Metastatic calcinosis cutis

Calcinosis cutis may be associated with metastatic calcification, dystrophic calcification, tumoral calcinosis, or may be deemed idiopathic. The association of cutaneous calcification with metastatic or tumoral calcinosis is quite rare. A case of metastatic calcinosis cutis in a woman with chronic renal failure and secondary hyperparathyroidism is presented. Other causes of calcinosis cutis are discussed briefly.     

A dystrophic calcinosis cutis case treated with CO2 laser

Abstract

Calcinosis cutis is the deposition of insoluble calcium salts within cutaneous tissue. It may be divided into four major subtypes: dystrophic, metastatic, idiopathic, and iatrogenic. The most common subtype is dystrophic calcinosis cutis. It can occur as a result of local tissue injury. We herein present a child with dystrophic calcinosis cutis developed following trauma and successfully treated with CO₂ laser.     

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.     

Dystropic Calcinosis Cutis Secondary to Intrauteriee Herpes Simplex

A neonate had numerous positive skin cultures for herpes simplex virus (HSV) as well as associated abnormalities strongly suggestive of a maternal intrauterine infection. In addition, he was noted to have dystrophic calcinosis cutis involving the back and buttocks. We believe the dystrophic calcinosis cutis occurred as a consequence of the HSV infection.     

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.     

Calcinosis cutis: a complication of intravenous administration of calcium glucanate

Calcinosis cutis, the deposition of calcium in the dermis, can be dystrophic, metastatic, iatrogenic, or idiopathic. Here, we describe a case of iatrogenic calcinosis cutis secondary to extravasation of an intravenous calcium-containing solution in a child. We also review the literature regarding the pathogenic mechanisms involved in the development of calcinosis cutis after extravasation injuries. While iatrogenic calcinosis cutis is generally a benign entity, it is important to recognize its unique clinical and histopathologic presentation to avoid complications from misdiagnosis.     

Dystrophic calcinosis cutis in subacute lupus

Dystrophic calcinosis cutis is known to be associated with various connective tissue disorders but to the best of our knowledge has never been reported in subacute cutaneous lupus erythematosus (SCLE), a distinctive cutaneous subset in the spectrum of lupus erythematosus. It occurs without calcium and phosphorus metabolic abnormalities and may be localized or generalized. We report a patient with SCLE who developed calcinosis cutis and had normal serum calcium and phosphorus levels and, interestingly, a normal concentration of blood ionized calcium. This latter, which represents the active form in the total amount of blood calcium, is a parameter only rarely assessed in patients with dystrophic calcinosis cutis. Thus, other pathogenic factors should be investigated to clarify the pathophysiology of the dystrophic type of calcification.     

Lack of response to intravenous sodium thiosulfate in three cases of extensive connective tissue disease‐associated calcinosis cutis

Dystrophic calcinosis cutis is a debilitating condition of calcium salt deposition in the skin often occurring in association with connective tissue disease (CTD). Available treatments for calcinosis cutis are unsatisfactory, but given the recent use of topical and intralesional sodium thiosulfate (STS) to treat calcifying disorders, we sought to describe the use of intravenous (IV) STS for CTD‐associated dystrophic calcinosis cutis. We report three patients with long‐standing and extensive CTD‐associated calcinosis cutis treated with IV STS after having failed multiple prior therapies. All three patients experienced fatigue and nausea with STS infusions, and none of the patients had notable clinical or symptomatic improvement of calcinosis. It remains to be seen whether the administration of IV STS earlier in the onset of calcinosis might be of benefit given that these patients all had long‐standing and refractory CTD‐associated calcinosis. Given the small number of patients in this series, further investigation into the use of IV STS in calcinosis cutis is warranted.     

An unusual adverse effect of nadroparin injections: Calcinosis cutis

In 1988, Tumiati et al described the first case of calcinosis cutis related to a calcium-containing heparin. Since then, only 18 cases have been reported in the literature; they usually have an altered calcium-phosphate product, an elevated parathyroid hormone (PTH), or both. We report a 33-year-old patient who developed calcinosis cutis at sites of nadroparin injections without any disturbance of calcium-phosphate product, PTH, or vitamin D. The pathogenesis of calcinosis cutis secondary to nadroparin injections remains controversial; Proposed causes included metastatic, dystrophic, iatrogenic, or multifactorial etiologies. This is the first case of multiple nodules of calcinosis cutis without alterations of calcium-phosphate product, PTH, or vitamin D, which supports an iatrogenic mechanism. We also suggest that calcinosis cutis could be more frequent than we thought and is probably an underdiagnosed entity.     

Self-healing dystrophic calcinosis following trauma with transepidermal elimination

An unusual case of dystrophic calcinosis that occurred following trauma is presented. Calcinosis cutis is the deposition of calcium phosphate into the skin. It is classified as dystrophic if calcium and phosphorous levels are normal and tissue damage is present, idiopathic if calcium and phosphorous levels are normal and no tissue damage is present, or metastatic if there is hypercalcemia or hyperphosphatemia. The numerous causes of underlying tissue damage associated with dystrophic calcinosis are discussed.     

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 in a patient with eosinophilia-myalgia syndrome: case report

Eosinophilia-myalgia syndrome (EMS) often is a disabling disorder caused by the consumption of contaminated L-tryptophan. Affected patients present with an array of symptoms, including cutaneous manifestations, peripheral eosinophilia, myalgias, and long-term neurocognitive disability. This article is the first reported case of a patient with EMS who developed calcinosis cutis. While many long-term sequelae of EMS are reported in the literature, there are no reports of the development of dystrophic calcification in these patients. The calcinosis cutis in this patient with EMS may represent a new manifestation of EMS that has not been documented to date. If more patients with EMS develop calcinosis cutis, it will present a therapeutic challenge to the physicians managing these patients.     

Dystrophic calcinosis cutis in pseudoxanthoma elasticum

Pseudoxanthoma elasticum (PXE) is a genetic disorder in which elastic fibers become calcified with prominent cutaneous, ocular, and cardiovascular features. Calcinosis cutis is an acquired disorder of calcium deposition in cutaneous tissues that occurs as one of the following forms: dystrophic, metastatic, idiopathic, and iatrogenic. We report a case of a woman with PXE who developed widespread dystrophic calcinosis cutis in areas affected by PXE. Although tumoral calcification and nephrolithiasis have been reported in patients with PXE, only one other case in the English-language literature of PXE and calcinosis cutis has been reported and this case was characterized by small, milia-like papules on the front of the neck, without significant discomfort, whereas our patient had widespread involvement that was very painful and pruritic. On 6-month follow-up, this patient had only mild improvement after treatment with an anti-itch lotion and aluminum hydroxide, with which she was noncompliant.     

Calcinosis cutis presenting years before other clinical manifestations of juvenile dermatomyositis: Report of two cases

Calcinosis cutis in dermatomyositis is dystrophic calcification appearing late in the course of the disease. Two cases are reported here of calcinosis cutis that presented years before other clinical manifestations of juvenile dermatomyositis. The first case was a 14-year-old Thai girl who had asymptomatic subcutaneous nodules that spontaneously ruptured, exuding a chalky discharge and healing with an atrophic scar 8 years before the onset of other clinical manifestations of juvenile dermatomyositis; that is, Gottron's papules, proximal muscle weakness grade IV/V with atrophy, slightly elevated serum creatinine phosphokinase level and an abnormal electromyogram compatible with myopathy. The second case was a 15-year-old Thai boy who had calcinosis cutis 3 years before the onset of other clinical manifestations of juvenile dermatomyositis, and the calcinosis cutis was so severe that it interfered with the movement of his extremities. Both cases responded well to aluminium hydroxide therapy.     

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.     

Nanobacteria and calcinosis cutis

BACKGROUND: The nanobacteria are a recently characterized group of extremely small bacteria capable of precipitating calcium salts implicated in the pathogenesis of urinary calculi and calcific atherosclerosis. The pathogenesis of calcinosis cutis and its significance in conjunction with a variety of unrelated scarring and pre-existing cutaneous entities are incompletely understood. METHODS: A series of cases, including basal cell carcinoma with dystrophic calcification, subepidermal calcified nodule, pilomatricoma, and tumoral calcinosis, were ultrastructurally examined for the presence of Nanobacteria sp. RESULTS: All cases, including three basal cell carcinomas, two subepidermal calcified nodules, three cases of pilomatricoma, and two cases of tumoral calcinosis, were negative for Nanobacteria. CONCLUSIONS: The dystrophic calcification that occurs in conjunction with the above entities does not likely involve a bacterial-induced etiology. The cause of these entities remains unknown.     

Dystrophic calcinosis cutis after subcutaneous administration of para‐aminosalicylic acid for treatment of pulmonary tuberculosis

An 81‐year‐old women presented with monstrous subcutaneous mobile masses on the ventral and ventrolateral surfaces of her thighs. Radiography as well as computer tomography showed extensive soft tissue calcifications. We interpreted these alterations as dystrophic calcinosis cutis, most likely resulting from repeated subcutaneous PAS infusions for the treatment of pulmonary tuberculosis.     

Childhood Calcinosis Cutis

Abstract: Calcinosis cutis, an uncommon disorder characterized by hydroxyapatite crystals of calcium phosphate deposited in the skin, has been described infrequently in childhood. Classically, it is divided into dystrophic, metastatic, and idiopathic types. We report an 8-year-old girl with hyperphosphatemia secondary to a tumor lysis syndrome, who developed a localized soft tissue calcification over a previous lesion of ec-thyma gangrenosum. Intravenous infusion of calcium gluconate was probably the precipitating factor. Our case illustrates that several etio-pathogenic mechanisms may be simultaneously involved in calcinosis cutis.     

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.     

Milia-like idiopathic calcinosis cutis

Milia-like idiopathic calcinosis cutis is a rare entity. Only 17 cases have been reported so far. Two-thirds of these have been associated with Down syndrome. We report the fifth case occurring in a child without Down syndrome. Milia-like idiopathic calcinosis cutis has long been regarded as a peculiar subtype of idiopathic calcinosis cutis. The pathogenesis of the disorder remains unclear.