Abstract
Sir, Lichen planus (LP) is categorized as a chronic inflammatory skin disease of unknown etiology that involves immune reactions. It is characterized by flat-topped, polygonal, violaceous papules and plaques. It has various clinical presentations, such as classical LP, hypertrophic LP, LP pigmentosus, and linear LP (LLP). Primary aldosteronism (PA) is known to pose a higher risk of causing multiple autoimmune diseases [1]. Herein, we report a case with LLP and PA present at the same time. A 72-year-old Japanese female presented herself to our hospital with a three-month history of slightly itchy skin lesions on the lower right leg. A physical examination revealed flat-topped plaques on the lower right limb extending from the middle of the leg to the dorsum of the foot (Fig. 1a). There was no oral or nail involvement. The patient had a history of hypertension from the age of 62 years and was diagnosed with PA afterward. The patient had been treated with an antihypertensive drug since then without change in internal medication. The patient had no history of a preceding trauma, dental metal fillings, hepatitis, metastatic cancer, or any other infections. A histopathological examination of a skin biopsy from a lesion on the right leg revealed hyperkeratosis, a saw-tooth appearance of the epidermis, and severe liquefaction degeneration. A band-like lymphocytic infiltration was present in the upper dermis (Figs. 2a and 2b), as well as lichenoid infiltration into the dermis composed of CD4+ and CD8+ T lymphocytes. Predominantly, CD8+ T lymphocytes infiltrated into the epidermis (Figs. 2c and 2d). Clinical and histological findings confirmed the diagnosis of LPP.
Highlights
The patient was treated with a topical corticosteroid
The patient had been taking eplerenone, an oral aldosterone antagonist, for eight years since the diagnosis of primary aldosteronism, but the medication remained unchanged after blood pressure became well controlled
The exact etiology of our patient’s linear LP (LLP) is unknown and we speculated that the coexistence of primary aldosteronism could have been one trigger
Summary
The patient was treated with a topical corticosteroid. The lesions improved after six months (Fig. 1c). Our case had no history of recent vaccination or episodes of allergic reaction to metals. The patient had been taking eplerenone, an oral aldosterone antagonist, for eight years since the diagnosis of primary aldosteronism, but the medication remained unchanged after blood pressure became well controlled. The lesions improved without change in drugs.
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