Background. We have observed an increasing number of patients referred to the Scottish Photobiology Service (SPS), who were later diagnosed with actinic folliculitis (AF) and had positive phototesting results. Treatment options for AF are limited, with only a few reports in the literature. The use of prophylactic narrowband ultraviolet B (NB-UVB) phototherapy for AF has not previously been described, and we report on this for the first time. Aim. To analyse the clinical characteristics, phototesting results and responses to treatment for patients with AF diagnosed by the SPS. Methods. We undertook a retrospective review over 10 years of all case notes of patients who were assessed and diagnosed with AF through the SPS, based at the Photobiology Unit, Dundee, UK. Results. All 10 patients were women. Mean age of onset was 25 years and mean time to referral for investigation was 7 years. The commonest site involved was the face, with the main clinical feature being monomorphic pustules appearing after sunlight exposure. The eruption could be provoked with iterative doses of broadband UVA irradiation in five patients. All patients were offered photoprotective advice and prophylactic NB-UVB phototherapy. Five patients proceeded with phototherapy; four of these completed the desensitization course and all four reported either a delay in symptom onset or total prevention of rash induction, with complete efficacy of desensitization maintained for 3 years in one patient. Conclusion. We demonstrate the successful use of UVA provocation testing as a diagnostic tool in AF. Additionally, we recommend the use of prophylactic NB-UVB phototherapy in AF as an effective and well-tolerated approach. MethodsThis case series included all patients with a diagnosis of AF who presented to the SPS between January 2010 and December 2019. We retrospectively

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observed. This infiltrate was composed of lymphocytes and of abundant mononuclear cells that showed large vesicular nuclei and scant eosinophilic cytoplasm, mimicking small histiocytes.Immunostaining showed that these cells were strongly positive for CD68KP1, with coexpression of myeloperoxidase (Fig. 2b,c). Immunohistochemical study for cytokeratin cam 5.2 was negative, thus excluding metastatic infiltration (Fig. 2d). Blood and skin biopsy cultures came back negative.The patient was diagnosed with HSS, probably associated with her medication. Palbociclib was suspended and oral prednisone 1 mg/kg daily was started, which resulted in complete resolution of symptoms. The patient continued treatment with letrozole as monotherapy with no relapse over a follow-up period of 6 months.The pathogenesis of drug-induced HSS is poorly understood. It has been proposed that in cases of drug-induced HSS, the culprit drug may cause a rise in endogenous levels of granulocyte colony-stimulating factor (G-CSF), 3 and idiosyncratic granulocytic maturation arrest may occur in the bone marrow. During the recovery phase from this acute bone marrow insult, elevated endogenous levels of G-CSF may induce release of myeloid precursors from the bone marrow into the skin, resulting in an SSlike reaction, with a histiocytoid inflammatory infiltrate histologically. 3 Palbociclib is a first-in-class, highly selective inhibitor of cyclin-dependent kinase (CDK) 4 and CDK6. It is indicated for the treatment of hormone receptor-positive and HER2-negative advanced or metastatic breast cancer, in combination with an aromatase inhibitor as initial endocrine-based therapy. 4 Palbociclib and other CDK4/6 inhibitors (e.g. ribociclib, abemaciclib) are usually well tolerated. Severe skin reactions (grade ≥ 3) occur in < 1% of patients and have rarely been reported in the literature. 4,5 To our knowledge, this is the first report of HSS induced by a CDK4/6 inhibitor.This case illustrates that HSS can mimic cellulitis, cutaneous infiltration by cancer or lymphangitis carcinomatosa in oncology patients. It should be considered as a possible diagnosis especially if protein kinase inhibitors are being administered.