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J J Body

Publications and source records attributed to J J Body.

At least 73 records · Page 4Linked to original sources
PubMed1996

Effects of secretory products of breast cancer cells on osteoblast-like cells.

The pathogenesis of breast cancer-induced osteolysis remains largely unknown. To evaluate the potential role of osteoblasts as target cells during this process, we incubated SaOS-2 human osteoblast-like cells (OBL) with culture media conditioned by proliferative (PM, 'Proliferation Media') or confluent (CfM, 'Confluence Media') MCF-7 human breast cancer cells. CfM decreased the growth of OBL by 26% (P < 0.01) while PM was without significant effect on this parameter. In contrast, both PM and CfM obtained from MCF-7 cultures increased the cyclic AMP (cAMP) response of OBL to the osteolytic agents PTH (10(-8) M) and PTH-related peptide (PTHrP, 10(-8) M) by a factor of about 3 (P < 0.001), and to prostaglandin E(2) (PGE(2),10(-6) M) by a factor of about 2 (P < 0.01). No significant modulation of OBL growth or sensitivity to PTH, PTHrP, or PGE2 was induced by media obtained from HBL-100 non-malignant immortalized breast epithelial cell cultures. 17betaestradiol (E(2), 10(-8) M) and the antiestrogen tamoxifen (Tam, 10(-7) M) added for 48 h to MCF-7 cultures before collecting conditioned media attenuated and potentiated, respectively, the PM- but not the CfM-induced increase in the response of OBL to PTH or PTHrP Along the same line, the addition to MCF-7 conditioned media of a polyclonal anti-transforming growth factor-beta (TGF-beta) antibody attenuated by about 25% (P < 0.01) the PM-induced increase in OBL response to PTH and PTHrP while abrogating the modulatory effects of E(2) and Tam on that response. Together, our results indicate that MCF-7 breast cancer cells secrete factors which inhibit the growth of OBL and increase their sensitivity to various osteolytic agents. TGF-beta was only partly responsible for these effects, and accounts for their modulation by E(2) and Tam. The identification of other osteoblast-modulatory factor(s) should contribute to a better understanding and treatment of breast cancer-induced osteolysis.

Adenocarcinoma↗
PubMed1996

Cyclical pamidronate infusions in postmenopausal osteoporosis.

OBJECTIVES: Until recently, two bisphosphonates, pamidronate (APD) and etidronate were available for clinical purposes. Contrary to etidronate, pamidronate was not extensively studied in osteoporosis. Therefore, we investigated the effect of cyclic intravenous APD treatment in postmenopausal osteoporosis. METHODS: Parameters of bone remodelling and lumbar spine bone mineral density (BMDL) were assessed in 36 postmenopausal women with osteoporosis (BMDL t-score < -2.5). They received five courses of APD. Intervals between courses were defined according to the fasting urinary calcium excretion (UCa/Cr, mg/mg creatinine) which was measured before each APD course and every 2 weeks after the first treatment. The patients were retreated when UCa/Cr had reached baseline levels. Serum biochemical parameters and urinary hydroxyproline (UOHPro/Cr, mg/mg) were measured before each APD. RESULTS: UCa/Cr decreased during 21-28 days after each course but UCa/Cr measured before APD infusion remained unchanged. UOHPro/Cr significantly fell after the third APD (P = 0.02). Serum calcium was however not modified. Parameters of bone remodelling decreased with time: bone-GLA protein (BGP) started to fall after the first APD (P = 0.0001) and continued to decrease until the fourth APD course, alkaline phosphatase (ALP) significantly decreased after the first APD (P = 0.005); intact PTH significantly increased at the fifth APD (P = 0.02). BMDL significantly increased after 1 year treatment: +2.9% of baseline value. CONCLUSIONS: Cyclical pamidronate treatment of postmenopausal osteoprosis appeared to be effective in reducing bone turnover assessed by BGP, ALP and OHPro/Cr. This effect is followed by an increase in vertebral BMD.

Adult↗
PubMed1996

Randomized phase II trial comparing different doses of the bisphosphonate ibandronate in the treatment of hypercalcemia of malignancy.

PURPOSE: To evaluate the hypocalcemic effect and safety of three different doses of the bisphosphonate ibandronate in tumor-associated hypercalcemia, and to identify factors predicting response. PATIENTS AND METHODS: One hundred seventy-four cancer patients with a serum calcium level greater than 2.7 mmol/L (10.8 mg/dL) were enrolled onto the trial. If hypercalcemia persisted after fluid repletion, patients were randomly assigned to treatment with 0.6 mg, 1.1 mg, and 2.0 mg of ibandronate. Response, defined as restoration of normocalcemia, was evaluated by an intent-to-treat analysis. RESULTS: One hundred seventy-three (99%) patients were assessable for toxicity and 151 (87%) for efficacy. The administration of 0.6 mg (group A), 1.1 mg (group B), or 2.0 mg (group C) of ibandronate led to response rates of 44%, 52%, and 67%, respectively. Significantly more patients in group C responded than in group A (P = .0276). Of the various parameters examined, only the initial serum calcium level (P < .0001; odds ratio, 0.083) and the dose of ibandronate (P = .0162; odds ratio, 2.094) correlated with response. One hundred ninety-five adverse events (AEs) were reported, 99 classified as serious and 96 as nonserious. Three serious and sixteen nonserious AEs were considered related to ibandronate treatment. The three serious AEs were one case with thrombocytopenia, one with nausea, and one with fever. CONCLUSION: Ibandronate therapy led to a dose-dependent reduction in serum calcium levels. The response to ibandronate treatment correlated negatively with the initial serum calcium level and positively with the dose administered. A dose of 2 mg was necessary to achieve a response rate comparable to that in previous studies with the bisphosphonates pamidronate and clodronate. Because the incidence of drug-associated AEs was low, a dose escalation of ibandronate can be recommended for further clinical trials.

Adult↗
PubMed1996

Technical and clinical validation of a new immunoradiometric assay for human osteocalcin.

The measurement of circulating osteocalcin or bone GLA protein (BGP) constitutes a well established and non-invasive means for evaluating preferentially the bone formation rate, but most available commercial assays suffer from several technical constraints, notably a rapid degradation of BGP at room temperature or after thawing and the inability to measure subnormal values. We evaluated, from a technical and a clinical viewpoint, a newly available two-site sandwich immunoradiometric assay (IRMA) using standard of human origin and two different monoclonal antibodies. The theoretical and functional assay detection limit was 0.3 ng/ml. Concentrations of BGP progressively decreased when the serum was left at 4 degrees C or at room temperature (mean apparent loss of 15% after 24 h). Two cycles of freezing-thawing only lightly reduced the BGP concentrations. The mean (+/- SD) BGP concentration was 19.6 +/- 7.9 ng/ml in healthy subjects (NI, N = 61); the normal range was 8.1-35.6 ng/ml. There was a marked difference between pre- and postmenopausal women: 15.1 +/- 4.4 vs 22.3 +/- 8.4 ng/ml, respectively (p < 0.05). The mean BGP concentration in patients with tumor-induced hypercalcemia (N = 29) was not significantly different from NI, but nine patients (31%) had subnormal levels and five (17%) had elevated BGP levels. Concentrations of BGP were significantly increased in patients with hyperparathyroidism (N = 14) (45.1 +/- 21.0 ng/ml) and significantly lower than NI in patients with hypoparathyroidism (N = 18) (7.3 +/- 4.6 ng/ml). Concentrations of BGP were also measured by a classical radioimmunoassay using bovine standards and tracer; the correlations between both sets of measurements were significant in all groups, except in patients with hypoparathyroidism. In summary, this newly available IRMA for measuring circulating human BGP appears to be quite sensitive, reproducible and robust. It should be especially useful for investigating clinical conditions characterized by a low bone formation rate.

Adult↗
PubMed1995

Intravenous pamidronate in patients with tumor-induced osteolysis: a biochemical dose-response study.

Bisphosphonates are used increasingly in normocalcemic patients for treating tumor-induced osteolysis (TIO) but little is known about the metabolic effects and the most appropriate therapeutic regimen. In 21 patients with breast cancer and TIO, we determined the biochemical effects of a single infusion of pamidronate given at 30 mg (n = 5), 60 mg (n = 5), 90 mg (n = 5), or 120 mg (n = 6). Patients received no other systemic antineoplastic therapy during the trial. We selected patients with baseline fasting urinary Ca/Creat (creatinine) > 0.105 mg/mg (median value of our normal range) and they were followed weekly for up to 14 weeks. The biochemical effects were maximal at day 7. For the whole group, mean (+/- SEM) Ca/Creat levels fell from 0.208 +/- 0.018 to 0.048 +/- 0.008 mg/mg on day 7 and remained significantly ( p < 0.01) lower than baseline up to day 56. Hydroxyproline excretion fell to a lesser degree, from 7.0 +/- 1.2 to 4.0 +/- 0.6 mg x 100/mg of Creat. The falls in Ca/Creat and hydroxyproline excretion were dose-related (ANCOVA, p < 0.05). Changes in serum parameters of calcium metabolism were, however, not significantly dose-related. Serum Ca levels fell from 9.3 +/- 0.1 to 8.7 +/- 0.1 mg/dl on day 7, but not patients developed symptomatic hypocalcemia, and the decrease within each dose group was significant only at 120 mg. Ca2+ levels followed a similar pattern. There was a slight increase in Mg levels and a pronounced fall in Pi levels, from 3.6 +/- 0.2 to 2.8 +/- 0.1 mg/dl. Intact PTH levels increased from 29 +/- 4 to 91 +/- 13 pg/ml and remained significantly (p < 0.05) elevated up to day 28.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Calcitonin for prevention and treatment of postmenopausal osteoporosis.

Prolonged calcitonin administration (intramuscular, subcutaneous, or intranasal) can prevent postmenopausal trabecular bone loss. Nasal administration constitutes a particularly attractive option for women who cannot tolerate or benefit from estrogen replacement therapy. The optimal schedule of administration still has to be precised, but 100 U/day of nasal calcitonin, combined with calcium supplements, can currently be recommended. Interrupted regimens are maybe favourable. Calcitonin can also prevent further bone loss in established osteoporosis particularly if bone turnover is increased. The anti-fracture efficacy of calcitonin is suggested by different types of studies but has not been formally demonstrated. Lastly, its analgesic efficacy in cases of painful vertebral compression fractures has been demonstrated in controlled studies.

Bone Density↗
PubMed1995

Clinical trials in metastatic breast cancer to bone: past--present--future.

The skeleton is the most common site of metastatic disease in breast cancer and the site of first distant relapse in almost one half of the cases. Bone metastases are the source of a considerable morbidity, including pain, long bone fractures in 10-20%, and hypercalcemia in 10-15% of the cases. The median survival after first relapse in bone is close to two years compared to three months after first relapse in liver. A review of endocrine and chemotherapy trials indicates that patients with metastatic bone disease have a lower response rate to antineoplastic therapy than patients with soft tissue or visceral metastases, but this probably reflects selection bias and the insensitivity of our current methods for evaluating bone response. Classical UICC criteria require radiological recalcification, implying not only tumor regression but also bone healing, which can take many months. Symptom evaluation, measurement of tumor markers and of biochemical parameters of bone turnover should be further investigated for early assessment of bone response. Pain relief could occur in more than half of the patients after radiotherapy, but uncertainty remains as to the relationship between radiotherapy dose or fractionation and the incidence duration of pain relief. Radioactive isotopes have been used successfully in patients with blastic bone metastases from prostate cancer, but controlled studies are lacking in breast cancer. The pathophysiology of metastatic bone destruction makes it logical to use osteoclast inhibitors. Bisphosphonates are potent inhibitors of bone resorption that have opened the way for a noncytotoxic medical treatment of bone metastases. Two large-scale studies in patients with breast cancer metastatic to the skeleton, one with clodronate and one with pamidronate, indicate that the prolonged administration of oral bisphosphonates, in addition to systemic antineoplastic therapy, can reduce the frequency of morbid skeletal events, including the incidence of hypercalcemic episodes and the need for radiotherapy, and probably the incidence of severe pain and of fractures. On the other hand, in patients with established tumor-induced osteolysis, intravenous pamidronate infusions can induce bone pain relief and an objective sclerosis of lytic lesions maybe in one-third and in one-fourth of the cases, respectively. These figures must, however, be taken with caution, and prospective placebo-controlled trials in large series of patients are needed.

Antineoplastic Agents↗
PubMed1994

Regulation of lymphocyte calcitonin receptors by interleukin-1 and interleukin-6.

We have reported the existence of specific and high-affinity calcitonin (CT) receptors on normal human T-lymphocytes. Because of the increasingly recognized importance of interleukin-1 (IL-1) and IL-6 in the control of bone metabolism, we have examined their influence on the binding parameters of labeled salmon calcitonin (sCT) on lymphocytes. After a 24-hour incubation, IL-1 at 100-5000 U/ml and IL-6, at 1-1000 U/ml, decreased the apparent number of CT binding sites (Bmax) on T-lymphocytes. The effects of IL-6 on purified T-lymphocytes were dose related and 100 U of IL-6/ml reduced sCT binding to 57 +/- 16% (mean +/- SD) of the control values (n = 6). There was no significant change in CT binding affinity (Kd, 0.71 +/- 0.54 x 10(-10) M for controls versus 0.90 +/- 0.55 x 10(-10) M after IL-6) and the decrease in Bmax was reversible after 48 hours. The effects of IL-1 appeared to be mediated through an increased production of IL-6 as they were neutralized by a polyclonal antiserum against IL-6. Added alone, the antiserum caused a slight increase in the apparent number of CT binding sites on T-lymphocytes to 115 +/- 5% of control values (n = 3). In summary, IL-1 and IL-6 can induce a marked apparent loss of CT binding sites on normal T-lymphocytes at concentrations known to be active on bone metabolism. The contributions of our observations to the osteolytic activity of these cytokines deserve further investigation.

Animals↗
PubMed1994

Circulating concentrations of interleukin-6 in cancer patients and their pathogenic role in tumor-induced hypercalcemia.

Circulating interleukin-6 (IL-6) concentrations correlate with disease activity in severe inflammatory conditions, in sepsis and in some hematological malignancies. On the other hand, IL-6 is a potent stimulator of osteoclastogenesis and has been implicated as a contributory factor in the genesis of osteopenic conditions. We measured circulating IL-6 levels by a sensitive (detection limit of 10 U/ml) and specific bioassay in 103 patients with advanced cancer, including 41 with tumor-induced hypercalcemia before any specific hypocalcemic therapy. We related IL-6 concentrations to clinical features and to biochemical parameters of bone metabolism, including blood Ca, Ca2+, Pi, intact parathyroid hormone, parathyroid hormone-related protein, osteocalcin, 1,25-(OH)2-vitamin D and, as markers of bone resorption, the fasting urinary excretion of calcium (Ca/creatinine) and hydroxyproline. IL-6 levels were increased, i.e. detectable, in 23% of the patients, 8/41 (20%) hypercalcemic and 16/62 (26%) normocalcemic patients (NS); the distribution of the values was similar in the two groups. The presence of increased IL-6 concentrations was not related to any clinical characteristic, notably not to the survival nor to the existence of bone metastases, whether in hypercalcemic or normocalcemic patients; e.g., only 3/12 (25%) hypercalcemic subjects without bone metastases had elevated IL-6 levels. We found no significant correlations between IL-6 concentrations and any of the biochemical parameters studied. Hypercalcemic subjects with increased IL-6 had higher urinary Ca/creatinine levels than patients with normal IL-6 levels (P < 0.005) but this was not the case in normocalcemic subjects. Mean concentrations of inflammatory or other bone metabolism markers were not significantly different between patients with normal or with elevated IL-6 levels. In summary, circulating IL-6 levels were increased in 23% of 103 patients with advanced cancer, but the frequency of increased IL-6 concentrations was not related to the presence of hypercalcemia or to any marker of calcium metabolism or bone turnover. The pathogenic importance of circulating IL-6 in patients with solid tumors remains to be demonstrated and our data indicate that increased circulating levels of IL-6, possibly reflecting the activation of the immune system, only contribute in a minor way to the osteolytic process in patients with tumor-induced hypercalcemia.

Adult↗
PubMed1994

Treatment of tumour-induced hypercalcaemia with the bisphosphonate pamidronate: dose-response relationship and influence of tumour type.

BACKGROUND: Patients with humoral hypercalcaemia of malignancy appear to respond less well to biphosphonate therapy than hypercalcaemic patients with osteolytic metastases. On the other hand, pamidronate is currently the most potent of the commercially available biphosphonates and it is recommended that its dose be increased as a function of pretreatment calcium levels. PATIENTS AND METHODS: We reviewed our experience with pamidronate in 160 patients with tumour-induced hypercalcemia (TIH) persisting after rehydration, particularly the influence of the dose administered, the tumour type and the presence of bone metastatic involvement on the calcaemic and calciuric response to pamidronate therapy. RESULTS: Serum Ca was normalized in 92% of the cases (87% when Ca was corrected for protein levels). After therapy, 59% of the patients developed asymptomatic hypocalcaemia (30% for Corr. Ca levels). A multiparameter regression analysis revealed that the response to pamidronate was significantly (P < 0.01) influenced by initial Ca levels up to days 5-7 and, thereafter, only by the dose received. To confirm the dose effect, we divided the patients into three groups according to the median dose received, namely 0.5 mg/kg (n = 35), 1.0 mg/kg (n = 52), and 1.5 mg/kg (n = 73). The differences among the three groups became significant (P < 0.05) from days 5-7 until the end of the evaluation (days 22-26). Similarly, the success rate, considering Corr. Ca levels, was 80% for the 0.5 and 1.0 mg/kg groups combined, compared to 94% for the 1.5 mg/kg group (P < 0.05). The duration of normocalcaemia was similarly more prolonged in the high-dose group. There was a dose-response relationship only in patients with Ca levels above 3.0 mmol/L and in patients with an elevated index of tubular calcium reabsorption. By contrast, the decrease in Ca levels and in fasting urinary calcium excretion, a sensitive index of bone resorption, were not significantly influenced by the primary tumour site or by the presence of bone metastatic involvement. CONCLUSIONS: Our data demonstrate a dose-response relationship for pamidronate in TIH over an efficient hypocalcaemic dose range, at least in patients with an elevated tubular calcium reabsorption, which helps to resolve conflicting data in the literature. We suggest that a dose of around 1.5 mg of pamidronate/kg is optimal for the treatment of TIH, except in patients with mild hypercalcaemia, for whom a dose of 1 mg/kg appears to be sufficient. At these dose levels, the efficacy of pamidronate is not significantly influenced by the tumour type or the degree of metastatic bone involvement.

Adult↗
PubMed1993

Circulating PTHrP concentrations in tumor-induced hypercalcemia: influence on the response to bisphosphonate and changes after therapy.

We studied the influence of circulating parathyroid hormone-related protein (PTHrP) concentrations on the response of hypercalcemic cancer patients to bisphosphonate therapy. We also examined the changes in circulating PTHrP levels during the normalization of serum Ca to determine if part of the increase in PTHrP concentrations is not secondary to hypercalcemia itself, as suggested by some in vitro data. We sequentially measured in 45 hypercalcemic cancer patients treated by pamidronate the circulating concentrations of PTHrP (by an amino-terminal RIA; normal values < 9 pmol/liter), Ca, Ca2+, Pi, intact PTH, and the fasting urinary excretion of Ca (Ca/Cr) and cyclic AMP (cAMP). Mean +/- SEM baseline PTHrP levels were 9.5 +/- 1.3, with a median (range) value of 6.0 (< 3.4-43) pmol/liter. PTHrP levels were elevated in 18 of 45 patients, more often in epidermoid than in glandular carcinomas (P < 0.05), and they were significantly (P < 0.05) correlated with the concentrations of Pi (r = -0.46), Ca/Cr (r = -0.31), and urinary cAMP (r = 0.47). Mean pretreatment Ca levels were not significantly different between patients with elevated and patients with normal PTHrP levels, 13.3 +/- 0.4 versus 12.9 +/- 0.4 mg/dl, but the concentrations became significantly different (P < 0.005) 4 days after therapy, 10.2 +/- 0.3 versus 9.2 +/- 0.1 mg/dl, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Medical treatment of tumor-induced hypercalcemia and tumor-induced osteolysis: challenges for future research.

Tumor-induced hypercalcemia (TIH) and tumor-induced osteolysis (TIO) are essentially due to a marked increase in osteoclast-mediated bone resorption. Parathyroid-hormone-like protein plays an essential role in TIH, and maybe in TIO, but other substances, such as growth factors or cytokines, could contribute to the osteoclast activation and osteoblast inhibition secondary to the neoplastic infiltration of the skeleton. Treatment of TIH essentially consists of volume repletion and administration of potent anti-osteolytic drugs. Intravenous administration of the bisphosphonate clodronate or pamidronate is particularly useful for this. Pamidronate at a dose of 1.0-1.5 mg/kg as a single 4- to 24-h infusion can normalize serum calcium in about 90% of hypercalcemic cancer patients. The apparently low response rate of bone metastases to systemic antineoplastic therapy seems essentially to reflect the relative insensitivity of our current methods for assessing response in TIO. Quantitative evaluation of pain and of newly developed biochemical markers of bone turnover could be particularly useful for early assessment of response. Prolonged administration of oral pamidronate could reduce by almost one-half the complications of TIO, and iterative bisphosphonate infusions could induce a dramatic relief of bone pain in one-third and a sclerosis of lytic lesions in one-fourth of the cases. These data must, however, be confirmed in randomized blind trials and many questions remain unanswered concerning the optimal therapeutic schemes. Despite these limitations, medical therapy of TIO by non-cytotoxic means has already become a reality.

Forecasting↗
PubMed1993

Calcitonin: from the determination of circulating levels in various physiological and pathological conditions to the demonstration of lymphocyte receptors.

This article summarizes our main findings concerning calcitonin (CT) physiology and pathology. We have devised a simple extraction method of circulating CT that much improves assay sensitivity and specificity for the measurement of the CT monomer. Combining this extraction method with newer immunometric assays permits a sensitive and exclusive measurement of monomeric CT. CT secretory capacity is 4-5 times lower in women than in men, but there is no significant fall in basal or calcium-stimulated CT levels with age. We also found no evidence for CT deficiency in postmenopausal osteoporosis. On the contrary, changes in circulating CT levels appear to be secondary to the changes in bone turnover, whether in postmenopausal osteoporosis, after estrogen replacement therapy or in renal stone formers. We found a marked CT deficiency after thyroidectomy, radioactive iodine treatment and in patients with congenital hypothyroidism or autoimmune primary hypothyroidism. The deleterious effects of CT deficiency on bone mass remain, however, essentially speculative. Lastly, we have found specific and high-affinity CT receptors on normal circulating T-lymphocytes. Their meaning remains to be demonstrated but we have recently found that the osteolytic cytokines IL-1 and IL-6 are able to markedly reduce the number of CT receptors on T-lymphocytes without changing their affinity.

Aging↗
PubMed1993

Circulating calcitonin levels in healthy children and subjects with congenital hypothyroidism from birth to adolescence.

Using an extraction-concentration technique of circulating calcitonin (exCT) that permits a sensitive and specific assessment of circulating CT monomer levels, we measured exCT levels in 115 healthy children (59 girls and 56 boys), aged 0-16 yr, and 25 patients (15 girls and 10 boys), aged 2 months to 22 yr, with congenital hypothyroidism (CH), a condition characterized by a marked CT deficiency in adults. We found a significant negative correlation between CT levels and age in healthy children (girls, r = -0.83; boys, r = -0.63; P < 0.001). There was a 5-fold decrease in CT levels from the neonatal period to adolescence. The fall in CT levels was particularly marked in early infancy (e.g. for the age category 1 day to 1 yr, 19.0 +/- 1.9 vs. 7.3 +/- 1.2 ng/L for the group 1-5 yr, P < 0.01), but less pronounced thereafter (for the group 5-10 yr, 4.7 +/- 0.8 ng/L; P < 0.001 vs. the group 1 day to 1 yr). The well established sex difference in CT levels in adults was significant only for the age category above 10 yr (2.7 +/- 0.4 ng/L for girls vs. 4.5 +/- 0.7 ng/L for boys, P < 0.05). In patients with CH, the mean exCT level was 2.0 +/- 0.3 ng/L under 3 yr of age (n = 9), whereas all CT values were undetectable after the age of 3 yr, which could contribute to the lower bone mass of adult CH patients. CT values were normal in 3 children with metabolic goiter. In healthy children, our results demonstrate the existence of an age-related decrease in circulating CT levels, which was particularly marked in infancy. The sex difference in CT levels progressively appeared in childhood, but was significant only after 10 yr of age. Such changes in CT levels could be important for neonatal calcium metabolism and contribute to the lower bone mass in females.

Adolescent↗
PubMed1992

Nasal human calcitonin for tumor-induced hypercalcemia.

We treated four hypercalcemic cancer patients by nasal hCT, 3 x 2 mg daily, which has been reported to be active in Paget's disease at lower doses. Only one patient became normocalcemic and mean (+/- SEM) calcium levels fell from 11.6 +/- 0.2 mg/dl before therapy to 10.7 +/- 0.6 mg/dl 2-3 days after starting hCT. The tolerance was excellent but, because of insufficient efficacy, we do not recommend this form of therapy for cancer hypercalcemia.

Adenocarcinoma↗