Photolocalized varicella in an adult

Sakiyama, Masayuki; Maeshima, Hirotaka; Higashino, Toshihide; Kawakubo, Yo

doi:10.1111/bjd.12814

Cited by 9 publications

(10 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although viral rashes aggravated by sun exposure, trauma, and inflammation have been described, photolocalized varicella is rare, and the typical distribution may not be seen. 1 As with our patient, a mild viral prodrome or constitutional symptoms are often reported. This case highlights the importance of including varicella in the differential diagnosis of a photolocalized eruption, especially in a patient with a known history of exposure and immunosuppression.…”

supporting

confidence: 73%

A photodistributed eruption in an immunosuppressed patient

2021

View full text Add to dashboard Cite

supporting

confidence: 73%

A photodistributed eruption in an immunosuppressed patient

2021

View full text Add to dashboard Cite

“…In varicella, it is known that eruptions sometimes localize in sunburned areas, called photolocalized varicella. 11,12 In this photolocalized varicella, vesicles appear earlier and more in sunburned areas. This phenomenon clearly indicates that vesicle formation is influenced by the condition of local skin, independent of systemic immunity.…”

Section: Correlation Between Onset-measurement Time Lapse and Antibodmentioning

confidence: 88%

“…The reason for the inter‐subject variation is yet unknown. In varicella, it is known that eruptions sometimes localize in sunburned areas, called photolocalized varicella . In this photolocalized varicella, vesicles appear earlier and more in sunburned areas.…”

Section: Discussionmentioning

confidence: 99%

Relationship between serum anti‐varicella zoster virus antibody titer and time from onset of herpes zoster

Ihara

Miyachi

Imafuku

2017

The Journal of Dermatology

View full text Add to dashboard Cite

Herpes zoster is an internal reactivation of varicella zoster virus, and its onset depends on immunity against this virus. We have previously reported that antiviral antibody titers are inversely correlated with patient numbers. In this study, we hypothesized that patients with higher titers may be late visitors to the clinic, whose antibodies were already boosted at presentation because of the time lapse between onset of zoster and measurement of antibodies. We analyzed antibody titers of patients with acute herpes zoster who visited Fukuoka University Hospital from January 2009 to May 2016 (n = 141, 62 males and 79 females). Varicella zoster virus-specific immunoglobulin G, M and complement fixation tests were positive in 93.9%, 12.0% and 64.2% of the patients, respectively. Immunoglobulin G and complement fixation titers were strongly correlated (Spearman's r = 0.8634, P < 0.0001). Patients with high immunoglobulin G and complement fixation titers were immunoglobulin M-negative. Unexpectedly, immunoglobulin G and complement fixation titers showed large inter-subject variation, and were only weakly correlated with onset-measurement time lapse. Patients with consecutive tests tended to show increasing immunoglobulin G and complement fixation titers. Our data suggest that herpes zoster preferentially occurs in patients with low immunoglobulin G and complement fixation titers, and subsequently causes antibody elevation. However, the timing of elevation varies and can be as late as 10 days after zoster. The large variation in antibody titer over the time from onset to testing suggests that some mechanism exists that resists the local breakthrough of virus in the skin, and so delays the onset of blisters.

show abstract

“…8,9 The potential mechanisms of photoaggravation in viral disease have been discussed. [8][9][10] Theoretically, ultraviolet radiation could trigger and/or aggravate eruptions in viral disease through the following mechanisms: (1) cutaneous inflammation with increased capillary permeability and deposition of viral particles, (2) immunosuppression, (3) increased viral proliferation caused by thermal cell membrane damage, (4) virus dissemination by infected melanocytes distributing melanin, and (5) binding of infected lymphocytes to keratinocytes as a result of enhanced expression of intercellular adhesion molecule 1. 9,10 The 2 reported cases demonstrate that viral disease may mimic a photodermatosis.…”

Section: Discussionmentioning

confidence: 99%