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.

SourceResearch connectionFrom yearThrough year

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

At least 163 records · Page 9Linked to original sources

PubMedDate not supplied

Extensive skin calcifications in an infant with chronic renal failure: metastatic calcinosis cutis.

Calcinosis cutis, one of the rare manifestations of systemic calcinosis, is characterized by the deposition of calcium and phosphate salts in the skin. Metastatic calcinosis, usually a late complication of chronic renal failure, arises from increased calcium or phosphate levels in the serum or both. Both sexes and all ages may be affected; however, cutaneous involvement is uncommon, particularly in children. We present the youngest patient, to our knowledge, with end-stage renal disease and cutaneous metastatic calcification resulting from secondary hyperparathyroidism. A 2-month-old infant presented to the pediatric service with anuria and uremia. A renal biopsy specimen showed chronic tubulo-interstitial nephritis. Indurated, firm, tender reddish papules were localized to both lower limbs, and extensive irregular nodules and plaques with ulceration and white stony contents were localized to the right upper limb. Topical antibiotic ointment was applied to the skin lesions to prevent secondary infection. However, acute peritonitis developed during peritoneal dialysis, and death occurred as a result of sepsis.

Calcinosis↗

PubMed1988

Scrotal calcinosis: origin from dystrophic calcification of eccrine duct milia.

Scrotal calcinosis is a rare benign disorder considered idiopathic by most recent authors, although an origin from dystrophic calcification of epidermoid cysts has been proposed. In 3 of 4 cases which were otherwise typical of scrotal calcinosis, there was calcification of the contents of small cysts lined by stratified squamous epithelium. These structures were identified as eccrine duct milia because some of them communicated with eccrine ducts and there were ultrastructural features of eccrine duct differentiation in one case. The eccrine nature of the milia was confirmed using the immunoperoxidase technique for the demonstration of carcinoembryonic antigen (CEA) which serves as a marker of eccrine sweat glands. Since a transition could be seen between degenerating calcified milia and typical nodules, it appeared that the calcific deposits of scrotal calcinosis result from the breakdown of such lesions. Staining of deposits unassociated with cyst walls with the technique for the demonstration of CEA supported this conclusion. An advanced stage of evolution of the disease could account for the absence of visible cysts in many cases. We propose the term "hidrocalcinosis of the scrotum" for this distinctive form of cutaneous calcification.

Adult↗

PubMed2001

Calcinosis circumscripta following an injection of proligestone in a Burmese cat.

A 9-month-old speyed Burmese cat was presented with a cutaneous lesion in the dorsal thoracolumbar region. The lesion was characterised by alopecia and whitish deposits within the subcutis and had occurred at the site of a previous progestogen injection (Covinan; Intervet). Excisional biopsy confirmed the diagnosis of calcinosis circumscripta. Recovery of the cat following surgical excision was excellent, with no recurrence of the lesion detected 12 months later. The classification of tissue calcification and the proposed aetiology of calcinosis circumscripta is reviewed. It is concluded that further work is required to determine any link between subcutaneous injections, especially of progestogens, and calcinosis circumscripta.

Animals↗

PubMed1998

Clinical significance of subcutaneous calcinosis in patients with systemic sclerosis. Does diltiazem induce its regression?

OBJECTIVE: To establish whether diltiazem reduces subcutaneous calcinosis (SCC) in patients with systemic sclerosis (SSc), and whether this calcinosis is related to other signs or symptoms. METHODS: 47 patients with SSc were evaluated and divided into two groups according to the presence or absence of SCC. RESULTS: Among the 12 patients with SCC who were treated with diltiazem and had sequential hand radiographs (differential time between the two radiographs: 7.8+/-4 years), there was a slight radiological improvement in three patients only. More patients with SCC had anticentromere antibodies than patients without (p = 0.003), fewer had anti-Scl 70 antibodies (p = 0.01), more had telangiectasia and giant capillaries ( p + 0.04 and 0.048 respectively), and SCC patients had significantly fewer capillaries at the nailfold (p = 0.03). CONCLUSION: These results do not clearly indicate that diltiazem is effective in calcinosis associated with SSc. Among the patients with SSc, those who also had SCC exhibited a distinctive autoimmune profile and more severe cutaneous capillary injury than those without SCC.

Autoantibodies↗

PubMed1972

Treatment of calcinosis circumscripta with probenecid.

A 23-year-old woman presented with an 11-year history of peripheral joint pains and stiffness slowly progressing to the development of gross calcinosis circumscripta. She had no definite evidence of systemic scleroderma. She was first treated for one year with frequent intravenous sodium EDTA, which increased urinary calcium and enhanced negative calcium balance but did not lessen her calcinosis. She was then treated with probenecid up to 2 g daily and her calcinosis lessened steadily over three years. Plasma levels of both phosphorus and urate fell during this time.

Adult↗

PubMed1999

Mobile intracardiac calcinosis: a new risk of thromboembolism in patients with haemodialysed end stage renal disease.

Cardiac calcinosis is a common complication of end stage renal disease. A newly observed risk of thromboembolism is reported in four patients with mobile cardiac calcinosis, treated with long term dialysis. Rapidly growing mobile calcification was confirmed by echocardiography. Each patient had an imbalance in serum calcium x inorganic phosphate (Ca x P product >/= 50); this imbalance could not be treated due to the sudden death of the patient or the need for surgical resection to prevent recurrent cerebral thromboembolism. Histological examination revealed intracardiac calcinosis in three cases, and each case showed haemodialysis hypoparathyroidism (intact PTH < 160 pg/ml). Thromboembolism in such cases is rare, however it indicates a need for cautious echocardiographic monitoring in end stage renal disease in patients with an uncontrolled Ca x P product.

Aged↗

PubMed1999

Dystrophic calcinosis cutis in subacute lupus.

Dystrophic calcinosis cutis is known to be associated with various connective tissue disorders but to the best of our knowledge has never been reported in subacute cutaneous lupus erythematosus (SCLE), a distinctive cutaneous subset in the spectrum of lupus erythematosus. It occurs without calcium and phosphorus metabolic abnormalities and may be localized or generalized. We report a patient with SCLE who developed calcinosis cutis and had normal serum calcium and phosphorus levels and, interestingly, a normal concentration of blood ionized calcium. This latter, which represents the active form in the total amount of blood calcium, is a parameter only rarely assessed in patients with dystrophic calcinosis cutis. Thus, other pathogenic factors should be investigated to clarify the pathophysiology of the dystrophic type of calcification.

Calcinosis↗

PubMed2000

Diffuse calcinosis cutis in a patient with congenital leukemia and leukemia cutis.

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.

Acute Disease↗

PubMed2004

Diffuse calcinosis and intradermal tophi in a uremic pateint: effect of low-calcium hemodialysis and mechanism of hypercalcemia.

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.

Adult↗

PubMed1979

Generalized cutaneous calcinosis and mixed connective tissue disease.

A 49-year-old female patient with a history of fever episodes, muscular weakness, Raynaud's phenomenon, cardiac insufficiency and increasing cutaneous calcinosis over a period of 4 years is reported. Based upon clinical as well as histological and immunological findings, the disease is diagnosed as mixed connective tissue disease with generalized cutaneous calcinosis in an extent yet unpublished, to our knowledge, in this 'overlap syndrome'. The pathogenesis of cutaneous calcinosis is discussed with particular reference to the phenomenon of calciphylaxis, and some therapeutic implications are considered.

Calcinosis↗

PubMed1991

Paradoxically decreased aortic wall stiffness in response to vitamin D3-induced calcinosis. A biphasic analysis of segmental elastic properties in conscious dogs.

We studied the aortic elastic behavior in response to vitamin D3-induced accelerated calcinosis in conscious dogs chronically instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. The two functional phases of the elastic segmental properties of the aorta in vivo were discriminated by computation on a beat-by-beat basis from the phasic pressure-diameter (P-D) hysteresis loops in basal conditions and during the transient state of a wide range of pressures obtained mechanically (aortic occlusion) or pharmacologically (angiotensin bolus). The overall P-D curve formed by all P-D hysteresis loops was comprised of two linear relations according to a model that assumes that only elastin is stretched at lower pressures, whereas both elastin and collagen are stretched at higher pressures. The slope of the first linear portion of the P-D curve was considered as the elastin P-D elastic modulus, and the slope of the curve obtained by subtraction between the P-D curve and the extrapolation of the elastin straight line was assumed to be the collagen P-D elastic modulus. After vitamin D3-induced calcinosis, the elastin elastic modulus was unaffected, whereas the collagen elastic modulus decreased significantly during occlusion maneuvers (58.6%, p less than 0.01) and during bolus injections of angiotensin (37.2%, p less than 0.05). The collagen elastic modulus correlated with the serum calcium concentration (r = -0.65, p less than 0.001) and with the aortic pulse pressure (r = 0.51, p less than 0.01), and this relation persisted at constant heart rate. Histopathologic analysis evidenced calcium-depositing elastic lamina, focal disappearance of collagen, and rupture of elastic fibers. The present study shows that accelerated, severe, experimental calcinosis-inducing calcium deposition inside the large artery walls is accompanied by a clear-cut paradoxical reduction in arterial rigidity that is mainly due to functional and structural modification of collagen elasticity.

Animals↗

PubMed2001

Tumoral calcinosis of the foot.

Tumoral calcinosis is characterized by periarticular deposition of calcium phosphate, usually in the setting of normocalcemia and hyperphosphatemia. The term tumoral calcinosis can be used to describe lesions with periarticular deposition of calcium phosphate resulting either from a primary disorder or a secondary disorder, such as renal failure with associated secondary hyperparathyroidism. Treatment entails phosphate deprivation, control of any primary disease processes such as secondary hyperparathyroidism, and resection for recalcitrant symptoms. We present a case of tumoral calcinosis involving the foot which required resection and ultimately hyperparathyroidectomy.

Adult↗

PubMed1985

Genetic transmission of tumoral calcinosis: autosomal dominant with variable clinical expressivity.

Tumoral calcinosis is a rare inherited metabolic disorder characterized by hyperphosphatemia, elevated serum 1,25-dihydroxyvitamin D levels and periarticular cystic and solid calcifications. Based on previous investigations, the inheritance of this disorder has been postulated to be autosomal recessive. This interpretation was based on finding clinically affected subjects in only single generations of kindreds. We investigated four generations of an affected kindred and found nine subjects with the disease. A unique dental lesion which is specific for this disorder and serves as a phenotypic marker was identified in two generations of the kindred. In all affected subjects, elevated serum 1,25-dihydroxyvitamin D levels were found, although each member did not have the classical clinical findings of tumoral calcinosis. The possibility that this disorder may be variably expressed and have multiple formes frustes has not been previously considered. Using the unique dental lesion as well as the classical clinical and biochemical abnormalities, we found that in this kindred, tumoral calcinosis is transmitted in an autosomal dominant mode, with variable clinical expressivity.

Adolescent↗

PubMed2005

Tumoral calcinosis of the filum terminale.

OBJECTIVE AND IMPORTANCE: Tumoral calcinosis is a rare disorder presenting with tumor-like masses of calcification, usually in soft tissues around large joints. Although this condition has been reported in the spine, this is the first reported instance of this uncommon lesion occurring in the intradural compartment, involving the filum terminale. CLINICAL PRESENTATION: A 55-year-old man presented with back and right leg pain. Initial investigations revealed no cause. A review of his original magnetic resonance imaging scans revealed an intradural calcified mass at L3 level. Surgical exploration was undertaken. INTERVENTION: A L3 laminectomy revealed a calcified mass adherent to the filum terminale. Frozen section from this mass revealed tumoral calcinosis involving the filum terminale. CONCLUSION: This is the first known case of intradural involvement by tumoral calcinosis. This is an uncommon disorder, and a high index of suspicion is required to diagnose the condition, which can recur if incompletely removed.

Calcinosis↗

PubMed1995

Oral presentation of metastatic calcinosis cutis.

An 80-year-old man presented with a hard swelling in the lower labial sulcus. Radiological investigation showed a mineralized mass on the labial aspect of an edentulous mandible which on excision, demonstrated the histological features of calcinosis cutis. No other sites seemed to be affected by calcific deposits in this patient, who appears to be the oldest reported case of metastatic calcinosis, and the first intra-oral case, to date. The different forms of calcinosis cutis are highlighted.

Aged↗

PubMed2001

Metastatic calcinosis circumscripta treated with an oral charcoal absorbent in a dog.

A five-year-old West Highland white terrier dog was admitted to the teaching hospital of Nippon Veterinary and Animal Science University due to swelling and pain of the foot pads. Examinations revealed that the dog had renal failure and calcinosis circumscripta on its foot pads. The diagnosis was metastatic calcinosis circumscripta secondary to renal failure. An oral charcoal adsorbent (Kremezin) was used to treat this condition. Following this treatment, a significant decrease in the Ca x P value (the serum calcium level x the serum phosphorus level) was observed, and the dog's condition improved dramatically. This case suggests that charcoal adsorbent (Kremezin) may be useful for treating metastatic calcinosis circumscripta in dogs.

Animals↗

PubMed1986

Pulmonary alveolar septal calcinosis causing progressive respiratory failure in acute lymphoblastic leukemia in childhood.

A syndrome of pulmonary alveolar septal calcinosis, pneumothorax, and pneumomediastinum, leading to rapidly progressive acute respiratory insufficiency and death was observed in 2 children with acute lymphoblastic leukemia (ALL). Primary clinical and radiological considerations in these patients were pulmonary edema and infection, and the diagnosis of pulmonary alveolar septal calcification was established only at autopsy. One patient, a 15-year-old girl, was found also to have parathyroid hyperplasia typical of familial hyperparathyroidism. The other, a 16-month-old girl, showed osteitis fibrosa of the bones and parathyroid hyperplasia of secondary type, suggesting that the pulmonary calcinosis resulted from hypercalcemia caused by a parathormone or prostaglandin-secreting tumor. The cause of pneumothorax and pneumomediastinum may have been rupture of calcified alveolar septa induced by high PEEP during ventilation of these patients. Other possible mechanisms contributing to hypercalcemia and pulmonary calcinosis in children with acute leukemia include bone resorption due to marrow infiltration, immobilization syndrome, renal failure, and administration of calcium, phosphate, or bicarbonate. This complication of acute leukemia in childhood is rare (2 patients in 430 autopsied over the period 1961-1982 at Childrens Hospital of Los Angeles). How often the process can be reversed if diagnosed before severe respiratory insufficiency is present is not known.

Adolescent↗

PubMed1979

Tumoral calcinosis in a patient undergoing hemodialysis.

Recently, tumoral calcinosis was found in a patient who had been undergoing haemodialysis in this hospital. The tumor was partially removed and subsequently regressed. The tumoral calcinosis of hemodialysis patients seems to be different from classical tumoral calcinosis.

Adult↗