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PubMed1987

Hypercalcemia of cancer in the digestive tract.

We made a retrospective review of the patients with cancer of the digestive organs who died between January 1, 1975 and December 31, 1985, at Shinshu University Hospital. Of 183 patients with such cancers 15 (8.2%) had hypercalcemia. Hypercalcemia was defined as serum calcium level greater than 11.0 mg/dl on at least two determinations. The incidence of hypercalcemia by site was 5 of 74 (6.8%) liver, 1 of 16 (6.3%) biliary tract, 4 of 33 (12.1%) pancreas, 3 of 15 (20.0%) esophagus, 0 of 37 stomach, 0 of 2 duodenum, 2 of 5 colon, and 0 of 1 rectum carcinomas. There was no sexual or age predisposition to hypercalcemia. Bone scans and/or x-ray results were positive in three of eight, negative in five of eight, and were not evaluated in the remaining seven patients. Of five patients tested, four had low to normal serum parathyroid hormone (PTH) levels, and one had a serum PTH level high by C-terminal assay but normal by N-terminal assay. Serum chloride levels at the late stage of hypercalcemia were less than 102 mEq/L in all patients. Therefore, hyperproduction of PTH was unlikely to be a causative factor for hypercalcemia. Indomethacin was given to four patients with hypercalcemia with no effect on serum calcium levels in any cases. Survival from the diagnosis of hypercalcemia ranged from 2 to 96 days (mean 33 days). We conclude that hypercalcemia is a complication not infrequent at the late stages of cancers of the digestive organs, with the exception of gastric cancer, and a portent of a poor prognosis.

Aged↗
PubMedDate not supplied

Hypercalcemia in children with rhabdomyosarcoma.

PURPOSE: Hypercalcemia complicating malignancy is a serious and frequent occurrence in adults but rare in children. The aim of this study was to determine the incidence, symptoms, outcome, and cause of hypercalcemia in children with rhabdomyosarcoma. PATIENTS AND METHODS: Among 93 children with rhabdomyosarcoma, six with hypercalcemia were identified and their clinical course, pathologic findings, treatment, and outcome were evaluated. In addition, serum and intratumor parathyroid hormone-related protein (PTHrP) concentrations were measured to ascertain the potential of hypercalcemia. RESULTS: All six patients with hypercalcemia had bone metastasis, and four with severe hypercalcemia had multiple bone metastases. Serum PTHrP levels were moderately elevated. There were no significant trends detected based on age, gender, primary site, and pathologic type. All patients achieved transient resolution of hypercalcemia after treatment. However, none survived for a long period of time because their original tumor eventually recurred. CONCLUSIONS: Hypercalcemia is not an uncommon complication in patients with rhabdomyosarcoma. Bone absorption seems to be the predominant factor that induces the hypercalcemia in rhabdomyosarcoma. However, PTHrP may be a powerful stimulator of bone absorption, which contributes to the growth of bone metastasis.

Adolescent↗
PubMed1997

Hypercalcemia stimulates expression of intrarenal phospholipase A2 and prostaglandin H synthase-2 in rats. Role of angiotensin II AT1 receptors.

In chronic hypercalcemia, inhibition of thick ascending limb sodium chloride reabsorption is mediated by elevated intrarenal PGE2. The mechanisms and source of elevated PGE2 in hypercalcemia are not known. We determined the effect of hypercalcemia on intrarenal expression of cytosolic phospholipase A2 (cPLA2), prostaglandin H synthase-1 (PGHS-1), and prostaglandin H synthase-2 (PGHS-2), enzymes important in prostaglandin production. In rats fed dihydrotachysterol to induce hypercalcemia, Western blot analysis revealed significant upregulation of both cPLA2 and PGHS-2 in the kidney cortex and the inner and outer medulla. Immunofluorescence localized intrarenal cPLA2 and PGHS-2 to interstitial cells of the inner and outer medulla, and to macula densa and cortical thick ascending limbs in both control and hypercalcemic rats. Hypercalcemia had no effect on intrarenal expression of PGHS-1. To determine if AT1 angiotensin II receptor activation was involved in the stimulation of cPLA2 and PGHS-2 in hypercalcemia, we treated rats with the AT1 receptor antagonist, losartan. Losartan abolished the polydipsia associated with hypercalcemia, prevented the increase in cPLA2 protein in all regions of the kidney, and diminished PGHS-2 expression in the inner medulla. In addition, losartan completely prevented the increase in urinary PGE2 excretion in hypercalcemic rats. Intrarenal levels of angiotensin II were unchanged in hypercalcemia. These data indicate that hypercalcemia stimulates intrarenal cPLA2 and PGHS-2 protein expression. Our results further support a role for angiotensin II, acting on AT1 receptors, in mediating this stimulation.

Angiotensin II↗
PubMedDate not supplied

Idiopathic hypercalcemia in cats.

Unexplained hypercalcemia has been increasingly recognized in cats since 1990. In some instances, hypercalcemia has been associated with calcium oxalate urolithiasis, and some affected cats have been fed acidifying diets. We studied the laboratory findings, clinical course, and treatment of 20 cats with idiopathic hypercalcemia. Eight (40%) of the cats were longhaired and all 14 cats for which adequate dietary history was available had been fed acidifying diets. Clinical signs included vomiting (6 cats), weight loss (4 cats), dysuria (4 cats), anorexia (3 cats), and inappropriate urinations (3 cats). Hypercalcemia was mild to moderate in severity. and serum parathyroid hormone concentrations were normal or low. Serum concentrations of phosphorus, parathyroid hormone-related peptide, 25-hydroxycholecalciferol, and calcitriol were within the reference range in most cats. Diseases commonly associated with hypercalcemia (eg, neoplasia, primary hyperparathyroidism) were not identified despite thorough medical evaluations and long-term clinical follow-up. Azotemia either did not develop (10 cats) or developed after the onset of hypercalcemia (3 cats), suggesting that renal failure was not the cause of hypercalcemia in affected cats. Seven of 20 cats (35%) had urolithiasis, and in 2 cats uroliths were composed of calcium oxalate. Subtotal parathyroidectomy in 2 cats and dietary modification in 11 cats did not result in resolution of hypercalcemia. Treatment with prednisone resulted in complete resolution of hypercalcemia in 4 cats.

Animal Feed↗
PubMed2001

[Hypercalcemia in the elderly].

UNLABELLED: A COMMON FINDING: Hypercalcemia is not rare among elderly patients. Hyperparathyroidism and neoplasia are the most frequent causes of hypercalcemia in old patients. Symptoms due to hypercalcemia are usually non specific in old subjects, leading to consider easily this diagnosis and to measure plasma calcium level. DIAGNOSIS: Biological diagnosis of hypercalcemia is not always obvious in old patients because of frequently decreased plasma albumin levels leading to lower plasma total calcium level. Thus, it is always necessary to calculate plasma total calcium level corrected by albumin in order not to underestimate hypercalcemia in elderly subjects. PROGNOSIS: The short-term risk of hypercalcemia is acute hypercalcemia, which may be lifethreatening. The long-term risk of hypercalcemia is renal failure. TREATMENT: When hypercalcemia is due to primary hyperparthyroidism, the treatment of choice is surgery. However, for old patients with high surgical risk surgery with local anesthesia or ultrasonically guided percutaneous ethanol injection into parathyroid adenoma can be proposed.

Age Factors↗
PubMed1992

Mechanisms of cancer-induced hypercalcemia.

Cancer-associated hypercalcemia is due to the: (a) elaboration of systemically-acting humoral factors by neoplasms which alter calcium metabolism in bone, kidney, and intestine; or (b) stimulation of bone resorption at sites of tumor metastasis to bone. It is likely that both mechanisms occur in the same patient with certain neoplasms. There are many humoral factors that can be produced by tumors, secreted into the circulation, and have distant effects which induce hypercalcemia. The stimulation of increased osteoclastic bone resorption is a principal feature of humoral hypercalcemia of malignancy, but the kidney also plays an important role. In addition, intestinal absorption of calcium may be a factor in the pathogenesis of hypercalcemia in certain neoplasms. Parathyroid hormone-related protein plays a dominant role in the pathogenesis of HHM. PTHrP alone is able to induce nearly all of the clinical signs of HHM in experimental animals, but other humoral factors, such as cytokines, can interact with PTHrP to contribute to the development of hypercalcemia. Neoplasms which metastasize widely to bone and induce local osteoclastic bone resorption, such as multiple myeloma, also are capable of inducing hypercalcemia. Based upon existing data it is not clear what percentage of neoplasms which metastasize to bone and stimulate local bone resorption also are capable of stimulating hypercalcemia by systemic factors. Future research is needed to delineate the systemic and local factors associated with CAH; to define interactions of humoral factors in the pathogenesis of hypercalcemia; and to investigate the regulation of transcription, translation, modification, and secretion of hypercalcemia-inducing factors in normal and neoplastic tissues.

Animals↗
PubMed1994

Familial benign hypercalcemia--from clinical description to molecular genetics.

Familial benign hypercalcemia (or familial hypocalciuric hypercalcemia), a syndrome of lifelong hypercalcemia inherited as an autosomal dominant trait, is distinct from the multiple endocrine neoplasia syndromes and other forms of inherited parathyroid disease. Familial benign hypercalcemia results from the inappropriate secretion of parathyroid hormone despite hypercalcemia, enhanced renal tubular reabsorption of calcium (independent of parathyroid hormone), and apparent tissue resistance to adverse effects of hypercalcemia. Heterozygosity for the familial hypercalcemia trait is benign, although homozygosity for the trait may lead to severe neonatal primary hyperparathyroidism. Genetic linkage studies show that most persons affected with familial hypercalcemia have a mutation on the long arm of chromosome 3 (3cen-q21), although one phenotypically indistinguishable family appears to have a mutation on the short arm of chromosome 19 (19p), and another family has neither 3q nor 19p mutations. One group has recently shown mutations in a putative parathyroid cell-surface calcium receptor that are plausible causes for the chromosome 3q variant of the familial hypercalcemia syndrome. Perhaps the other genes for this syndrome encode proteins representing hitherto-unknown regulators of systemic calcium metabolism independent of parathyroid cell calcium sensing or proteins involved in signal transduction from the calcium receptor.

Genetic Linkage↗
PubMed1993

[Medical treatment of malignant hypercalcemia].

Hypercalcemia is one of the life-threatening paraneoplastic syndromes and urgent medical treatments are needed since malignant hypercalcemia progresses very rapidly. The intravenous administration of sufficient quantities of isotonic saline sometimes with loop diuretic agents is the first and fundamental step in the management of malignant hypercalcemia. As hormonal therapeutic agents for malignant hypercalcemia, calcitonin and/or glucocorticoid are the usual candidates. Calcitonin exerts calcium-lowering effects both through its direct inhibitory effect on osteoclastic bone resorption and prevention of calcium reabsorption from renal tubulus. Among the anticalcemic agents available, calcitonin has the most rapid onset of action; the hypocalcemic effects appear within a few hours after administration. But continued usage diminishes its effect which is called the "escape phenomenon". The usual dosage of calcitonin is 80-160 unit/day. Glucocorticoid alone has sometimes calcium-lowering effects for malignant hypercalcemia, even in the case of solid cancer such as lung cancer, though the mechanism is not clear. In lymphocytic proliferative disorders, a direct inhibitory effect on the proliferation of malignant cells accounts for the calcium-lowering effects. Glucocorticoid is known to prolong the calcium-lowering effect of calcitonin. So, the combination of calcitonin and glucocorticoid is the most effective hormonal treatment for malignant hypercalcemia. Calcitonin is used for initial several days and glucocorticoid (30-40 mg/day) is continued along with calcitonin from the beginning of the treatment. Most effective and safe hypocalcemic agents for malignant hypercalcemia are the newly developed bisphosphonate compounds, which are not yet available in Japan. These agents interact chemically with hydroxyapatite on the bone surface and prevent osteoclastic function and activity. According to the data of our own investigation, pamidronate, one of the relatively new generation of bisphosphonates, showed clearly hypocalemic effects for malignant hypercalcemia due to various kinds of malignancy by one intravenous administration (30-60 mg) without any adverse effect. In near future, the combination of calcitonin and bisphosphonates will also be the most effective medical management for malignant hypercalcemia in Japan.

Aged↗
PubMed1993

Pathophysiology and management of severe hypercalcemia.

The principal pathophysiologic alteration in severe hypercalcemia accompanying hyperparathyroidism and malignancy is enhanced osteoclastic bone resorption. Hypercalcemia impairs renal mechanisms that lead to sodium and calcium excretion; PTH and PTHrP acting on renal tubules enhance further calcium reabsorption. Although rehydration is often necessary as an initial therapy of hypercalcemia, the cornerstone of therapy is to inhibit osteoclastic bone resorption. The bisphosphonates, plicamycin, gallium, and calcitonin all inhibit osteoclastic bone resorption. Calcitonin is the most rapidly acting agent. Toxicities of calcitonin are minimal, yet its therapeutic efficacy is limited by lack of potency and tachyphylaxis. The second-generation bisphosphonates such as pamidronate represent a class of compounds that are extremely effective in inhibiting the metabolic function of the osteoclast. Given in a single infusion, a significant majority of patients will have normalization of corrected serum calcium lasting, on average, 1-2 weeks. Therapeutic benefit will be of greater duration because most patients remain only minimally symptomatic until corrected serum calcium rises above 11.5 mg/dL. Side effects of low-grade fever, hypophosphatemia, hypomagnesemia, and hypocalcemia may occur. Gallium nitrate is a potent inhibitor of bone resorption and may be of increased clinical value when more efficient administration protocols can be developed. Plicamycin, available for two decades, has cumulative toxicities and is less potent than the aminobisphosphonates. Renal insufficiency often accompanies severe hypercalcemia. The nephrotoxicity of gallium nitrate and plicamycin should preclude their use when there is moderate impairment of renal function, and amino bisphosphonates become the treatment of choice in these patients. Although several authors have advocated individualized approaches to the management of hypercalcemia, the potency and duration of action of the aminobisphosphonates make them a reasonable treatment choice for most patients with symptomatic hypercalcemia. Most importantly, the most effective therapy for hypercalcemia is to recognize and treat the underlying disease. Acute primary hyperparathyroidism requires surgery. The effective treatment of hypercalcemia of malignancy allows the introduction of tumor-specific therapy, limits morbidity, and shortens and deintensifies hospitalization. At times, the most appropriate and compassionate decision (particularly in patients with malignancy who have exhausted all therapeutic options and have relentless bone pain) is to withhold therapy for hypercalcemia. Future therapies directed at the osteoclast, such as more potent later-generation bisphosphonates; inhibitors of osteoclast attachments and inhibitors of peptides, which stimulate osteoclastic bone resorption, may permit safe, easily administered, outpatient therapies that will improve the quality of life for hypercalcemic patients.

Diagnosis, Differential↗
PubMed1995

Hypercalcemia associated with the use of human growth hormone in an adult surgical intensive care unit.

BACKGROUND: The anabolic properties of human growth hormone (HGH) may prove beneficial in critically ill surgical patients. Potential effects of hypercalcemia with HGH therapy have not been addressed for adult patients in the intensive care unit. METHODS: We performed a retrospective review of the past 100 patients treated with HGH in a surgical intensive care unit. Laboratory data, including serum calcium levels, were recorded at baseline and during HGH therapy. Additionally, calcium levels in 27 burn patients receiving HGH were compared with calcium levels in a well-matched group of 27 burn patients not receiving HGH. The incidence and severity of hypercalcemia were recorded, with attention to contributing factors and overall outcome. RESULTS: There was a statistically significant increase in the mean +/- SD serum calcium level with the institution of HGH therapy (2.50 +/- 0.20 mmol/L [10.0 +/- 0.8 mg/dL] before HGH vs 2.74 +/- 0.27 mmol/L [11.0 +/- 1.1 mg/dL] during HGH, P < .05). Before HGH, 14% of the patients had hypercalcemia, defined as a calcium level greater than 2.74 mmol/L (11.0 mg/dL). During HGH, 43% of the patients developed hypercalcemia. Before HGH, no patient exhibited severe hypercalcemia, defined as a calcium level greater than 3.12 mmol/L (12.5 mg/dL). However, during HGH, 10% of the patients developed severe hypercalcemia. Elevations in serum calcium levels were correlated with the duration of HGH therapy and renal dysfunction. Burn patients receiving HGH exhibited significantly higher mean +/- SD calcium levels than controls (2.87 +/- 0.32 mmol/L [11.5 +/- 1.3 mg/dL] vs 2.50 +/- 0.17 mmol/L [10.0 +/- 0.7 mg/dL], P < .001). Studies performed in selected patients demonstrated that alterations in parathyroid function, vitamin D metabolism, and thyroid function did not appear to contribute to this effect. CONCLUSION: Prolonged HGH therapy in critically ill surgical patients may result in severe hypercalcemia, particularly in patients with altered renal function. Possible mechanisms for HGH-induced hypercalcemia include increased intestinal absorption and decreased urinary excretion. Outcome was not adversely affected by this biochemical alteration, but careful monitoring of calcium levels should be undertaken in this population receiving HGH.

Adult↗
PubMed1993

Hypercalcemia complicating childhood malignancies.

BACKGROUND: Hypercalcemia complicating malignancy is a frequent complication in adults, but little has been published about the pathogenesis or the true incidence of hypercalcemia in children with cancer. METHODS: Hypercalcemia developing in childhood malignancies was studied retrospectively at St. Jude Children's Research Hospital to determine its incidence, the timing of its presentation, and its response to therapy. RESULTS: Over a 29-year period, 25 children (median age, 9.5 years) had been diagnosed and treated for hypercalcemia that occurred during the course of their malignancy. These 25 represented 0.4% of the total number of children treated for cancer at the institution during that period. Their malignancies comprised acute leukemias (11; 0.6%), rhabdomyosarcoma (4; 1.2%), malignant rhabdoid tumor (2), Hodgkin disease (1), non-Hodgkin lymphoma (1), hepatoblastoma (2), neuroblastoma (1), brain tumor (1), angiosarcoma (1), and a solid malignant tumor of undetermined type. CONCLUSIONS: Patients with acute lymphoblastic leukemia were more likely to present with hypercalcemia at the time of their initial diagnosis and to achieve resolution of this complication, whereas patients with solid tumors presented with hypercalcemia later in the course of their disease and had hypercalcemia that was more resistant to therapy. In contrast to adults with cancer, hypercalcemia of malignancy is extremely rare in children.

Adolescent↗
PubMed1984

The incidence of hypercalcemia in squamous cell carcinoma of the head and neck.

Hypercalcemia is a well-recognized phenomenon in squamous cell carcinoma of the head and neck, but the incidence of hypercalcemia in this group of patients is not clear. We have reviewed the records of 166 patients with squamous cell carcinoma of the head and neck presented at the Boston VA Medical Center over a 2-year period (October 1981 to September 1983). Hypercalcemia (greater than 11 mg/dl), for which a benign etiology could not be identified, occurred in the clinical course of seven patients (4.2%). Of the hypercalcemic patients, 5/7 (71.4%) had advanced stage IV disease and serum calcium levels ranging from 11.2 to 15 mg/dl at presentation. The incidence of hypercalcemia in this stage IV group was 5/78 (6.4%). On the basis of concomitant serum alkaline phosphatase, x-ray films, and radionuclide bone scans in these patients, bone metastases or a humoral factor were felt to be the etiologic agent. Six of the seven patients died within 77 days of the onset of the hypercalcemia despite vigorous antihypercalcemic and chemotherapeutic measures, and the remaining patient is under chemotherapy at present. We conclude that hypercalcemia is a late manifestation of advanced squamous cell carcinoma of the head and neck and is an ominous prognostic sign. Hypercalcemia without bone metastases is presumably due to the production of ectopic parathormone (PTH)-like substances from the tumor. To control this hypercalcemia, the underlying tumor must be treated vigorously in conjunction with symptomatic treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Herbimycin A, a tyrosine kinase inhibitor, impairs hypercalcemia associated with a human squamous cancer producing interleukin-6 in nude mice.

Interleukin-6 (IL-6) is a multifunctional cytokine that is produced not only by a variety of normal cells but also by cancer cells. IL-6 produced by cancer cells stimulates the proliferation of these cancer cells in an autocrine/ paracrine manner and causes paraneoplastic syndromes including hypercalcemia, cachexia, and leukocytosis. We have reported previously that a human oral squamous cancer associated with hypercalcemia produces large amounts of IL-6, that animals bearing this cancer exhibit elevated levels of plasma IL-6, and that neutralizing antibodies to human IL-6 reverse hypercalcemia in tumor-bearing animals, indicating an important role of IL-6 in the hypercalcemia in this model. Because these cancer cells overexpress epidermal growth factor receptors (EGFR) with intrinsic tyrosine kinase (TK) activity similar to many other squamous cancers, we examined the effects of herbimycin A, a tyrosine kinase inhibitor, on IL-6 production and hypercalcemia in animals bearing this cancer to develop a new approach to treat the hypercalcemia associated with malignancy. Intraperitoneal administration (once a day for 2 days) of herbimycin A to cancer-bearing hypercalcemic mice reduced the plasma levels of human IL-6 and impaired the hypercalcemia. During 2-day treatment with herbimycin A, no changes were observed in tumor size. Of interest, plasma levels of mouse, but not human, soluble IL-6 receptors were also elevated. However, herbimycin A showed no effects on plasma levels of mouse soluble IL-6 receptors. Herbimycin A suppressed the tyrosine autophosphorylation of EGFR and IL-6 mRNA expression and production, all of which were stimulated by EGF. The data raise the possibility that TK inhibitors may be potential mechanism-based therapeutic agents for the treatment of hypercalcemia associated with squamous cancers which overexpress EGFR.

Animals↗
PubMed1990

Incidence and pathophysiology of hypercalcemia.

Hypercalcemia occurs for various reasons in patients with malignant diseases. Most of these patients show a relative increase in bone resorption over bone formation. Increased renal tubular calcium reabsorption is also important for maintaining hypercalcemia in the majority of patients. Calcium absorption from the gut is usually decreased. In a few patients, fixed impairment of glomerular filtration contributes to hypercalcemia. Because the pathophysiology of hypercalcemia is heterogeneous, it may be considered as three separate syndromes: the humoral hypercalcemia of malignancy caused by systemic mediators; the hypercalcemia associated with localized osteolytic disease; and the hypercalcemia associated with myeloma and related hematologic malignancies. Increased bone resorption is a key feature in each of these syndromes. In malignant disease, bone resorption is enhanced because osteoclast activity is increased by the production of humoral mediators. These mediators are often produced by the tumor cells but are also produced by normal host cells that have been activated by the presence of the tumor. some of these mediators of hypercalcemia are systemic factors, but some act only locally. They include parathyroid hormone-related protein, transforming growth factor alpha, lymphotoxin, tumor necrosis factor, interleukin-1 alpha and 1,25-dihydroxyvitamin D.

Animals↗
PubMed1986

Implications of hypercalcemia with respect to diagnosis and treatment of lung cancer.

This study had two objectives. The first was to determine if hypercalcemia presents as an isolated finding in patients with lung cancer prior to the development of abnormalities on chest radiography. The second was to correlate the presence of hypercalcemia with survival after surgical therapy. A review of clinical material over a seven-year period yielded 67 patients with diagnoses of hypercalcemia and lung cancer. No patient presented with surgically curable lung cancer associated with hypercalcemia. A review of the literature disclosed only four cases in which a putative cure occurred in the presence of hypercalcemia. Review of the clinical material and the literature revealed no instance in which hypercalcemia per se led to the diagnosis of clinically occult lung cancer. Hypercalcemia was almost always associated with large tumor masses. Median survival after the discovery of hypercalcemia complicating carcinoma of the lung was one month.

Adenocarcinoma↗
PubMed1989

Three cases of oral squamous cancer associated with leukocytosis, hypercalcemia, or both.

Three examples of malignant neoplasms primary to the oral cavity and associated with paraneoplastic syndromes are presented. The first case is a squamous cell carcinoma of the maxilla associated with leukocytosis. The second case is a mandibular squamous cell carcinoma associated with hypercalcemia in the absence of bony metastases. The third case is a squamous cancer of the tongue that metastasized to the lumbar vertebrae and right second rib and was associated with both hypercalcemia and leukocytosis. There was no evidence of acute infection or leukemia that could be expected to account for leukocytosis. Hypercalcemia in the second case was defined as humoral hypercalcemia of malignancy by biochemical and clinical evaluations. To our knowledge, this is the first definitive report of a carcinoma primary to the oral cavity associated with humoral hypercalcemia of malignancy. In each case, the severity of hypercalcemia, leukocytosis, or both very closely correlated with tumor growth. Surgical excision of the tumors or regression of tumor mass due to aggressive anticancer drug administration resulted in decreases in leukocyte number, serum calcium level, or both. In contrast, recurrence or regrowth of tumors induced further development of hypercalcemia, leukocytosis, or both. It is therefore likely that humoral factors released by these oral carcinomas are responsible for the hypercalcemia, leukocytosis, or both.

Adult↗
PubMed1996

Reversibility of deoxycholate-induced cellular hypercalcemia in rabbit gastric mucosal cells.

BACKGROUND: Bile acid exposure produces cellular hypercalcemia in gastric and hepatic cells. It is not known, however, whether this event contributes to cell injury or if it results from passive equilibration of calcium ion concentrations across the membranes of irreversibly damaged cells. This study was performed to determine whether the cellular hypercalcemia produced by bile acid exposure in gastric cells is reversible and to determine whether the source of this hypercalcemia is from intracellular stores of calcium, extracellular sources, or both. METHODS: Cytosolic free calcium concentrations ([Ca]i) were measured in rabbit gastric mucosal cells that had been loaded with the intracellular probe FURA-2. Measurements were performed in suspensions of dispersed cells by using standard spectrofluorometry and in primarily cultured cells by using fluorescence videomicroscopy. Measurements were made before and after exposure to 0.2, 0.5, and 1.0 mmol/L deoxycholic acid (DC). These measurements were made in the presence of 1 mmol/L extracellular calcium and in the absence of any extracellular calcium (0.5 mmol/L EGTA). RESULTS: In experiments with dispersed cells and spectrofluorometry, [Ca]i increased from a pretreatment level of 194 +/- 8 nmol/L to 396 +/- 21 nmol/L within 3 minutes of exposure to 0.2 mmol/L DC. When these cells were washed and resuspended in DC-free medium, [Ca]i] decreased to 180 +/- 5 nmol/L. In experiments with cultured cells and fluorescence videomicroscopy, rapid, reversible hypercalcemia was observed after exposure to 0.5 and 1.0 mmol/L DC. Removal of extracellular calcium from the incubating medium reduced both the magnitude and duration of the observed hypercalcemia. CONCLUSIONS: These data show that the cellular hypercalcemia that accompanies DC-induced injury in gastric cells is a reversible event. The initial increase in [Ca]i appears to come from both intracellular and extracellular sources, although sustained hypercalcemia requires a source of extracellular calcium. As a reversible event, cellular hypercalcemia may be an important pathophysiologic feature of bile acid induced injury of the upper gastrointestinal tract.

Animals↗
PubMed2001

Hypercalcemia associated with extracorporeal life support in neonates.

BACKGROUND/PURPOSE: Disturbances in calcium homeostasis are common at initiation of extracorporeal life support (ECLS). At the authors' institution many neonates undergoing ECLS have developed hypercalcemia. To determine the frequency of hypercalcemia in neonates during ECLS we performed retrospective chart review of neonates that required ECLS at our neonatal intensive care unit. METHODS: The authors identified 76 consecutive neonates who underwent ECLS before 10 days of age at Cincinnati Children's Hospital Medical Center from July 1, 1991 to June 30, 1996. The hospital charts and ELSO forms were reviewed. Demographic, clinical, and laboratory data for each of the patients were reviewed, both before initiation and during ECLS. Hypercalcemia was defined as total serum calcium concentration of greater than 11 mg/dL (2.74 mmol/L) on at least one occasion beyond the first 24 hours of ECLS. RESULTS: The hospital charts and ELSO forms from 70 patients were available for review. One patient was excluded because he was only on ECLS for 33 hours, and there were no calcium levels obtained after 24 hours of ECLS and until death. Twenty-five (36%) neonates undergoing ECLS had hypercalcemia (serum Ca > 11 mg/dL [2.74 mmol/L]). Hypercalcemia was associated with longer duration of ECLS (hypercalcemia group, 243 +/- 115 hours and normocalcemia group, 139 +/- 64 hours) and greater requirements for platelet transfusions (hypercalcemia group, 538 +/- 282 mL and normocalcemia group, 372 +/- 233 mL). This could not be explained by differences in primary diagnosis, amounts of calcium administered, and acid-base status. CONCLUSIONS: Hypercalcemia was found to be common in neonates that require ECLS and is associated with longer duration of ECLS support. Conservative calcium administration for neonates while on ECLS may be warranted.

Analysis of Variance↗