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PubMed1994

Systemic calciphylaxis.

Systemic calciphylaxis is a rare, poorly understood syndrome of progressive ischemic necrosis, usually associated with hyperparathyroidism. The combination of hyperparathyroidism, usually secondary or tertiary, and chronic renal failure seems to produce a particular biochemical environment conducive to the development of an unusual progressive form of ischemia. Early recognition and diagnosis, appropriate therapy including wound care, and expeditious parathyroidectomy often will halt the progression of the disease, minimize limb loss, and prevent subsequent sepsis and death.

Calciphylaxis↗
PubMed1988

Epidermal and follicular calciphylaxis.

A patient with secondary hyperparathyroidism due to chronic renal failure developed epidermal and follicular calcification without concomitant dermal calcification in the lesions of toxic epidermal necrolysis. We propose that the combination of keratinocyte necrosis and an elevated serum calcium-phosphorus product resulted in epidermal calciphylaxis.

Adult↗
PubMed1969

Calciphylaxis in man.

A patient with renal failure developed widespread calcification in the thighs after the injection of iron-dextran (Imferon). This is considered as an example of calciphylaxis, a process in which calcium is laid down in parts of the body following the administration of a "challenger." Iron-dextran is a known challenger, and should be used with caution in uraemic subjects, who may be sensitized by high serum parathyroid hormone levels. Contributing factors may have been a high calcium/phosphate product, steroids, and the patient's immobility.

Adult↗
PubMed1981

Systemic calciphylaxis revisited.

A syndrome characterized by rapidly progressive ischemic necrosis involving large areas of the skin and muscle, and by peripheral gangrene associated with extensive vascular calcifications was observed in a patient with end-stage renal failure on chronic hemodialysis. In an effort to control the disease, parathyroidectomy was performed which resulted in rapid improvement of tissue perfusion. However, the patient eventually died from sepsis within 2 months after admission. This case presents the typical features of the syndrome of systemic calciphylaxis. The literature is reviewed searching for similar cases of this poorly recognized, but life-threatening, clinical syndrome. The pathogenesis, clinical manifestations, and therapy of this unusual and rapidly progressive, but potentially reversible, condition are reviewed with emphasis on its prompt recognition and appropriate management.

Adult↗
PubMed1990

Calciphylaxis and systemic calcinosis. Collective review.

The phenomenon of calciphylaxis as defined by Selye is a condition of hypersensitivity that results in acute local calcification of various organs, with a whole host of morbid processes. Nephrocalcinosis and cutaneous calcifications have long been recognized in patients with chronic renal failure, but they have not often been reported in acute hyperparathyroidism or other causes of calcium-phosphate metabolism aberrations. The pathogenesis is not clear, and both the sensitizer and challenging agent in the hypersensitivity theory are often elusive, though hypercalcemia is the most consistent factor. The clinical features vary according to the organs affected and often mimic a gamut of more common conditions. Treatment is primarily supportive, with specific measures only possible when a sensitizer or challenger is identified. Correction of the hypercalcemia is, however, imperative. It is important to recognize this rare condition to avoid the more serious end results often reported.

Calcinosis↗
PubMed1990

[Systemic calciphylaxis and acquired perforating disease in a uremic patient].

We show the case of a patient suffering from a chronic renal failure in hemodialysis. He had a ischemic necrosis that was quickly progressive in his fingers and toes. It was necessary to amputate them. Diffuse vascular calcifications were recorded so radiologically than pathologically. PTH and phosphocalcic product were raised. Parathyroidectomy was practised with a quick initial improvement but immediately new distal ischemic lesions and keratotic papules with histologic perforation, that became necrosed, appeared in his buttocks and inferior extremities. The coexistence of acquired perforating disease and calciphylaxis in uremic patients has not been reported until now.

Calciphylaxis↗
PubMed1990

[Idiopathic arterial calcification: its link with calciphylaxis].

The attempt to establish the connection of the idiopathic arterial calcification (IAC) with calciphilaxy is made on the basis of the published data analysis and 11 observations of IAC in children. Apart from known morphological manifestations of IAC, the authors found mast cells in the cellular infiltrate, vesicular transformation of smooth cells in the arteries affected. This together with the elastic membrane changes in the arteries and massive iron and oxyapatite deposits in the arterial wall suggests the development of calciphylactic reaction. The similarity of the morphological and clinical manifestations, and IAK therapy in the clinics and experiment is shown. Special emphasis is made on the possibility of the calciphylaxy development in children under conditions of the vitamin D wide use for the prevention of rickets and iron preparations use for anemia treatment. The conclusion is drawn on the multicausal character of IAK and possibility to distinguish congenital, acquired and combined forms of the disease. The necessity of through analysis of each case of IAK is stressed in order to reveal iatrogenic factors capable to produce sensibilization and/or to provoke the disease.

Animals↗
PubMed1993

Calcifying panniculitis and systemic calciphylaxis in an end-stage renal patient.

A patient with a history of end-stage renal failure who had been receiving hemodialysis for approximately six months experienced painful plaques bilaterally on the medial aspects of her thighs. A biopsy specimen of the affected subcutaneous tissue demonstrated calcification in the subcutaneous tissue. In this case of calcifying panniculitis, the conditions for systemic calciphylaxis appear to have been present.

Calcinosis↗
PubMed1983

Calcergy and calciphylaxis: timed appearance of gamma-carboxyglutamic acid and osteocalcin in mineral deposits.

gamma-Carboxyglutamate (Gla), a calcium binding amino acid whose synthesis depends on vitamin K, has been found in association with pathologic calcifications. It is of interest therefore to examine the role of Gla-containing proteins in the formation of nonskeletal mineralized tissues. Calcergy and calciphylaxis, experimentally induced models of pathologic calcification, offer the opportunity to study the formation of mineral deposits in the absence of an endochondral sequence of bone formation. Before induction of subcutaneous calcinosis by topical treatment with the direct calcergen, KMnO4, or by challenging dihydrotachysterol-sensitized animals with FeCl2, control specimens contain no gamma-carboxyglutamic acid. With the initial formation of cytoplasmic vesicles, calcium content of the tissues increases and Gla is detected. Gla levels are further elevated with the appearance of poorly crystalline apatite-like crystallites. Origin of protein bound Gla was established by positive identification of osteocalcin by radioimmunoassay. Gla and osteocalcin appear concomitant with the earliest mineral deposits observed by electron microscopy and micro X-ray analysis. The formation of organized extracellular pattern by X-ray diffraction allowed sufficient mineral accumulation for detection with calcium, Gla, and osteocalcin increasing allowed sufficient mineral accumulation for detection of an apatite-like pattern by X-ray diffraction with calcium, Gla, and osteocalcin increasing proportionately as mineral is deposited.

1-Carboxyglutamic Acid↗
PubMedDate not supplied

[Cutaneous calcinosis induced by topical calciphylaxis in rats. I. Ultrastructural aspcts].

Skin calcification induced by topical calciphylaxis was provoked by a subcutaneous injection of iron chloride in rats previously sensitized by D.H.T. and studied by electron microscope. The evolution of the calciphylatic response can be resumed as follows: -- early appearance of numberous granules in the mitochondria of the cells of the connective tissue; their inorganic nature was revealed by microincineration and it is highly probable that they are a reserve of mineral ions; -- between the 6 hr, and the 18 hr, stages the interfibrillar matrix contained rounded vesicular structures, enclosed by a triple mambrane, which must surely be of cellular origin; they progressively incorporated more and more mineral particles which confirm their primordial role in the initial phases of mineralization; -- from the 14 hr. stage onward, mineral rodlets composed of chains of little dots appeared in the intercellular matrix and then on the collagen fibrils, probably in contact with the mucopolysaccharides; -- starting at the 24 hr, stage, the mineralization progressed without a vesicular intermediary forming increasingly dense and widespread plaques; the presence of needles of homogenous aspect indicated the appearance of a crystalline mineral deposit; an intrafibrillar mineral deposit becomes visible later. These results are compared with those obtained previously in other studies of experimental or pathological calcinosis and of mineralization of skeletal tissues.

Animals↗
PubMed1976

Calciphylaxis in man. A syndrome of tissue necrosis and vascular calcification in 11 patients with chronic renal failure.

Eleven patients with chronic renal failure and presumed secondary hyperparathyroidism developed a syndrome of medial calcinosis of the arteries and painful ischemic ulcers of the fingers, legs, or thighs, or any combination of the three. Five patients required maintenance hemodialysis; six had functioning renal homografts. Severe hyperphosphatemia had existed in each; seven showed roentgenographic evidence of subperiosteal resorption. Similarities are evident between the lesions and experimentally produced calciphylaxix. The lesions demonstrated a relentless, progressive course, with serious morbidity and mortality. Hyperplastic or adenomatours parathyroid tissue was removed from ten of 11 patients unergoing surgical procedures; healing followed in seven patients. Treatment with phosphate-binding antacids to lower serum phosphorus levels may prevent this syndrome. Total or subtotal parathyroidectomy should be considered when ischemic skin lesions appear in uremic patients or in renal transplant recipients.

Adolescent↗