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.     

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 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 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 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.     

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.     

Calcinosis cutis following contact with calcium chloride solution

Calcinosis cutis is the deposition of insoluble calcium in the cutaneous tissue. Calcinosis cutis can be classified as metastatic, dystrophic, idiopathic or exogenous. We report a 48‐year‐old white man who was dismantling a portable ice skating rink when calcium chloride solution from the pipes spilt onto his clothing. Several days later, he started to develop mildly pruritic erythematous papules, some studded with white deposits and some with umbilication over the exposed areas corresponding to the spillage of the calcium chloride solution. Histological features revealed interstitial fibrohistiocytic reaction with calcium‐encrusted degenerated collagen bundles in the dermis which was further confirmed by von Kossa stain. He was commenced on topical corticosteroid cream twice daily and the lesions cleared completely between 6 to 10 weeks.     

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.     

Case of dystrophic calcinosis cutis in epidermal cyst arising from verrucous epidermal nevus

Dystrophic calcinosis cutis is diagnosed when calcium is deposited into previously damaged tissue by connective tissue disease, panniculitis, pseudoxanthoma elasticum or trauma. We report a case of dystrophic calcinosis cutis arising from the lesion of an epidermal cyst on the verrucous epidermal nevus. A 20‐year‐old woman presented with a polypoid pinkish tumor on a brownish, verrucous plaque. Histopathological findings of the pinkish tumor showed calcium deposits as amorphous, basophilic material lining the true epidermis in the upper dermis, which were compatible with dystrophic calcinosis cutis and the plaque was diagnosed as a verrucous epidermal nevus.     

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.     

Diffuse cutaneous calculi (subepidermal calcified nodules): Case study

Four forms of calcinosis cutis exist: metastatic calcinosis, dystrophic calcinosis, idiopathic calcinosis, and subepidermal calcified nodules, usually referred to as cutaneous calculi because single, small, raised, hard nodules are present. Occasionally, there are two or three nodules, and in some instances there are numerous or even innumerable nodules. Most patients are children, but in some patients, a nodule is present already at birth or does not appear until about adult life; in some instances, the surface of the nodule is verrucous, but it may be smooth. The most common location of the nodule is the face. A 12‐year‐old Yemeni child patient presented with warty, hard‐ and smooth‐surface, white, and small and large non‐itchy numerous nodules in the face and in the four extremities, which started at 4 years after birth, of 8 years' duration. Serum levels of calcium, phosphorous, and parathyroid hormones were normal. Plain chest X‐ray, abdominal ultrasonography, and complete blood count picture were normal. Skin biopsy followed by histopathological examination was diagnostic. The patient was treated with curettage and surgical removal.     

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.     

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.     

Acquired perforating calcific collagenosis in a drug addict with rhabdomyolysis and transient hypercalcemia

Acquired perforating calcific collagenosis (APCC), which is characterized by the calcification of dermal collagen fibers with subsequent transepidermal elimination and perforation, is an extremely rare entity. Thus far, it has only been reported in a patient with direct contact exposure to calcium chloride. Here, we report a unique case of APCC occurring in a drug addict admitted for rhabdomyolysis. The present case is a 20‐year‐old male patient hospitalized for drug‐related rhabdomyolysis and multiple organ damage. During hospitalization, he gradually developed unusual skin rashes. There were multiple confluent umbilicated and keratotic erythematous to brownish papules and plaques with scratch‐like linear plaques on his lower abdomen, inguinal areas and gluteal sulci. Also, multiple well‐demarcated flesh‐colored rough, hard and thin plaques with a “crepe paper”‐like texture were found on the bilateral popliteal fossae, olecranon fossae and axillae. The histopathology of two biopsied lesions demonstrated acquired perforating calcific collagenosis. The lesions appeared during the rhabdomyolysis‐related hypercalcemia phase and resolved spontaneously after the calcium level returned to normal. This is the first reported case of disseminated APCC occurring during transient hypercalcemia due to rhabdomyolysis.     

Clinical pearls and therapeutic challenges in connective tissue disease

ABSTRACT: The management of autoimmune skin disease is extremely challenging. This article provides the clinician with clinical pearls and highlights novel/anecdotal treatments for the management of recalcitrant discoid lupus erythematosus, lupus profundus, calcinosis cutis associated with dermatomyositis and scleroderma, and intractable pruritus in autoimmune disease. The disfigurement that occurs as a result of autoimmune skin diseases may be great. This article includes a discussion of the cosmetic and psychosocial concerns of patients. Lastly, wounds and wound care in autoimmune diseases are addressed along with practical management of challenging cases such as digital ulcers in Raynaud's disease, pyoderma gangrenosum, and ulcerating striae and leg ulcers in scleroderma and dermatomyositis.     

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.