Background: HIV infection leads to depletion of intestinal CD4+ T cells, mucosal barrier dysfunction, increased gut permeability and microbial translocation even among patients on suppressive ART. Previous studies suggest probiotics may help restore intestinal function. Methods: In this double-blind, placebo-controlled pilot study, we enrolled HIV-infected patients on suppressive ART with poor CD4+ recovery to address the effect of daily oral use of Lactobacillus casei Shirota (LcS) on CD4+ T-cell count and CD4+/CD8+ ratio at 6 and 12 weeks after treatment initiation; immune activation and intestinal microbiome composition were addressed as secondary outcomes. Results: From January 2015 to July 2016, 48 patients were randomized (1 : 1) to active intervention or placebo. Groups had comparable demographic and clinical characteristics; only CD4+ T-cell nadir was statistically different between groups. All participants were virologically suppressed under ART. At week 6, the increment in CD4+ T-cell count was 17 cells/μl [interquartile range (IQR) −33 to 74] in the active intervention arm and 4 cells/μl (IQR −43 to 51) in the placebo arm (P = 0.291); at week 12, the change in CD4+ T-cell count was 8 cells//μl (IQR −30 to 70) in the active arm and 10 cells//μl (IQR −50 to 33) among participants allocated to placebo (P = 0.495). Median change in CD4+/CD8+ ratio at week 6 compared with baseline was 0 (IQR −0.04 to 0.05) in the active intervention arm and −0.01 in the placebo arm (IQR −0.06 to 0.03; P = 0.671). At week 12, the change in CD4+/CD8+ ratio was higher in the active product group compared with placebo (respectively 0.07 and 0.01), but this difference failed to reach statistical significance (P = 0.171). We found no significant effects of LcS on immune activation markers, CD4+ and CD8+ subpopulations, sCD14 levels or NK cells at week 12. Finally, we found no statistically significant differences between groups in the change of enteric microbiome at week 12. Conclusion: In this pilot study, we found no statistically significant effect of LcS probiotic on CD4+ T-cell counts, CD4+/CD8+ ratio, immune activation or intestinal microbiome among HIV-infected patients on suppressive ART with poor CD4+ recovery.

Aniridia-associated cytogenetic rearrangements suggest that a position effect may cause the mutant phenotype. Hum Mol Genet 1995;4:415-22. 3 Nishimura DY, Swiderski RE, Alward WL, et al. The forkhead transcription factor gene FKHL7 is responsible for glaucoma phenotypes which map to 6p25. Nat Genet 1998;19:140-7. 4 Flomen RH, Vatcheva R, Gorman PA, et al. Construction and analysis of a sequence-ready map in 4q25: Rieger syndrome can be caused by haploinsufficiency of RIEG, but also by chromosome breaks approximately 90 kb upstream of this gene. Genomics 1998;47:409-13. 5 Gardner RJM, Sutherland GR. Chromosome abnormalities and genetic counselling.

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Background:Adverse drug reactions are important determinants of inpatient and outpatient morbidity. Thiocolchicoside is a semisynthetic derivate of naturally occurring colchicoside, which is largely used in humans as a centrally acting muscle relaxant. Epileptic seizures after thiocolchicoside intake have been reported in individuals with a history of epilepsy, acute brain injury or possible blood–brain barrier disruption.Case report:We report the case of a 66-year-old male patient presenting a sudden epileptic seizure temporally related to the intake of thiocolchicoside for muscle contracture and pain. The probably causes of the seizures were thiocolchicoside intake and cerebral microhemorrhages attributed to cerebral amyloid angiopathy.Discussion:Drugs only rarely cause focal seizures. Our case indicates that thiocolchicoside can precipitate seizures in predisposed patients, and that its use should be avoided in patients with brain diseases (and therefore lower seizure thresholds) or blood–brain barrier disruption. This information should be provided in the drug package insert.