PATIENT HISTORY

A 35-year-old man with HIV who is highly compliant with his antiretroviral regimen is otherwise healthy and presents with small bumps all over his body as seen in Figures 1 and 2. These lesions are not particularly pruritic and are otherwise asymptomatic. A review of systems was negative, and he denies close contacts with similar findings. He notes the bumps mainly on the abdomen and arms but is most concerned about the lesions on his penis. On examination, the penile lesions are 1- to 3-mm monomorphic papules, highly concentrated on the head of the penis, over the entire mucosal surface (not only the corona), with a few lesions on the shaft of the penis. He is concerned that the lesions are warts and may be contagious.

FIGURE 1. Linear array of 1- to 3-mm flesh-colored papules on the right forearm.

FIGURE 2. One- to 3-mm flesh-colored papules on the abdomen.

MULTIPLE-CHOICE QUESTION

Which of the following is true of his diagnosis?

a. The lesions are contagious and due to a cutaneous fungal infection.

b. The lesions are benign and not contagious.

c. The lesions are secondary to a bacterial infection; he is at an increased risk due to HIV status.

d. The lesions are of autoimmune origin and require immunosuppressive therapy.

e. The lesions are malignant.

DISCUSSION

Lichen nitidus (LN) is an inflammatory skin disease with lesions that are classically described as highly uniform, flat-topped, grouped, flesh-colored papules. Most commonly, LN occurs in school-aged children and is predisposed to the upper extremities, trunk, and head of the penis (Payette, Weston, Humphrey, Yu, & Holland, 2015). The Koebner phenomenon is a hallmark of this disorder and occurs in almost all cases of LN, where trauma can induce linear lesions as seen in Figure 1 (Tilly, Drolet, & Esterly, 2004). LN is generally asymptomatic and only sometimes pruritic. Less common features reported include palmoplantar hyperkeratosis and nail changes including ridging and dystrophy (Munro, Cox, Marks, & Natarajan, 1993).

LN lesions, which are typically flesh colored, may also vary in color from yellow to brown to violaceous, a feature that helps distinguish LN from lichen planus (LP), which is more consistently violaceous. LN lesions are classically 1 to 3 mm or pinhead sized, smaller than those of LP, and are also less likely to have scale compared with LP. The distinction between LN and LP should be made clear as the two diseases often coincide; nearly a third of patients with LP also have LN-like lesions (Wilson & Bett, 1961). Histologically, LP and LN share certain features including vacuolization of basal keratinocytes and an inflammatory infiltrate, similar to many lichenoid reactions. One striking histologic feature distinguishes LN from LP. In LN, the infiltrate in the papillary dermis is typically a focal, well-circumscribed, heterogeneous collection of lymphocytes as well as macrophages (Payette et al., 2015). Surrounding this structure are elongated rete ridges, giving rise to a characteristic "ball-in-claw" appearance.

LN is rarely associated with systemic disease but is speculated to have an association with diseases that affect immune function. For example, generalized LN, which is rare, has been described in patients with Crohn's disease (Wanat, Elenitsas, Chachkin, Lubinski, & Rosenbach, 2012). LN has also been reported to present as a lichenoid photoeruption in patients with HIV (Berger & Dhar, 1994). In populations with darker skin, LN can present seasonally in the summertime as a photodistributed lichenoid eruption, also called actinic LN (Hussain, 1998).

LN is typically asymptomatic. Although the lesions may last a year or longer, they tend to eventually resolve spontaneously. Therefore, treatment of LN is usually unnecessary. In some cases, topical high-potency to midpotency corticosteroids, as well as avoidance of sun exposure in cases of actinic LN, have hastened resolution (Hussain, 1998).

Regarding the clinical question, Options a and c are incorrect because LN is not due to a cutaneous infection, despite a relationship with HIV. LN is not malignant, so Option e is incorrect. LN is not considered strictly autoimmune (although it may be part of the pathogenesis), and treatment is often not necessary (d). The correct answer is that LN is benign (b); no additional treatment is usually needed other than topical corticosteroids for pruritus, as discussed above.

REFERENCES