Inguinal Ulcers in a Patient with HIV Infection

Dear Editor, A 21-year-old male patient was admitted with mild traumatic brain injury following a traffic accident. During hospitalisation, he developed sepsis of pulmonary origin, which was managed with antibiotics. Additionally, he was diagnosed with de novo human immunodeficiency virus (HIV) infection, with a viral load of 894,685 copies/mL and a CD4 T lymphocyte count of 195 cells/µL. Additionally, opportunistic infections such as tuberculosis, histoplasmosis, cryptococcosis, cytomegalovirus infections, syphilis, and viral hepatitis were ruled out. Since admission, the patient reported the presence of round, painful ulcerated plaques in both inguinal folds [Figure 1a and b], with no known temporal onset. Due to the possibility of a deep fungal infection or pyoderma gangrenosum, a histopathological examination was performed, revealing an epidermal ulcer with a neutrophilic infiltrate, thus confirming the diagnosis of pyoderma gangrenosum [Figures 2 and 3]. Antiretroviral therapy consisting of dolutegravir, tenofovir, and emtricitabine was initiated, leading to improvement in the inguinal lesions. After 4 months, the lesions had fully healed [Figure 1c], establishing the diagnosis of pyoderma gangrenosum associated with HIV.Figure 1: (a and b) Ulcers with well-defined edges in the inguinal folds, deep, with a fibrinous base. (c) Hypopigmented scars in the inguinal folds 4 months laterFigure 2: H and E. 4X. Irregular acanthosis in the epidermis, with a polymorphonuclear inflammatory infiltrate in the deep dermis extending to the hypodermis. There are areas of necrosis and haemorrhage with the formation of microabscessesFigure 3: H and E. 20X. Neutrophils in the deep dermisPyoderma gangrenosum is a non-infectious inflammatory dermatosis characterised by painful, undermined ulcers with defined borders, which can appear in various anatomical locations following minimal trauma (pathergy phenomenon). Its incidence is <1/100,000, with a mean age of onset of 59 years and no sex predilection. Approximately 50% of cases are associated with immune-mediated diseases such as inflammatory bowel disease, rheumatoid arthritis, and hematologic malignancies.[1,2] The pathophysiology involves trauma, which leads to damage of keratinocytes and the release of pro-inflammatory cytokines, primarily interleukin-36 and interleukin-8. The latter promotes neutrophil chemotaxis, enhancing local inflammation and ulcer formation. Furthermore, it has been linked to inflammatory syndromes involving genetic alterations in genes coding for key proteins in the inflammasome pathway and the synthesis of pro-inflammatory proteins like interleukin-1 beta. Clinically, a painful ulcer with well-defined borders is typically observed. However, other forms of pyoderma gangrenosum, such as bullous, pustular, vegetative, periostomal, and post-surgical forms, can present diagnostic challenges.[1] For initial management, the 2018 Delphi consensus criteria are currently used, which recommend that, in addition to a biopsy confirming a neutrophilic infiltrate, at least four of the following minor criteria should be met: exclusion of infection; history of pathergy; personal history of inflammatory bowel disease or inflammatory arthritis; history of papules or pustules evolving into an ulcer early on; erythema around the ulcer with a well-defined, painful border; multiple ulcers, at least one of which is located on the anterior aspect of the legs; a cribriform appearance in previous scars; and improvement of lesions with immunosuppressive treatment.[3] Our patient met the major criterion and four minor criteria. Although pyoderma gangrenosum associated with HIV is rare, it is suggested that immunodeficiency may alter the immune response, predispose to an exaggerated inflammatory reaction, and give rise to these typical clinical manifestations.[4] Treatment for pyoderma gangrenosum may include topical steroids or calcineurin inhibitors for small ulcers, systemic steroids either orally or intravenously for more severe cases, systemic immunomodulators such as cyclosporine, methotrexate, or azathioprine, and biologics such as tumour necrosis factor inhibitors and interleukin-1 beta, 12/23, 17, and 23 inhibitors. Some small molecules, such as JAK/STAT inhibitors, are also under investigation.[5] In our patient, the lesions resolved with antiretroviral therapy, as previously reported.[4] We present the case of an HIV-infected patient who developed inguinal ulcers clinically and histologically compatible with pyoderma gangrenosum and whose condition improved with antiretroviral therapy alone. Pyoderma gangrenosum should be considered as a differential diagnosis for genital and inguinal ulcers in HIV patients during the initial evaluation. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.