All participants were of black African descent

All participants were of black African descent. Participants who presented with organ Atopaxar hydrobromide failure and fulfilled intensive care admission criteria were referred to the intensive care unit where they were co-managed with critical care specialists and the dermatology team. Data collection and classification The review of patients clinical records during admission, weekly after discharge for the first month and then monthly for the following 3 months were recorded. assessed management in a general dermatology ward without implementing wound debridement. Methods This was a retrospective cohort study of 36 HIV-infected adults with SJS/TEN admitted to a tertiary dermatology unit between 1st January 2010 and Atopaxar hydrobromide 31st July 2011. Standard-of-care protocols included identification and elimination of the possible causative drug, meticulous wound care without debridement, initiation of oral prednisone (1 mg/kg/day) on admission for 3 consecutive days, and the addition of IVIG (1 g/kg/day) for 3 consecutive days to those with TEN. Results Of the 36 patients in the study, 32 were female. Nevirapine was the commonest drug implicated. A diagnosis of tuberculosis did not increase the case fatality rate. Complications included infections, anaemia, drug-induced hepatitis, ocular involvement, renal impairment, deep vein thrombosis, respiratory distress, Leucopenia, gastritis and hypernatremia. The overall survival rate was 97%. Conclusion HIV-infected SJS and TEN patients were treated in a tertiary dermatology ward with a treatment plan of skin care, and a combination of systemic corticosteroids and IVIG respectively had a survival rate of 97%. Keywords: StevensCJohnson syndrome, Toxic epidermal necrolysis, Systemic steroids, Intravenous immunoglobulins Introduction Rabbit polyclonal to TGFB2 StevensCJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe life-threatening mucocutaneous reactions characterised by epithelial sloughing and systemic symptoms.1,2 StevensCJohnson syndrome is characterised by mucous membrane erosions and epidermal detachment, which involves less than 10% of the body surface area (BSA) in the Bastuji-Garin classification. Atopaxar hydrobromide StevensCJohnson syndromeCtoxic epidermal necrolysis overlap represents 10% C 30% BSA involvement, and TEN involves over 30% BSA involvement.3 The worldwide incidence rate of SJS is 1.2C6 per million persons per year with a mortality rate of 5%, while the incidence rate of TEN is 0.5C1.2 per million per year with a mortality Atopaxar hydrobromide rate of up to 30%.4 In South Africa, there are no published data on the incidence of SJS and TEN. With the current HIV epidemic and increased use of HIV treatment in South Africa, the number of patients with SJS/TEN has increased.5 The incidence of SJS/TEN is 1000-fold higher in patients with HIV.6 The high incidence of SJS/TEN in immunocompromised patients is likely multifactorial. It may be due to polypharmacy in the management of HIV, slow acetylation of drugs, glutathione deficiency, altered lymphocyte function and cytotoxic sulfamethoxazole metabolites in the Atopaxar hydrobromide case of trimethoprim/sulfamethoxazole.7,8 In addition, the high rates of tuberculosis co-infection in individuals with HIV leads to the use of a vast array of drugs to treat these infections. This results in greater susceptibility to SJS/TEN and an associated increase in mortality.9 Other factors that contribute to mortality included lymphopenia, neutropenia and hypernatremia, as well as low-serum haemoglobin and hypoalbuminemia.9,10 The use of systemic corticosteroids in the treatment of SJS/TEN is controversial.11 Systemic steroids in the setting of SJS/TEN has immune-modulating anti-apoptotic effects which downregulate Fas-Fas L binding.12 This results in anti-inflammatory properties which inhibit interleukin 2, tumour necrosis factor (TNF) and interferon (IFN), and immunosuppressant properties which inhibit T cells.12,13 Intravenous immunoglobulins (IVIGs) contain anti-Fas antibodies that block the Fas-Fas L interactions on the keratinocyte and thus prevent apoptosis that results in epidermal detachment.14 Studies have shown that IVIG arrests disease progression and reduces time to skin healing.14,15,16 By combining systemic corticosteroids and IVIG, the inflammatory cascade and the undesirable adverse effects are prevented. Systemic corticosteroids and IVIG abort the inflammatory cascade in SJS/TEN and, hence, the deleterious effects that ensue. Therefore, this retrospective cohort study assessed the outcomes of intensive supportive care combined with systemic corticosteroids and IVIG for 3 consecutive days in HIV-infected patients with TEN. In addition, we assessed the outcome of managing these patients in a general dermatology ward without implementing wound debridement. Some centres treat SJS/TEN as a partial thickness burn17 as the clinical presentation is similar to a burn wound, although it is an immune-mediated hypersensitivity reaction. However, SJS/TEN should not be managed strictly as a burn but rather in a specialised dermatology ward without debridement.1,18,19 We believe the treatment of SJS/TEN should differ from that of burn treatment because of the different aetiology and pathophysiological mechanism.1,20 Methods The study was undertaken at the Greys Hospital Department of Dermatology, a tertiary referral centre in Pietermaritzburg, KwaZulu-Natal, South Africa. It is a 530-bed tertiary hospital, serving 3.5 million people in the western part of KwaZulu-Natal. Study population The clinical records of all 39 participants with SJS/TEN admitted to a general dermatology ward from 01 January 2010 until July 2011 were retrospectively reviewed. Three patients were HIV-negative and were thus excluded from the study. All participants were of black African descent. Participants who presented with organ failure and fulfilled intensive care admission criteria were referred to the intensive care unit where they were co-managed with critical care specialists and the dermatology team. Data collection and.

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