Histologic features of long-lasting chilblain-like lesions in a paediatric COVID-19 patient.

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None reported.

Dear Editor,

Since the beginning of the pandemic of coronavirus disease 2019 (COVID‐19), an increasing number of skin manifestations have been reported. , Most reports concern adult patients and describe various patterns of skin eruptions, in most of cases with low specificity and no univocal temporal association with the onset of systemic symptoms of COVID‐19. , ,

Recently, few papers describe chilblain‐like lesions (CLL) as a possible skin clue of COVID‐19 among young patients and children, mostly in the absence of systemic symptoms and with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) swab negativity. , , , , This observation is consistent with the atypical outbreak of CLL reported in high endemic COVID‐19 Italian regions among paediatric and dermatological networks.

We hereby report a case of an adolescent boy with a reverse transcriptase (RT)‐PCR‐confirmed COVID‐19 who developed long‐lasting CLL.

A 16‐year‐old boy presented to our emergency room with multiple asymptomatic erythemato‐oedematous, partially eroded, macules and plaques on dorsal aspects of the fingers (Fig. 1) and a single similar plaque on the second right toe. A complete skin examination was otherwise unremarkable.

Figure 1

(a) Multiple erythemato‐oedematous macules and plaques on dorsal aspects of the fingers. (b) Partially eroded papules. (c) Erythematous–oedematous macula on the palmar aspect of the fifth finger.

The acral findings appeared 20 days earlier preceded by about 3 days of transient dysgeusia and mild diarrhoea. He denied association with cold exposure, Raynaud's phenomenon or similar episodes in the past. The patient's mother was hospitalized due to COVID‐19 a few days after the appearance of the CLL in our patient.

Because of this anamnestic data, blood tests, nasopharyngeal swab and skin biopsy were performed despite the patient's good health. Routine blood tests including coagulation, autoimmunity, cryoglobulins and viral serologies were either within normal limits or negative. RT‐PCR for SARS‐CoV‐2 resulted positive on nasopharyngeal swab.

Histopathologic examination showed oedema of the papillary dermis, superficial and deep lymphocytic infiltrate in a perivascular and strong perieccrine pattern (Fig. 2); there were no signs of endothelial damage.

Figure 2

(a) Oedema of the papillary dermis, superficial and deep lymphocytic infiltrate in a perivascular and strong perieccrine pattern (haematoxylin–eosin stain; original magnification: ×20). (b) Higher magnification of perieccrine lymphocytic infiltrate (haematoxylin–eosin stain; original magnification: ×40).

Clinico‐pathological findings were consistent with a diagnosis of chilblains. In particular, the absence of autoimmune disorders and some pathological clues (oedema, deep infiltrate with perieccrine involvement) come out in favour of idiopathic chilblains rather than lupus erythematous chilblains. ,

The temporary connection with general mild symptoms and the positivity of RT‐PCR for SARS‐CoV‐2 has led us to suppose that CLL in our patient could be related to COVID‐19. Our case reflects the prototype reported in the literature: an adolescent in good health with occasional history of systemic symptoms preceding cutaneous lesions. , , , ,

Interestingly, we observed in our patient long‐lasting skin lesions several weeks after the first showings of the symptoms, concurrently with the positivity of the nasopharyngeal swab.

These findings may suggest that young patients with long‐lasting CLL could be carriers of the virus also in the late stage of skin eruption and so they would be crucial for containment strategies. Further clinical and pathological studies are mandatory to better know the relation between SARS‐CoV‐2 infection and CLL and the possible pathogenetic link.