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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↗
PubMed1997

[Calciphylaxis in a patient on long-term dialysis].

Calciphylaxis is a special form of soft tissue calcification (in particular blood vessels), affecting specially patients with chronic renal insufficiency and associated secondary hyperparathyroidism. Most severely affected are small arteries with a diameter of 0.2-0.5 mm at the interface of the corium and subcutaneous layer. Calcification of the vascular media with subsequent narrowing of the lumen causes ischaemic changes manifested by the development of painful reddish-violet spots on the skin with necrosis and ulcerations. The authors describe the case of a 73-year-old diabetic female patient with regular dialyzation treatment. The patient developed reddish-violet spots on the lower extremities shortly before admission to hospital. At the site of the spots rapidly progressing necroses developed. The cause of these ischaemic changes were calciphylactic changes confirmed on post-mortem examination and by histological examination.

Aged↗
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↗
PubMed2002

The amino bisphosphonate ibandronate prevents calciphylaxis in the rat at doses that inhibit bone resorption.

The present experiments were carried out to test the hypothesis that there is a common underlying biochemical mechanism that accounts for the different kinds of soft tissue calcification observed in animals that are treated with toxic doses of vitamin D. In previous studies we showed that lethal doses of vitamin D cause extensive calcification of arteries, lungs, kidneys, and cartilage, and that doses of the amino bisphosphonate ibandronate that inhibit bone resorption completely inhibit each of these soft tissue calcifications and prevent death. In the present experiments we have examined the effect of ibandronate on an entirely different type of calcification, the calciphylaxis induced by administration of a challenger to rats previously treated with sub-lethal doses of vitamin D. These studies show that ibandronate doses that inhibit bone resorption completely inhibit artery calcification as well as, in the same rat, the calciphylactic responses to either subcutaneous injection of 300 mg FeCl3 or intrascapular epilation. Since the vitamin D-treated animals had dramatically increased levels of bone resorption, and concurrent treatment with ibandronate normalized resorption, these results support the hypothesis that soft tissue calcifications in the vitamin D-treated rat may be linked to bone resorption. The ability of ibandronate to inhibit all vitamin D-associated calcifications in the rat cannot be explained by an effect of ibandronate on serum calcium, since serum calcium remained 30% above control levels in the vitamin D-treated animals that also received ibandronate.

Animals↗
PubMed2005

[Calciphylaxis: a severe but unrecognized complication in end-stage renal disease patients. A review of 2 cases].

Calciphylaxis presents like subcutaneous lesions with livedo reticularis leading to necrotic and painful ulcers, predominantly in the lower limbs and the abdomen. They initially simulate dermohypodermitis. Biology reveals secondary hyperparathyroidism, phosphocalcic metabolism abnormalities and state of hypercoagulability. Histological signs are constant: calcifications in the media of small and sub-cutaneous arteries, intimal hyperplasia and intravascular thrombosis. This complication occurs in 4% of end-stage renal disease patients. Its prognostic is awful with a rate of mortality of 60% due to sepsis. Treatment is based upon the normalization of phosphocalcic rates and local debridement.

Aged↗
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↗
PubMed1964

CALCIPHYLAXIS: PASSIVE TRANSFER.

Rats were sensitized by mouth with dihydrotachysterol and subsequently challenged by a subcutaneous injection of ferric dextran. Mineralization at the injection site is barely detectable 17 hours after challenge. If, at this time, the challenged skin is transplanted onto a normal recipient, mineralization continues in the nonsensitized host. Sensitization is indispensable only for the initiation of the calciphylactic response and, once "triggered," the mechanism for this type of mineralization is transferable.

Calcification, Physiologic↗