Background: In March 2020 our clinics providing three monthly interval sexually transmitted infection(STI) testing for HIV pre-exposure- prophylaxis( PrEP) users closed due to COVID-19. In absence of funding for commercially available solutions we planned a home sampling kit(HSK) to screen for HIV and syphilis on our existing laboratory platform. We proposed a self-obtained capillary blood sample of >0.6mls in a paediatric sample tube would be achievable and sufficient to conduct a 4th generation HIV test, enzyme-immunoassay( EIA) for treponemal(IgG) and if EIA positive, a non-treponemal( RPR) test. A rapid service evaluation was implemented. Method: Written instructions were drafted, consumables sourced and an evaluation form developed. Ten patients were invited for observed self-sampling in lieu of their routine testing appointment. Both patients, and clinicians observing the self-sampling, completed an evaluation form which was used to refine the technical procedure, instructions and evaluation process. Subsequently postal HSK's were implemented with a telephone evaluation completed for the first forty patients. Results: In face-to- face evaluation, 5/9 obtained sufficient blood for testing and 7/9 reported they would use the HSK method if offered. Satisfactory HSK results for HIV and syphilis testing were obtained in 25/40 patients. 15/40 required further testing, 5/40 samples were not processed, 2/40 were unlabelled, 4/40 were insufficient for both tests and 4/40 had a positive EIA but inadequate blood for RPR. In patient evaluation: 32/40 agreed the test was easy to perform, 29/40 agreed HSK's were a good option, 37/40 felt instructions were clear. Conclusion: Technical challenges included the relatively high volume of blood required for the existing laboratory platform. This issue was more marked in a cohort with high rates of new and previous syphilis infection, thus requiring both EIA and RPR testing from the sample. 8/29 had a positive EIA but there was only sufficient blood to perform RPR in 4/8. Consequently, the screening test for syphilis in the HSK was changed from EIA to RPR. Even with a relatively high rate of insufficient samples requiring follow up, the rate of attendance to the clinic is dramatically reduced at a consumable cost of around £8 per full testing panel.

Summary Among patients presenting with diverse neurological problems at a single center, cerebrospinal fluid discordance or escape was observed in 15% and was associated with diffuse white matter signal abnormalities on cranial magnetic resonance imaging.

The objective was to evaluate the efficacy of a HIV targeted-testing teaching session in improving knowledge and confidence at a London medical school. A survey assessing knowledge of HIV testing guidelines, confidence to offer testing and outcomes of targeted-testing teaching was developed and distributed to fifth year medical students. Results were compared for students who had completed GU/HIV modules (GU+) and those who had not (GU−) and chi-squared testing was performed; 100 and 119 questionnaires were returned by GU+ and GU− students (response rate of 92.6% and 97.5%), respectively. For the three knowledge-based questions, GU+ students were significantly more likely to provide correct answers for two ( p < 0.001). Similarly, they were significantly more likely to feel confident in offering an HIV test ( p < 0.001). After targeted-testing teaching 92%, 98% and 62% felt more confident about when to test, how to discuss testing and more knowledgeable about testing, respectively. Most students were happy to offer HIV testing in different medical settings; significantly fewer reported this for an acute admissions unit compared with antenatal clinic (79% vs 96%). Students who had received targeted-testing teaching demonstrated better knowledge and confidence about HIV testing. We hope this study raises awareness of the need to include HIV testing teaching in medical school curricula.

© 2016 Haddow et al. This work is published by Dove Medical Press Limited, and licensed under a Creative Commons Attribution License. The full terms of the License are available at http://creativecommons.org/licenses/by/4.0/. The license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. © 2016 Haddow et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms. php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Neurobehavioral HIV Medicine 2016:7 31–41 Neurobehavioral HIV Medicine Dovepress

White matter (WM) abnormalities are frequently seen on brain MRI of HIV positive (HIV+) patients. We aimed to determine the prevalence of unexplained WM abnormalities and their associations with HIV disease and cardiovascular risk factors. We conducted a retrospective, cross-sectional study of brain MRI of HIV+ patients conducted between 2004 and 2009 at our center. Clinical and laboratory data were compiled, and images were independently reviewed for WM lesions. Images were obtained from 254 patients: 70% male, 53% white, 40% black, mean age 42 years, median current CD4 count 240 cells/mm3, and 41% not taking antiretroviral therapy (ART). Hyperintense WM lesions were present in 161 patients (63.4%): 89 scans (35.0%) showed diffuse WM signal abnormality (DWMSA), 61 (24.0%) were consistent with small vessel disease (SVD, graded by Fazekas' scale), and 37 (14.6%) showed large asymmetrical focal WM lesions. SVD changes were associated with age and cardiovascular risk factors, and while cerebral SVD may be related to HIV infection, the MRI findings were not associated with HIV-related factors. The only risk factor for DWMSA was black race, and no correlation with cardiovascular risk factors, CD4 count, or clinical presentation was identified. DWMSA are therefore of uncertain neurological significance in HIV+ patients and could represent more than one clinicopathological entity.

The field of HIV medicine has changed rapidly in the last two decades since effective and tolerable antiretroviral treatment became available. As a result, although classical opportunistic infections of the brain have become less common, clinicians need to be aware of a wider range of acute and chronic complications of HIV and its treatment. In this article, we summarise major opportunistic infections, immune reconstitution inflammatory syndrome, HIV-associated neurocognitive disorders, and cerebrovascular disease in HIV positive patients. We also emphasise the preventability and reversibility of most of the central nervous system complications of HIV, and hence the importance of early diagnosis of HIV and involvement of clinicians with special expertise in HIV medicine.

Background UK guidance recommend all acute medical admissions be offered an HIV test. Our aim was to determine whether a dedicated staff member using a multimedia tool, a model found to be effective in the USA, is an acceptable, feasible, and cost-effective model when translated to a UK setting. Design Between 14th Jan to 12th May 2010, a Health advisor (HA) approached 19–65 year olds at a central London acute medical admissions unit (AAU) and offered a rapid HIV point of care test (POCT) with the aid of an educational video. Patients with negative results had the option to watch a post-test video providing risk-reduction information. For reactive results the HA arranged a confirmatory test, and ensured linkage into HIV specialist care. Feasibility and acceptability were assessed through surveys and uptake rates. Costs per case of HIV identified were established. Results Of the 606 eligible people admitted during the pilot period, 324 (53.5%) could not be approached or testing was deemed inappropriate. In total 23.0% of eligible admissions had an HIV POCT. Of the patients who watched the video and had not recently tested for HIV, 93.6% (131/140) agreed to an HIV test; four further patients had an HIV test but did not watch the video. Three tests (2.2%, 3/135) were reactive and all were confirmed HIV positive on laboratory testing. 97.5% felt HIV testing in this setting was appropriate, and 90.1% liked receiving the information via video. The cost per patient of the intervention was £21. Discussion Universal POCT HIV testing in an acute medical setting, facilitated by an educational video and dedicated staff appears to be acceptable, feasible, effective, and low cost. These findings support the recommendation of HIV testing all admissions to AAU in high prevalence settings, although with the model used a significant proportion remained untested.

Multicentric Castleman's disease is a lymphoproliferative disorder manifesting with fever, lymphadenopathy, splenomegaly, raised inflammatory markers, and cytopenias. The clinical course ranges from indolent to fulminant [1,2]. The proliferation of polyclonal but often monotypic lymphoplasmocytoid cells is thought to be driven by human herpesvirus 8 [2–5]. Multicentric Castleman's disease can result in death by complex immune dysregulation leading to sepsis-induced and/or cytokine-induced multiorgan failure [2,6]. An optimal treatment algorithm for fulminant multicentric Castleman's disease is unknown because of the absence of controlled trials, and the outcome is usually fatal. We report on two patients who developed multicentric Castleman's disease-associated multiorgan failure. One of them achieved complete remission on treatment with corticosteroids and chemotherapy after failing to respond to rituximab monotherapy. Case 1 A 36-year-old man presented with a 4-month history of night sweats and fever. He had been diagnosed with HIV infection 3 years earlier and had been on highly active antiretroviral therapy (HAART); [most recently emtricitabine (200 mg), tenofovir (300 mg), and efavirenz (600 mg) daily] since diagnosis. Examination revealed generalized lymphadenopathy and hepatosplenomegaly. Left inguinal lymph node excision biopsy showed plasma cell multicentric Castleman's disease (MCD) associated with perifollicular HHV8-positive cells. His HIV viral load on presentation was less than 50 copies/ml, the white blood cell count (WBC) was 8.4 × 109/l, and the CD4 count 280 × 106/l. HHV8 plasma viral DNA load was 26 400 copies/ml but it increased to 104 000 copies/ml in another measurement performed 7 days later. He was commenced on rituximab 375 mg/m2. Four days later, he developed ascites, acute renal failure, cholestatic liver impairment, bilateral chest infiltrates with type I respiratory failure, and pancytopaenia. Haemofiltration was initiated, and the next day he suffered two asystolic cardiac arrests. He was successfully resuscitated but remained intubated and dependent on inotropic support. HAART medications were stopped due to worsening liver function and lactic acidosis. During the acute episode, the WBC and CD4 counts decreased to 1.3 × 109/l and 120 × 106/l, respectively, and the HIV viral load increased moderately to 2900 copies/ml. Treatment with prednisolone (100 mg daily) and reduced-dose ganciclovir (3 mg/kg daily) was started and the patient also received a single dose of vincristine (0.5 mg). As there was a marked improvement, he was extubated and discharged from intensive care unit. He continued chemotherapy with vincristine, bleomycin, rituximab, and ganciclovir (Fig. 1a). After recommencement of HAART [Kaletra (lopinavir/ritonavir) four capsules once daily], the CD4 count recovered to 490 × 106/l, the HIV viral load decreased to less than 50 copies/ml, and HHV8 viral load became undetectable. The patient remained well and without any MCD-related symptoms with a follow-up of 11 months.Fig. 1: Clinical course and the treatment of fulminant multicentric Castleman's disease. Clinical course as reflected by C-reactive protein (CRP) levels, platelet counts, and serum human herpesvirus 8 (HHV8) viral load and the treatment of fulminant multicentric Castleman's disease (MCD) in patient 1 (a) and patient 2 (b). HAART, highly active antiretroviral therapy; PLT, platelet.Case 2 A 32-year-old man diagnosed with HIV infection 6 years earlier presented with generalized body aches, lethargy, anorexia, and intermittent high fever. There was palpable hepatomegaly, splenomegaly, and generalized lymphadenopathy. He had never been on HAART as his CD4 count had always been greater than 300 × 106/l despite a very high plasma HIV load in excess of 500 000 copies/ml. In the previous year, the CD4 count had been decreasing steadily from 680 × 106/l to 360 × 106/l, with WBC within the normal range. Histology of a lymph node revealed the presence of HHV8-positive Kaposi sarcoma but this was not deemed to be a sufficient explanation for his problems and he went on to have a diagnostic splenectomy. Histological examination of the spleen and a hilar lymph node showed HHV8-positive plasma-cell MCD. His HHV8 load at this time was 96 000 copies/ml. After the splenectomy, his HHV8 viral load decreased to 3600 copies/ml but he continued to have fever and fatigue. We started treatment with rituximab (375 mg/m2) weekly, ganciclovir (5 mg/kg) twice daily, and Kaletra (lopinavir/ritonavir) capsules once daily (Fig. 1b). However, his condition continued to deteriorate with thrombocytopenia and hypoalbuminaemia, and we decided to start vincristine (0.5 mg) and dexamethasone (16 mg) daily. On this therapy, he became afebrile, and peripheral blood cell counts and inflammatory markers normalized. However, the CD4 count continued to decrease to 130 × 106/l. The patient developed severe cachexia, became completely bed-bound, and died 1 month after the onset of fulminant MCD. Autopsy was not permitted by the family. Discussion Rituximab has recently emerged as a promising agent for the treatment of MCD and is recommended as the first-line treatment in many centres. Despite its activity in relapsing MCD, rituximab alone may not be sufficient in fulminant MCD. In a report by Marcelin et al.[7], the two patients who developed haematological failure died on treatment with rituximab alone. Our experience shows that the combination of nonmyelotoxic chemotherapy and high-dose corticosteroids together with intensive care support is capable of reversing MCD-associated multiorgan failure even in patients progressing on rituximab and should be considered as the next step in the treatment algorithm for fulminant MCD.

A profoundly immunosuppressed HIV-infected man developed sepsis syndrome with multi-organ failure. A septic screen failed to identify a bacterial or fungal cause and despite empirical treatment for these pathogens the patient remained unwell. Investigations revealed disseminated tuberculosis. With specific anti-tuberculosis therapy the patient rapidly recovered. Although most cases of sepsis syndrome in HIV-infected patients are due to bacteria, tuberculosis should be added to the differential diagnosis of this presentation.

Background: Long-term antiretroviral therapy, while dramatically reducing HIV-related morbidity and mortality, is associated with metabolic and morphological changes. Peripheral fat loss, lipoatrophy, appears most associated with prolonged therapy with thymidine nucleoside analogues. Methods: A randomized, open-label, comparative study of switching from a thymidine nucleoside analogue to either tenofovir disoproxil fumarate (DF) or abacavir in 105 individuals on successful antiretroviral therapy with clinically evident moderate to severe lipoatrophy. Results: Individuals were randomized to tenofovir DF (52) or abacavir (53). The switch was well tolerated and the majority of patients completed 48 weeks of study. One individual in the tenofovir DF group and three in the abacavir group discontinued due to drug-related adverse events. Both groups similarly maintained virological control. Limb fat mass increased similarly in both groups: mean increases by week 48 of 329 and 483 g in tenofovir DF and abacavir groups, respectively [mean 95% confidence interval for difference, −154.3 (range −492.8 to 184.3)]. This change from baseline was statistically significant in both groups (tenofovir DF, P = 0.01; abacavir, P = 0.0001). Mean total cholesterol, low density lipoprotein cholesterol and triglycerides improved modestly with switching to tenofovir DF but were unchanged with abacavir. The changes in these parameters were significantly greater in the tenofovir DF arm relative to abacavir. Conclusions: Switching from a thymidine nucleoside analogue to either tenofovir DF or abacavir leads to significant improvement in limb fat mass over 48 weeks. Tenofovir DF may have modest advantages over abacavir for changes in lipids. Peripheral lipoatrophy, when clinically apparent, resolves slowly following treatment switching.