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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcemia is a rare complication of chronic lymphocytic leukemia (CLL), mostly seen in the context of advanced disease, for which different pathogenetic mechanisms have been postulated. A CLL patient who developed hypercalcemia in the setting of Richter's syndrome is reported. She was a 69-year old woman with stage B (II) CLL of 28-month duration, who presented with mental confusion, anorexia, vomiting, and diffuse bone pain, with hypercalcemia being subsequently found. A lymph node biopsy demonstrated evolution of CLL into Richter's syndrome. Serum levels of parathyroid hormone (PTH), PTH-related peptide and several cytokines were normal. The hypercalcemia initially responded to conventional treatment and chemotherapy, but it reappeared coincidentally with disease progression and the development of osteolytic lesions. Richter's syndrome should be kept in mind in CLL patients with hypercalcemia.
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PMID:Hypercalcemia in a patient with chronic lymphocytic leukemia evolving into Richter's syndrome. 917 22

Primary hyperparathyroidism (PHP) is an infrequently diagnosed disorder in cats. In this report the signs and symptoms of two cats with hypercalcaemia due to PHP are described, together with diagnostic approach, results of treatment, and immunohistochemical findings. A 9-year-old and a 13-year-old neutered male domestic shorthair cat were presented with signs of lethargy, anorexia, and vomiting. Both cats had persistent hypercalcaemia and normo- to hypophosphataemia. Cytological examination of a fine-needle aspiration biopsy sample of a palpable cervical mass revealed groups of benign glandular-epithelial cells in one cat. In the other cat no cervical mass was palpable. In this cat plasma parathyroid hormone (PTH) levels were measured repeatedly and these values exceeded the maximum reference value on two occasions. Following exclusion of other causes of hypercalcaemia both cats were subjected to neck surgery and in both a solitary parathyroid adenoma was removed. The adenomas contained an abundance of PTH, as demonstrated by immunohistochemical techniques. Plasma calcium and phosphate concentrations returned to within, reference ranges postoperatively. Recovery was uncomplicated and there were no signs of recurrence on follow-up examinations.
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PMID:Primary hyperparathyroidism in two cats. 922 38

The objective of the study was to evaluate the phosphate-binding efficacy, side effects, and cost of therapy of calcium ketoglutarate granulate as compared with calcium carbonate tablets in patients on chronic hemodialysis. The study design used was a randomized, crossover open trial, and the main outcome measurements were plasma ionized calcium levels, plasma phosphate levels, plasma intact parathyroid hormone (PTH) levels, requirements for supplemental aluminum-aminoacetate therapy, patient tolerance, and cost of therapy. Nineteen patients on chronic hemodialysis were treated with a dialysate calcium concentration of 1.25 mmol/L and a fixed alfacalcidol dose for at least 2 months. All had previously tolerated therapy with calcium carbonate. Of the 19 patients included, 10 completed both treatment arms. After 12 weeks of therapy, the mean (+/-SEM) plasma ionized calcium level was significantly lower in the ketoglutarate arm compared with the calcium carbonate arm (4.8+/-0.1 mg/dL v 5.2+/-0.1 mg/dL; P = 0.004), whereas the mean plasma phosphate (4.5+/-0.3 mg/dL v 5.1+/-0.1 mg/dL) and PTH levels (266+/-125 pg/mL v 301+/-148 pg/mL) did not differ significantly between the two treatment arms. Supplemental aluminum-aminoacetate was not required during calcium ketoglutarate treatment, while two patients needed this supplement when treated with calcium carbonate. Five of 17 (29%) patients were withdrawn from calcium ketoglutarate therapy within 1 to 2 weeks due to intolerance (anorexia, vomiting, diarrhea, general uneasiness), whereas the remaining 12 patients did not experience any side effects at all. The five patients with calcium ketoglutarate intolerance all had pre-existing gastrointestinal symptoms; four of them had received treatment with cimetidine or omeprazol before inclusion into the study. Calculations based on median doses after 12 weeks showed that the cost of the therapy in Denmark was 10 times higher for calcium ketoglutarate compared with calcium carbonate (US$6.00/d v US$0.65/d). Calcium ketoglutarate may be an effective and safe alternative to treatment with aluminum-containing phosphate binders in patients on hemodialysis who are intolerant of calcium carbonate or acetate because of hypercalcemia. However, care must be exercised when dealing with patients with pre-existing gastrointestinal discomfort. Due to the high cost of the therapy, calcium ketoglutarate should be used only for selected patients.
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PMID:Randomized crossover study comparing the phosphate-binding efficacy of calcium ketoglutarate versus calcium carbonate in patients on chronic hemodialysis. 946 96

A previously well 70 year old woman was admitted to hospital following a three day history of vomiting and confusion. Her serum calcium was 6.58 mmol/l, phosphate 1.09 mmol/l, and alkaline phosphatase 91 iu/l. The mechanism of this hypercalcaemia was not obvious as there was no evidence of a primary malignancy, lymphadenopathy or hepatosplenomegaly. The calculation of indices of urinary excretion of calcium and phosphate suggested the presence of excessive parathyroid hormone (PTH) activity as the mechanism of hypercalcaemia. Plasma intact PTH, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol were not raised suggesting the presence of PTH related peptide (rP). This led to a systematic search for a malignancy, which revealed the presence of a high grade B cell non-Hodgkin's lymphoma confined to the bone marrow. Plasma PTH-rP was subsequently shown to be raised confirming the interpretation of the initial urinary and calcium excretion indices. This case highlights the value of standard laboratory measurements such as urinary calcium and phosphate excretion in cases of hypercalcaemia of obscure aetiology, which can complement measurements of PTH and other calcitropic hormones.
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PMID:Value of assessing parathyroid hormone-like activity in a case of extreme hypercalcaemia. 965 76

In 1990 Scopinaro's technique of biliopancreatic diversion with distal gastrectomy (DG) and gastroileostomy was modified. A sleeve gastrectomy with duodenal switch (DS) was used instead of the distal gastrectomy; and the length of the common channel was made 100 cm instead of 50 cm. A questionnaire and a prescription for blood work were sent to 252 patients who underwent DG a mean 8.3 years ago (range 6-13 years) and 465 patients who underwent DS 4.1 years ago (range 1.7-6.0 years). The questionnaire response rate was 93%, and laboratory work was completed for 65% of both groups. The mean weight loss after DG was 37 +/- 21 kg and after DS 46 +/- 20 kg. There were fewer side effects after DS: The number of daily stools was lower (p < 0.0002), as was the prevalence of diarrhea (p < 0.01), vomiting (p < 0.001), and bone pain (p < 0.001). Greater benefits related to several aspects of life were reported after DS than DG (p < 0.0001). The mean serum levels of ferritin, calcium, and vitamin A were higher (p < 0.001), and parathyroid hormone was lower. The yearly revision rate for excessive malabsorption was 1.7% per year after DG and 0.1% per year after DS. The two procedures were equally efficient for treating co-morbid conditions such as diabetes, hypertension, and hypercholesterolemia. Biliopancreatic diversion with sleeve gastrectomy/duodenal switch and a 100-cm common limb was shown to produce greater weight loss with fewer side effects.
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PMID:Biliopancreatic diversion with duodenal switch. 971 20

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

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.
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PMID:Idiopathic hypercalcemia in cats. 1111 Mar 84

Current treatment of secondary hyperparathyroidism in chronic kidney failure with calcium and active vitamin D is potentially limited by hypercalcemia and hyperphosphatemia. AMG 073 represents a new class of compounds for the treatment of hyperparathyroidism known as calcimimetics, which reduce parathyroid hormone (PTH) synthesis and secretion by increasing the sensitivity of the parathyroid calcium-sensing receptor (CaR) to extracellular calcium. The current study evaluates the efficacy and safety of AMG 073 when added to conventional treatment of secondary hyperparathyroidism in end-stage renal disease (ESRD). Seventy-one hemodialysis patients with uncontrolled secondary hyperparathyroidism, despite standard therapy with calcium, phosphate binders, and active vitamin D sterols, were treated in this 18-wk, dose-titration study with single daily oral doses of AMG 073/placebo up to 100 mg. Changes in plasma PTH, serum calcium, serum phosphorus, and calcium x phosphorus levels were compared between AMG 073 and placebo groups. Mean PTH decreased by 33% in the AMG 073 patients compared with an increase of 3% in placebo patients (P = 0.001). A significantly greater proportion of AMG 073 patients (44%) had a mean PTH < or = 250 pg/ml compared with placebo patients (20%; P = 0.029). Also, a significantly greater proportion of AMG 073 patients (53%) had a decrease in PTH > or =30% compared with placebo patients (23%; P = 0.009). Calcium x phosphorus levels decreased by 7.9% in AMG 073 patients compared with an increase of 11.3% in placebo patients (P = 0.013). Adverse event rates were low and mostly mild to moderate in severity; however, the incidence of vomiting was higher in AMG 073 patients. In this study, the calcimimetic AMG 073 at doses up to 100 mg for 18 wk provided a safe and effective means to attain significant reductions in PTH and calcium x phosphorus levels in ESRD patients. AMG 073 represents a novel and promising therapy to improve the management of secondary hyperparathyroidism.
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PMID:The calcimimetic AMG 073 as a potential treatment for secondary hyperparathyroidism of end-stage renal disease. 1259 92

Primary hyperparathyroidism is a life-threatening rare disorder. It is seen as a result of neonatal primary hyperparathyroidism, familial hypocalciuric hypercalcemia, increased vitamin D levels and inactivation of calcium sensing receptor mutations. The clinical findings are hypotonia, bone demineralization, hypercalcemia and parathyroid hyperplasia. We present a six-month-old female patient, the first child of nonconsanguineous parents, who was referred for the investigation of failure to thrive, vomiting, constipation, fever, abdominal distention and hypotonia. Physical examination revealed weight under 3rd percentile, height 3rd-10th percentile, decreased subcutaneous fat, and distention of the abdomen. In neurological examination, hypotonia, motor-mental retardation, and active deep tendon reflexes were found. The biochemical values at the time of admission revealed primary hyperparathyroidism. Since hypercalcemia did not respond to calcitonin therapy and due to the mortality of hypercalcemia, parathyroidectomy was performed. Because hyperparathyroidism and hypercalcemia continued, angiography was done which revealed increased parathyroid hormone levels in the periphery of the innominate vein. Exploratory surgery followed, but hyperparathyroidism and hypercalcemia persisted after all of these procedures. Calcium-sensing receptor mutations and supernumerary gland were considered. Because hypercalcemia persisted, pamidronate therapy was initiated on a monthly basis.
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PMID:Persistent elevated serum levels of intact parathyroid hormone after reoperation for primary hyperparathyroidism and after pamidronate therapy. 1469 11

A 12-year-old girl was admitted to ward because of persistent left flank pain, vomiting, and hematuria. A stone was located at the ureteropelvic junction of the left kidney, as determined by means of abdominal sonography. Metabolic investigation for a renal stone revealed that she had hypercalcemia, hypophosphatemia, and hypercalciuria. Hyperparathyroidism was diagnosed based on the hypercalcemia and inappropriately elevated serum parathyroid hormone level. A parathyroid adenoma was successfully diagnosed by using thallium/technetium subtraction parathyroid scanning. Extracorporeal shock wave lithotripsy was performed to treat the renal stone, and the parathyroid adenoma was successfully removed. The patient's postoperative course was uneventful. This case is presented because urolithiasis and hyperparathyroidism are rare in children. Metabolic evaluation is mandatory in children with a renal stone. Further investigation for the hyperparathyroidism should be performed if hypercalcemia associated with hypercalciuria is documented.
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PMID:Urolithiasis and primary parathyroid adenoma: report of one case. 1498 62


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