Oral lichenoid lesions as a sign of Good’s syndrome

Abstract

basement membrane zone with C3 (Figure 3). In addition, there were few colloid bodies in the upper dermis staining with IgG, IgM, and IgA. Systemic steroids were instituted at a dose of 1 mg/kg, which was gradually tapered over a period of 3 months.The disease responded well to the treatment.LPP was earlier thought to be an overlap of bullous pemphigoid and LP but is increasingly considered a unique disease entity in itself. As the majority of cases of LPP have lesions of LP preceding bullous eruption, it is proposed that the lichenoid inflammation might actually promote the development of an autoimmune response, which targets proteins of the epidermal basement membrane. 1-3 Differential diagnoses having similar clinical and histopathological features include bullous lichen planus, erythema multiforme, atypical subacute cutaneous lupus erythematosus, and paraneoplastic pemphigus. Diagnosis is made by a thorough history taking, examination, histopathology, immunofluorescence, and immunoblotting.The case reported is typical of LPP with classical clinical features with lesions having a propensity to appear more on the peripheral sites rather than in a generalized fashion. 4 The histopathology and direct immunofluorescence were also suggestive of LPP. Unfortunately, immunoblotting could not be performed because of unavailability at the institute. We postulate that the Wickham striae (WS) visualized on dermoscopy corresponds to the beaded hypergranulosis seen on histopathology, which is visible as the cleft is subepidermal in nature. WS is considered the hallmark of LP and is pathognomic of the disease. 5 The central dimple, that is, structured white globule, might correspond to the infundibulum of hair.