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

Hyperprostaglandin E syndrome (HPS) is the antenatal variant of Bartter syndrome and characterized by polyhydramnios and preterm delivery in the antenatal period and salt-wasting, isosthenuric or hyposthenuric polyuria, hypercalciuria and nephrocalcinosis in the postnatal period. We report a one-month-old infant with HPS with a 15-year-old sister with Bartter syndrome. The infant's birth weight was 2750 g and she had severe dehydration on the 2nd day of life. She had hypercalcemia, hyponatremia, hypokalemia, metabolic alkalosis and elevated plasma renin and aldosterone levels. We instituted indomethacin therapy accompanied by steroid therapy for hypercalcemia. However, the patient developed abdominal distention on the 30th day, which was due to diffuse pneumatosis in sigmoid colon revealed by a subsequent surgical intervention. Following surgery, the patient developed fever, electrolyte abnormalities and subsequently sepsis. The patient died due to sepsis 10 days after surgery. We conclude that indomethacin and steroid therapy must be used cautiously in infants with HPS.
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PMID:Hyperprostaglandin E syndrome: use of indomethacin and steroid, and death due to necrotizing enterocolitis and sepsis. 1901 56

Hypercalcaemic crisis is a rare endocrine emergency. Often, an acute renal failure develops due to hypercalcaemia-induced polyuria. The molecular causes comprise stimulation of the calcium-sensing receptor in the ascending Henle loop and a reduced aquaporin expression in the collecting ducts. We report on a 54-year-old woman who was admitted for hypercalcaemic crisis and acute renal failure. Immediate rehydratation, bisphosphonate administration, and slow-extended daily dialysis (SLEDD) were initiated leading to a marked reduction of serum calcium. Endocrine work-up revealed primary hyperparathyroidism due to a parathyroid adenoma, which was treated by emergency surgery. Haemodialysis was continued in the first post-operative weeks for prolonged acute renal failure.
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PMID:[Hypercalcaemic crisis and acute renal failure due to primary hyperparathyroidism]. 1918 Apr 12

We retrospectively studied seven children (six girls, one boy) aged from 7.5 to 25 months who presented to our institution after taking large doses of vitamin D (900 000-4 000 000 U) prescribed by medical practitioners for wrong indications like failure to thrive, etc. The clinical manifestations were constipation, decreased appetite, lethargy, polyuria, dehydration and failure to thrive. All patients had hypercalcemia (serum calcium ranging from 12 to 16.8 mg/dl), high 25[OH]D levels (ranging from 96 to >150 ng/ml), suppressed intact parathyroid hormone (ranging from <3 to 8.1 pg/ml). Hypercalciuria (urinary calcium/creatinine ranging from 1 to 2.45) was found in all patients, while nephrocalcinosis was present in five patients. All were treated with intravenous fluids, oral prednisolone, restriction of calcium in diet, while four patients received pamidronate infusion for reducing hypercalcemia.
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PMID:Hypercalcemia due to hypervitaminosis D: report of seven patients. 1933 14

Lithium use in mental diseases has changed over the years but remains a cornerstone of treatment in bipolar disorders. In two companion papers, we have reviewed existing (and especially recent) data on lithium efficacy and updated basic knowledge regarding the practical fundamentals of lithium therapy. The present paper reviews safety data on lithium available to date. Gastrointestinal pain or discomfort, diarrhoea, tremor, polyuria, nocturnal urination, weight gain, oedema, flattening of affect and exacerbation of psoriasis are typical complaints of patients receiving long-term lithium therapy. Renal involvement results in a reduced urinary concentrating capacity, expressed as obligate polyuria, with secondary thirst. With long-term therapy, this may result in nephrogenic diabetes insipidus. In addition, glomerular filtration rate falls slightly in about 20% of patients. The view that only a few patients receiving long-term lithium are at increased risk of glomerular impairment and progressive renal insufficiency should be regarded with caution. The risk is increased in case of concomitant diseases or medications. Lithium treatment may inhibit thyroid hormone release and induce goitre. Consequently, the prevalence of both overt and subclinical hypothyroidism is increased, with circulating thyroid auto-antibodies frequently being found. Much less commonly, thyrotoxicosis may also develop in association with lithium therapy. Long-term lithium treatment may also be associated with persistent hyperparathyroidism and hypercalcaemia, as well as with hypermagnesaemia. Overweight of up to 4-10 kg is found in approximately 30% of lithium-treated patients. Most neurological manifestations are benign, for example, the fine postural and/or action tremor present in 4-20% of patients. This is increased by high caffeine consumption and concomitant use of other psychotropic agents. A number of rare, potentially serious neurological adverse effects have been reported, including extrapyramidal symptoms, 'pseudotumour cerebri' or occasionally cerebellar symptoms. Severe neurological sequelae are exceptional. Cognitive disturbances are often mentioned as a lithium-related adverse effect. The few controlled studies do show a statistically significant negative effect of lithium on memory, vigilance, reaction time and tracking. There are frequent reports of mild effects of lithium on cognition at therapeutic serum concentrations. A number of deaths associated with lithium treatment have been reported. The most serious issue is that of non-accidental overdose, i.e. either long-term overdosage or acute overdose on long-term treatment. Progressive renal insufficiency, an exceptional complication of long-term lithium therapy, may also have a fatal outcome. In relation to pregnancy, lithium salts are rated as category D (positive evidence of risk). Therefore, prescription of lithium should be avoided during the first trimester of pregnancy unless the benefit to the mother exceeds the risk to the fetus. Although lithium transfer into breast milk is well established, the long-term fate of babies breast-fed by mothers receiving lithium therapy is unknown. Whether lithium therapy is safe in breast-feeding women is controversial. Although there is no absolute contraindication, it is known that the kidney is particularly sensitive to lithium just after birth. Intoxication in patients on long-term treatment with lithium in the absence of history of acute ingestion is not rare. Contributing factors include change in daily dose, long-term high dosage, kidney disease or drug interaction. In suspected cases, serum concentrations should be obtained early and repeatedly. In addition to supportive measures, haemodialysis is the treatment of choice for severe cases. Thorough knowledge of the limitations and drawbacks of lithium therapy is mandatory for its optimal use, especially at a time when its risk/benefit profile needs to be compared accurately with that of antiepileptic drugs and other mood stabilizing medications.
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PMID:Lithium: updated human knowledge using an evidence-based approach: part III: clinical safety. 1945 1

Primary hyperparathyroidism is a fairly frequent pathologic diagnosis characterized by hypersecretion of parathyroid hormone, which results from adenomas in 80% to 85% of all cases. At clinical onset, the most common symptoms are hypercalcemia-related and some of them are pain due to kidney stones, polyuria, gastrointestinal, and neurologic disorders, whereas rarer symptoms are due to brown tumors and expansive lesions often found in fibrocystic osteitis. Brown tumors represent the terminal stage of the remodeling processes caused by an increased osteoclastic activity and fibroblastic proliferation during primary or secondary, albeit more seldom, hyperparathyroidism. The manifestation of primary hyperparathyroidism as skeletal disease has nearly disappeared in the last 2 decades. Cases are now most often diagnosed by the coincidental finding of asymptomatic hypercalcemia. Advanced screening techniques have made clinical evidence of bone disease rare. This article contains a case of brown tumor on the maxilla, palate, and mandible in addition to nephrectomy and proximal femur fracture, which are probably associated with primary hyperparathyroidism although less common nowadays. The diagnosis was suggested by the clinical history and confirmed by biochemical, radiologic, and histopathologic evidence. Excision of a parathyroid adenoma normalization of the metabolic status was then realized.
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PMID:Primary hyperparathyroidism presenting as a palatal and mandibular brown tumor. 1988 50

Patients with calcium concentrations above 3 mmol/L typically start to develop symptoms of hypercalcaemia, which can include nausea, vomiting, thirst and polyuria, malaise, confusion, lowered pain threshold and coma. Milder hypercalcaemia (calcium concentrations <3 mmol/L) is often asymptomatic, and the problem is therefore usually discovered as an incidental finding on routine biochemical screening. Primary hyperparathyroidism is a common cause of hypercalcaemia. Here, we consider the recognition and further management of patients presenting with asymptomatic primary hyperparathyroidism in primary care.
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PMID:Managing primary hyperparathyroidism in primary care. 2020 Jan 46

Lithium continues to be the standard for acute and maintenance treatment of bipolar mood disorders despite the availability of alternative agents. Lithium has a narrow therapeutic index and can result in considerable toxicity. Acute renal intoxication is well-known but chronic kidney disease should be in each doctor's mind. The main manifestations are nephrogenic diabetes insipidus (NDI) and tubulointerstitial nephritis. For NDI, the potassium sparing diuretic amiloride or a thiazide diuretic can improve polyuria. Lithium-induced ESRD in chronic tubulointerstitial nephritis is not uncommon and more prevalent (> 1% among long-term lithium patients) than previously thought. The risk of renal failure may persist even after lithium discontinuation. Additional kidney manifestations of lithium exposure include renal tubular acidosis and hypercalcemia.
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PMID:[Lithium and chronic kidney disease: a pathology which remains relevant]. 2034 95

This report describes a primary clitoral adenocarcinoma in a dog with secondary hypercalcemia of malignancy. A 10-year-old, spayed female basset hound was evaluated for a mass protruding from the vulva. The mass was excised, and a histological diagnosis of clitoral adenocarcinoma was made. No evidence of metastasis on thoracic radiographs or abdominal ultrasound was seen. Preoperative hypercalcemia resolved following excision of the mass. Cellular features were similar to an apocrine gland anal sac adenocarcinoma, and immunohistochemistry exhibited features noted with apocrine gland anal sac adenocarcinoma. No further treatment was elected by the owner. Internal iliac lymph-node metastasis was identified 4 weeks postoperatively, and hypercalcemia recurred 8 weeks postoperatively. The dog was euthanized 22 weeks postoperatively for signs related to hypercalcemia, including polyuria/polydipsia, lethargy, and weakness. A necropsy was performed and confirmed the presence of internal iliac lymph-node metastasis. The colon, rectum, and anal sacs were grossly and histologically normal. To our knowledge, this is the first reported case of clitoral neoplasia in the dog.
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PMID:Primary clitoral adenocarcinoma with secondary hypercalcemia of malignancy in a dog. 2043 43

A 13-year-old spayed Labrador Retriever cross dog presented for polyuria and polydipsia. Serum total calcium, free calcium, and intact parathyroid hormone concentrations were elevated. Surgical exploration of the ventral neck revealed a grossly enlarged right external parathyroid gland. The histopathological diagnosis for the excised right parathyroid gland was an incompletely resected parathyroid carcinoma. Parathyroid carcinoma in the dog is an infrequent cause of hypercalcemia and primary hyperparathyroidism.
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PMID:Diagnosing the etiology of hypercalcemia in a dog: a case of primary hyperparathyroidism. 2047 10

An 11-year-old, male, neutered crossbred Collie dog was presented for a history of polydipsia and polyuria. Diagnostic investigations revealed total and ionized hypercalcemia and an increased concentration of parathyroid hormone-related peptide. Abdominal ultrasonography and contrast-enhanced computed tomography of the abdomen revealed a right-sided, cystic-appearing renal mass. Cytological examination of ultrasound-guided aspirates of the mass revealed high numbers of spindle cells. The mass was removed en bloc via an ureteronephrectomy. Histopathological examination of the mass revealed neoplastic spindle cells in loosely packed and interlacing streams within a myxomatous stroma. Immunohistochemical examination with vimentin, von Willebrand Factor, and alpha-smooth muscle actin confirmed the mass to be a renal angiomyxoma. A minority of the neoplastic spindle cells showed positive cytoplasmic parathyroid hormone-related peptide immunostaining. The hypercalcemia resolved following surgery, and the parathyroid hormone-related peptide concentration returned to within the reference interval. The dog was no longer polydipsic or polyuric 1 year following surgery. The present report describes a previously unreported renal neoplasm causing paraneoplastic hypercalcemia and highlights the possibility of paraneoplastic hypercalcemia being caused by a benign neoplasm.
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PMID:Paraneoplastic hypercalcemia in a dog with benign renal angiomyxoma. 2080 42


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