Cefuroxime-induced pemphigus erythematosus in a young boy

Abstract

Pemphigus erythematosus (Senear-Usher syndrome) is a variant of superficial pemphigus with features of both lupus erythematosus and pemphigus. It affects mainly middle-aged adults, and is rarely observed before the age of 20 years. The case of a 14-year-old boy who showed cutaneous lesions suggestive for pemphigus erythematosus is described. Not all laboratory and histopathological investigations confirmed the hypothesis, so a diagnosis of clinical pemphigus erythematosus was made. Systemic steroid therapy was effective in controlling the disease. This case is interesting because of the rare occurrence of pemphigus erythematosus in adolescence and the possibility of another drug being added to the list of pemphigus inducers.

Pemphigus vegetans possible association with enalapril

“…Antibiotics are another group of drugs that could induce bullous diseases. Baroni et al report a case of pemphigus vulgaris possibly associated with the use of amoxicillin and clavulanic acid [14], in another paper and the same authors report cefuroxime as a inducer of the disease [15]. An example of pemphigus caused by biologicals may be found in the paper by Hayashida et al, who indicated that the disease was triggered by secukinumab [16].…”

“…Baroni i wsp. przedstawili przypadek pęcherzycy zwykłej o możliwym związku z przyjmowaniem amoksycyliny z kwasem klawulanowym [14], natomiast w kolejnym opracowaniu ten sam autor wymienił cefuroksym jako induktor choroby [15]. Przykład pęcherzycy wywołanej przez leki biologiczne można odnaleźć w publikacji Hayashida i wsp., którzy jako lek indukujący chorobę wskazali sekukinumab [16].…”

Angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers induced pemphigus: A case series and literature review

“…Several mechanisms have been postulated in the pemphigus onset due to non-thiol and non-phenol drugs as overexpression of target antigens on keratinocyte membrane, hyperactivation of the immune system, increase of the local immune response and release of plasminogen activators by keratinocytes (Wolf et al, 1991). Literature data showed increasing evidence of cases of pemphigus due to several systemic drugs penicillamine (Popadic, Skiljevic, & Medenica, 2009), penicillin (Heymann, Chodick, Kramer, Green, & Shalev, 2007), ampicillin (Hodak, Ben-Shetrit, Ingber, & Sandbank, 1990), amoxicillin/clavulanic acid (Baroni, Russo, Faccenda, & Piccolo, 2012), some cephalosporins (Baroni et al, 2009;Pellicano, Iannantuono, & Lomuto, 1993;Scardina, Conti, & Messina, 2004), quinolones (Anadolu, Birol, Bostanci, & Boyvatt, 2002), most nonsteroidal anti-inflammatory drugs (Durdu, Baba, & Seckin, 2011;Kanitakis, Souillet, Faure, & Claudy, 2001;Laing, Sheretz, & Flowers, 1988;Pompeova, 1981), nifedipine (Ameen, Harman, & Black, 2000), (Parfrey, Clement, Vandenburg, & Wright, 1980). Penicillamine was the first drug described to cause pemphigus (Popadic et al, 2009) and have a similar chemical structure to captopril (Parfrey et al, 1980).…”

“…Recently, it has also been hypothesized the potential role of amides in the pathogenesis of pemphigus (Lo Schiavo, Sangiuliano, Puca, Brunetti, & Ruocco, 2009;Wolf et al, 1991). Literature data showed increasing evidence of cases of pemphigus due to several systemic drugs penicillamine (Popadic, Skiljevic, & Medenica, 2009), penicillin (Heymann, Chodick, Kramer, Green, & Shalev, 2007), ampicillin (Hodak, Ben-Shetrit, Ingber, & Sandbank, 1990), amoxicillin/clavulanic acid (Baroni, Russo, Faccenda, & Piccolo, 2012), some cephalosporins (Baroni et al, 2009;Pellicano, Iannantuono, & Lomuto, 1993;Scardina, Conti, & Messina, 2004), quinolones (Anadolu, Birol, Bostanci, & Boyvatt, 2002), most nonsteroidal anti-inflammatory drugs (Durdu, Baba, & Seckin, 2011;Kanitakis, Souillet, Faure, & Claudy, 2001;Laing, Sheretz, & Flowers, 1988;Pompeova, 1981), nifedipine (Ameen, Harman, & Black, 2000), Literature data showed increasing evidence of cases of pemphigus due to several systemic drugs penicillamine (Popadic, Skiljevic, & Medenica, 2009), penicillin (Heymann, Chodick, Kramer, Green, & Shalev, 2007), ampicillin (Hodak, Ben-Shetrit, Ingber, & Sandbank, 1990), amoxicillin/clavulanic acid (Baroni, Russo, Faccenda, & Piccolo, 2012), some cephalosporins (Baroni et al, 2009;Pellicano, Iannantuono, & Lomuto, 1993;Scardina, Conti, & Messina, 2004), quinolones (Anadolu, Birol, Bostanci, & Boyvatt, 2002), most nonsteroidal anti-inflammatory drugs (Durdu, Baba, & Seckin, 2011;Kanitakis, Souillet, Faure, & Claudy, 2001;Laing, Sheretz, & Flowers, 1988;Pompeova, 1981), nifedipine (Ameen, Harman, & Black, 2000),…”

Pemphigus erythematosus relapse associated with atorvastatin intake

“…The antibodies recognize the pemphigus foliaceus antigen, desmoglein 1; in addition, immunoglobulin G (IgG) and C3 deposition on cell surface of keratinocytes can be revealed in a group of patients. A positive antinuclear antibody (ANA) is detected in 30%–80% of PE patients but only a few patients have been reported to have PE and lupus erythematosus concurrently 2,3. As for pemphigus vulgaris, several exogenous factors are able to induce PE in genetically predisposed individuals, including drug intake, viral infections, exposure to physical agents, and others.…”