Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCINOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1997

[Perforating milia-like idiopathic calcinosis of the extremities in Down syndrome].

INTRODUCTION: Several skin diseases can be seen in patients with trisomy 21. We report a case of miliary calcinosis of the extremities. CASE REPORT: A 15-year old adolescent with Down's syndrome presented small papular miliary lesions which had developed over 18 months and tended to discharge a chalk-like substance via the epidermis. Approximately 15 lesions were present on the hands and feet. Histologically, there was a well-delimited calcium deposit in the superficial dermis. There was no alteration in phosphorus/calcium metabolism. Brain CT-scan and cardiac echography did not reveal any calcifications. DISCUSSION: Miliary calcinosis cutis may not be exceptional in Down's syndrome, although only 9 observations have been reported. Preferential localizations include the hands, wrists and feet. Association with syringoma has been noted but would appear to be fortuitous. Transepidermal elimination of the calcium deposits is frequent. Pathogenic hypotheses include precipitation of calcium salts in sudation products and/or increased synthesis by fibroblasts. The association with trisomy 21 appears to be significant since only three cases have been reported in patients with normal karyotypes. This entity should be individualized as perforating milia-like idiopathic calcinosis cutis of the extremities.

Adolescent↗
PubMed1999

Uremic tumoral calcinosis in patients receiving longterm hemodialysis therapy.

OBJECTIVE: To analyze a series of uremic tumoral calcinosis (UTC) in patients receiving longterm dialysis therapy. METHODS: Twelve patients receiving longterm hemodialysis affected by tumoral calcinosis were analyzed. Clinical, radiological, and pathological features were evaluated and pathogenic factors were reviewed. RESULTS: The most common sites for UTC were the elbow, hip, hand, and wrist. The lesions were multiple (67%, n = 8), of large size, and symptomatic with joint mobility impairment (75%, n = 9) as well as nerve compression (33%, n = 4). High serum calcium and phosphate concentrations were detected in 50% (n = 6) and 100% of the patients, respectively. An increased calcium-phosphorus product (Ca x P) was observed in all patients, either due to overt secondary hyperparathyroidism (42%, n = 5), or secondary to iatrogenic hypercalcemia and/or severe hyperphosphoremia of multifactorial etiology (i.e., prolonged and excessive administration of calcitriol and calcium carbonate, insufficient dialysis and inadequate phosphorus chelating therapy, etc.) (58%, n = 7). Several treatment strategies were followed (surgical excision, parathyroidectomy, renal transplant) in combination with aggressive medical therapy to decrease Ca x P product, achieving complete remission in 83% of the patients. CONCLUSION: UTC lesions show clinical and pathogenic features that differ from those of idiopathic tumoral calcinosis. The most important pathogenic factor involved in UTC is an increase in Ca x P, not necessarily related to hyperparathyroidism. Combined treatment strategies allow complete remission in a high proportion of patients. A low Ca x P is necessary to prevent development of UTC.

Adult↗
PubMed1983

Childhood systemic lupus erythematosus. Association with pancreatitis, subcutaneous fat necrosis, and calcinosis cutis.

Pancreatitis developed in a 12-year-old girl with a one-year history of systemic lupus erythematosus. The pancreatitis was first manifested by panniculitis of the lower extremities. Calcinosis cutis subsequently developed, both in areas of panniculitis and in areas free of panniculitis. The patient's medications at the time of onset of pancreatitis included prednisone, hydrochlorothiazide, and azathioprine, all of which have been reported to be causes of pancreatitis. We wish to alert physicians that pancreatitis associated with cutaneous panniculitis and calcinosis cutis may develop in children with systemic lupus erythematosus.

Adipose Tissue↗
PubMed1996

Ocular tumoral calcinosis. A clinicopathologic study.

Tumoral calcinosis is a rare systemic disorder characterized by para-articular ectopic soft-tissue calcification. This case report describes the ophthalmic features (palpebral conjunctival calcific nodules, the white limbal girdle of Vogt, disc drusen, and angioid streaks) in a 38-year-old Asian woman who had tumoral calcinosis associated with hyperphosphatemia. A morphologic study of the calcified nodules on the palpebral conjunctiva disclosed deposition of hydroxyapatite crystals in an extracellular matrix (deposit) containing alcianophilic mucopolysaccharides. Excision of the eyelid nodules was not followed by recurrence.

Adult↗
PubMed1985

Elevated serum calcitriol concentrations do not fall in response to hyperphosphatemia in familial tumoral calcinosis.

Five affected members in two branches of a Druze Arab kindred presented with calcified deposits in or about the hips and knees, indicating the diagnosis of tumoral calcinosis. Serum vitamin D metabolite concentrations, immunoreactive parathyroid hormone, and the tubular reabsorption of phosphate were measured in three affected siblings, as well as in their parents and an unaffected sibling. Normocalcemia and hyperphosphatemia with an elevated tubular maximum for phosphate per glomerular filtration rate were found in the affected patients. Levels of serum immunoreactive parathyroid hormone were normal, and the calcitriol value (1,25-dihydroxyvitamin D) was normal or elevated in the three affected patients. A trial of a low-phosphorus diet and oral aluminum hydroxide gel did not lower serum phosphate levels or improve the calcified deposits. These findings suggest that serum calcitriol values do not decline in response to hyperphosphatemia in tumoral calcinosis and that hyperphosphatemia with elevated tubular reabsorption of phosphate is a constant feature of this disorder because the kidney fails to excrete the increased filtered load of phosphate.

Adult↗
PubMed2000

Fine-needle aspiration cytology of the breast in a case with abundant acellular calcific material indicative of soft-tissue calcinosis.

Since calcific deposits in soft tissue may clinically resemble a tumor, it is feasible to investigate them by fine-needle aspiration (FNA) cytology. In this presentation we describe a case in the breast with extensive accumulation of acellular liquid calcific material which was sampled by the noninvasive technique of FNA, and which was indicative of nonfamilial soft-tissue calcinosis. A 48-yr-old, perimenopausal woman on a routine mammogram showed a well-defined, 1-cm partially cystic opacity in the left upper quadrant of the breast. All other investigations were normal, and no significant family or medical history was present. Under ultrasound guidance FNA was done, and about 1 ml of thick whitish fluid was obtained. Cytopreparations only showed abundant acellular calcium. The patient refused any further treatment and elected to be under the care of her family physician, according to whom she was clinically well with no changes in mammograms for the last 2 yr. The case is interesting, since the cytohistologic findings in aspirate sample appeared to be strongly indicative of soft-tissue calcinosis, which to our knowledge has not been previously reported.

Biopsy, Needle↗
PubMed1992

Bilateral striopallidodentate calcinosis: cerebrospinal fluid, imaging, and electrophysiological studies.

We report the genetic, clinical, electrophysiological, and imaging studies in a family with bilateral striopallidodentate calcinosis (Fahr's disease). The intracerebral calcium deposits occurred before onset of the symptoms in the third decade of life. Progressive neurological deterioration occurred in the fifth decade of life in the proband. Cerebrospinal fluid homocarnosine, a central nervous system-specific peptide, was increased twofold in patients with autosomal dominant bilateral stripallidodentate calcinosis; in sporadic cases, there was no detectable homocarnosine and a decreased level of histidine. With advancing age, the amount of calcification increases, but it has not been determined if a critical amount must be reached before symptoms occur. Computerized tomography is superior to magnetic resonance imaging for radiological diagnosis. Despite diffuse striatal calcification, striatal 6-[18F]fluoro-L-dopa uptake did not reveal any difference between patients and control subjects, from which we infer persisting integrity of the nigrostriatal dopaminergic pathway.

Adult↗
PubMed1995

Aspiration cytology of a case of tumoral calcinosis.

The fine-needle aspiration (FNA) cytologic findings in a case of non-familial tumoral calcinosis are described. These include abundant calcific amorphous deposits, mononuclear histiocytes, osteoclast-type multinucleated giant cells, and fragments of tissue consisting of osteoblast-type cells with atypical epithelial-like features mimicking an epithelial malignancy. This is the first reported case describing the cellular morphology of tumoral calcinosis in an FNA specimen. A previously reported case described the evacuation of acellular calcific fluid only. In the present case, vigorous aspiration of the solid portions of the lesion yielded cellular material representative of the histology of the lesion. Points of caution for a correct interpretation of the cytologic findings are discussed.

Biopsy, Needle↗
PubMed1975

The ultrastructure of topical cutaneous calcinosis.

Mineralized plaques, which develop at the site of repeated subcutaneous injections of 100 mug KMnO4/0.2 H2O in rats, were investigated by electron microscopy. The newly formed, delineated, white plaque tissue at the injection site consisted of numerous, mostly unaltered fibroblasts and collagen fibers, without participation of inflammatory cells. Some signs of cell injury were found in the center of the lesions. Numerous, irregularly distributed, small, mineralized foci were seen near the fibroblasts. These were formed by aggregation of small needle-like units (50 A in diameter and 0.05-2.0 mum long). These needle-shaped units were found either in vesicular, cell derived structures, considered to be shed cell fragments, or on collagen fibers. Intramitochondrial deposits of such needle like units were seen frequently. Fusion of smaller mineralized foci to larger plaques occured and then needle-shaped units were seen at the periphery of the electron-dense lesions. Hypotheses concerning the mechanism of experimental cutaneous calcinosis (soft tissue mineralization) are discussed and related to the findings of this study. Probable intracellular crystal deposition and mineralization in cell-derived structures were shown for the first time in topical cutaneous calcinosis.

Animals↗
PubMed1988

Tumoral calcinosis revisited--common and uncommon features. Report of ten cases and review.

Familial cutaneous and subcutaneous tumoral calcifications are a recognized entity of unknown pathogenesis. The course of calcinosis and various treatments are discussed and the literature concerning the aetiology is reviewed. Our ten cases provided some experience in dealing with tumoral calcinosis and demonstrated, in addition, some clinical phenomena unrecognized previously, such as involvement of the mucous membranes and an erythematous rash preceding the development of calcified nodules.

Adolescent↗
PubMed1992

Tumoral calcinosis of the ischium.

The authors report on a case of tumoral calcinosis of the ischium in a 63-year-old female. By means of this particular case a general review of the literature on pathogenesis, histological characteristics, the possible way of treatment and the prognosis of tumoral calcinosis is presented.

Bone Diseases↗
PubMed1980

Tumoral calcinosis: evidence for concurrent defects in renal tubular phosphorus transport and in 1 alpha,25-dihydroxycholecalciferol synthesis.

A 50-year-old Latin American man with tumoral calcinosis presented with hyperphosphatemia (6.62 +/- 1.04 SD mg/dl), elevated renal threshold phosphorus concentration (TmP) (7.3 mg/GFR), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] (69 pg/ml) hypercalciuria (239 mg/day), and a high fractional intestinal calcium (Ca) absorption (0.74). Sodium cellulose phosphate therapy (20 g/day) lowered urinary Ca, and partially reduced serum phosphorus (P) and TmP to 5.91 +/- 0.63 mg/dl and 6.2 mg/GFR, respectively. Serum 1,25-(OH)2D remained elevated at 58-64 pg/ml. Amphojel therapy (4 oz/day) decreased urinary P to 23 +/- 21 mg/day and lowered serum P to 5.75 +/- 0.36 mg/dl (P < 0.05). TmP increased to a value of 8.0 mg/GFR while serum 1,25-(OH)2D continued to remain elevated at 53 pg/ml. This case illustrates the probable operation of dual abnormalities in tumoral calcinosis represented by augmented renal conservation of P and an elevation in the circulating concentration of 1,25-(OH)2D.

Calcinosis↗
PubMed1982

Focal mineralization defect during disodium etidronate treatment of calcinosis.

The use of disodium etidronate (EHDP) for the treatment of calcinosis is complicated by the threat of drug-induced inhibition of skeletal mineralization. Adults with Paget's disease of bone treated for 6 months with 10-20 mg/kg/day of EHDP have been reported to show both a marked delay in mineralization and a diffuse excess of unmineralized bone matrix. Drug-induced bone disease is, however, a function of growth as well as of the dose and duration of therapy. Therefore, children treated with EHDP may respond differently to the drug-induced mineralization defect. A 10-year-old girl with dermatomyositis developed incapacitating ectopic calcification. After 9 months of therapy with 12 mg/kg/Day of EHDP, a small decrease in the calcinosis was accompanied by a dramatic increase in joint mobility. Bone mineral content of the radial diaphysis showed a failure to gain mineral density as expected with prepubertal growth (8 cm/year). Bone biopsy revealed a patchy excess of osteoid. Although the percentage of osteoid surface labeled by tetracycline was reduced, normal mineralization was evident in the double-labeled areas. In children, the mineralization defect occurring with EHDP treatment may be focal.

Bone Diseases↗
PubMed2005

Tumoral calcinosis with hyperphosphatemia.

Tumoral calcinosis is a rare disorder of mineral metabolism among adolescents and young adults characterized by deposition of calcific masses around large joints. It is less commonly reported in pediatric population and commonly mistaken for bone tumors. Typical lab parameters include hyperphosphatemia with normal levels of serum calcium, parathyroid hormone (PTH) and alkaline phosphatase. A ten-year-old boy with typical features of tumoral calcinosis is presented.

Alkaline Phosphatase↗
PubMed1994

Scrotal calcinosis.

Calcinosis is a rare benign lesion of the scrotum. A new case with scrotal calcinosis is presented and the relevant literature is reviewed.

Calcinosis↗
PubMed1989

Effects of the acute subcutaneous administration of synthetic salmon calcitonin in tumoral calcinosis.

We examined the effects of the acute administration of salmon calcitonin on phosphate metabolism in tumoral calcinosis. On two different days, 200 MRC U of the synthetic hormone were administered sc to a 38-year-old patient, either as twice daily 100 MRC U injections, or as a continuous sc infusion via a portable pump. Both ways of calcitonin administration elicited a phosphaturic effect and a lowering of serum phosphate level comparable with that observed after an iv infusion of calcitonin. 1,25 dihydroxyvitamin D level, which was in the normal range during a control study, increased after calcitonin administration. In our patient, long term therapy with diet, a phosphate-binding agent and calcitonin prevented the occurrence of new ectopic calcifications. Owing to its phosphaturic activity, synthetic salmon calcitonin may be a useful adjunct to diet and aluminium-containing antacids in long-term management of tumoral calcinosis.

Adult↗
PubMed1999

Familial tumoral calcinosis: association with cerebral and peripheral aneurysm formation.

Two siblings with histologically and radiologically proven tumoral calcinosis presented with cerebral and peripheral aneurysms. The brother died of a ruptured subclavian artery aneurysm after surgical repair of brachial, iliofemoral and coeliac axis aneurysms. Magnetic resonance and catheter angiography in the sister demonstrated marked carotid dysplasia and a left ophthalmic segment aneurysm, not amenable to treatment. We believe this is the first reported case of familial aneurysms in association with tumoral calcinosis.

Aneurysm↗
PubMed2004

Severe calcinosis cutis in an infant.

We report on an infant with severe asphyxia and persistent pulmonary hypertension as a newborn. The baby received prolonged intravenous calcium gluconate therapy for hypocalcemia. At 5 weeks of age, multiple firm, indurated areas (armor-like lesions) were palpable in the subcutaneous tissues of the trunk, arms, legs, and face, particularly in skin folds. Roentgenographic study showed generalized soft-tissue calcifications throughout the body, extremities, and face. Calcinosis cutis occurs through a variety of pathogenetic mechanisms. Case reports on calcinosis cutis in infants are uncommon, and the calcifications are mostly localized. In our patient, they are generalized.

Asphyxia Neonatorum↗