The effect of intravenous magnesium therapy on serum and urine levels of potassium, calcium, and sodium in patients with ischemic heart disease, with and without acute myocardial infarction

Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.(ABSTRACT TRUNCATED AT 400 WORDS)     

Graves病治疗前及治疗中血清游离钙与血,尿钙磷代谢异常

46例Graves病患者治疗前血清游离钙(Ca~( ))、磷(P)、碱性磷酸酶(AKP)及24小时尿钙(Ca)、P、羟脯氨酸(Hyp)排量水平都显著高于正常对照组。经治疗2—3个月甲亢病情控制后,血Ca~( )、P及24小时尿Ca、P亦随之恢复正常,但血AKP与24小时尿Hyp仍高于对照组。高钙血症比率在血Ca、校正钙与Ca~( )测定中分别为11.2％、16.3％与30.0％。前臂骨密度呈现骨量减少和腰椎相示骨质疏松者分别为29.0％和13.3％。本文对Graves病患者的钙、磷和骨代谢改变及其发生作了初步讨论。     

The effect of hypermagnesaemia on serum immunoreactive calcitonin levels in normal human subjects

The effect of hypermagnesaemia on serum levels of immunoreactive calcitonin was studied in normal human subjects. After iv administration of magnesium sulphate over 120 min, the mean (+/- SEM) serum magnesium concentration rose from the baseline level of 0.9 +/- 0.1 to 2.6 +/- 0.3 mmol/l (P less than 0.01), and thereafter remained higher than the baseline level. The magnesium infusion caused a significant increase in serum immunoreactive calcitonin levels (P less than 0.01). The rise in serum magnesium concentration was accompanied by a significant decrease in the concentrations of corrected serum calcium and whole blood ionized calcium (P less than 0.01, P less than 0.01 respectively). Our results suggest that hypermagnesaemia causes an increase in serum immunoreactive calcitonin levels in normal human subjects despite a decrease in the concentrations of corrected serum calcium and whole blood ionized calcium.     

Relationship of thyroid hormones and norepinephrine to the lateral hypothalamic syndrome

The role of thyroid hormones and norepinephrine in the elevated thermogenesis seen following lateral hypothalamic (LH) lesions was investigated by measuring serum thyroid hormone levels and urinary norepinephrine excretion during the 24 hours following placement of LH lesions and again one month later when body weight had stabilized at a reduced level. During the first 24 hours following LH lesions, serum thyroxine (T4) and triiodothyronine (T3) were significantly depressed. By one month postlesion, both T4 and T3 had returned to normal. In contrast, urinary excretion of norepinephrine (NE) was increased 100% during the 24 hours following LH lesions. By one month postlesion, NE had returned to normal levels. These results indicate that the elevated thermogenesis seen shortly following LH lesions does not reflect enhanced thyroid activity, but is probably a consequence of sympathetic nervous system stimulation. The return of NE to normal levels after one month is consistent with the observation that LH-lesioned rats are by one month postlesion no longer hypermetabolic, but display levels of heat production appropriate to the reduced body weight they then maintain.     

PRIMARY HYPERPARATHYROIDISM WITH INTERMITTENT HYPERCALCAEMIA: SERIAL OBSERVATIONS AND SIMPLE DIAGNOSIS BY MEANS OF AN ORAL CALCIUM TOLERANCE TEST

Ten patients with subtle primary hyperparathyroidism and intermittent hypercalcaemia were followed serially for periods of 2--18 months (mean 10 months). Fasting serum calcium was elevated (greater than 10.6 mg/dl) in only 20% of determinations and fluctuated widely (9.1--11.2 mg/dl), yet the patients displayed a continuous, rather than episodic, basic disease process as defined by increases in nephrogenous cyclic AMP and serum iPTH. Identical findings were noted in short-term (2--3 successive days) studies in twelve patients. In response to a 1000 mg oral calcium tolerance test, twelve patients with primary hyperparathyroidism and intermittent hypercalcaemia (basal serum calcium 10.2 +/- 0.2 mg/dl, mean +/- SD) displayed: (1) hyperabsorption of calcium (mean calciuric response twice normal); (2) induced-hypercalcaemia (mean serum calcium 11.4 mg/dl, with a mean increase of 1.2 mg/dl versus 0.2 mg/cl in normal subjects); and (3) abnormal parathyroid suppressibility (nephrogenous cyclic AMP 2.66 +/- 0.57 nmol/100 ml GF versus 0.95 +/- 0.40 nmol/100 ml GF in normal subjects, mean +/- SD). The patients demonstrated striking hypercalciuria (452 +/- 123 mg/24 h) on a 1000 mg metabolic calcium diet. Serum levels of 1,25(OH)2D3, measured in ten patients, were markedly elevated at 90 +/- 20 pg/ml (mean +/- SD), and there was a strong positive correlation between the values for 1,25(OH)2D3 and the calciuric response to the calcium tolerance test (r = 0.75, P less than 0.001). These results (1) indicate that the calcium tolerance test is a simple and reliable technique for diagnosis of patients with primary hyperparathyroidism and intermittent hypercalcaemia, and (2) emphasize the important pathophysiologic features of this subtle clinical variant of primary hyperparathyroidism.     

Calcium metabolism and parathyroid function in primary aldosteronism

Calcium and magnesium metabolism was investigated in 10 hypertensive subjects with primary aldosteronism (seven adenomatous, three idiopathic). Serum levels of total calcium (9.03 +/- 0.2 mg/dl) and ionized calcium (2.06 +/- 0.06 meq/liter) were in the low-normal range, except for two patients who had levels of serum ionized calcium clearly above normal. Furthermore, both serum total (n = 6, p less than 0.01) and ionized calcium levels (n = 3) rose postoperatively in the patients who had an aldosterone-producing tumor removed. Dramatic elevations of parathyroid hormone levels (mean, 645 +/- 109 pgeq/liter; normal, less than 150 to 375 pgeq/liter) were seen in the majority of patients, including those two with frank ionized calcium elevations. Magnesium levels were within normal limits (2.07 +/- 0.07 meq/liter). These results indicate that parathyroid hypersecretion is a common feature of primary aldosteronism and also suggest a physiologic relationship between the activity of the renin-aldosterone system and parathyroid physiology. Sodium-volume expansion and negative calcium balance induced by aldosterone excess may predispose to hyperparathyroidism.     

Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.     

Increased prevalence of primary hyperparathyroidism in treated breast cancer.

Hypercalcemia occurring in patients with advanced breast cancer (BC) is generally due to osteolytic metastases or to the activity of circulating tumor-derived products. In these conditions, the production of endogenous PTH is reduced. The frequency of hypercalcemia due to primary hyperparathyroidism in breast cancer is unknown. We examined the occurrence of primary hyperparathyroidism in a large group of women with treated BC. A total of 100 consecutive women aged 28-80 years with treated breast cancer were enrolled. One hundred and two healthy age-matched women and 60 age-matched female patients with differentiated thyroid carcinoma examined before thyroidectomy were used as controls. Intact serum PTH and serum calcium were measured in all patients and controls. Hypercalcemia associated with elevated serum PTH concentration indicating primary hyperparathyroidism was found in 7 BC patients (7%) and in none of healthy women or patients with thyroid cancer. The pre-operative staging of BC patients with primary hyperparathyroidism was I in six and II in one of them, and no patient had evidence of distant metastases. A parathyroid adenoma was found in all 6 BC patients submitted to neck exploration, one patient refused surgery. Serum calcium and PTH concentrations returned to normal levels after surgery. Two BC patients had increased serum PTH and normal calcium concentrations. One of them had low serum 25-hydroxyvitamin D [25(OH)D]. One patient with spread bone metastases had neoplastic hypercalcemia with undetectable serum PTH concentration. All remaining 90 BC patients had serum calcium and PTH concentrations within normal limits, but their mean (+/-SD) values (9.6+/-0.5 mg/dl for serum calcium, 38.0+/-16.4 mg/dl for serum PTH ) were slightly but significantly greater than in normal controls (9.3+/-0.5 mg/dl, p=0.003 and 27.9+/-10.6 pg/ml, p=0.0001, respectively) and in patients with thyroid cancer (9.2+/-0.6 mg/dl, p=0.001 and 26.2+/-11.0 pg/ml, p=0.001), with no relationship with clinical staging or anti-tumor therapy. In conclusion: 1) an increased frequency of parathyroid adenoma was found in BC patients with mildly aggressive neoplastic disease; 2) in BC patients with no evidence of primary hyperparathyroidism mean serum PTH and calcium concentrations were significantly greater than in healthy controls and in patients with thyroid carcinoma; and 3) this finding was unrelated to clinical staging or anti-tumor therapy. Thus, primary hyperparathyroidism should be considered as a possible cause of hypercalcemia in patients with non-aggressive breast cancer. We suggest that serum PTH should be determined in all BC patients with increased serum calcium concentration, especially in those with no evidence of metastatic disease.     

SERUM CALCIUM CONCENTRATION IN HYPERTHYROIDISM AT DIAGNOSIS AND AFTER TREATMENT

In a large, mainly outpatient, series of hyperthyroid patients who attended a district general hospital the serum concentrations of calcium and albumin were measured before and in many cases after treatment. The calcium level (mean +/- SD) before treatment (2.41 +/- 0.21 mmol/l, n = 437) was significantly higher (P less than 0.01) than afterwards (2.36 +/- 0.15 mmol/l, n = 232) and the albumin level rose when the patients became euthyroid (from 40.5 +/- 3.1 g/l to 44.0 +/- 2.4 g/l; P less than 0.01). After treatment neither value differed from those of an unselected group of out-patients. The usual relation between the serum concentrations of calcium and albumin did not hold in the hyperthyroid subjects but reverted to normal on treatment; the variation, probably due to an increase in ionized calcium, leads to an overestimate of the 'corrected calcium' when conventional methods are used to calculate this figure. Thus, using a conventional formula 8.5% of our hyperthyroid patients would appear to have a calcium greater than 2.65 mmol/l (normal mean plus 2 standard deviations) whereas using a correction factor specific for the hyperthyroid situation the figure is reduced to 5.7% which is only twice the expected proportion. The calcium level was significantly greater (P less than 0.001) in those patients in whom initial T3 concentration was high (greater than 7.2 nmol/l). There was no effect of T4 upon serum calcium which could not be accounted for by the action of T3. In this series of 437 patients there was no case of symptomatic hypercalcaemia. The maximum value was 2.80 mmol/l in a patient with coincident primary hyperparathyroidism. Significant hypercalcaemia is rare in hyperthyroidism.     

Parathyroid hormone secretion in magnesium deficiency.

The effect of an acute elevation of the serum magnesium concentration on the concentrations of serum immunoreactive parathyroid hormone (IPTH) were studied in hypocalcemic hypomagnesemic patients, hyperparathyroid patients, and normal individuals. Basal serum IPTH concentrations in the hypomagnesemic patients ranged from undetectable to 3 times the upper limit of normal. All hypomagnesemic patients were observed to have an immediate rise in the serum IPTH concentration after magnesium administration regardless of the basal IPTH concentration. In contrast, normal individuals and patients with primary and secondary hyperparathyroidism responded to magnesium administration with either a decrease or little change in the serum IPTH concentration. These date indicate that an acute stimulation of PTH secretion induced by magnesium is characteristic of the magnesium-deficient state. The consistency of this response suggests that impaired PTH secretion is a significant factor contributing to the hypocalcemia of magnesium deficiency.     

EFFECTS OF ARTIFICIAL MENOPAUSE ON PLASMA AND URINE CALCIUM AND PHOSPHATE

Plasma and urine calcium and phosphate were determined in nine patients before and after oophorectomy and in eleven patients before and after simple hysterectomy. Oophorectomy was followed by a significant rise in the mean plasma and fasting urine calcium, and a mean rise of 37 mg in the 24 hr calcium which, however, was not significant. Hysterectomy alone caused no significant change in plasma or urine calcium. In both groups only small changes were observed in plasma and urine phosphate and these did not reach the level of significance. The mean urine hydroxyproline/creatinine ratio rose significantly in six patients after oophorectomy but did not change after hysterectomy. It is suggested the rise in plasma and urine calcium following oophorectomy is due to increased bone resorption which does not occur after simple hysterectomy.     

Thyroid hormone metabolism in nonthyroidal illness. I. Changes in thyroid hormone metabolism in dogs with experimental myocardial infarction and effect of thyroid hormone administration on their hemodynamics

To asses the changes in thyroid hormone metabolism after the onset of acute myocardial infarction (AMI), serum T4 and T3 levels were serially measured for 24 hours after the coronary artery ligation in dogs. The effect of thyroid hormone administration on hemodynamics in these dogs were also studied to clarify the possible usefulness of thyroid hormone therapy in nonthyroidal illness (NTI). Dogs were anesthetized with ketamine using "Micro-Mini" drip administration. Coronary artery ligation was performed in 8 dogs (MI group) Open chest operation was performed in 8 dogs, but their coronary arteries were not ligated and were used as control (cont. group). Blood samples were drawn before and 1, 3, 6, 12, 18 and 24 hours after coronary artery ligation, and serum levels of T4 and T3 were measured using the TDX T4 system and a commercial RIA kit, respectively. Various hemodynamic parameters (heat rate, mean blood pressure, max dp/dt, left ventricular end-diastolic pressure, cardiac output) were measured at the same time mentioned above. All the hemodynamic parameters remained within normal range for 24 hours in the control group. Serum T4 and T3 levels, however, showed slight, but significant decreases due to general anesthesia and open chest operation in the control group. On the other hand, hemodynamic parameters were maintained in the normal ranges only for 12 hours, and gradually deteriorated in the MI group. Moreover, it was remarkable that both T4 and T3 levels were decreased immediately after the ligation in this group, T4 being less than 0.1 micrograms/dl and T3 less than 10 ng/dl. They continued to show the low values thereafter. When T4 (30 micrograms/24 hours), and T3(7, 14 or 21 micrograms/24 hours) were continuously infused intravenously for 24 hours after the coronary artery ligation in 10 dogs, serum T4 levels were maintained in the normal range of the dog (1.5-3.6 micrograms/dl) and the serum T3 levels were increased to the low normal range. However, there were no significant differences in hemodynamic indices between the thyroid hormone treated groups and the non-treated group. These data show that T4 and T3 concentrations decrease prior to the deterioration of cardiac function. Moreover, the present findings also suggest that administration of thyroid hormone has no benefit in patients with NTI associated with low T4 and T3 levels.     

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.     

Studies on the pituitary and thyroid function in patients with nonthyroid illnesses

Serum thyroid hormone and TSH concentrations were determined in patients with nonthyroidal illnesses (NTI) including 26 patients with chronic renal failure on hemodialysis, 15 patients with end-stage malignancy and 21 normal controls. Serum TSH levels were measured by a highly sensitive immunoradiometric assay Kit (RIA-gnost hTSH) and free-T4 levels were determined not only by both back-titration method and T4 derivative method, but also by magnesium precipitation method using equilibrium dialysis. TSH levels in normal controls ranged from 0.6 to 2.4 microU/ml. In 40 of 41 patients with NTI, serum T3 levels were less than 100 ng/dl, and 37 patients had diminished T3 levels, as compared with those in normal controls. Moreover, serum T4 levels were also diminished in 19 patients with NTI, and T4 levels related significantly to serum TBG levels in all patients with NTI (r = +0.76, p less than 0.01), suggesting that the diminution of T4 levels in patients with NTI can be explained partly by decreased TBG levels. However, it was remarkable that free T4 levels in serum, determined by RIA kits, were decreased in approximately half of the patients with NTI. Free T4 levels by the magnesium precipitation method were still lower in these patients when compared with those in normal controls. Serum TSH levels in patients with NTI showed a wide scattering from below to above the normal range, and the mean value was not significantly different from that in normal controls. No significant relations were found between TSH levels and T4, T3, or free T4 levels in patients with NTI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Studies on the factors affecting serum thyrotropin levels in healthy controls and on the thyroid function in depressed patients using a highly sensitive immunoassay

With a highly sensitive time-resolved fluorometric immunoassay (TR-FIA), serum thyrotropin (TSH) levels were determined in various conditions in healthy subjects. In addition, we compared the thyroid function in 10 depressed female patients with that in 27 female controls. 1) We evaluated a highly sensitive time-resolved fluorometric immunoassay kit for serum TSH. The lower limit of detection of TSH in serum was 0.008 less than U/ml. The intraassay and interassay variances were 3.0 greater than 3.6% and 3.4 greater than 5.1%, respectively. There was a significant correlation between basal TSH levels and maximum TSH values after TRH administration (r = 0.797, p less than 0.01). 2) The mean TSH levels in 31 healthy controls of both sexes was 1.26 +/- 0.96 less than U/ml, but TSH levels in women were significantly higher than in men (p less than 0.01). A large intra-individual variation of serum TSH levels determined on different days was found equally in both men and women. The nyctohemeral elevation of TSH levels was not clearly seen prior to the onset of normal sleep, but the nocturnal rise of TSH levels was remarkably accentuated by sleep deprivation. 3) The serum TSH levels in depressed female patients were significantly lower than those in healthy female controls when the post-menopausal subjects were excluded. For the serum thyroid hormone concentrations, serum T4 levels were normal. Serum free T3 levels tended to be lower, although the reduction was not significant. The serum levels of these 3 thyroid hormones were not related to serum TSH values. The present study demonstrated a large variation of TSH levels in various conditions, even in the same individuals, indicating the necessity of strictly controlled conditions in the study of TSH secretion. A significant reduction in TSH levels was observed in the depressed female patients when the post-menopausal subjects were excluded. Our results suggest that the dysfunction of the regulating mechanism of the pituitary-thyroid axis in depression may occur at a pituitary or a suprapituitary level.     

Ⅱ型糖尿病肾病和非肾病患者甲状旁腺激素和钙磷代谢关系的初步探讨

测定４６例Ⅱ型糖尿病患者（肾病２５例，非肾病２１例）和２４例正常人血清甲状旁腺激素（ＰＴＨ）、钙（Ｃａ）、磷（Ｐ）、碱性磷酸酶（ＡＫＰ）、肌酐（Ｃｒ）和尿白蛋白（Ａｌｂ），发现糖尿病患者血ＰＴＨ、ＡＫＰ和尿Ｐ浓度较正常人增高，血Ｃａ、Ｐ浓度较正常人降低，其中肾病患者ＰＴＨ值又较非肾病组增高，差异有显著性。相关分析示糖尿病肾病的ＰＴＨ值与血Ｃｒ、ＡＫＰ和尿Ｐ有较好的相关性。作者认为糖尿病患者存在钙、磷代谢异常，体钙缺乏，这种代谢异常在糖尿病肾病患者尤为明显，血清ＰＴＨ值、ＡＫＰ和尿Ｐ浓度是反映糖尿病肾病钙、磷代谢异常的有意义指标。     

THE ACUTE BIOCHEMICAL EFFECTS OF FOUR PROPRIETARY CALCIUM PREPARATIONS

Abstract Changes in serum and urine biochemical indices have been studied in ten normal subjects in the four hours following the ingestion of four proprietary calcium supplements. Each was taken in a dose containing 1 gram of elemental calcium. The four preparations were ranked according to the amount of calcium absorbed in the order Spar-Cal and Calcium Sandoz> Os-Cal> Ossopan. There were no significant differences between the four preparations in the changes in parathyroid hormone (PTH) and urine hydroxyproline levels. For this reason, the four results from each subject were averaged. Following the calcium load there was a reduction in mean PTH from 0.16 ± 0.01 to 0.10 ± 0.02 μg/l (p<0.001) and a decline in urine hydroxyproline/creatinine ratio from 20 ± 1 to 17 ± 1 (p<0.02), suggesting that bone resorption responds immediately to dietary calcium intake. There was a rise in urine sodium excretion which correlated with the indices of calcium absorption (r= 0.63, p<0.01) but not with the sodium content of the calcium preparations. This effect could be important, particularly in elderly patients on borderline sodium intakes.     

Parathyroid hormone responsiveness in hypoparathyroidism with hypomagnesemia.

The failure to respond normally to parathyroid hormone (PTH) administration has been reported in patients with severe hypomagnesemia. A patient with hypoparathyroidism and a markedly decreased serum concentration of magnesium (0.7 mEq/liter), but a normal red blood cell magnesium level, is described who increased serum calcium concentration and decreased per cent renal tubular reabsorption of phosphate when parathyroid extract was given. It is suggested that PTH responsiveness in hypomagnesemic patients may, at least in part, be dependent upon the adequacy of intracellular magnesium stores. This interpretation is supported by the normal cellular (red blood cell) magnesium concentrations observed in this patient and in comparable studies in which PTH responsiveness in the presence of hypomagnesemia was demonstrated. In addition, a failure of optimal renal conservation of magnesium was noted to occur in this patient since, despite hypomagnesemia, urinary magnesium excretion was greater than the 1 mEq/day loss that is seen when magnesium conservation is induced by means such as dietary restriction.     

Reciprocal changes in parathyroid hormone and thyroid function after radioiodine treatment of hyperthyroidism

Hyperthyroidism is associated with negative calcium balance, normal to increased serum calcium concentrations, and decreased cortical bone mass. There is no agreement concerning serum PTH levels in such patients. In this study, we measured serum PTH concentrations using a newly developed sensitive 2-site immunoradiometric assay in 17 hyperthyroid patients before and after radioiodine therapy. The mean serum PTH and calcium concentrations were 28 +/- 15 (+/- SD) ng/L (normal range, 12-65 ng/L) and 2.4 +/- 0.5 mmol/L (normal range, 2.1-2.6 mmol/L) before therapy. After therapy serum PTH concentrations increased in 16 of the 17 patients. The increase in serum PTH was greater in the 9 patients who became hypothyroid rapidly (29 +/- 15 to 75 +/- 29 ng/L) compared with that in the 8 patients who became euthyroid gradually (26 +/- 16 to 45 +/- 24 ng/L). Serum PTH rose along with TSH as the patients became hypothyroid after radioiodine, and both serum PTH and TSH fell when L-T4 therapy was given. The reciprocal changes in serum PTH concentrations and thyroid function over time suggest a strong association of bone mineral metabolism and thyroid status.