Seborrhoea Herpeticum: A distinct entity or mere coincidence

Dear Editor,

Seborrheic dermatitis (SD) is a frequently encountered chronic inflammatory skin condition. Its manifestations span a spectrum from mild scaling of the scalp to erythematous papules and plaques adorned with greasy yellowish scales in regions rich in sebaceous glands such as the scalp, face, and trunk.[1]

The predominant approach to treatment focuses on addressing the commensal yeast Malassezia along with symptomatic relief with anti-inflammatory therapies.[2] Despite employing all such modalities, certain individuals still experience persistent and widespread SD that proves challenging to manage. We hereby present one such challenging case that propelled us to dig deeper into the triggers of this inflammatory dermatosis, revealing an unlikely pathogen and shedding new light on the possible underlying mechanism of this condition.

A 29-year-old male with no known co-morbidities, presented with recurrent episodes of itchy scaly lesions on his scalp for the past 3 years. The scale on the scalp varied in appearance, ranging from thin white and flaky to thick, yellow, and greasy looking. He reported frequent exacerbations occurring more than six times a year, during which the area of involvement extended to the eyebrows, forehead, nasal crease, and chest region with red raised lesions covered with thick dirty-looking greasy scales. He did not give any history of photosensitivity, thick silvery scaly plaques with winter exacerbation, itchy oozy lesions, exacerbation of lesions with spicy or hot food intake, or drug intake before the onset of lesions. There was no history of involvement of any mucosa, fever, joint pains or weight loss.

Dermatological examination revealed multiple polysized well defined erythematous plaques involving the scalp, anterior hairline, eyebrows, glabella region of forehead, nasal alar creases, nasolabial, mentolabial folds, chin, and central chest (sternum area) [Figure 1]. The plaques were covered with thick yellowish-greasy scales in some areas and thin fine white scales in other areas. Seborrheic Dermatitis Area and Severity Index (SEDASI) score was 52 (suggestive of severe SD). Dermoscopy using 3Gen Dermlite DL4 Polarised dermoscope revealed dirty yellow scales (yellow arrow) on a pinkish background with dotted vessels (black star) and uniform cylindrical, solid, off-white-coloured deposits encircling normal hair follicles in the nasal crease suggestive of sebaceous filaments (green arrow) [Figure 2]. Palms, soles, and mucosae were uninvolved.

Figure 1.

Multiple polysized well-defined erythematous plaques involving the scalp, anterior hairline, eyebrows, glabella region of forehead, nasal alar creases, nasolabial, mentolabial folds, chin, and central chest

Figure 2.

Dermoscopy using 3Gen Dermlite DL4 Polarised dermoscope revealed dirty yellow scales (yellow arrow) on pinkish background with dotted vessels (black star) and uniform cylindrical, solid, off-white-colored deposits encircling normal hair follicles in the nasal crease suggestive of sebaceous filaments (green arrow)

Based upon the highly distinctive area of involvement, and clinical and dermoscopic features, a diagnosis of SD was reached. Routine hematological and biochemical investigations were within normal limits. Serology for human immunodeficiency virus, hepatitis C virus and hepatitis B surface antigen were negative. The individual was initially managed with oral antifungals (capsule itraconazole 100 mg twice a day) along with mild topical desonide lotion to control the flare followed by topical antifungals and antifungal shampoo. There was partial remission with treatment; however, the disease recurred with increased severity even before stopping treatment.

Despite good compliance to treatment and adequate precautions to prevent flare, the individual continued to have frequent severe recurrent episodes. He was then thoroughly re-evaluated and antibodies against Herpes simplex virus (HSV) were tested given reference of one previous case report of recalcitrant SD in an infant with high anti-HSV titers.[3] IgM HSV was negative and IgG anti-HSV was elevated at 700.92 [>19 AU (Arbitary units)/ml is positive]. He was then started on suppressive antiviral therapy (Tab acyclovir 400 mg twice a day) with which he had significant improvement with a SEDASI score of 5.4 within a month [Figure 3] and complete clearance after two months. Presently the patient is on follow-up and no recurrence of disease is observed after 6 months of starting antiviral therapy.

Figure 3.

Improvement in lesions after one month of treatment with acyclovir suppressive therapy

Seborrhoea herpeticum, an arcane term, has only one mention in literature by Steadman et al.[3] that too in an infant. In our case, the characteristic vesiculo-pustules on an erythematous base or erosions as mentioned in literature for eczema herpeticum were not seen. However, the marked improvement in SD lesions on starting antivirals and decrease in the frequency and severity of recurrences on suppressive therapy with acyclovir led us to hypothesize that there is a probable causative link between HSV and SD.

We did a thorough review of the literature to look for possible correlation between the two entities. We found several possible mechanisms for how SD can create a fertile ground for HSV [Figure 4a][4,5,6,7,8,9] and a few mechanisms as to how HSV can aggravate SD [Figure 4b].[4,5,10] Also, both conditions have common triggers like sunlight, psychological stress, fever, or illness, which can explain the co-occurrence.[1,10,11]

Figure 4.

(a) Effect of seborrheic dermatitis or Malassezia on HSV. (b) Effect of HSV on seborrheic dermatitis or Malassezia

Even after adequate treatment with antifungals and steroids which are the mainstay of therapy in SD, symptoms kept recurring in our case which outlined the importance of a much broader understanding of SD, beyond the central key role of Malassezia to develop a long-term cure and prevention of SD recurrence. It is suggested that the role of HSV be considered in cases of recalcitrant SD and further studies may be taken up to confirm this association.

Declaration of patient consent

The patient in this manuscript has given written informed consent to the publication of his case details and photographs.

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Funding Statement

Nil.