ABSTRACT
BACKGROUND: The incidence of sexually transmitted infections (STIs) is unbridled and on the rise. Extragenital STIs (anal and pharyngeal infections) are commonly asymptomatic, resulting in delayed diagnosis and treatment and consequently higher chances of onward transmission. OBJECTIVE: The aim of this observational single-centre study was to determine the prevalence of STIs at extragenital sites in symptomatic and asymptomatic patients presenting at an STI outpatient clinic. METHODS: We conducted a retrospective analysis of patients who presented between October 2019 and February 2021 at the STI outpatient clinic of a tertiary centre in Central Europe. Patients were included in the study if they received at least one pharyngeal and/or anorectal swab in addition to a genital swab for multiplex-PCR STI diagnostics. Demographic data, symptoms and serological results were collected and analysed. RESULTS: Data collected from 440 patients were analysed (mean age: 33.9 years, male: n = 345, 78.4%, female: n = 95, 21.6%). Ninety-seven males reported having sex with men (MSM); 174 patients identified as heterosexual (132 males, 42 females), and 10 females as bisexual. The sexual orientation was not reported in 159 cases. An STI was confirmed in 195 patients (44.3%) and, among those, 109 patients (55.9%) tested positive for an STI at extragenital sites. Seventy-one patients had a pharyngeal STI whereas 61 were infected in the anorectal region. Of those suffering from an extragenital STI, 64.2% (70 out of 109) tested negative for relevant pathogens at genital sites. The most frequently detected extragenital pathogen was Neisseria gonorrhoeae (71.8% of all pharyngeal STIs [51 out of 71], 55.7% of anorectal STIs [34 out of 61]), followed by Chlamydia trachomatis (41.0% of all anal infections [25 out of 61], 5.6% of pharyngeal infections [4 out of 71]). Pharyngeal and anorectal infections were asymptomatic in 88.7% [63 out of 71] and 65.6% [40 out of 61] of the cases, respectively. CONCLUSION: These results underline the need to perform multisite testing, regardless of the presence of symptoms.
ABSTRACT
BACKGROUND: HIV/HCV co-infected patients show accelerated fibrosis progression and higher risk for complications of portal hypertension (PHT). AIM: To assess the effects of interferon-free therapy on portal pressure, liver histology and plasma biomarkers in HIV/HCV-coinfected patients with PHT. METHODS: Twenty-two patients with paired hepatic venous pressure gradient (HVPG) measurements prior and after successful treatment (SVR) with interferon-free regimens were included. Liver stiffness was assessed by transient elastography and biopsies were scored according to METAVIR. Plasma biomarkers were determined by ELISA. RESULTS: Overall, HVPG decreased from 10.7 ± 4.1 mmHg at baseline to 7.4 ± 4.2 mmHg after HCV treatment (Δ:-3.3 ± 2.7 mmHg; p < 0.001). In patients with clinically significant PHT (HVPG≥10 mmHg, n = 11), HVPG decreased from 14.1 ± 2.9 to 10.4 ± 3.9 mmHg (Δ:-3.7 ± 3.3 mmHg; p = 0.004) and a haemodynamic response (HVPG decrease ≥10%) was observed in 73%. In 64% of patients with subclinical PHT (HVPG 6-9 mmHg, n = 11), portal pressure normalised at SVR. Mean liver stiffness decreased from 20.8 kPa to 11.5 kPa (Δ:-8.8 ± 7.4 kPa; p < 0.001). Fifty percent (7/14) of patients with cirrhosis were re-classified as METAVIR ≤F3 and all patients with decompensated cirrhosis improved their Child-Pugh stage. After successful HCV treatment, 39% still had persistent histological necroinflammatory activity (METAVIR A1), which correlated with less HVPG response and more steatosis. While most biomarkers improved with SVR, METAVIR A1 patients had significantly higher plasma levels of fibrogenic (PDGF, TGF-ß) and angiogenic (VEGF, Angiopoietin1) biomarkers. CONCLUSIONS: Interferon-free therapy reduces PHT and halts histological necroinflammatory activity in the majority of HIV/HCV-coinfected patients after SVR, which may lead to re-compensation of liver function in cirrhosis. Biomarkers could identify patients with persisting hepatic necroinflammation.