No abstract

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is the virus responsible for coronavirus disease 2019 (COVID‐19), which manifests as a flu‐like respiratory infection affecting multiple organ systems, including the gastrointestinal system, central nervous system, cardiovascular system, skin, and mucosa. In this review, we investigated the literature on specific manifestations of COVID‐19 in the oral mucosa. An online literature search in PubMed, Scopus, Google Scholar, and Medline was conducted to retrieve relevant studies on confirmed COVID‐19 patients with oral mucosa findings published between December 31, 2019, and April 07, 2021. After an independent review by two authors, 39 articles considering 59 laboratory‐confirmed cases of SARS‐CoV‐2 infection were included in the final analysis. The most common finding, reported in 29 patients (43.9%), was Kawasaki‐like syndrome. In addition, oral ulcers including aphthous, hemorrhagic, and necrotic ulcers were reported in 24 patients (36.3%). Other lesions reported included pustules, macules, bullae, maculopapular enanthema, and erythema multiforme‐like lesions. Concomitant skin lesions were present in 60.6% of patients. Fever was reported in 86.2% of patients. Forty‐eight patients (76.1%) were hospitalized. Loss of taste and smell was present in 30.8% of the patients. A comprehensive understanding of the dermatologic manifestations of COVID‐19 can improve and facilitate patient management and referrals.

Orf (contagious ecthyma) is a zoonotic infection caused by a dermatotropic parapoxvirus that commonly infects sheep, goats, and oxen. Parapoxviruses are transmitted to humans through contact with an infected animal or fomites. Orf virus infections can induce ulceration, and papulonodular, pustular, or ecthymic lesions of the skin after contact with an infected animal or contaminated fomite. Rarely, orf virus provokes extensive vasculo-endothelial proliferation as a skin manifestation. Here, we present the case of an 8-year old female with poxvirus-induced vascular angiogenesis that developed 10 days after a thermal burn. An 8-year-old female presented at our outpatient clinic with red swellings and a yellow-brown crust on them. After a thermal burn with hot water, she went to a clinic and the burn was dressed with nitrofurazone and covered for 2 days. When the dressing was removed after 2 days, nodules were seen in the burnt areas. When the clinical findings were considered with the histopathological features, a reactive vascular proliferation due to a viral agent was suspected. Following PCR, parapoxvirus ovis was detected. Viral infections such as pox virus can trigger pyogenic granulomas or pyogenic granuloma-like vascular angiogenesis. Infectious agents must be considered when dealing with pyogenic granuloma-like lesions.

The most severe side effect of prolonged MTX treatment is hepatotoxicity. The aim of this study is to investigate the effect of lactulose treatment on MTX-induced hepatotoxicity in a rat model. Twenty-four male rats were included in the study. Sixteen rats were given a single dose of 20 mg/kg MTX to induce liver injury. Eight rats were given no drugs. 16 MTX-given rats were divided into two equal groups. Group 1 subjects were given lactulose 5 g/kg/day, and group 2 subjects were given saline 1 ml/kg/day for 10 days. The rats were then sacrificed to harvest blood and liver tissue samples in order to determine blood and tissue MDA, serum ALT, plasma TNF-α, TGF-β, and PTX3 levels. Histological specimens were examined via light microscopy. Exposure to MTX caused structural and functional hepatotoxicity, as evidenced by relatively worse histopathological scores and increased biochemical marker levels. Lactulose treatment significantly reduced the liver enzyme ALT, plasma TNF-α, TGF-β, PTX3, and MDA levels and also decreased histological changes in the liver tissue with MTX-induced hepatotoxicity in the rat model. We suggest that lactulose has anti-inflammatory and antifibrotic effects on an MTX-induced liver injury model. These effects can be due to the impact of intestinal microbiome.