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.     

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.     

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 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.     

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.     

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.     

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.     

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.     

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 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.     

A case of idiopathic vulvar calcinosis: the first in Japan.

Idiopathic calcinosis of the scrotum is a rare condition of unknown etiology. As counterparts of this male disorder, only two female cases have been reported. We report a third case, the first of its kind, in Japan. Histochemical stains revealed acid mucopolysaccharide (acid-MPS) within the calcinosis and many infiltrated mast cells near it; these might histogenese the calcium deposition. Immunohistochemically, polyclonal carcinoembryonic antigen (CEA) and keratin stains revealed no positive cells near the calcium depositions.     

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.     

病理性瘢痕的研究和治疗现状

病理性瘢痕是创伤后皮肤结缔组织异常修复愈合的结果,其组织病理学特点为成纤维细胞大量异常增生、胞外基质(胶原、蛋白多糖、糖蛋白等)过度沉积及各类胶原纤维排列紊乱。病理性瘢痕不仅影响美观,严重者会引起畸形及功能障碍。目前治疗方法主要包括:药物治疗、物理治疗、手术治疗等,但大多数难以取得满意疗效。近年来,二氧化碳点阵激光、浅层X线放疗和瘢痕防治动态方案的实施为瘢痕治疗带来了新曙光,国内外对病理性瘢痕的形成机制以及其基因缺陷研究也取得大量成果,使其从基因水平突破性治疗有了理论支持。该文将从生物学特征、形成机制以及临床治疗3方面对病理性瘢痕的研究和治疗现状进行综述。     

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.     

Subcutaneous calcification of the lower legs in a patient with mixed connective tissue disease

A 56-year-old woman who had been treated for mixed connective tissue disease (MCTD) noticed a skin ulcer on the lower leg. There was no history of trauma. X-rays of the lower legs showed extensive calcification in the soft tissue. Biopsied tissue from the ulcer showed marked calcium deposition with necrosis. Laboratory findings revealed normal serum calcium and phosphate levels and normal parathyroid function. On the basis of these findings, we diagnosed skin ulcer due to subcutaneous dystrophic calcification associated with MCTD. The ulcer was gradually reduced in size and epithelialized by treatment with local debridement and antibiotics.     

A failure of mucocutaneous lymphangiogenesis may underlie the clinical features of lipoid proteinosis

Lipoid proteinosis (LiP) (OMIM 247100) is a rare autosomal recessive disease caused by loss of function mutations in the extracellular matrix protein 1 gene, ECM1, on chromosome 1q21. LiP is characterized clinically by hoarseness in early infancy, followed by waxy papules and plaques on the face and body along with pox-like and acneiform scars. We studied a 20-year-old Japanese woman with LiP. She was born of consanguineous parents. Biopsy specimens obtained from a nodule on the elbow were used for histopathology, immunohistology and electron microscopy. Exons 6 and 7 of ECM1 were amplified by polymerase chain reaction (PCR) from genomic DNA from the proband, her parents, her brother and an unrelated person. PCR products were sequenced to detect the mutation. Histopathological examination revealed an irregular mass of calcium beneath deposits of a hyaline material in the dermis. Immunofluorescence double staining showed that the CD31-positive microvascular density was increased but that staining for the lymphatic-specific hyaluronan receptor LYVE-1 was drastically diminished in lesional compared with nonlesional skin of the patient and with normal skin. Electron microscopy revealed marked concentric reduplication of basal laminae not only around blood vessels but also around solitary dermal cells positive for Weibel-Palade bodies scattered in the hyaline material. Sequencing of the PCR products revealed a homozygous frameshift mutation, 507delT, in exon 6. This led to a premature stop codon 23 bp downstream. The results of immunopathological and ultrastructural characterization suggest that a failure of mucocutaneous lymphangiogenesis may underlie the clinical features of LiP. Identification of mutation 507delT in a Japanese patient with LiP further supports the thesis that this mutation represents a recurrent mutation in ECM1 in patients with LiP. To our knowledge, this case represents the first report of calcinosis cutis occurring in LiP.     

皮肌炎伴钙质沉着一例并国内外105例回顾分析

报道1例皮肌炎伴钙质沉着并总结相关文献。共分析总结105例皮肌炎伴钙质沉着患者,其中女59例,男46例,1~12岁患者最多,21%的患者皮损局限,以臀部、四肢为主。除典型结节、斑块外,3.8%的患者可形成钙性液体或钙化性囊性病灶,14.3%患者伴严重关节挛缩、畸形。皮肌炎伴钙质沉着多有危险因素,如持续活动性炎症反应、局部隐性损伤、抗NXP-2抗体阳性等。患者多采用多种药物联合,或者药物与外科手术联合治疗。TNF-α抑制剂等生物制剂正逐步应用于临床个案治疗。     

Ⅰ型先天性皮肤再生不良3例并文献复习

例1女,出生时头顶旋涡旁圆形皮肤缺损,表面有透明薄膜,光滑似水疱,皮损周围发红;3个月后随访,创面呈略红色菲薄纸样瘢痕愈合,触之有囊样感。例2男,例3女,出生时均于头顶旋涡中央出现椭圆形皮肤缺损,表面鲜红色、肉芽肿样,湿润有渗出物;例2于10个月后随访,创面呈肤色膜状瘢痕性愈合,例3于19个月后随访,创面呈灰白色羊皮纸样瘢痕性愈合,质地均柔软。3例瘢痕性愈合处均光滑无毛发。例1诊断为膜性Ⅰ型先天性皮肤再生不良,例2、例3诊断为非膜性Ⅰ型先天性皮肤再生不良。