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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Squamous cell carcinoma with hypercalcemia and leukocytosis arising from burn scars in a 45-year-old man is reported. Hypercalcemia and leukocytosis improved with pepleomycin treatment and worsened with recurrence of the tumor. Serum levels of parathyroid hormone, prostaglandin E and 25-OH-Vitamin D were within normal limits. Autopsy did not disclose any bone metastases or abnormalities of the parathyroid glands. It is suggested that hypercalcemia and leukocytosis were due to factors produced by the squamous cell carcinoma. This is the fifth reported case of cutaneous squamous cell carcinoma associated with hypercalcemia in the absence of bone metastasis or parathyroid gland abnormalities.
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PMID:Squamous cell carcinoma with hypercalcemia and leukocytosis. 242 67

Malignancy-related hypocalcaemia has received less attention in the literature than the opposite perturbation, hypercalcaemia. Only, scarce and contradictory data exist about hypocalcaemia associated with bone metastases (BMH). We have reviewed the clinical records of 155 patients with bone metastases of solid tumours, 122 of which were followed during the whole course of the disease until death. The frequency of hypocalcaemia ranged from 5 to 13%, depending on the formula used to correct calcium values for protein concentration. BMH was almost exclusively limited to patients with osteoblastic metastases. The frequency of BMH among patients with prostate carcinoma was 13-27%, depending on the formula used. Only two of 60 patients with lytic bone lesions presented hypocalcaemia, and in both cases it was rather mild. The development of hypocalcaemia did not seem to imply a worse prognosis, at least in patients with carcinoma of the prostate. Thus, the prevalence of BMH appears to be higher than is usually considered. Adequate attention should be given to this disorder because of the potentially deleterious effects on several organ systems.
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PMID:The clinical spectrum of hypocalcaemia associated with bone metastases. 248 31

Atypical carcinoid tumors of the bronchial tree are uncommon. Their tendency to metastasize is well recognized, characteristically producing osteoblastic bone deposits without disturbance of calcium homeostasis. We report two patients who presented with hypercalcemia and osteolytic bone metastases following surgical removal of atypical bronchial carcinoid tumors. In one of the patients, chemotherapy induced remission and controlled the hypercalcemia.
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PMID:Hypercalcemia in atypical bronchial carcinoid tumors. 255 47

A review of 208 cases of surgically treated squamous cell carcinoma of the esophagus revealed 16 (7.7%) with hypercalcemia. There was no evidence of bone metastases in 13 (6.3%) of the patients with hypercalcemia. Pathogenesis of this hypercalcemia without bone metastases was suggested to be multifactorial. Anastomotic leakage and malnutrition because of fasting were the most possible causes of mild hypercalcemia, and moderate to severe hypercalcemia was thought to be due to subclinical and clinical recurrence of the tumor, probably with PTH-like hormonal activity. Overall survival rates in the groups with and without hypercalcemia were 18.2 and 61.7% at the 12th postoperative month and 9.1 and 37.8% at the 24th month, respectively. Thus hypercalcemia is a significant prognostic factor linked to an unfavorable clinical course even in patients with no evidence of bone metastases.
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PMID:Hypercalcemia related to the poor prognosis of patients with squamous cell carcinoma of the esophagus. 259 66

Hypercalcaemia in malignancy is a major clinical problem. It contributes significantly to morbidity and mortality and can present difficult diagnostic and management dilemmas. Direct bony invasion by tumour cells rather than humorally mediated hypercalcaemia is probably the most common cause of malignant hypercalcaemia. Yet even in this situation the mechanism of bone resorption or the reason that the normal homeostatic mechanisms cannot cope with the calcium load are poorly understood. It is likely that the humoral and paracrine factors produced by tumours which result in hypercalcaemia or in osteosclerotic bone metastases, are interposing themselves into the normal regulatory processes and deranging them. Humoral hypercalcaemia of malignancy is an important model for studying these questions, and it also provides some insight into the normal regulation of bone turnover. This review will examine the animal models and human syndromes of malignant hypercalcaemia and show how animal models, although helpful, fail to delineate the relative importance of the various potential humoral factors. A most interesting recent development in this area is the description of a new hormone, the parathyroid hormone-related peptide, which may explain many of the cases of humoral hypercalcaemia of malignancy. It is also a useful model with multiple sites of action within the bone and calcium homeostatic process. The active hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3, may also be involved in a small proportion of cases, but again it is a useful model of some of the factors that may operate. Of considerable interest are the tumour derived factors, such as the transforming growth factors, and the cytokines, such as tumour necrosis factors, interleukins, and haemopoietic colony stimulating factors. Prostanoids are seldom of major importance, but may be important in certain tumour types. Osteosclerotic metastases, although seldom associated with hypercalcaemia, may provide insight into osteoblast regulating factors. Treatment of hypercalcaemia is discussed to show ways in which response to treatment may shed light on underlying pathophysiological mechanisms. Most effective treatments have many potential modes of action, and further study of the interactions of these agents and tumour types may help to unravel some of the enigmas in this human syndrome. The major advances in this complex problem involve the realisation of the necessity of multiple sites of action, including renal calcium handling as well as relative increases in bone resorption and/or intestinal calcium absorption.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypercalcaemia of malignancy. 266 84

The effect of long-term bisphosphonate (APD) treatment on the morbidity from bone metastases in breast cancer patients was studied in a controlled clinical trial. 131 patients were randomized between treatment with APD (300 mg/day orally) or control. Systemic treatment for breast cancer was left to the discretion of the physician. The distribution of cases according to age, receptor status and previous treatment was similar in both groups. Patients were examined at 3-month intervals, while bone scans and radiography of relevant lesions in the skeleton were performed every 6 months. After a median follow-up of 13 months, the morbidity in the treated group was significantly less than in the controls. This concerned the occurrence of hypercalcemia, bone pain and fractures, and the need for radiotherapy of osteolytic lesions. In this interim analysis, APD treatment more than halved the requirement for specific treatment of bone lesions. The treatment is simple and well tolerated at a relatively low dosage. A higher oral dose was precluded due to gastrointestinal toxicity. Because the effect of APD on skeletal morbidity was not complete, efforts should be made to develop more effective and less toxic bisphosphonates.
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PMID:Effect of long-term bisphosphonate treatment on morbidity due to bone metastases in breast cancer patients. 266 67

Bisphosphonates, associated with rehydration, became the treatment of choice of malignant hypercalcemia when it became apparent that these compounds normalized plasma calcium in most cases within a few days and with almost no side effects, and that their effect was prolonged. Dichloromethylene bisphosphonate and aminobisphosphonate, especially APD, were shown to inhibit bone resorption with no noticeable inhibition of bone formation, and were highly effective in the long-term treatment of Paget's disease. APD was used in almost 300 patients with malignant hypercalcemia published in the literature and has been used in the medical clinic at Lausanne for several years. When given to 14 patients with malignant hypercalcemia at the dose of 25 mg/day until plasma calcium became normal for two consecutive days, APD had to be given for 4-11 days, severe hypercalcemia needing longer treatment than mild hypercalcemia (Adami et al. 1982). When given for a fixed period of 6 days, again plasma calcium normalized in all patients, whether APD was given i.v. (30 mg/day, ten patients) or orally (1200 mg/day, ten patients) (Adami et al. 1985). Further shortening of the treatment to one single infusion given over 24 h did not decrease the efficacy, as long as high enough doses were given (Blomqvist 1986). For severe hypercalcemia of above 3.5 mmol/liter 60-90 mg had to be given, while 30-45 mg was sufficient in milder cases (Body 1984). Otherwise, mild, transient, and asymptomatic hypocalcemia could occur. Normalization of plasma calcium went along with clinical improvement, sometimes even with correction of coma. Renal function was improved, even when the initial plasma creatinine levels were up to twice normal. Hypercalcemia could reoccur, but the duration of the effect of APD (1 week to several months) depended among other things on the dose administered. The decrease in plasma calcium was accompanied by a decrease in urinary calcium and hydroxyproline, both showing inhibition of bone resorption. In the case of recurrency, the treatment could be repeated with almost unaltered efficacy, except in end-stage cancer disease. When given to 13 normocalcemic patients with bone metastases from breast cancer, hydroxyproline and urinary calcium again decreased. Bone pains and radiologic signs of metastatic bone resorption also showed significant improvement, although these latter effects could also be explained by the antitumoral treatment, in this uncontrolled open trial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment of tumor-induced osteolysis by APD. 276 65

A 50-year-old male with unresectable hepatocellular carcinoma (HCC) had a hypercalcemic crisis with a serum calcium concentration of 7.8 mEq/zeta, without any evidence for bone metastases or parathyroid lesions. The hypercalcemia was thought to be due to increased renal reabsorption of calcium and increased bone resorption, which was probably caused by humoral factors derived from the HCC, some being parathyroid hormone-like factors. Since conservative therapy for hypercalcemia was not sufficiently effective and was accompanied by progressive exacerbation of ascites and leg edema, transcatheter arterial chemo-embolization (TACE) was performed. On the following day, serum calcium concentration decreased from 6.3 mEq/zeta to the normal range, although serum alpha-fetoprotein levels decreased only slightly. Thereafter hypercalcemia did not develop for about 4 weeks. The results demonstrated that TACE can be effective for humoral hypercalcemia of HCC.
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PMID:Transcatheter arterial chemo-embolization for humoral hypercalcemia of hepatocellular carcinoma. 283 39

An autopsy case of prostaglandin E-producing hepatocellular carcinoma with hypercalcemia is presented in this article. A 72-year-old man showed high serum calcium levels (14.2 to 17.3 mg/100 ml) and hypophosphatemia. The plasma level of immunoreactive parathyroid hormone was below the normal range. Administration of oral indomethacin 50 mg daily was effective in decreasing the serum calcium concentration. However, this effect lasted only 5 days, after which it returned to pretreatment levels. The patient died in a hypercalcemic coma. By an autopsy, hepatocellular carcinoma was found in the right lobe of the liver. However, no obvious bone metastases nor abnormalities in the parathyroid glands were detected. The immunoreactive prostaglandin E level assayed in the neoplastic tissue (2278 ng/g) was significantly high when compared with level in the nonneoplastic liver tissue (194 ng/g). The production of prostaglandin E by the tumor itself appears to be the most likely mechanism for the hypercalcemia in this patient.
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PMID:Prostaglandin-E-producing hepatocellular carcinoma with hypercalcemia. 283 40

The controversial prognostic significance of serum calcitonin in small-cell lung cancer (SCC) prompted this retrospective study relating serum levels to (1) stage of disease [limited disease (LD) vs. extensive disease (ED)], (2) imaging studies of metastases to bone, liver, and brain, and (3) survival. Of the 127 previously untreated patients with SCC presenting from 1979 to 1984, calcitonin levels could be compared to the stage of the disease in 69 patients (25 LD and 44 ED) and to various staging procedures including 99mTc methylene diphosphonate bone scans (63 patients), 99mTc sulfur colloid liver-spleen scans (64 patients), computed tomography of the head (63 patients) and serum calcium (61 patients). 71% (49/69) of patients had elevated calcitonin of whom 65% (32/49) had ED. 29% (20/69) had normal levels of whom 60% (12/20) had ED. 40% (18/45) of patients with raised calcitonin had liver metastases. 100% (19/19) with normal calcitonin had no liver involvement. Two patients with hypercalcemia and increased calcitonin had extensive bony metastases. The survival experiences of patients with normal and elevated serum calcitonin levels were analyzed. No significant differences were found within each stage or in the group overall. The positive correlation of serum calcitonin to liver metastases was statistically significant. No such relationship could be demonstrated with stage of disease, bone metastases, brain metastases, or survival.
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PMID:Imaging studies and the prognostic value of serum calcitonin in staging small-cell lung cancer. 283 15


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