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Diffuse Lacy Reticular Calcinosis in Juvenile Dermatomyositis.

A 14-year-old girl presented with multiple tender skin-colored to hyperpigmented firm-to-hard nodules over lower abdomen, buttocks, and thighs (Fig. 1A), along with proximal muscle weakness affecting both upper and lower limbs. There was history of periorbital erythema and edema, suggestive of a heliotrope rash. Her laboratory parameters were significant for positive antinuclear antibody (1:100, 1+ speckled pattern) and elevated lactate dehydrogenase level (708 U/L; reference range, 200–420 U/L) and erythrocyte sedimentation rate (45 mm/h). Complete blood cell count, liver and renal function tests, serum calcium, and creatine phosphokinase were within normal limits. Electromyography showed an inflammatory myopathic pattern. Histopathology from the nodule on left thigh showed irregular basophilic calcium deposits in the deep dermis and subcutis, along with foci of hyalinization in the lobular panniculus (Fig. 1B). Radiographic imaging demonstrated subcutaneous calcification in a lacy reticular pattern encasing the lower trunk, thighs, and legs (Fig. 2). The patient was initiated on monthly pulsed corticosteroids (dexamethasone 50mg daily for 3 days), weeklymethotrexate 10mg, hydroxychloroquine sulphate 100 mg/d, and intravenous pamidronate (1 mg/kg per day for 3 days every month), along with supportive physiotherapy. There was good improvement in muscle strength in the next 3 months, but only minimal improvement in calcinosis cutis. Juvenile dermatomyositis is characterized by a combination of cutaneous lesions such as heliotrope rash, Gottron's papules and confluent violaceous macular erythema, and symmetrical proximal myopathy. Unlike its adult counterpart, juvenile dermatomyositis has a higher incidence of calcinosis, vasculopathy, and metabolic abnormalities such as insulin resistance. Calcinosis cutis occurs due to dystrophic deposition of insoluble calcium salts in the skin, subcutaneous tissues, fascia, and muscle, and has been reported to occur in 10% to 70% of patients with juvenile dermatomyositis. It is usually related to longstanding and severe disease, delayed initiation of treatment, or inadequately treated disease, and is potentially linked to genetic polymorphisms in TNF-α-308 allele. Radiologically, 4 patterns of calcinosis in juvenile dermatomyositis have been described: