Clofazimine-induced pigmentation in a breastfed infant of a mother with chronic erythema nodosum leprosum

Dear Sir,

Clofazimine is an important component of multidrug therapy for multibacillary leprosy and is also frequently administered in higher doses for chronic erythema nodosum leprosum (ENL). Cutaneous reddish-brown to black pigmentation is a well-recognized adverse effect of clofazimine therapy in adults, resulting from drug accumulation within macrophages and subcutaneous tissues. However, pigmentation occurring in breastfed infants secondary to passive exposure through breast milk is rarely reported.

We report a one-year-old male infant who presented with diffuse reddish-brown hyperpigmentation predominantly involving the face and upper trunk [Figure 1]. The child was developmentally normal with appropriate anthropometric parameters (weight 9.2 kg, length 77 cm, and head circumference 45 cm). There was no history suggestive of systemic illness, drug intake, or familial pigmentary disorder.

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Figure 1: Diffuse reddish-brown facial pigmentation in a one-year-old breastfed infant secondary to passive exposure to maternal clofazimine therapy administered for chronic erythema nodosum leprosum (ENL).

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The infant’s mother had been diagnosed with lepromatous leprosy during the third trimester of pregnancy. Slit-skin smear examination revealed acid-fast bacilli with a bacillary index of 5+. Histopathological examination of a skin biopsy was consistent with lepromatous leprosy. Three months after initiation of multidrug therapy, she developed painful erythematous nodular lesions suggestive of ENL. Fine-needle aspiration cytology from a thigh lesion showed inflammatory infiltrates consistent with active ENL, while repeat slit-skin smear demonstrated a bacillary index of 6+. She was treated with multidrug therapy, including high-dose clofazimine (200 mg/day) along with intermittent corticosteroids.^[1,2] The infant was predominantly breastfed during this period.

Clinical examination of the child revealed diffuse reddish-brown pigmentation over the face and trunk without mucosal involvement. Hair, nails, and systemic examination were normal. Ophthalmological evaluation did not reveal conjunctival or retinal pigmentation.

The infant was evaluated to exclude alternative causes of generalized hyperpigmentation. Complete blood count, liver and renal function tests, iron profile, serum vitamin B12, folate levels, serum electrolytes, and glucose-6-phosphate dehydrogenase screening were within normal limits. A skin biopsy was not performed because the pigmentation was gradually improving, and the parents did not consent to an invasive procedure.

Considering the temporal association with maternal high-dose clofazimine therapy during breastfeeding, absence of alternative etiologies, and gradual spontaneous improvement after reduction of exposure, a diagnosis of clofazimine-induced hyperpigmentation secondary to passive exposure through breast milk was made.^[3] Pigmentation began to fade over 6–8 weeks and showed marked improvement by 3 months [Figure 2]. This case highlights a rare yet benign and reversible adverse effect of clofazimine exposure in breastfed infants. Recognition of this entity is important to avoid unnecessary investigations and to reassure caregivers regarding the self-limiting nature of the pigmentation.

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Figure 2: Marked resolution of facial hyperpigmentation following discontinuation of maternal clofazimine therapy after 3 months, supporting the diagnosis of transient clofazimine-induced pigmentation in the infant.

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