gastrins and Hypocalcemia

Topics: Adrenocorticotropic Hormone; Calcitonin; Calcium; Feedback; Gastrins; Gastrointestinal Hormones; Hypercalcemia; Hypocalcemia; Melanocyte-Stimulating Hormones; Pancreatic Neoplasms; Thyroid Gland; Zollinger-Ellison Syndrome

Topics: Calcium; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Hyperparathyroidism; Hypocalcemia; Injections, Intravenous; Peptic Ulcer

Topics: Animals; Calcitonin; Calcium; Dog Diseases; Dogs; Gastrins; Hormones; Hypercalcemia; Hypocalcemia; Mammals; Parathyroid Glands; Perfusion; Phosphates; Rats; Rodent Diseases; Species Specificity; Stimulation, Chemical; Swine; Swine Diseases; Thyroid Gland

We analyzed gastrin, PTH, and calcitonin responses to oral calcium and peptones in hypocalciuric hypercalcemia, mild primary hyperparathyroidism, and normal controls. We observed diverse hormonal responses that may help in the differential diagnosis of these conditions.. Hypocalciuric hypercalcemia (HH) is consequent to calcium-sensing receptor (CaSR) genetic mutations or anti-CaSR antibodies. CaSR is expressed in parathyroid tissue, thyroid C cells, and gastrin-secreting cells, where it has been suggested that on calcium and/or amino acid allosteric activation, promotes gastrin secretion.. We evaluated gastrin, PTH, and calcitonin responses to oral calcium (1 g) and peptones (10 g) in 10 patients with HH (mean age, 58.5 +/- 10.3 years; F/M = 9/1), 15 patients with primary hyperparathyroidism (PH; mean age, 60.4 +/- 8.3 years; F/M = 11/4), and 30 healthy controls (mean age, 60.3 +/- 8.1 years). Statistical analyses for differences during oral loading tests were calculated with ANOVA for repeated measurements and comparisons between two groups were performed with Student's t-test.. PTH response to peptones was markedly increased in patients with PH compared with flat responses in controls and HH patients (p < 0.05). Gastrin increase after oral calcium was absent in HH and PH subjects (p < 0.05 versus controls), and gastrin responses to peptones were blunted in HH and PH subjects compared with controls (p < 0.05). PTH drop and calcitonin increase after calcium load observed in controls were absent in HH and PH subjects (p < 0.05).. The marked difference in PTH response elicited by peptones observed in PH compared with subjects with HH may help in the differential diagnosis of these conditions without genetic studies. Peptones may stimulate CaSR-controlled hormones as an allosteric regulatory pathway. CaSR abnormalities may help to explain the different calcium- and peptones-induced hormonal responses observed in PH and HH compared with normal subjects.

Topics: Aged; Calcitonin; Calcium; Diagnosis, Differential; Female; Gastrins; Humans; Hyperparathyroidism; Hypocalcemia; Male; Middle Aged; Parathyroid Hormone; Peptide Hormones; Peptones

Our previous study revealed that the gastric vagus nerve plays an etiologic role in immobilization (IMB) stress-induced hypocalcemia. The purpose of the present study is to identify exactly what parts of the stomach are involved in the development of IBM-induced hypocalcemia and to determine whether or not gastric acid secretion is involved. A total gastrectomy, but not a resection of the upper intestine, eliminated the hypocalcemic effect of IMB. In addition, either an antrectomy (removal of the source of gastrin) or a fundectomy (depriving the origin of gastric histamine and gastric acid) was sufficient for eliminating IMB-induced hypocalcemia, while a partial (50%) fundectomy failed to suppress it. An intraperitoneal injection of galanin (an inhibitor of gastrin release) or ranitidine (a blocker of histamine H2-receptor) also suppressed the calcium-lowering effect of IBM, whereas omeprazole (an inhibitor of the proton pump) had no effect. These findings suggest that the antrum and the fundus of the stomach play essential roles in IMB-induced hypocalcemia through the vagus-induced release of gastrin and histamine but not through the secretion of gastric acid per se.

Topics: Animals; Female; Gastrectomy; Gastric Fundus; Gastrins; Histamine H2 Antagonists; Hypocalcemia; Immobilization; Intestines; Ion Pumps; Omeprazole; Protons; Pyloric Antrum; Rats; Rats, Inbred Strains; Rats, Wistar; Stomach

The involvement of the parasympathetic nervous system in the etiology of stress-induced hypocalcemia was investigated in the rat. Atropine methyl bromide (0.1 and 0.6 mg/kg ip) given 20 min before immobilization (IMB) was observed to suppress the induction of hypocalcemia in a dose-dependent manner. A vagotomy of the bilateral cervical trunks also abolished the IMB-induced hypocalcemia. A vagotomy on either the thyroid/parathyroid branches or the celiac branches had no effect on the IMB-induced hypocalcemia, but a vagotomy on the gastric branches completely abolished it. Pretreatment with either secretin (2 and 6 micrograms/kg ip), an inhibitor of gastrin release, or cimetidine (5 and 10 mg/kg ip), a histamine H2-receptor antagonist, diminished the IMB-induced hypocalcemia. The concentration of serum gastrin increased significantly during IMB. It is thus concluded that the decreased levels of plasma calcium caused by IMB are due to the activation of the vagus innervating the stomach. Gastrin and histamine are also involved as a consequence of the activation of the vagus.

Topics: Animals; Atropine Derivatives; Cimetidine; Female; Gastrins; Hypocalcemia; Immobilization; Rats; Rats, Inbred Strains; Rats, Wistar; Secretin; Stomach; Vagus Nerve

To study Ca metabolism in critically ill children, we measured ionized Ca (Ca2+), parathyroid hormone (PTH), calcitonin, 25 hydroxycholecalciferol (25[OH] D3), 1-25 dihydroxycholecalciferol (1-25[OH]2D3, and gastrin levels in critically ill children and in healthy controls. Patients were considered hypocalcemic if Ca2+ was less than 1.1 mmol/L. Six (14%) of 45 patients were hypocalcemic. Five hypocalcemic patients were studied and were found to have higher calcitonin levels than normocalcemic patients and healthy controls and higher PTH levels than healthy controls. 25(OH)D3 and 1-25(OH)2D3 were not significantly different in the three groups of patients. Gastrin levels were low in critically ill patients, whether or not they were hypocalcemic. We conclude that hypocalcemia occurs frequently in critically ill children. It is associated with raised levels of calcitonin and PTH. The mechanism for the increase in calcitonin is unknown.

Topics: Acute Disease; Adolescent; Calcifediol; Calcitonin; Calcitriol; Calcium; Child; Gastrins; Humans; Hypocalcemia; Parathyroid Hormone; Radioimmunoassay

Gastrin-17 induces hypocalcemia in the rat without stimulating calcitonin release. The gastrin-induced hypocalcemia persisted after thyroparathyroidectomy or parathyroidectomy. In contrast, gastrectomy or extirpation of the acid-producing part of the stomach prevented the hypocalcemic effect, suggesting the involvement of the proximal stomach in the gastrin-evoked lowering of blood calcium. The drop in blood calcium upon injection of gastrin-17 did not reflect a loss of calcium via the gastric juice or via the urine. Extracts of the acid-producing mucosa of the rat stomach had a hypocalcemic effect. The extracts were purified by gel chromatography and reversed-phase high-performance liquid chromatography. Digestion with leucine aminopeptidase destroyed the hypocalcemic activity, while trypsin had no effect, suggesting a peptide (or peptides) with an unprotected NH2 terminus and without basic amino acid residues (or with protected basic amino acids). Both gastrin-17 and the mucosal extract stimulated the uptake of 45Ca into bone (radius and sternum). Gastrin-17 was without effect in rats that had undergone gastrectomy, while the mucosal extract was equally effective in gastrectomized and unoperated rats. We suggest that the effects of gastrin-17 on blood calcium and on calcium transfer into bone are indirect and that gastrin-17 stimulates the release of a peptide hormone, tentatively named gastrocalcin, from the acid-producing mucosa of the stomach. Gastrocalcin stimulates the uptake of 45Ca into bone, thereby causing hypocalcemia.

Topics: Animals; Bone and Bones; Calcium; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Hypocalcemia; Male; Peptides; Rats; Rats, Inbred Strains

In 64 maternal-infant pairs, we tested the hypotheses that serum calcitonin, serum gastrin, and plasma glucagon concentrations are elevated in infants at risk for early neonatal hypocalcemia, and that elevated serum gastrin and plasma glucagon result in elevated serum calcitonin and low serum calcium values in neonates. Serum Ca declined significantly in neonates at 24 hours of age, and was inversely correlated with serum calcitonin. Cord serum calcitonin, gastrin, and plasma glucagon concentrations rose significantly at 24 hours of age. Cord calcitonin was significantly higher in preterm compared with term infants, and there was no significant difference between asphyxiated and nonasphyxiated preterm neonates; in term neonates cord calcitonin concentration was inversely correlated with Apgar scores at 1 and 5 minutes. Cord calcitonin was not correlated with cord gastrin or glucagon. Cord and 24-hour gastrin and glucagon values were not related to prematurity; cord glucagon, but not gastrin, was related to birth asphyxia. We conclude that (1) serum calcitonin, gastrin, and plasma glucagon values rise postnatally; cord calcitonin is elevated in preterm and in asphyxiated term infants; serum calcitonin concentration does not correlate with the elevated serum gastrin and plasma glucagon values; and at 24 hours of age, decreased serum Ca is correlated with serum calcitonin, and hence calcitonin might play a role in the pathogenesis of early neonatal hypocalcemia.

Topics: Apgar Score; Asphyxia Neonatorum; Calcitonin; Fetal Blood; Gastrins; Gestational Age; Glucagon; Humans; Hypocalcemia; Infant, Newborn; Minerals; Prospective Studies

The hypocalcaemic action of ethanol (3 g/kg body weight) was investigated in intact, thyroparathyroidectomized and antrectomized rats. It was found that ethanol administered either intraperitoneally or orally reduced plasma calcium concentrations within 30 min and that this response lasted for 8 h. Additional studies performed in antrectomized and thyroparathyroidectomized rats indicated that neither gastrin nor the hormones parathormone and calcitonin had any effect on the hypocalcaemic effect of ethanol. Investigation of the mechanism of action of ethanol-induced hypocalcaemia involved measurements of calcium efflux from and influx into the plasma pool. Ethanol did not have any effect on the disappearance from plasma of 45Ca administered intravenously at 0 min. In contrast, ethanol was found to enhance the disappearance of 45Ca administered intraperitoneally 17 h prior to the experiment. The interpretation of 45Ca studies was discussed and it was concluded that ethanol-induced hypocalcaemia resulted from a decrease in calcium influx into the plasma. Additional in vitro studies did not indicate the suppressive action of ethanol on the release of calcium from tibias. In conclusion, our results show that the mechanism of hypocalcaemia caused by ethanol is the suppression of calcium release from some tissue(s) into the plasma.

Topics: Animals; Bone and Bones; Calcitonin; Calcium; Ethanol; Female; Gastrins; Hypocalcemia; In Vitro Techniques; Parathyroid Glands; Pyloric Antrum; Rats; Rats, Inbred F344

The hypocalcemia effect of gastrin and the possible role of the hormone in calcium homeostasis have been demonstrated in our previous study. The mechanism involves neither the gastrointestinal absorption nor the removal of calcium from plasma but is possibly due to the suppression of the calcium influx into blood. In searching for the organ(s) involved in the action of gastrin, the following were tested and not found to be directly responsible: stomach, intestine, pancreas, liver, spleen, adrenal gland, kidney, lung, muscle, and red blood cell. After 17 hr of 45Ca administration, the turnover of 45Ca in the tibia was measured. Gastrin was found to suppress the release of 45Ca by 25% within 1 hr. The suppressive effect of gastrin on 45Ca release was also demonstrated in an in vitro preparation which showed that the 45Ca released from prelabeled tibia into the incubating medium was also reduced by gastrin. It was thus concluded that the gastrin-induced hypocalcemia in rat was the result of a suppression of the release of calcium from bone.

Topics: Animals; Bone and Bones; Calcium; Female; Gastrectomy; Gastrins; Hypocalcemia; Intestines; Nephrectomy; Pancreatectomy; Rats; Splenectomy

Oral calcium supplements (80 mg/kg per 24 h) were given to 23 preterm infants, and the course of serum calcium, magnesium, immunoreactive calcitonin, and gastrin was compared with a control group of 23 matched infants. In the supplemented group, serum calcium concentrations remained at the baseline level (2.31 mmol/l +/- 0.18 SD) while a fall (from 2.27 +/- 0.18 to 1.91 +/- 0.24 mmol/l) was observed at 12-16 hours of age in the control group, with 4 values < 1.75 mmol/l. There was no change in serum magnesium concentration in either group. The postnatal rise of serum immunoreactive calcitonin concentrations in the control group (from 171 +/- 135 to 493 +/- 273 pg/ml at 12-48 hours of age) was not found in the supplemented group. There was a negative correlation between serum calcium and immunoreactive calcitonin levels in the control group, but not in the supplemented group. There was no correlation between serum immunoreactive calcitonin and gastrin concentrations. These data show that oral calcium supplementation can prevent early neonatal hypocalcaemia, and suggest that this effect is achieved at least in part through a reduction of the postnatal rise of serum immunoreactive calcitonin.

Topics: Calcitonin; Calcium; Food, Fortified; Gastrins; Humans; Hypocalcemia; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature; Magnesium

The influence of restraint stress on serum calcium (Ca) and phosphate was studied in normal and thyroidectomized rats. In addition the response of gastric stress ulcer index, blood gastrin and glucagon to exogenous Ca was investigated. In intact as well as in thyroidectomized animals serum total, ionised and previously injected radioactive Ca decrease during an 8h stress period, whereas inorganic phosphate increases. Together with a constant specific activity these findings are consistent with hypoparathyroidism and calcitonin independent hypocalcemia during stress. Intragastric infusion of 45 mg/kg Ca-gluconate per 8h proves to be a potent anti-stress ulcer regimen in intact and neck-sham operated, but not in thyroidectomized rats without and with additional adrenal demedullation. Gastrin and glucagon were not correlated with calcemia during either stress alone or stress combined with intragastric Ca infusion. It is suggested that the development of gastric stress ulcerations can be prevented by a Ca-mediated release of endogenous calcitonin.

Topics: Adrenal Medulla; Animals; Calcitonin; Calcium; Calcium Carbonate; Calcium Gluconate; Gastrins; Hypocalcemia; Lactates; Male; Rats; Restraint, Physical; Stomach Ulcer; Stress, Physiological; Thyroidectomy

Topics: Animals; Bile; Calcium; Female; Gastric Juice; Gastrins; Hypocalcemia; Parathyroid Glands; Rats; Thyroid Gland

Calcium excretion from rat intestine was measured by placing distilled water in an intestinal loop in situ and measuring the calcium content after various intervals. More calcium was excreted from the intestine of 18-month-old rats than that of 1-month-old rat. Acute hypocalcemia failed to change the intestinal calcium excretion significantly. Parathyroidectomy decreased intestinal calcium excretion and administration of Parathyroid Extract reversed it. Renal damage produced by injection of Na-sulfacetylthiazole increased the intestinal calcium excreation but dihydrotachysterol reversed it. Gastrin at 200 microng/kg increased the intestinal calcium excretion. Calcium excretion, like calcium absorption, appears to be controled by various endocrine factors and the method of intestinal loop in situ appears to be useful to study the part played by these factors.

Topics: Animals; Calcium; Dihydrotachysterol; Gastrins; Hypocalcemia; Intestinal Mucosa; Male; Parathyroid Glands; Parathyroid Hormone; Rats; Thiazoles

The AA., on the basis of their recent studies, offer a new hypothesis on the role of calcitonin, as a regulator of phosphorus metabolism. In addition the AA. confirm the clear interrelationship between calcitonin and other hormones as gastrin and autonomous nervous system.

Topics: Autonomic Nervous System; Calcitonin; Calcium; Ethanol; Gastrins; Humans; Hypocalcemia; Insulin; Insulin Secretion; Kidney Diseases; Phosphorus; Propranolol

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.

Topics: Acute Disease; Calcitonin; Gastrins; Glucagon; Homeostasis; Hypocalcemia; Magnesium; Pancreas; Pancreatitis; Parathyroid Hormone; Phosphorus; Prospective Studies; Triglycerides

Topics: Animals; Calcium; Depression, Chemical; Gastrins; Humans; Hypocalcemia; Male; Parathyroid Glands; Rats; Swine; Thyroid Gland

Topics: Animals; Gastric Mucosa; Gastrins; Glucagon; Hypocalcemia; Male; Oxygen; Rats; Regional Blood Flow; Stomach Ulcer; Stress, Physiological

Topics: Animals; Atropine; Calcium; Electric Stimulation; Gastrins; Hypocalcemia; Injections, Intravenous; Phosphorus; Sheep; Vagus Nerve

It is suggested that there are two hormonal syndromes associated with noninsulin-secreting islet cell tumours and this case is an example of the non-gastrin-secreting type with watery diarrhoea and hypokalaemia. The patient had histamine-fast achlorhydria and a normal gastric biopsy and no gastrin was recovered from the tumour tissue. The watery diarrhoea was isosmotic with plasma and was increased by an intravenous saline load. There was a dramatic response to steroids.

Topics: Achlorhydria; Adenoma, Islet Cell; Aldosterone; Cortisone; Dexamethasone; Diarrhea; Feces; Gastrins; Humans; Hypocalcemia; Hypokalemia; Neoplasms; Pancreatic Neoplasms; Potassium; Prednisone; Sodium; Surgical Procedures, Operative; Urine; Water-Electrolyte Balance; Zollinger-Ellison Syndrome