Calcinosis cutis universalis

We report the case of a 49-year-old female who complained of hardening of the skin, with onset about 1.5 years before presentation. The laboratory data showed normal biochemistry profile. Routine haematochemical examinations showed slight anaemia, an increased erythrocyte sedimentation rate and negative rheumatological markers. Calcium excretion in a 24-h urine sample was normal, but the phosphate excretion was slightly low. The clinical diagnosis was verified by soft tissue ultrasound examination showing subcutaneous calcifications. X-ray examination of bones evidenced no abnormal calcification. Mammography revealed deep seated bilateral reticular calcifications, even in the axillary region. Histological examination showed calcinosis cutis. On these grounds, the diagnosis of idiopathic universal calcinosis cutis was made. The authors describe the clinical and histological picture and discuss the laboratory findings.     

Calcinosis cutis of the fingertip associated with Raynaud's phenomenon

Cutaneous calcification may be divided into four major categories: (i) dystrophic; (ii) metastatic; (iii) idiopathic; and (iv) iatrogenic. Dystrophic calcification is the most common type of calcinosis cutis and is associated with a variety of diseases. It most notably occurs in connective tissue diseases. Diffuse and limited cutaneous systemic sclerosis is an example of connective tissue diseases that frequently show calcinosis. We experienced a case of fingertip calcinosis cutis associated with Raynaud's phenomenon. The patient had no previous trauma, skin lesion or systemic connective tissue disease. We propose that calcinosis cutis of the fingertip may result from chronic ischemic injury caused by Raynaud's phenomenon.     

Calcinosis cutis following extravasation of calcium chloride

A 27-year-old woman with hypoparathyroidism developed multiple firm white-yellow papules along the path of an infiltrated calcium chloride intravenous infusion. A biopsy specimen obtained ten days after the extravasation revealed an urticarial reaction. A subsequent biopsy specimen, obtained 25 days after the extravasation, showed diffuse dermal calcification, confirmed by roentgenographic analysis, with incipient transepidermal elimination. A biopsy specimen obtained 40 days after the extravasation was consistent with an elimination reaction. An increase in mast cells was not noted. Electron microscopy showed mineral deposits along collagen fibrils without significant collagenous degeneration. In this report we describe a complication of intravenous calcium chloride infusion.     

Calcinosis cutis dermatologic toxicity associated with fibroblast growth factor receptor inhibitor for the treatment of Wilms tumor

Small‐molecule inhibitors (nibs) have revolutionized cancer therapy with the emergence of clinically efficacious treatment for advanced‐stage malignancies. Fibroblast growth factor receptor (FGFR) inhibitors have shown therapeutic efficacy in malignancies with molecular‐genetic alterations in the FGFR/fibroblast growth factor pathway. In a phase 1 clinical trial, erdafitinib, a pan FGFR inhibitor, was well tolerated with a manageable toxicity profile. Hyperphosphatemia was a frequent adverse event in patients treated with erdafitinib; however, no serious complications were observed with this therapy. Here, we report the development of calcinosis cutis dermatologic toxicity in a patient with hyperphosphatemia while treated with a novel selective FGFR inhibitor, INCB 54828‐101. Awareness of this form of dermatologic toxicity from an FGFR inhibitor will be important for close monitoring of serum levels of phosphate, FGF23, vitamin D, and calcitriol, the management of adverse serum chemistry with chelators, and treatment decisions to either reduce dose or withhold FGFR inhibitor.     

Solitary Milialike Idiopathic Calcinosis Cutis: A Case Unassociated with Down Syndrome

We report a unique case of solitary milialike idiopathic calcinosis cutis (MICC) in a healthy Korean woman, which is not associated with Down syndrome. This case of MICC would be a form of idiopathic calcinosis cutis, which can be solitary or multiple, sporadic or associated with Down syndrome.     

Calcinosis cutis in systemic lupus erythematosus: a case report and review of the published work

Calcinosis cutis is a common clinical feature of dermatomyositis and scleroderma but rarely reported in association with systemic lupus erythematosus (SLE). Calcinosis cutis in SLE occurs without calcium and phosphorus metabolic abnormalities and may be localized or generalized. The pathophysiology remains unclear and no effective therapy is currently available. We report a 30-year-old woman with a 13-year history of SLE who developed multiple calcinosis cutis around both knees and we review the relevant published work.     

Two cases of dystrophic calcinosis cutis in burn scars

Dystrophic calcinosis cutis is defined as the abnormal deposition of insoluble calcium salts in dead or degenerated cutaneous tissues in the absence of abnormal serum calcium or phosphate concentrations. Although dystrophic calcification can occur in various diseases, its occurrence on a burn scar has rarely been reported in the dermatologic literature. Herein we describe two patients who presented with a solitary non-healing ulcer in a postburn scar, with histopathologic evidence of calcium deposition in the dermis.     

Disseminated linear calcinosis cutis associated with the Koebner phenomenon in an infant with congenital acute monocytic leukaemia

We present a unique case of an infant with acute monocytic leukaemia who presented at birth with multiple rubbery, erythematous to violaceous subcutaneous nodules secondary to leukaemia cutis. As these infiltrates regressed with chemotherapy, numerous white to yellow linear confluent papules appeared in a scratch-like pattern. These lesions were widely disseminated but were concentrated across her face, trunk and extremities with relative sparing of the napkin area and back. We propose that these lesions represent a form of dystrophic calcinosis cutis that occurred secondary to koebnerization in an infant with congenital leukaemia cutis.     

Calcinosis Cutis in Juvenile Dermatomyositis Responsive to Aluminum Hydroxide Treatment

Calcinosis cutis is a frequent complication of juvenile dermatomyositis; however, its treatment remains unsatisfactory. We report a case of calcinosis cutis in juvenile dermatomyositis which was successfully treated with oral aluminum hydroxide. Almost complete clearing of calcinosis was observed after 8 months of therapy. There were no adverse effects from therapy. Aluminum hydroxide is worth trying in treating calcinosis cutis.     

Calcinosis cutis following the administration of intravenous calcium therapy

Calcinosis cutis, the cutaneous deposition of calcium salts in the dermis, can occur through a variety of pathogenetic mechanisms, and can be associated with both normal and elevated calcium levels. Iatrogenic causes of calcinosis cutis include extravasation of intravenously administered calcium chloride or calcium gluconate, and traumatic deposition of calcium in the skin, subsequent to electromyography or electroencephalography. We report two cases of calcinosis cutis following intravenous infusion of a calcium-containing salt.     

Milialike idiopathic calcinosis cutis and syringoma in Down's syndrome

A 6-year-old girl with Down's syndrome presented milialike whitish small papules on her hands and feet and periorbital syringoma. Histopathological examination of the hand lesion revealed small localized calcium deposits and syringoma in the adjacent upper dermis. This is a very rare but typical case of calcinosis cutis with syringoma in a patient with Down's syndrome.     

Two cases of gigantic dystrophic calcinosis cutis caused by subcutaneous and/or intramuscular injections.

We describe two female patients with gigantic dystrophic calcinosis cutis caused by a large number of subcutaneous and/or intramuscular injections which they received when they were much younger. Laboratory data and physical examinations were generally within normal limits, and we detected no disease which might induce cutaneous calcification. There are many reports of dystrophic calcinosis cutis caused by injection of several kinds of drugs. However, we found no previous report describing a patient with calcinosis cutis induced by local tissue injury from a large number of injections and with extraordinarily widespread calcification at the injection sites. Because we do not know the exact drugs injected, it is difficult to say if a specific ingredient in the injections was related to this condition. We do know that a large number of subcutaneous or intramuscular injections were frequently administered to patients who had difficulty in maintaining venous infusions in the past, so there may be similar cases of dystrophic calcinosis cutis which have not been reported.     

A case of hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber's disease) with dystrophic calcinosis cutis and retinal lesions

A 65-year-old Japanese female developed a nodule on the distal interphalangealjoint of her right thumb. She also had multiple telangiectasias on her face, oral mucosa, tongue, nasal mucosa and upper extremities. A lip biopsy showed irregularly dilated capillaries and venules lined by flat endothelial cells. The nodule in the right thumb was resected. Histopathology revealed calcium deposits in the dermis. This case was diagnosed as dystrophic calcinosis cutis within hereditary hemorrhagic telangiectasia. Ophthalmologic examination showed bilateral retinal vascular lesions with dilated and tortuous retinal venules.     

Study of a myo-inositol hexaphosphate-based cream to prevent dystrophic calcinosis cutis

Background Calcinosis cutis is a disorder caused by abnormal deposits of calcium phosphate in the skin and is observed in diverse disorders. Myo‐inositol hexaphosphate (InsP₆) is a diet‐dependent molecule found in all mammalian fluids and tissues, which exhibits an extraordinary capacity as a crystallization inhibitor of calcium salts. Objectives To establish the effects of topically administered InsP₆ cream on artificially provoked dystrophic calcifications in soft tissues. Methods Fourteen male Wistar rats were randomly assigned into two groups: control and treated groups. Rats were fed with an InsP₆‐free or phytate diet. Plaque formation was induced by subcutaneous injection of 0·1% KMnO₄ solution. From 4 days before plaque induction to the end of the experiment, control rats were treated topically with a standard cream, whereas treated rats were treated with the same cream with 2% InsP₆ or phytate (as sodium salt). Calcification of plaques was allowed to proceed for 10 days. InsP₆ in urine was determined. The plaques were excised and weighed. Results It was found that when InsP₆ was administered topically through a moisturizing cream (2% InsP₆‐rich), the plaque size and weight were notably and significantly reduced compared with the control group (1·6 ± 1·1 mg InsP₆‐treated, 26·7 ± 3·0 mg control). The InsP₆ urinary levels for animals treated with the InsP₆‐enriched cream were considerably and significantly higher than those found in animals treated topically with the cream without InsP₆ (16·96 ± 4·32 mg L^?1 InsP₆‐treated, 0·06 ± 0·03 mg L^?1 control). Conclusions This demonstrates the important capacity of InsP₆ as a crystallization inhibitor and also demonstrates that it is possible to propose topical use as a new InsP₆ administration route.