Aims and Background. We assessed long-term clinical outcomes and prognostic factors for liver disease progression after sustained viral response (SVR) with direct-acting antivirals (DAAs) in HIV/HCV coinfected patients with advanced fibrosis (AdF) or cirrhosis. Approach and Results. A total of 1,300 patients who achieved SVR with DAAs from 2014 to 2017 in Spain were included: 1145 with chronically advanced liver disease (cACLD) (384 AdF and 761 compensated cirrhosis [CoC]) and 155 with decompensated cirrhosis (DeC). The median follow-up was 40.9 months. Overall, 85 deaths occurred, 61 due to non-liver non-AIDS-related (NLNA) causes that were the leading cause of death across all stages of liver disease. The incidence (95% confidence interval [CI]) of decompensation per 100 person-years (py) was 0 in patients with AdF, 1.01 (0.68–1.51) in patients with CoC, and 8.35 (6.05–11.53) in patients with DeC. The incidence (95% CI) of hepatocellular carcinoma (HCC) per 100 py was 0.34 (0.13–0.91) in patients AdF, 0.73 (0.45–1.18) in patients with CoC, and 1.92 (1.00–3.70) per 100 py in patients with DeC. Prognostic factors for decompensation in patients with cACLD included serum albumin, liver stiffness measurement (LSM), and FIB-4. In this population, LSM and LSM-based posttreatment risk stratification models showed their predictive ability for decompensation and HCC. Conclusions. NLNA events were the leading causes of morbidity and mortality after DAA cure among coinfected patients with AdF/cirrhosis. Among those with cACLD, baseline LSM and posttreatment LSM-based models helped to assess decompensation and HCC risk. Export

Background: Hepatitis C virus (HCV) has significantly impacted people with human immunodeficiency virus (HIV). Harm reduction programs, changing transmission patterns, and direct-acting antivirals (DAAs) have profoundly altered HIV/HCV coinfection trends. This study evaluates HCV prevalence among people with HIV in Spain over 2 decades. Methods: We conducted 9 cross-sectional studies (2002–2023) in 39–43 centers. Sampled individuals were randomly sampled from people with HIV actively followed up at these centers, with proportional allocation. Main outcomes included the prevalence of anti-HCV antibody and active HCV infection (HCV RNA­–positive result). Results: The reference population ranged from 31 800 to 47 006, with sample sizes of 1260–1867. HIV transmission patterns shifted from 2002 to 2023, with injection drug use decreasing from 55% to 21% and the proportion of men who have sex with men increasing from 17% to 46%. HCV seroprevalence fell from 60.8% to 27.4%, and active infection from 46.3% to 0.9%. In the DAA era (2015–2023), active HCV infection dropped by 100% in heterosexuals, 94% in people who inject drugs, and 71% in men who have sex with men. Treatment uptake increased from 23% in 2002 to 99% by 2023 with all-oral DAAs. The prevalence of cirrhosis among active HCV cases peaked at 23.1% in 2015 but fell to 0% by 2021. Among those achieving sustained virologic response, cirrhosis prevalence was 20.4% in 2023. Conclusions: HIV/HCV coinfection has drastically declined in Spain, with active HCV infection prevalence <1% since 2021. DAAs were pivotal in this achievement. However, cirrhosis remains a concern among those with sustained virologic response. Ongoing surveillance and prevention efforts are essential to sustain these gains and address residual risks.

Mitochondrial DNA (mtDNA) haplogroups have been associated with advanced liver fibrosis and cirrhosis in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV). Our aim was to determine whether mtDNA haplogroups are associated with liver-related events (LREs) in HIV/HCV-coinfected patients. We carried out a retrospective cohort study in HIV/HCV-coinfected patients who were potential candidates for therapy with interferon and ribavirin (IFN/Rib) between 2000 and 2009. The primary endpoint was the occurrence of LREs (decompensation or hepatocellular carcinoma). mtDNA genotyping was performed using the Sequenom MassARRAY platform. We used Fine and Gray proportional hazards model to test the association between mtDNA haplogroups and LREs, considering death as a competitive risk. The study population comprised 243 patients, of whom 40 had advanced fibrosis or cirrhosis. After a median follow-up of 7.7 years, 90 patients treated with IFN/Rib achieved sustained viral response (SVR), 18 patients had LREs, and 11 patients died. Patients with haplogroup H had lower cumulative incidence than patients with other haplogroups (p = 0.012). However, patients with haplogroup T had higher cumulative incidence than patients with other haplogroups (p = 0.074). In the multivariate analysis, haplogroup T was associated with an increased hazard of developing LREs [adjusted subhazard ratio (aSHR) = 3.56 (95% CI 1.13;11.30); p = 0.030]; whereas haplogroup H was not associated with lower hazard of LREs [aSHR = 0.36 (95% CI 0.10;1.25); p = 0.105]. When we excluded patients who achieved SVR during follow-up, we obtained similar SHR values. European mitochondrial haplogroups may influence the natural history of chronic hepatitis C.

Lipoprotein(a) [Lp(a)] has emerged as an important cardiovascular risk factor. However, the prevalence and determinants of elevated Lp(a) in people living with HIV (PLHIV) remain insufficiently characterised. Since PLHIV have an increased cardiovascular risk even under effective virological control, our aim was to explore the prevalence of elevated Lp(a) and its association with cardiovascular risk in this population. We conducted a single-centre observational study in adult PLHIV with sustained virological suppression and without active oncological or infectious comorbidities. According to most international consensus statements, elevated Lp(a) was defined as levels >50mg/dL. A total of 186 PLHIV were included. Of these, 21% had Lp(a) levels >50mg/dL. Individuals with elevated Lp(a) had significantly higher total cholesterol, Low-density lipoprotein cholesterol (LDL-C), and apolipoprotein B levels, as well as a higher odds of a cardiovascular event (OR 5.3, p = 0.018). Although the proportion of patients receiving lipid-lowering therapy was significantly higher among those with elevated Lp(a), the percentage achieving LDL-C targets according to cardiovascular risk was significantly lower compared with patients with Lp(a) <50mg/dL. No association was observed between elevated Lp(a) and antiretroviral therapy regimens, CD4 count, CD4/CD8 ratio, or duration of HIV infection. In our study, elevated Lp(a) was present among 21% of virologically suppressed PLHIV and was associated with an adverse lipid profile and cardiovascular events, whereas no association was observed with HIV-related factors. Lp(a) may represent a marker of residual cardiovascular risk in this population and could help refine cardiovascular risk stratification beyond traditional lipid parameters.

Introducción: Desde que se inició la pandemia por el SARS-CoV-2, se han descrito numerosos casos de síndrome de Guillain-Barré secundario a la COVID-19. Su presentación típica es la triada de parestesias, debilidad muscular ascendente y arreflexia, aunque hay diversas variantes regionales como la diplejía facial. Presentación del caso: Mujer de 35 años que, dos semanas después de un contacto estrecho con un caso confirmado de COVID-19, ingresa por miopericarditis probablemente viral, con estudio de autoinmunidad negativo, múltiples serologías virales negativas y positividad para IgG anti-SARS-CoV-2 con PCR negativa. Una semana tras el alta presenta paresia de ambos nervios faciales sin otras alteraciones neurológicas. Se realiza TAC craneal sin hallazgos y EMG que evidencia afectación bilateral de los nervios faciales. La paciente rechaza realización de punción lumbar Discusión: La diplejía facial puede ocurrir en el contexto de diversas patologías, como tumores meníngeos o troncoencefálicos, agentes infecciosos, síndrome de Guillain-Barré, patologías autoinmunes, traumatismos, causas metabólicas o causas congénitas. En el caso descrito tras descartar mediante pruebas de imagen y analíticamente el resto de etiologías, y dada la presentación clínica, permanece como causa más probable el síndrome de Guillain-Barré, posiblemente secundario a infección por SARS-CoV-2 dada la positividad de IgG anti-SARS-CoV-2 tras un contacto con un caso confirmado. Conclusión: Este caso apoya la hipótesis de que la COVID-19 puede desencadenar el síndrome de Guillain-Barré, específicamente en forma de diplejía facial, una variante atípica que se debe conocer para su identificación y manejo precoz como parte de este síndrome.

In a patient on immunosuppressant treatment, SARS-CoV-2 RNA was documented in different extra-respiratory samples over several months in the absence of positive determinations in upper respiratory samples. Whole-genome sequencing of these samples showed the acquisition of different single-nucleotide polymorphisms over time, suggesting viral evolution and thus viral viability.