Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report an unusual case of congenital leukemia with leukemia cutis (LC) and diffuse calcinosis cutis. A newborn girl presented with widespread dusky red and yellowish cutaneous nodules and papules. Bone marrow morphology was consistent with the diagnosis of acute monocytic leukemia of the FAB M5 type. Skin biopsy specimens confirmed the presence of a leukemic infiltrate and revealed calcium salt deposition in the papillary and reticular dermis. Calcinosis was diffuse in the whole skin but spared other organs. Vascular calcification was not present. Serum calcium levels oscillated between 2.5 and 2.86 mmol/l, and phosphorus, parathyroid hormone and 25-hydroxyvitamin D(3) levels were normal. There were diffuse osteoporosis and spontaneous fractures of small tubular bones. The patient responded to chemotherapy but, following consolidation treatment, developed sepsis and died at 120 days of age. Congenital leukemia is rare and LC is uncommon. Hypercalcemia may be a complication of leukemia, which leads to multiorgan metastatic calcification. Despite the absence of frank hypercalcemia, the presence of bone lesions suggests that the patient's calcinosis cutis was of the metastatic type. However, the cutaneous leukemic infiltrate may also represent a triggering factor for calcium deposition in the skin.
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PMID:Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis. 1077 6

The extracellular fluid is a metastable system with regard to calcium and phosphate ions. Active inhibitors of calcification must be present in serum to prevent the spontaneous formation of Ca2+.Pi solid phases which could otherwise precipitate to cause renal calcinosis and block small blood vessels. alpha 2-HS glycoproteins/fetuins, AHSGs, are ideal candidates for this function. AHSGs are ubiquitous and highly abundant in serum; they bind calcium and efficiently prevent de novo formation of apatitic mineral. Normocalcemic AHSG-deficient mice develop sporadic perivascular calcification. Hypercalcemia induced by dietary means or by hormone treatment results in lethal calcinosis in Ahsg-/-mice. A mineral binding structure is proposed for domain D1 of AHSG suggesting that the proposed EF-hand motif for calcium binding does not exist in AHSG. Unlike serum albumin, AHSG does not preferentially bind ionic Ca2+, but rather in the form of apatitic microcrystals.
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PMID:Systemic inhibition of spontaneous calcification by the serum protein alpha 2-HS glycoprotein/fetuin. 1137 33

A 2 month-old male infant presented with severe hypercalcemia due to parathyroid hyperplasia. A total parathyroidectomy and partial heterotopic autotransplantation were carried out. Hypercalcemia recurred two months later. Normocalcemia was re-established after removing one half of the implanted tissue. Despite two separate surgical explorations and several imaging studies, including 99mTc-sestamibi scintigraphy, ultrasonography, and MRI, only three parathyroid glands were found. Severe pulmonary calcinosis has not previously been reported in children with PHPT. In conclusion, developmental variations of the parathyroid glands may be difficult to identify with present imaging techniques. This may pose difficulties in management of PHPT. The present report describes pulmonary calcinosis as a sequela which can cause additional morbidity in these infants.
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PMID:Primary hyperparathyroidism in an infant with three parathyroid glands and pulmonary calcinosis. 1159 79

The calcinogenic plants are among the most noxious plants to animals in the world. The pathological and biochemical effects of calcinogenic plants in cattle, sheep, goats, pigs, horses, buffalo and laboratory animals have been determined. The chemical nature of the toxic agents and the precise mechanism by with the calcinogenic plants induces calcinosis have been defined. Most of the active principle present as steroidal glycoside is hydrolyzed in intestine, rumen and other tissues or by the bacterial flora releasing the steroidal fragment, in most cases 1,25(OH)(2)D(3). The excess of vitamin D stimulates CaBP synthesis and calcium and phosphate absorption, producing hypercalcemia and/or hyperphosphatemia. The excessively absorbed mineral cannot be physiologically accommodated, and the deposition in soft tissues results in calcinosis. The different means of treatment of calcinosis and control of calcinogenic plants are discussed with regards to their effectiveness. A number of potential uses of calcinogenic plants have been suggested but none has been exploited on a large scale. The understanding of the mechanisms involved with calcinosis contributed enormously to the compression of vitamin D mechanism. Research methods were developed and improved but a lot is to be done in this fascinating subject.
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PMID:Calcinosis--calcinogenic plants. 1246 55

Hypercalcemic nephropathy has been classified as a tubulointerstitial renal disease. The presence of glomerular pathologic findings attributable to hypercalcemia has been observed in only a few patients and therefore has been considered an unusual finding. In the current study, calcium deposition within glomeruli was investigated in 2 patients with extreme elevations in serum calcium levels and hypercalcemic nephropathy. The study material consisted of a renal biopsy specimen from a 31-year-old woman (patient 1) who had T-cell lymphoma/leukemia and a serum calcium level of 20.2 mg/dL (5.0 mmol/L) and autopsy kidney specimens from a 19-year-old woman (patient 2) who was being evaluated for primary hyperparathyroidism and a calcium level of 18.4 mg/dL (4.6 mmol/L). The renal biopsy specimen for patient 1 exhibited calcium deposits present in the glomerular capillary basement membranes, where they were associated with segmental sclerosing lesions (21% of glomeruli). Nine percent of the cortical tubules contained calcifications. In patient 2, calcium was found in the mesangial areas in 95% of glomeruli, filling the Bowman space in 7% of glomeruli, or associated with capillary basement membranes and segmental sclerosing lesions (12% of glomeruli). Fifteen percent of cortical tubules, 4% of outer medullary tubules, and 40% of inner medullary tubules were calcified. In neither case was there immunofluorescence or electron microscopic evidence of primary glomerular disease. Thus, glomerular calcification may exceed that occurring in the cortical and outer medullary tubules and may play a significant role in the loss of renal function in hypercalcemic nephropathy. Glomerular calcinosis may also be recognized as an additional cause of segmental glomerulosclerosis and nephrotic range proteinuria in patients with extremely high levels of serum calcium.
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PMID:Glomerular calcification in hypercalcemic nephropathy. 1256 59

We report the case of a 58-year-old woman with metastatic pulmonary calcinosis who presented with bronchial hyperreactivity. She was receiving calcium and vitamin D supplementation following total bilateral thyroidectomy with parathyroidectomy and had a history of episodes of symptomatic hypercalcemia secondary to exogenous administration. Lung function testing showed slight obstruction that was reversed by bronchodilators. Images showed a bilateral micronodular pattern mainly in the upper fields (x-ray and high resolution computed tomography of the thorax) and abnormal calcium deposition in the lungs (bone scintigraphy). The diagnosis was established by transbronchial biopsy. The clinical course was favorable. Metastatic pulmonary calcinosis is rare and usually asymptomatic and evolution is good. This entity should be taken into account in the differential diagnosis of interstitial lung diseases involving micronodular infiltrates in patients at risk.
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PMID:[Metastatic pulmonary calcification: a rare cause of interstitial lung disease]. 1271 61

Soft tissue calcification is a frequent complication in end-stage renal disease (ESRD) patients with a high serum calcium-phosphate product, but systemic involvement of both the visceral organs and skin is rarely seen. We report on a newly diagnosed ESRD patient with gouty nephropathy who had initial presentations of extensive intradermal tophi, diffuse calcinosis, and hypercalcemia. He received maintenance hemodialysis (HD) with low-calcium dialysate (1.25 mEq/l) for 11 months. Although the above complications diminished, serum calcium remained elevated. Thereafter, unexpected cervical lymphadenitis from a Mycobacterium tuberculosis (TB) infection with high extra-renal production of calcitriol was found. Serum calcium levels normalized only after anti-TB treatment for 2 months. We thought that this patient might have had occult TB infection before the start of HD, which resulted in calcitriol production and hypercalcemia. In addition, concomitant hyperphosphatemia in chronic renal failure contributed to severe diffuse calcinosis. After the initiation of HD therapy, both the elevated serum calcitriol levels and accelerated resolution and mobilization of diffuse calcinosis from low-calcium HD contributed to persistent hypercalcemia.
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PMID:Diffuse calcinosis and intradermal tophi in a uremic pateint: effect of low-calcium hemodialysis and mechanism of hypercalcemia. 1504 22

We report a 72-year-old man who presented to our emergency room with congestive heart failure that was resistant to initial medical therapy. He had suffered from anterior myocardial infarction 20 years prior. Echocardiography and computed tomography revealed marked cardiac calcification including myocardium, chordal structures, mitral annulus, and aortic valve. Neither chronic renal insufficiency nor hypercalcemia were present in our patient. Bone resorption markers were increased and bone mineral density was consistent with severe osteoporosis. We suggested a novel mechanism, that increased bone resorption may lead to accumulation of calcium into avascular tissues in the heart (ie, chordal structures, mitral annulus, aortic valve, and fibronecrotic myocardium) especially in the setting of high left ventricular end-diastolic pressure. Dystrophic cardiac calcinosis, an age-related cardiomyopathy, is associated with elevated bone resorption markers and it may cause alterations in cellular calcium hemostasis with initiation of deleterious events leading to aggravate dilated and restrictive cardiomyopathy and may result in intractable congestive heart failure. The implication of this case report needs to be reemphasized.
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PMID:A case of massive dystrophic cardiac calcinosis with increased bone resorption markers: a novel pathophysiologic link? 1547 67

We have studied the deposition of calcium salts in the autopsied intestines which have not been described previously as far as we were able to determine. In order to clarify the incidence, predisposing conditions, mineral compositions of the deposited materials and clinical significance of this phenomenon, we examined 76 cases of consecutive autopsied small intestines by von Kossa's staining. Deposited calcium salts were further examined by electron microscopically, energy-dispersive X-ray spectroscope and electron diffraction analysis. Deposition of calcium salts was observed in the small intestines of 13 cases. Among them, 10 cases were accompanied by hypercalcemia. Deposition of calcium salts was mainly observed in smooth muscle cells of the proper muscle layers and ganglion cells of the Auerbach's myenteric plexus. Intestinal calcinosis was frequently accompanied by deposition of calcium salts in the proper muscle layers of esophagus and large intestine, renal tubules and cardiac myocardial cells. Electron microscopically, the calcium salts were identified as needle-shaped crystals and located on the surface of the extracellular-collagen bundles, in the cytoplasm, mitochondria and nucleus of the smooth muscles cells. Energy-dispersive X-ray spectroscope and electron diffraction analysis suggested the deposited calcium salts as hydroxyapatite. Two patients among the six cases with moderate to severe calcium deposition showed clinical manifestation of paralytic ileus. In conclusion, intestinal calcinosis was frequently observed mostly associated with hypercalcemia. Calcium salts of hydroxyapatite were deposited to the smooth muscle cells and the Auerbach's myenteric plexus of the muscular layer. Deposition of calcium salts might occasionally causes the paralytic ileus but clinical significance of this lesion requires further examination.
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PMID:Identification of hydroxyapatite deposits in the smooth muscle cells and ganglion cells of autopsied small intestines. 1550 21

Uremic Tumoral Calcinosis (UTC) is a rare complication of chronic kidney disease on dialysis, characterized by large periarticular calcification. Among some cases, hypercalcemia with no conventional etiologies has been reported. We present a case of UTC in which hypercalcemia occurred after parathyroidectomy and introduction of low-calcium containing dialysate. Work-up of hypercalcemia did not reveal any conventional etiology, but hypercalcemia resolved after debulking of the tumor. This change in serum calcium gives us an insight into the mechanism of hypercalcemia, occasionally seen among cases with UTC.
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PMID:Improved hypercalcemia after debulking of uremic tumoral calcinosis in a parathyroidectomized patient. 1598 44


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