IntroductionUntreated syphilis may lead to severe complications. This infection has recently re-emerged in developed countries with a high number of cases coinfected with human immunodeficiency virus. In these patients, the skin lesions of secondary syphilis can be very atypical.Case presentationWe report the case of a 38-year-old Bulgarian homosexual man who was coinfected with human immunodeficiency virus and syphilis. His skin contained multiple extensive necrotic lesions with abundant purulent secretion that covered his face, lips, scalp, and torso. Initial clinical diagnoses included varicella pustulosa and staphylococcal dermatitis. Human immunodeficiency virus infection in our patient had been established 2 years earlier in prophylactic studies, but had not been treated. Due to lack of penicillin, he was successfully treated with ceftriaxone, and the skin lesions underwent complete reversal. He also began antiretroviral therapy, which resulted in a significant effect on his immune status. Three months after the onset of antiretroviral therapy, he also achieved optimal viral suppression.ConclusionThis case emphasizes the importance of considering cutaneous secondary syphilis in the differential diagnosis of any inflammatory cutaneous disorder in individuals infected with human immunodeficiency virus.

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We present a case of a necrotising disease of the orofacial tissues, the so-called noma, in a female patient with AIDS in a stage of severe immune deficiency. To our knowledge, this is the first time a case like that has been reported in Bulgaria. The patient received an antibiotic course of treatment with a triple combination to good effect on the inflammatory process, and began also HAART. Within 3 weeks, the patient’s general condition improved. However, despite the treatment, a demarcation line was formed, and a defect on the lower lip occurred. Noma is a manifestation of severe immune deficiency with lasting adverse consequences for the patient: severe deformation of the maxilo-facial region and functional impairment (i.e. difficulties eating and speaking, and salivary leak).

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Today the HIV infection is a chronic disease with significantly longer duration of the life of the patients. Problems of pressing interest are the persistent immune activation and chronic inflammation during the treatment with antiretroviral therapy. Taking this into account, different factors which could affect the immune system and the progress of the HIV infection are being researched. Vitamin D (25(OH)D) is one of those factors if we take note of its effect on the innate and acquired immunity. The aim of this study was to assess 25-hydroxyvitamin D (vitamin D) status in one part of the Bulgarian HIV-infected adult population and to assess connection between 25-hydroxyvitamin D (vitamin D) status and plasma levels of some major cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α and IFN-γ). The study includes 145 HIV-positive patients, who are being monitored in the Department for acquired immune deficiency at Specialized Hospital for Infectious and Parasitic Diseases "Proff. Ivan Kirov"-Sofia. From all of the monitored patients only in 15% of the tested we found normal 25(OH)D serum levels, and in 12% of the patients we found deficiency. The largest group is that of patients with insufficiency of vitamin D. We didn't discovered significant difference in the 25(OH)D average values between men and women. There were no significant differences in the average values of the 25(OH)D serum levels when dividing the patients according to their antiretroviral therapy, but after separating the patients by gender, we found that the untreated women had average values of 25(OH)D higher than that of the women treated with EFV. On the next stage of the survey on the 60 HIV-infected patients, who are from the first tested group, we additionally defined the cytokine profile. Our results suggests that increasing 25(OH)D deficiency worsens the damaging of the cellular immune response. The lower levels of vitamin Dare associated with inN. Yancheva et al. 183 creased levels of IL-6, decreased levels of IL-10, IFN-γ and TNF-α. There's active immune inflammation when there are reduced 25(OH)D serum levels and it leads to stimulated secretion of the regulatory cytokines and suppression of the Th1 antiviral response. The phase of advanced 25(OH)D deficiency is characterized by parallel depletion of the regulatory and effecter capabilities of CD4 lymphocytes. The recovery of the CD4 lymphocyte pool is difficult because of the lower than average 25(OH)D serum levels, regardless of the conducted antiretroviral therapy.