Comparison of predictive scores of symptomatic intracerebral haemorrhage after stroke thrombolysis in a single centre

Peer reviewedPublisher PD

Viral load rebound in presumed elite controllers: a small case series of the potential use of non-prescribed HAART in African patients

Introduction: HIV elite controllers are rare with an incidence of <1/300 [1]. We report 4 cases of presumed elite control with subsequent viral load rebound possibly due to non-prescribed HAART. Case 1: A 37-year-old African woman trafficked to the UK was diagnosed HIV-positive with viral load (VL) <40 copies/mL and CD4 count of 436 cells/cmm. She denied prior diagnosis and was presumed an elite controller until a rise in VL to 26,5205 copies/mL 6 months later (Table 1). A resistance test reported HIV-1 subtype C with a minor protease inhibitor mutation (A71T). It was subsequently disclosed she was given unidentified tablets by traffickers. Case 2: A 31-year-old African woman presented 37 weeks pregnant and was diagnosed HIV-positive with VL 147 copies/mL and CD4 count of 1065 cells/cmm. She denied prior diagnosis, however stated an African doctor visited her ex-partner's home and supplied tablets identified as lopinavir/ritonavir and zidovudine/lamivudine. Clinics in this area were contacted but had no record of this patient. There was a rise in VL with a resistance test reporting HIV-1 subtype C/D with no mutations. Case 3: A 53-year-old African woman presented 6 weeks after a sexual assault in her home country and was diagnosed HIV-positive with VL<40 copies/mL and CD4 count of 609 cells/cmm. She denied prior diagnosis but stated her employers gave her unidentified tablets after the assault. Over 3 months VL increased to 390,751 copies/mL (Table 2). A resistance test reported HIV-1 subtype A with no mutations. Case 4: A 42-year-old African man was diagnosed HIV positive with VL 269 copies/mL and CD4 count of 562 cells/cmm. A resistance test reported HIV-1 subtype B with minor PI and NRTI mutations (L10V and V118L respectively). HIV parameters remained stable until 20 months later with an increase in VL to 1,463,132 copies/mL (Table 3). A resistance test excluded super-infection reporting a similar sequence and no new mutations. Co-existing pathology was also excluded. He subsequently disclosed taking medication supplied by his family but denied this was HAART. Conclusion: The viral load rebound seen in these cases may be due to a viral or immune mediated phenomenon; however, the possibility of non-prescribed HAART has to be considered. Home test kits for HIV are widely available and there are reports of counterfeit HAART in the developing world [2]. The HIV community has to be vigilant in reporting cases of this nature which create many anxieties regarding toxicity and resistance

Guillain-Barré syndrome following SARS-CoV-2 vaccination in the UK: a prospective surveillance study.

ObjectiveTo investigate features of Guillain-Barré syndrome (GBS) following SARS-CoV-2 vaccines and evaluate for a causal link between the two.MethodsWe captured cases of GBS after SARS-CoV-2 vaccination through a national, open-access, online surveillance system. For each case, the certainty of GBS was graded using the Brighton criteria, and the relationship to the vaccine was examined using modified WHO Causality Assessment criteria. We compared age distribution of cases with that of prepandemic GBS cases and clinical features with the International GBS Outcome Study (IGOS).ResultsBetween 1 January and 30 June 2021, we received 67 reports of GBS following the ChAdOx1 vaccine (65 first doses) and three reports following the BNT162b2 vaccine (all first doses). The causal association with the vaccine was classified as probable for 56 (80%, all ChAdOx1), possible for 12 (17%, 10 ChAdOx1) and unlikely for two (3%, 1 ChAdOx1). A greater proportion of cases occurred in the 50-59 age group in comparison with prepandemic GBS. Most common clinical variants were sensorimotor GBS (n=55; 79%) and facial diplegia with paraesthesias (n=10; 14%). 10% (n=7/69) of patients reported an antecedent infection, compared with 77% (n=502/652) of the IGOS cohort (pInterpretationMost reports of GBS followed the first dose of ChAdOx1 vaccine. While our study cannot confirm or refute causation, this observation, together with the absence of alternative aetiologies, different than expected age distribution and the presence of unusual clinical features support a causal link. Clinicians and surveillance bodies should remain vigilant to the possibility of this very rare adverse event and its atypical variants