery pressure and flow (during AHX: -16.1 +/- 1.38 and -23.3 +/- 1.73 mmHg.l-1.min-1, both P = 0.0001 vs. AHX alone, and during PG: -17.05 +/- 1.95 and -8.4 +/- 1.78 mmHg.l-1.min-1, P = 0.0001 vs. PG alone). Two principal conclusions emerge. First, the pulmonary vessels are minimally sensitive to changes in ionized calcium throughout the clinical hypercalcemia and hypocalcemia ranges; extreme hypocalcemia is required to produce vasodilation, which was reversed with calcium infusion. Second, whereas the pulmonary vasodilator effects of extreme hypocalcemia were independent of the intervention inducing pulmonary vasoconstriction (AHX vs. PG), those of nifedipine were much more pronounced with AHX.

Animals↗
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↗
PubMed1991

Hysteresis of the parathyroid hormone response to hypocalcemia in hemodialysis patients with low turnover aluminum bone disease.

During the study of parathyroid function in 19 hemodialysis patients with low turnover aluminum bone disease, it was observed that serum parathyroid hormone (PTH) levels were higher during the induction of hypocalcemia than during the recovery from hypocalcemia. This type of PTH response has been termed hysteresis. Hypocalcemia was induced during hemodialysis with a calcium-free dialysate. When the total serum calcium level decreased to 7 mg/dL, the dialysate calcium concentration was changed to 3.5 mEq/L and the dialysis session was completed. One week later, hypercalcemia was induced during hemodialysis with a high-calcium dialysate. The mean basal PTH level was 132 +/- 37 pg/mL (normal, 10 to 65 pg/mL; immunoradiometric (IRMA), Nichols Institute, San Juan Capistrano, CA) and increased to a maximal PTH level of 387 +/- 91 pg/mL during hypocalcemia. For the same ionized calcium concentration, the PTH level was higher during the induction of hypocalcemia than during the recovery from hypocalcemia. Conversely, for the same ionized calcium concentration, the PTH level was greater when hypercalcemia was induced from the nadir of hypocalcemia than when hypercalcemia was induced from basal serum calcium. The set point of calcium (defined as the serum calcium concentration required to reduce maximal PTH by 50%) was greater during the induction of hypocalcemia than during the recovery from hypocalcemia (4.44 +/- 0.10 versus 4.25 +/- 0.09 mg/dL; P = 0.03). The mean basal ionized calcium concentration and the mean ionized calcium concentration at the intersection of the two PTH-calcium curves were the same (4.61 +/- 0.13 versus 4.61 +/- 0.12 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Parturient paresis and hypocalcemia in ruminant livestock.

Parturient paresis (hypocalcemia) is most likely to affect dairy cattle around the time of parturition. It causes progressive neuromuscular dysfunction and flaccid paralysis. Older dairy cows, cows with a history of parturient paresis during a previous lactation, high-producing cows, and cows from the Jersey and Guernsey breeds are at highest risk for developing parturient paresis. Nonparturient hypocalcemia may also occur and is related to events other than parturition, such as severe stress, that temporarily overwhelm the mechanisms of calcium homeostasis. Beef cattle, sheep, and goats are affected less frequently by hypocalcemia than are dairy cows. Because these species are not as stressed for milk production as dairy cattle, nonparturient hypocalcemia makes up a higher proportion of cases in nondairy ruminants. Clinical signs of hypocalcemia in beef cattle, sheep, and goats tend toward hyperesthesia and tetany rather than the classic flaccid paralysis that occurs in dairy cattle with parturient hypocalcemia. Prompt and effective treatment of hypocalcemia helps to reduce the incidence of secondary complications, such as muscle damage or mastitis. The standard treatment regimen of 500 ml of 23 per cent calcium gluconate, administered intravenously, will elicit a favorable response in approximately 75 per cent of recumbent cows within 2 hours of treatment. Relapses following successful initial therapy are common and may be prevented in part by supplementation of intravenous treatment with an additional 500 ml of 23 per cent calcium gluconate administered subcutaneously. Proper nursing care following treatment speeds recovery and reduces the incidence of secondary complications owing to hypocalcemia.

Animals↗
PubMed2002

Low parathyroid hormone levels after thyroid surgery: a feasible predictor of hypocalcemia.

BACKGROUND: Selecting patients with a low risk of hypocalcemia is mandatory if patients are to be discharged on the first day after bilateral thyroidectomy. This study investigated the predictive value of intraoperative parathyroid hormone (PTH). METHODS: Thirty-eight patients underwent total or near-total thyroidectomy. Patients with or without biochemical and symptomatic hypocalcemia were compared regarding intraoperative PTH levels and previously suggested risk factors. The accuracy of intraoperative PTH to predict patients at risk for postoperative hypocalcemia was compared with a calcium concentration of less than 2.00 mmol/L (8.0 mg/dL) on the first postoperative day. RESULTS: PTH levels after resection of the second lobe, age, and number of parathyroid glands identified intraoperatively were independently associated with the reduction in serum calcium concentration measured at nadir on the first or second postoperative day. PTH levels after resection of the second lobe were lower among patients who developed biochemical (P <.001) and symptomatic hypocalcemia (P <.01) compared with those who did not. Low levels of intraoperative PTH identified the 3 patients who required intravenous calcium during the first 24 postoperative hours. An intraoperative PTH level below reference range and a calcium concentration of less than 2.00 mmol/L measured 1 day postoperatively both predicted biochemical hypocalcemia with a similar sensitivity (90% vs 90%) and specificity (75% vs 82%). Intraoperative PTH was slightly better than a serum calcium concentration of less than 2.00 mmol/L on postoperative day 1 to predict symptomatic hypocalcemia, with a sensitivity of 71% vs 52% and a specificity of 81% vs 76%, respectively. CONCLUSIONS: Parathyroid gland insufficiency is the main determinant of transient hypocalcemia after bilateral thyroid surgery. Low intraoperative PTH levels during thyroid surgery are therefore a feasible predictor of postoperative hypocalcemia.

Adolescent↗