Lichen Planus

Why Stop hydrochlorothiazide and substitute another antihypertensive is correct

• This is a lichenoid drug eruption (drug-induced lichen planus): lichen planus-like violaceous, flat-topped papules that began months after starting hydrochlorothiazide and are concentrated on sun-exposed skin (extensor forearms, dorsal hands, V of the neck) with the photoprotected upper inner arms spared, the pattern expected from a photosensitizing drug such as a thiazide
• Features that favor a drug cause over idiopathic lichen planus: photodistribution, sparing of the oral mucosa (which is involved in about half or more of idiopathic cases), and eosinophils with focal parakeratosis on biopsy (idiopathic lichen planus classically shows orthokeratosis without eosinophils)
• Withdrawing the culprit is the definitive treatment; without it, any skin-directed therapy only suppresses an eruption that keeps being driven
• His hypertension still needs treatment, so an agent from another first-line class (for example, amlodipine) replaces the diuretic rather than simply stopping therapy; a thiazide-like diuretic such as chlorthalidone is avoided
• Lesions resolve over weeks to months after withdrawal, often leaving postinflammatory hyperpigmentation; a topical corticosteroid may be added for itch once the drug is stopped

Why the others are wrong

• Continue hydrochlorothiazide and apply clobetasol 0.05% cream - a superpotent topical steroid relieves itch and flattens idiopathic lichen planus, but continuing the drug leaves the cause in place, so the eruption persists or recurs (the trap is treating the rash as idiopathic lichen planus and never asking about the medication list)
• Start narrowband UVB phototherapy three times weekly for 12 weeks - phototherapy is an option for widespread idiopathic lichen planus, but this eruption is concentrated on sun-exposed skin in a patient still taking a photosensitizing drug, so light treatment can aggravate it and it leaves the culprit in place (the trap is picking a standard lichen planus therapy without noticing that the distribution points to the medication)
• Start a 3-week oral prednisone taper beginning at 40 mg daily - short systemic steroid courses are reserved for severe or widespread lichen planus, including a severe drug-induced eruption after the culprit is withdrawn, or nail disease at risk of scarring (his nails are normal); they do not address the culprit, the eruption returns when the taper ends if the drug is continued, and prednisone raises blood pressure and glucose in a hypertensive patient
• Stop hydrochlorothiazide and recheck blood pressure in 3 months - withdrawing the culprit is the right first move, but his blood pressure is controlled because of the drug; stopping it without substituting an agent from another first-line class leaves his hypertension untreated for months while the rash resolves (the trap is treating the eruption and forgetting the condition the drug was prescribed for)

Additional high-yield points

• Common culprits of lichenoid drug eruption: thiazides, ACE inhibitors, beta-blockers, antimalarials (hydroxychloroquine), gold, and PD-1/PD-L1 checkpoint inhibitors
• Latency is long, typically months to more than a year after the drug is started, so a medication begun long before the rash can still be responsible
• Idiopathic lichen planus favors the flexor wrists, shins, and buccal mucosa with Wickham striae; drug-induced lichenoid eruptions are more often photodistributed, more eczematous or scaly, and usually spare the mouth
• Nail involvement occurs in only about 10% of idiopathic lichen planus, so normal nails do not help separate idiopathic from drug-induced disease
• Oral acitretin is a systemic option for widespread or refractory idiopathic lichen planus; it is not a first step while a triggering drug is still being taken
• Hydrochlorothiazide also causes subacute cutaneous lupus erythematosus, which is annular or papulosquamous and anti-Ro (SSA) positive rather than violaceous and flat-topped
• Rechallenge with the culprit is not recommended because the eruption typically recurs

Why Lichen planus is correct

• The vignette shows the classic "6 P's": pruritic, planar (flat-topped), purple (violaceous), polygonal papules on the flexor wrists and ankles.
• The fine lacy white lines on the papule surface are Wickham striae, which are essentially pathognomonic for lichen planus when seen with side lighting or dermoscopy.
• Reticular white striations on the buccal mucosa indicate oral lichen planus, which frequently accompanies cutaneous disease.
• Lesions appearing along a scratch mark demonstrate the Koebner phenomenon, also characteristic of lichen planus.

Why the others are wrong

• Psoriasis — well-demarcated plaques with thick silvery scale on extensor surfaces (elbows, knees, scalp) and nail pitting; lesions are not violaceous, lack Wickham striae, and do not produce buccal reticular striae.
• Pityriasis rosea — a self-limited eruption with a herald patch followed by salmon-colored oval plaques in a "Christmas tree" distribution on the trunk; lesions are non-violaceous and spare the oral mucosa.
• Secondary syphilis — generalized papulosquamous eruption that characteristically involves the palms and soles, with mucous patches, lymphadenopathy, and condylomata lata; it lacks Wickham striae, and serology (RPR/FTA) is positive.
• Lichen sclerosus — shares the lichen name and intense pruritus, but it produces porcelain-white, thin, wrinkled atrophic plaques that favor the anogenital skin of women; it lacks violaceous polygonal papules with Wickham striae and rarely involves the oral mucosa.