Factors associated with the healing time of pemphigus vulgaris oral lesions: A prospective study

Abstract

Objectives This study determines the healing time of lesions on different locations and the contributing factors to the healing time in patients with pemphigus. Methods In this prospective study, newly diagnosed patients with mucosal lesions were included. A dermatologist evaluated the lesions, disease status, side effects and assigned the PDAI. Follow‐up visits were conducted monthly until the patient reached complete remission and every three months thereafter. A Tzanck smear was performed on lesions clinically suspected to be herpetic in origin. Results Sixty patients enrolled in the study with a mean age of 45.9 ± 11.7 years. The buccal lesions took the longest to resolve (73[33.5–105.5] days). However, the posterior pharynx lesions showed the shortest healing time (20[13.0–25.5] days). The likelihood of improvement in buccal and soft palate lesions decreased by 5% and 3% with each additional year of age, respectively. Also, the resolution duration of soft palate lesions was significantly shorter in female patients than males (median of 24.0 days vs. 38.5 days). In contrast, lower gingival lesions resolve significantly faster in male patients by a median of 9 days. Herpes simplex virus infection increases the healing time of lesions by 26 days (median of 55 days vs. 29 days, hazard ratio 2.62, 95% CI: 1.04–5.92). Conclusions Buccal and lower gingival lesions are more recalcitrant to treatment, while posterior pharynx lesions heal most rapidly. Furthermore, older age was also associated with a lower rate of lesion improvement.

Detection of herpes simplex viruses in the oral lesions of patients with pemphigus vulgaris: Is it diagnostic or predictive of disease severity?

“…However, this hypothesis has not yet been fully documented by evaluating HSV infection in immunocompetent PV patients using reliable gold standard methods in a large sample size and control group. Furthermore, the findings of previous studies on the relationship between HSV infection and PV were controversial 10–13 . In the present study, we evaluated HSV positivity in oral mucosal lesions of patients with new onset PV using the molecular gold standard method (PCR) in comparison with the control group consisting of a wide range of PV‐unrelated oral mucosal lesions.…”

“…Considering the contradictory findings of previous studies, 9–12 it is not yet clear whether tracking HSV genome in tissue or evaluating serum levels of HSV antibodies can predict PV severity. Nevertheless, what we found in our study was that the existence of HSV genome in oral lesions could not be a predictor of PV severity.…”

“…Viral infections have been shown to stimulate disease‐related autoimmunity. In this context, the central role of herpes viruses in the incidence and exacerbation of PV has been widely studied 9,10 . For the first time, the close link between herpes simplex viruses (HSVs) and the risk for PV was described by Krain and colleagues in 1974.…”

“…Based on the detection of HSV‐specific DNA in swabs taken from PV oral lesions, it was hypothesised that antiviral therapeutic regimens could improve the disease‐related lesions 12,13 . Furthermore, HSV infection was found to be related to exacerbation of PV manifestations 10,11 . Although previous studies have reported a promising role for HSV infection and PV, this hypothesis was not evaluated using gold‐standard methods, including molecular evaluation of PV lesions , in the majority of the studies 11–13 .…”

“…Although previous studies have reported a promising role for HSV infection and PV, this hypothesis was not evaluated using gold‐standard methods, including molecular evaluation of PV lesions , in the majority of the studies 11–13 . Furthermore, the findings of previous studies regarding the relationship between HSV and PV severity or exacerbation were contradictory 5,9–14 . Since oral lesions are among the common findings in PV, identifying the presence of HSV infection in PV oral lesions can provide valuable justification for the pathogenesis of HSV infection in the formation of PV lesions.…”