Plasma Immunoreactive Calcitonin Research Articles

Chronic Electrical Stimulation of the Superior Laryngeal Nerve in the Rat: A Potential Therapeutic Approach for Postmenopausal Osteoporosis.

Electrical stimulation of myelinated afferent fibers of the superior laryngeal nerve (SLN) facilitates calcitonin secretion from the thyroid gland in anesthetized rats. In this study, we aimed to quantify the electrical SLN stimulation-induced systemic calcitonin release in conscious rats and to then clarify effects of chronic SLN stimulation on bone mineral density (BMD) in a rat ovariectomized disease model of osteoporosis. Cuff electrodes were implanted bilaterally on SLNs and after two weeks recovery were stimulated (0.5 ms, 90 microampere) repetitively at 40 Hz for 8 min. Immunoreactive calcitonin release was initially measured and quantified in systemic venous blood plasma samples from conscious healthy rats. For chronic SLN stimulation, stimuli were applied intermittently for 3–4 weeks, starting at five weeks after ovariectomy (OVX). After the end of the stimulation period, BMD of the femur and tibia was measured. SLN stimulation increased plasma immunoreactive calcitonin concentration by 13.3 ± 17.3 pg/mL (mean ± SD). BMD in proximal metaphysis of tibia (p = 0.0324) and in distal metaphysis of femur (p = 0.0510) in chronically SLN-stimulated rats was 4–5% higher than that in sham rats. Our findings demonstrate chronic electrical stimulation of the SLNs produced enhanced calcitonin release from the thyroid gland and partially improved bone loss in OVX rats.

Influence of estrogen replacement therapy on endogenous calcitonin production rates.

Calcitonin is now a well-accepted therapy for inhibition of bone loss, both in the first years of menopause and in established osteoporosis. However, its exact role in the pathogenesis of that disease as well as the interactions between calcitonin production and estrogen metabolism remain unsolved. In order to clarify the influence of estrogen replacement therapy (ERT) on calcitonin secretory capacity, we measured whole plasma immunoreactive calcitonin basal levels, metabolic clearance rates and production rates in a group of postmenopausal women, before and after a daily intake for 28 days of 0.625 mg/day of conjugated equine estrogens, and again 4 weeks after the withdrawal of that estrogen replacement therapy. No significant changes appeared in immunoreactive calcitonin or immunoreactive calcitonin metabolic clearance rate but the production rate significantly increased over the 28 days (mean +/- SEM, from 21.3 +/- 5.1 pg/ml to 25.2 +/- 5.9 pg/ml, p less than 0.05), and then decreased 4 weeks after therapy was withdrawn to the initial level (17.9 +/- 3.6 pg/ml). We concluded that estrogen replacement therapy significantly increases calcitonin secretory capacity. This confirms the interactions between calcitonin production and estrogen metabolism, and may provide an explanation concerning the mode of action of estrogen replacement therapy in prevention of postmenopausal bone loss.

Plasma immunoreactive calcitonin in the frog ( Rana pipiens)

1. 1. Plasma immunoreactive calcitonin (iCT) and ionic calcium ([Ca]i) were measured in intact frogs ( Rana pipiens) within complete 24 hr light-dark cycles over an 18 month period. 2. 2. Plasma iCT exhibits an annual periodicity about the annual mean of 10.0ng/ml, with an amplitude of 5.4 ng/ml that peaks in October. 3. 3. Within an annual cycle, a significant inverse association exists between the basal monthly levels of plasma iCT and [Ca]i for animals maintained in freshwater control conditions. 4. 4. When subjected to a high calcium environment during the latter half of the year, plasma [Ca]i and iCT were elevated above control levels but exhibited independent cyclic patterns. 5. 5. A distinct seasonal response of increased iCT in a high calcium environment may be related to the secretory activity of the ultimobranchial glands and physiological responsiveness to other calcémie hormones; e.g. parathyroid hormone and vitamin D.

Results of early thyroidectomy for medullary thyroid carcinoma in children with multiple endocrine neoplasia type 2

Children with multiple endocrine neoplasia type 2 (MEN2) often develop medullary carcinoma of the thyroid (MCT) or its precursor, C-cell hyperplasia. Survival results are improved if malignancy is diagnosed early from the results of plasma immunoreactive calcitonin (iCT) measurement. The effect of early detection and thyroidectomy in children with MEN2 syndrome was determined by reviewing the experience between 1975 and 1985. Seventeen children with MEN2 who were 12 years old or younger underwent a total thyroidectomy for MCT or C-cell hyperplasia. iCT was measured in all patients preoperatively and postoperatively. Of the 17 children, 14 (82%) had MEN2a and 3 (18%) had MEN2b. There were 14 (82%) female and three (18%) male patients; their mean age was 6.97 years (range 1.5 to 12 years). In all patients, the diagnosis of MCT was made from initial elevated levels of iCT after stimulation with pentagastrin. Three patients had clinical evidence of disease preoperatively. All patients underwent a total thyroidectomy and lymph nodes were removed from the central zone; a neck dissection was performed in the three with clinically obvious disease. MCT with C-cell hyperplasia was found in 11 children and C-cell hyperplasia alone in six. Of the 11 with carcinoma, eight had bilateral disease and three unilateral. Six children had bilateral C-cell hyperplasia. All 17 children were alive and feeling well at the time of this report; however, three had evidence of metastatic disease according to iCT measurements. None of the children had recurrent nerve injuries; one had evidence of hypoparathyroidism. All 14 children with occult disease diagnosed by iCT determinations survived and remained free of disease at follow-up. The three children with clinical disease when first examined, although alive, are presumed to have persistent metastatic disease. The youngest child with C-cell hyperplasia at operation was 20 months old, and the youngest with MCT was 3 years old. Therefore, we recommend initiating screening at age 1 year and total thyroidectomy when the diagnosis is made.

Plasma calcitonin in primary hyperparathyroidism: failure of C-cell response to sustained hypercalcemia.

An acute increase in serum calcium stimulates calcitonin (CT) secretion, but the effects of chronic hypercalcemia are controversial. Histopathological studies have shown C-cell hyperplasia in primary hyperparathyroidism (1 degree HPT), although circulating levels of CT have been variously reported to be normal, elevated, or depressed. We reexamined this relationship using CT RIA in conjunction with a silica extraction technique that conveys improved sensitivity and specificity for monomeric CT. Nine men and seven women with surgically documented 1 degree HPT were studied preoperatively before and after a short calcium infusion (2 mg Ca/kg, for 5 min), as were 72 normal men and 76 normal women. Basal whole plasma immunoreactive CT and silica-extractable CT concentrations in 1 degree HPT were indistinguishable from normal, regardless of sex. In addition, the whole plasma and silica-extractable CT responses to calcium stimulation were normal or blunted in patients with 1 degree HPT. We conclude that hypercalcemia resulting from 1 degree HPT is not associated with augmented CT secretion in response to an iv calcium infusion.

Secretion and metabolism of monomeric human calcitonin: effects of age, sex, and thyroid damage.

Some data suggest that human calcitonin (CT) secretion is lower in women than in men, decreases with age and the menopause, and is absent in thyroidectomized persons. To further explore CT secretory physiology, we have studied basal and calcium-stimulated plasma immunoreactive CT (iCT) and silica-extractable monomeric CT concentrations in 148 healthy volunteers and 33 patients with a history of thyroid damage (total or subtotal thyroidectomy, radioiodine treatment for thyrotoxicosis). Both whole-plasma iCT and extractable CT levels were lower basally and after calcium infusion in women than in men, basal levels being reduced about 50% and calcium-stimulated values about 75% from those of male subjects. There were no significant changes in basal iCT or extractable CT concentrations with age, and CT secretory capacity (CT response to calcium infusion) likewise did not change with age. Infusion of monomeric CT to constant concentration in 27 persons permitted estimates of CT metabolic clearance rates (MCRs) and secretion rates (SRs). Calculated MCRs of about 9 ml/min.kg-1 (persons aged 21-30 yr) and 6 ml/min.kg-1 (persons aged 54-70 yr) were in good agreement with published data, and did not differ between the sexes. SRs were dependent upon the assay method used to estimate basal plasma CT concentrations, being highest when whole-plasma iCT values were used. Based on estimates of plasma monomeric CT from the silica extraction procedure, the SR of CT was 59 +/- 6 (SE) ng/d.kg-1 in men, and 22 +/- 3 ng/d.kg-1 in women. Thyroid damage reduced, but did not abolish, apparent CT immunoreactivity, even in silica extracts of plasma. However, all subsets of thyroid-damaged patients had absent-to-markedly-impaired CT secretion in response to calcium infusion. We conclude that CT secretion is substantially lower both basally and after stimulation in women than in men, and that this difference in CT immunoreactivity probably reflects differences in circulating CT bioactivity. The sex difference in plasma CT concentrations probably results from lower rates of CT secretion in women, not increased MCR. There is no age-related decrease of plasma CT concentrations (or CT secretory reserve), calling into question the concept that a progressive deficiency of CT is partly responsible for age-related ("senile") osteoporosis. Surgical or radiation damage to the thyroid gland commonly abolishes C-cell response to calcium; such CT-deficient patients form a population suitable for determining whether or not reduced CT secretion can impair skeletal homeostasis.

Plasma ionic calcium regulation by anuran parathyroid glands

1. 1. Plasma ionic calcium ([Ca]i), directly measured by a calcium specific electrode, was measured in 7-day post-operative parathyroidectomized (PTX) frogs ( Rana pipiens) over complete 24 hr light-dark (L-D) cycles during February, June and October. 2. 2. [Ca]i in PTX frogs was depressed about 20% from control levels at each monthly interval, with a maximal depression of plasma total calcium ([Ca]t) in October, and a minimal depression of [Ca]t in June. 3. 3. Over 24 hr L-D cycles [Ca]i is depressed in PTX frogs during the nocturnal period in February with short light periods; but maximally depressed during the light period in June/October with equivalent or long light periods. 4. 4. Hypocalcemia of [Ca]i in PTX frogs is concomitant with a decline in nonprotein-bound calcium in October and February; while protein-bound calcium will increase in February and June. 5. 5. Plasma immunoreactive calcitonin (iCT) decreased from 10.8 ± 7.2, in controls, to 4.8 ± 3.9 ng/ml, in PTX frogs, in October and February with no difference observed in June.

Non Small Cell Lung Cancer and Elevated Plasma Immunoreactive Calcitonin

Non Small Cell Lung Cancer and Elevated Plasma Immunoreactive Calcitonin

Transpulmonary Levels of Plasma Immunoreactive Calcitonin in Man

Conference Abstract| December 01 1985 Transpulmonary Levels of Plasma Immunoreactive Calcitonin in Man J.P. McCann; J.P. McCann 1Wellcome Research Laboratories, Department of Medicine, The Queen's University of Belfast, N. Ireland Search for other works by this author on: This Site PubMed Google Scholar C.F. Johnston; C.F. Johnston 1Wellcome Research Laboratories, Department of Medicine, The Queen's University of Belfast, N. Ireland Search for other works by this author on: This Site PubMed Google Scholar J.E.S Ardill; J.E.S Ardill 1Wellcome Research Laboratories, Department of Medicine, The Queen's University of Belfast, N. Ireland Search for other works by this author on: This Site PubMed Google Scholar W.W. Dinsmore; W.W. Dinsmore 1Wellcome Research Laboratories, Department of Medicine, The Queen's University of Belfast, N. Ireland Search for other works by this author on: This Site PubMed Google Scholar C.M. McKee; C.M. McKee 1Wellcome Research Laboratories, Department of Medicine, The Queen's University of Belfast, N. Ireland Search for other works by this author on: This Site PubMed Google Scholar K.D. Buchanan K.D. Buchanan 1Wellcome Research Laboratories, Department of Medicine, The Queen's University of Belfast, N. Ireland Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1985) 69 (s12): 15P. https://doi.org/10.1042/cs069015P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation J.P. McCann, C.F. Johnston, J.E.S Ardill, W.W. Dinsmore, C.M. McKee, K.D. Buchanan; Transpulmonary Levels of Plasma Immunoreactive Calcitonin in Man. Clin Sci (Lond) 1 December 1985; 69 (s12): 15P. doi: https://doi.org/10.1042/cs069015P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu nav search search input Search input auto suggest search filter All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1985 The Biochemical Society and the Medical Research Society1985 Article PDF first page preview Close Modal You do not currently have access to this content.

"Nonspecific" Increases in Plasma Immunoreactive Calcitonin in Healthy Individuals: Discrimination from Medullary Thyroid Carcinoma by a New Extraction Technique

Occasional seemingly healthy individuals have above-normal concentrations of calcitonin-like immunoreactivity in their plasma, which can lead to mistaken diagnosis of thyroidal or other cancer. We measured immunoreactive calcitonin (CT) before and after extracting the plasma on columns of silica (to improve sensitivity and specificity of the assay for monomeric calcitonin) in five "healthy high-CT" men (I), five patients with known medullary thyroid carcinoma (II), and 30 normal controls (III). Median (and range) values (pg/mL = ng/L) for whole-plasma immunoreactive CT in these groups were, respectively, 379 (157-526), 429 (174-563), and 33 (less than 25-92). Dose-dilution curves for plasma samples from group I did not parallel the standard curve, in contrast to samples from the other two groups. Values for extractable CT from plasma from groups I and III, however, were indistinguishable, but remained significantly increased in group II. Infusions of Ca, 2 mg/kg body wt. in 5 min, produced the expected (normal) increases in extractable CT in group I. The occasional factor (or factors) in plasma of healthy persons that interferes in assays for CT is eliminated by the silica extraction method, and in this way such cases can be distinguished from cases of medullary thyroid carcinoma.

"Nonspecific" increases in plasma immunoreactive calcitonin in healthy individuals: discrimination from medullary thyroid carcinoma by a new extraction technique.

Abstract Occasional seemingly healthy individuals have above-normal concentrations of calcitonin-like immunoreactivity in their plasma, which can lead to mistaken diagnosis of thyroidal or other cancer. We measured immunoreactive calcitonin (CT) before and after extracting the plasma on columns of silica (to improve sensitivity and specificity of the assay for monomeric calcitonin) in five "healthy high-CT" men (I), five patients with known medullary thyroid carcinoma (II), and 30 normal controls (III). Median (and range) values (pg/mL = ng/L) for whole-plasma immunoreactive CT in these groups were, respectively, 379 (157-526), 429 (174-563), and 33 (less than 25-92). Dose-dilution curves for plasma samples from group I did not parallel the standard curve, in contrast to samples from the other two groups. Values for extractable CT from plasma from groups I and III, however, were indistinguishable, but remained significantly increased in group II. Infusions of Ca, 2 mg/kg body wt. in 5 min, produced the expected (normal) increases in extractable CT in group I. The occasional factor (or factors) in plasma of healthy persons that interferes in assays for CT is eliminated by the silica extraction method, and in this way such cases can be distinguished from cases of medullary thyroid carcinoma.

Effect of plasma calcium concentration on the metabolic clearance rate of calcitonin in the dog.

Plasma immunoreactive calcitonin (iCT) levels generally are not elevated in chronic, nonmalignant, hypercalcemic states. Normocalcitoninemia might occur despite increased CT secretion if hypercalcemia itself accelerated the clearance of CT from the circulation. Therefore, we have measured the metabolic clearance rate (MCR) of human CT (hCT), infused to constant plasma levels in thyroparathyroidectomized dogs, under conditions of acute and chronic hypo- and hypercalcemia. Acute increases of plasma calcium were without significant effect on the MCR of hCT, but chronic hypercalcemia, induced by dihydrotachysterol treatment, reduced the MCR of hCT by 30% (P less than 0.05) and glomerular filtration rate (GFR) by 40% (P less than 0.02). There was a significant, positive correlation (r = 0.60, P less than 0.02) between GFR and the MCR of CT. The data suggest that failure to detect elevated iCT levels in chronic hypercalcemia is not the result of an increased MCR of CT. In fact, hypercalcemia should exaggerate the effect of increased CT secretion by decreasing the renal clearance of the hormone.

Lack of influence of isoproterenol, propranolol, and dopamine on immunoreactive parathyroid hormone and calcitonin in normal man.

Available evidence in vitro and in vivo suggests that pharmacologic doses of isoproterenol stimulate the secretion of parathyroid hormone (PTH) and calcitonin (CT) and propranolol inhibits secretion. However, the findings in man are either quite modest or inconsistent. In view of this controversy, we examined the effects of isoproterenol, 0.15 micrograms intradermally (i.d.), dopamine, 5 micrograms/kg body weight over 60 min intravenously (i.v.), and propranolol, 1 mg over 5 min followed by 60 micrograms per min for 2 i.v. in normal human subjects. It was found that these agents did not alter serum calcium, serum immunoreactive PTH, or plasma immunoreactive CT. The findings do not support a physiologic role for biogenic amines in the control and regulation of PTH or CT secretion in normal man.

Epinephrine is a hypophosphatemic hormone in man. Physiological effects of circulating epinephrine on plasma calcium, magnesium, phosphorus, parathyroid hormone, and calcitonin.

The physiologic effects of epinephrine on mineral metabolism are not known. In six healthy men, insulin-induced hypoglycemia, a potent stimulus to endogenous epinephrine secretion, resulted in a decrement of 0.9+/-0.1 mg/dl (mean+/-SE, P < 0.001) in serum inorganic phosphorus and smaller increments in magnesium and total and ionized calcium. Plasma immunoreactive parathyroid hormone (iPTH) decreased and plasma immunoreactive calcitonin (iCT) increased appropriately with the increments in calcium and magnesium. We wished to determine to what extent these changes in mineral metabolism might be attributable to epinephrine. Therefore, in the same protocol, we infused the hormone over 60 min in these six men, in doses that resulted in steady-state plasma epinephrine concentrations ranging from 52 to 945 pg/ml (levels that span the physiologic range), for a total of 25 studies. Serum ionized calcium, iPTH, and iCT concentrations were unaltered by these physiologic elevations of plasma epinephrine. However, epinephrine resulted in dose-dependent decrements in serum inorganic phosphorus of 0.6+/-0.1 mg/dl (P < 0.005) for the highest epinephrine infusion rate. The plasma epinephrine concentration threshold for this hypophosphatemic effect was approximately 50-100 pg/ml. Thus, the sensitivity of the hypophosphatemic response to epinephrine is comparable to that of the cardiac chronotropic, systolic pressor, and lipolytic responses to epinephrine, and considerably greater than that of the diastolic depressor, glycogenolytic, glycolytic, and ketogenic responses to the hormone in human beings. In view of its rapidity, the hypophosphatemic effect of epinephrine is probably the result of a net shift of phosphate from the extracellular compartment to intracellular compartments. We suggest that it is a direct effect of epinephrine, in that it is not mediated by changes in availability of the primary regulatory hormones PTH and CT, although indirect effects mediated by changes in other hormones, such as insulin, cannot be excluded. The hypophosphatemic response is also not attributable to increments in plasma calcium. These data indicate that epinephrine in physiologic concentrations is a hypophosphatemic hormone in man.

The Surgical Management of Medullary Thyroid Carcinoma

Medullary carcinoma of the thyroid may occur in three patient groups: multiple endocrine neoplasia, type 2b (MEN2b), MEN2a, and sporadic. The prognosis is best in MEN2a and worst in MEN2b. Multicentric disease occurs in approximately 90% of patients in the MEN groups and in 20% of the patients in the sporadic group. The minimal surgical procedure advocated is total thyroidectomy with dissection of the central compartment nodes. When neck dissection is performed, there appears to be no advantage in resecting the internal jugular vein or the sternomastoid muscle. Primary relatives of all patients with medullary carcinoma should be screened by measurement of plasma immunoreactive calcitonin to identify C-cell disease in a generally unsuspecting group/reservoir and because it results in earlier diagnosis, which leads to a less extensive surgical procedure and a higher percentage of patients with a disease-free state.

An estimate of the endogenous secretion rate of calcitonin in man.

1. The metabolic clearance rate (MCR) of human calcitonin was measured in 12 normal subjects and four patients with Paget's disease by the infusion of synthetic human calcitonin (15-40 microgram/h for 2-24 h), and in 10 additional patients with Paget's disease from the disappearance rate of immunoreactive calcitonin from plasma after the intravenous injection of large doses of synthetic human calcitonin (0.5-1.0 mg). 2. The estimated MCR during the infusion studies (range 531-1224 litres/day) was similar to that calculated from the disappearance of large doses of synthetic human calcitonin injected intravenously in patients with Paget's disease (mean = 1035 litres/day; range = 593-1408 litres/day). 3. An eightfold range in the basal values of plasma immunoreactive calcitonin, in spite of the presence of a relatively constant MCR, suggests that the variation in basal plasma calcitonin was due principally to variation in the endogenous secretion rate for calcitonin. 4. The results suggest that the endogenous secretion rate for calcitonin is low in normal subjects (mean 124 +/- SEM 24 microgram/day), and give a basis for selecting the doses of calcitonin which can be considered physiological.

Clinical and biological effects of low doses of (3 amino-1 hydroxypropylidene)-1,1-bisphosphonate (APD) in Paget's disease of bone.

Abstract. At doses varying between 500 and 1500 mg/day, the disodium salt of (3 amino‐1 hydroxypro‐pylidene)‐1,1‐bisphosphonate (APD) has been shown to induce rapid and complete biochemical responses in Paget's disease of bone, but a short‐lived and self‐limited fever has been observed in 30–40% of patients. The present study is an open and unrandomized trial, performed to explore the use of lower doses of APD (250 and 50 mg/day) given for 6 months to fourteen patients suffering from Paget's disease of bone. Subjective clinical improvement and complete biochemical remission (as assessed by normalization of urinary hydroxyproline excretion and plasma alkaline phosphatase concentration) was observed in ten out of eleven patients given 250 mg/day, but fever did not occur. Thus, a significant decrease in urinary hydroxyproline excretion was noted as early as 15 days after the beginning of the treatment (from 4.5 to 1.3 μmol/l GF; P &gt; 0.05) whereas plasma alkaline phosphatase concentration fell significantly only 1 month later (from 330 to 195 IU/ml; P &gt; 0.05). Both mean (± SEM) urinary hydroxyproline excretion (0.98 ± 0.08 μmol/l GF) and plasma alkaline phosphatase concentration (70 ± 8 IU/ml) were in the normal range after 6 months of treatment. Plasma calcium and phosphorus concentration, urinary calcium excretion and TmP/GFR decreased whereas plasma immunoreactive parathyroid hormone concentration increased. These changes were statistically significant (P &lt; 0.05) only transiently and disappeared at the time when bone formation (assessed by plasma alkaline phosphatase) returned to normal. An increase in total body retention of 47Ca during the second month of treatment was documented in five patients (P &lt; 0.05), compatible with a positive calcium balance. Plasma immunoreactive calcitonin did not change (P &gt; 0.05). After 6 months of treatment at 50 mg/day, APD also induced significant decreases in urinary hydroxyproline excretion (from 4.23 to 1.73 μmol/l GF; P &lt; 0.05) and plasma alkaline phosphatase concentration (from 360 to 162 IU/ml; P &lt; 0.05) but biochemical remissions were not complete and these two variables were significantly higher than the corresponding values in the group of patients receiving 250 mg APD/day. Less marked changes were also noted in all the other variables measured. Biological and clinical tolerance was good in all the patients. It is concluded that 250 mg/day of APD is an effective dose schedule, capable of reducing to normal levels the indirect indices of bone turn‐over, but in contrast with higher doses, without inducing fever.

DEFICIENT CALCITONIN RESPONSE TO CALCIUM STIMULATION IN POSTMENOPAUSAL OSTEOPOROSIS?

To test whether mobilisation of immunoreactive calcitonin in response to calcium challenge is reduced in postmenopausal osteoporosis, seventeen postmenopausal osteoporotic women with compression fractures and ten normal agematched women were given intravenous infusions of 3 mg/kg elemental calcium over a 10 min period. Blood samples were obtained 5 min before and at 0, 10, 20, and 60 min after start of infusion for the measurement of serum calcium and plasma immunoreactive calcitonin. Serum calcium increased significantly from baseline in both normal and osteoporotic groups; immunoreactive calcitonin increased significantly in the controls 10 min and 20 min after the start of infusion, but in the women with osteoporosis calcitonin levels did not change significantly at any time. 20 min after the start of infusion the change in immunoreactive calcitonin from baseline was significantly less in osteoporotic women than in the controls. These data are consistent with a decreased immunoreactive calcitonin response to calcium infusion in postmenopausal osteoporotic women, and suggest that calcitonin deficiency may be involved in the development of postmenopausal osteoporosis.

Correction of abnormal bone and mineral metabolism in chronic streptozotocin-induced diabetes mellitus in the rat by insulin therapy.

Mineral homestasis and skeletal morphology were studied in freely fed control, streptozotocin-induced diabetic, and insulin-treated diabetic rats 7 weeks after the induction of diabetes. The untreated diabetic animals were characterized by modest hypercalcemia, hyperphosphatemia, and striking hypercalciuria and phosphaturia. Insulin treatment corrected the hypercalcemia and markedly reduced the calciuria (P < 0.001), but had no significant effect on the urinary phosphate levels. Circulating immunoreactive parathyroid hormone (iPTH) was detectable in only 6% of untreated diabetic animals compared to 30% of controls. Furthermore, in untreated diabetic animals, the circulating levels of iPTH, when detectable, approximated the lower limits of the assay. The urinary cAMP levels of untreated diabetic animals were markedly decreased. Both iPTH and urinary cAMP approximated control levels in insulin-treated rats. Conversely, plasma immunoreactive calcitonin was increased in the diabetic rats compared to control a...

Basal plasma immunoreactive calcitonin in postmenopausal osteoporosis

Calcitonin (CT) deficiency has been suggested as an etiologic factor in postmenopausal osteoporosis (PM-OP). Basal immunoreactive calcitonin (iCT) was measured with a sensitive radioimmunoassay (RIA) in 62 PM-OP women with compressin fractures (CF) and in 28 normal age-matched women. Mean iCT values in the two groups were not significantly different (43.5 and 45.1 pg/ml, p > 0.10). In the 62 PM-OP females, no significant correlation was noted between basal plasma iCT levels and (1) age; (2) severity of disease as assessed by number of CF; (3) serum calcium, phosphorus, alkaline phosphatase, and immunoreactive parathyroid hormone; and (4) total bone mass as assessed by neutron activation analysis determinations of total body calcium (TBC). In 20 PM-OP patients treated for 24 mo with 100 Medical Research Council (MRC) units daily of synthetic salmon CT, no correlation was observed between basal plasma iCT and response of bone mass (TBC) to therapy. These data suggest that basal CT is not decreased in women with PM-OP, and that the level of circulating CT does not influence therapeutic changes in bone mass during CT therapy. CT is probably not a major etiologic or pathogenetic factor in PM-OP.