Prurigo nodularis with predominant palmar involvement

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Prurigo nodularis (PN) is a chronic condition characterised by itchy hyperkeratotic nodules.¹ Typically, PN lesions are symmetrically distributed on the extensor surfaces of the extremities and trunk, and they rarely affect the face or palms.² This disease is often difficult to treat and has both psychological and physical consequences.³

A 58-year-old woman was referred to our dermatology clinic with a 15-year history of persistent pruritic nodules on her palms. She had previously been diagnosed with palmoplantar pustulosis at a local clinic and treated with betamethasone butyrate propionate ointment (very strong class; in Japan, topical steroids are classified into ‘strongest’, ‘very strong’, ‘strong’, ‘mild,’ and ‘weak’), oral antihistamine, and oral prednisolone. However, the pruritic nodules persisted and gradually spread to her extensor surfaces of the extremities due to chronic scratching. She had no family history of atopic dermatitis. She had no history of diabetes, thyroid diseases, and psychiatric disorders. There was no history of drug exposure or occupational irritants affecting her palms. Physical examination revealed multiple papulonodular, hyperkeratotic lesions on both palms, easily eroded by scratching [Figure 1a]. Additional nodular eruptions were observed on the dorsum of the hands [Figure 1b], forearms, and lower legs with no lesions on the trunk or other body areas. The pruritus numerical rating scale (NRS) score was 9/10, and the total nodule count was approximately 200. Laboratory tests revealed markedly elevated IgE (2728 IU/mL; normal level: 0-170 IU/mL) and thymus and activation-regulated chemokine (TARC, 2678 pg/mL; normal level: 0-450 pg/mL). Eosinophil count was slightly elevated (536/µL; normal level: 70-440/µL). The rest of the complete blood count was normal. Renal and liver function tests were normal. Blood sugars and thyroid functions tests were within normal limits. HCV serology was non-reactive. A skin biopsy from a nodule on the right palm demonstrated hyperkeratosis, parakeratosis, and irregular epidermal hyperplasia. Vertically oriented collagen fibres were noted in the upper dermis [Figure 2]. Direct immunofluorescence (DIF) was negative. Based on these findings, we diagnosed the hyperkeratotic nodules as PN.

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Figure 1:

(a) Severely pruritic nodules on the palms at the first visit. (b) Intensely itchy nodules observed on the dorsum of the hands.

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Figure 2:

Hyperkeratosis, parakeratosis and irregular epidermal hyperplasia in the epidermis. Vertically oriented collagen fibers in the upper dermis (white asterisk) (Haematoxylin and eosin, 40×).

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She was treated with clobetasol propionate ointment 0.1% (strongest class) applied twice daily, and occlusive dressing therapy (ODT) was continuously performed using plastic wrap as the occlusive material. Since pruritus was insufficiently controlled with a single oral antihistamine (olopatadine 10mg twice a day), oral therapy was combined with olopatadine (10mg) twice a day and rupatadine fumarate (10 mg) nightly. After 3- weeks, the lesions showed marked improvement with a significant reduction in both size and pruritus [Figure 3a, b]. No recurrence has been observed during 15 months of follow-up.

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Figure 3:

(a) Marked improvement of palmar lesions after three weeks of treatment. (b) Flattened nodules with healed excoriation on the dorsum of the hands.

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PN is a subtype of chronic prurigo (CPG).³ The three core diagnostic criteria for CPG are: (1) the presence of multiple pruriginous lesions; (2) chronic pruritus, defined as itching lasting longer than 6 weeks; and (3) a history and/or clinical signs of prolonged scratching.³ In our case, all three criteria were met, and the patient exhibited numerous pruriginous, dome-shaped nodules over 1 cm in diameter, confirming the diagnosis of PN.

PN is characterised by multiple, firm, hyperkeratotic nodules accompanied by intense pruritus.¹ PN lesions commonly affect the trunk and extensor surfaces symmetrically.² In our case, the lesions were predominantly localised to the palms, which is a rare presentation. Rowland et al. reported that, among 46 cases of PN, only four involved the palms.⁴ Although cases of acral-limited PN have been described,⁵ published clinical photographs of palmar lesions remain very limited, making recognition and diagnosis particularly challenging.

The exact pathogenesis of PN remains unclear but is believed to involve a complex interplay between neural and immune pathways, leading to a chronic itch-scratch cycle.⁶ Previous studies have suggested that Th2 cytokine-producing cells, such as Th2 cells and basophils, play a role in the development of PN.^1,7 In our case, pruritus was triggered by chronic scratching behaviour. The occlusive dressing protected the lesions from further scratching. facilitating improvement of both the eruptions and the pruritus. Elevated IgE and TARC levels supported prior reports implicating Th2 immune responses in PN pathogenesis.⁷

Differential diagnoses for palmar nodular lesions include palmoplantar pustulosis, verruca vulgaris, and pemphigoid nodularis. Histopathological examination and DIF are essential for accurate diagnosis.² In our case, the absence of immunoreactants and the presence of characteristic histological features supported the diagnosis of PN.

This case of PN with predominant palmar involvement highlights the importance of considering PN in the differential diagnosis of nodular lesions on the palms, despite its rarity.