BackgroundPre-exposure prophylaxis (PrEP) is a highly effective method for preventing HIV transmission among at-risk patients. There is limited and conflicting data regarding the risk of other STIs following PrEP initiation. The objective of this study was to compare the incidence of STIs before and during PrEP therapy.MethodsA retrospective observational study of patients seeking PrEP therapy at an inner-city clinic in Newark, New Jersey, between May 1, 2016 and March 30, 2018. Patients who were MSM, intravenous drug users, or heterosexual with multiple or HIV-positive partners were considered at risk for HIV and offered PrEP. Patients were initially screened and tested every 3 months for HIV, Chlamydia trachomatis, Neisseria gonorrhoea, syphilis, hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis A virus (HAV), herpes simplex virus (HSV), medication adherence and continued high-risk behavior. Patients were also counseled on risk-reduction behaviors. STI incidence before and during PrEP was compared.ResultsBetween May 1, 2016 to March 30, 2018, 125 patients were considered at risk. Fifty-one (41%) patients were lost to follow-up after the initial visit and were excluded. Seventy-four (59%) patients completed screening and were included in the study. The mean age was 35.0 ± 11.6 years. The majority of the patients were males 74% (54). 29 (40%) were MSM, and 33 (45%) had HIV-positive partners. The mean duration of PrEP was 386 ± 183 days. Upon initial screening 14 (19%) patients were positive for at least one STI; 3 (21%) patients had HCV, 3 (21%) had chlamydia, 2 (14.3%) had HBV, 2 (14.3%) had gonorrhea, 2(14.3%) had syphilis, one had HSV II and one was found to have HIV. Two patients acquired a new STI on PreP. One tested positive for chlamydia and gonorrhea 1 month after initiating prep and another contracted syphilis after 6 months. No patient had recurrent STIs nor acquired HIV while on PrEP therapy.ConclusionThe use of PrEP not only reduces the transmission of HIV but also appears to reduce the incidence of other STIs. Frequent STI screenings and behavioral counseling on risk reduction likely contributed toward lower STI incidence. Larger studies examining similar data over longer durations are needed to confirm these findings.Disclosures All authors: No reported disclosures.

Kaposi sarcoma (KS) was first described by Moritz Kaposi as a vascular tumor that mainly involves the skin but can affect any organ system. It is typically an acquired immunodeficiency syndrome defining illness but has emerged as a neoplasm also seen in patients on immunosuppressive therapy. Few KS cases have been reported in the literature associated with inflammatory bowel diseases. We report the case of a 39-year-old male with well-controlled human immunodeficiency virus (HIV) and ulcerative colitis (UC) who presented to the hospital with new skin lesions shortly after the initiation of vedolizumab to treat his refractory UC. Immunohistochemistry of the skin lesions was consistent with Kaposi's sarcoma secondary to human herpesvirus-8. This is a rare case of iatrogenic KS in a well-controlled HIV patient secondary to immunosuppressive therapy.

No abstract

No abstract

INTRODUCTION: Hepatitis B (HB) virus is a global public health problem as it affects more than 300 million patients around the world. It's well known that once we have Anti-HBs, seroconversion takes place, and that's a marker of viral clearance and immunity. In view of their important protective role, occurrence of anti-HBs and HBsAg is perplexing. Although this has been reported in 5-20% of cases of Chronic Hep B, it remains a confusing finding to many physicians who are unaware of the existence, explanation and implications of this finding. Herein, we will present a case of such a pattern. CASE DESCRIPTION/METHODS: A 49-year-old male with diabetes and hypertension was found to have elevated liver enzymes on routine blood work. Further workup resulted in diagnosing chronic hepatitis B. The patient’s viral serology results were positive for HB core antibody, HB surface antibody, HB surface antigen, HB e antigen, and a viral load of 1,500,000 IU/ml. Liver enzymes were elevated with ALT of 250U/L and AST of 180U/L. No masses were detected on liver ultrasound. Blood sample was sent to Center for Disease Control and analysis revealed a mutation G130N within the major hydrophilic region of surface antigen. The patient was started on Entecavir. After 12 months, the VL became undetectable. Serology was still positive for both HB s Ag and Ab but he successfully achieved HB e Ab +ve status. Liver enzymes normalized. DISCUSSION: The expected pattern in chronic HB is the presence of HBsAg and lack of anti-HBs. The mechanism underlying the coexistence of HBsAg and anti-HBs remains unclear. Mutations in the viral DNA were initially suggested by researchers to explain how the subtypes of the HBsAg and anti-HBs were heterologous. It was shown that there is a relation between this special serological profile and mutations in S gene region, particularly in the 'a' determinant of the major hydrophilic region of the surface antigen, including one located at G130N. Aside from mutations in the S gene region, the presence of heterologous subtype-specific antibodies, superinfection with a new HB strain, occult HB reactivation and false positivity for anti-HBs are other possible explanations. These patients might harbor an augmented HBV replicative capacity and HBV reactivation upon receiving immunosuppression. Antiviral prophylaxis must be considered before starting immunosuppressive drugs. It was also reported that coexistent HBsAg and anti-HBs independently increased the risk of advanced fibrosis and hepatocellular carcinoma.