Publications by authors named "Juan R Larrubia"

Purpose: To explore visual outcomes in patients with extreme myopia receiving an implantable collamer lens (ICL) at -18.00 diopters (D), with central port, followed by bioptics by laser vision correction (laser in situ keratomileusis [LASIK] or photorefractive keratectomy [PRK]) to address residual myopia or myopic astigmatism.

Setting: Clínica Baviera (Aier Eye Hospital Group), Bilbao, Spain.

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Background: The evaluation of bictegravir, emtricitabine, and tenofovir alafenamide (BIC/FTC/TAF) in clinical trials has shown high rates of virological suppression but information about its use in real-life settings is scarce.

Objective: To evaluate the effectiveness, safety, durability, and predictive variables of therapeutic failure of BIC/FTC/TAF in a real-life cohort.

Methods: This observational, retrospective, multicentered cohort study included treatment-naive (TN) and treatment-experienced (TE) adult patients living with HIV (PLWH) who started treatment with BIC/FTC/TAF from January 1, 2019, to January 31, 2022.

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Hepatitis C virus (HCV) infection is an excellent immunological model for understanding the mechanisms developed by non-cytopathic viruses and tumors to evade the adaptative immune response. The antigen-specific cytotoxic T cell response is essential for keeping HCV under control, but during persistent infection, these cells become exhausted or even deleted. The exhaustion process is progressive and depends on the infection duration and level of antigenemia.

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Background: Antiviral treatment of patients with chronic hepatitis B (CHB) in the grey zone of treatment comands risk management in order to optimize the health outcome. In this sense, the identification of HBV mutants related with an increased risk of hepatocellular carcinoma (HCC) could be useful to identify subpopulations with potential indication of antiviral treatment.

Aim: To analyze the prevalence/persistence of hepatitis B virus (HBV) preS and basal core promoter (BCP)/precore/core variants associated to HCC development in CHB patients in the grey zone.

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Chronic hepatitis B (CHB) remains a challenging global health problem, with nearly one million related deaths per year. Nucleos(t)ide analogue (NA) treatment suppresses viral replication but does not provide complete cure of the hepatitis B virus (HBV) infection. The accepted endpoint for therapy is the loss of hepatitis B surface antigen (HBsAg), but this is hardly ever achieved.

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HDV infection may occur within a primary HBV infection (co-infection) or by sub sequent acquisition ofthe virus in patients with chronic hepatitis B (superinfection). Acute HDV infection is rarely diagnosed. Since cero conversion usually takes place about six weeks after viral infection, early diagnosis requires the use of direct diagnostic techniques, such as antigen HD V (HDAg) detection, or genomic amplification by means of molecular biology methods (RT-PCR).

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Background & Aims: The addition of protease inhibitors (PIs) changed the hepatitis C virus (HCV) treatment standards and improved sustained viral response (SVR) rates in patients with genotype 1 HCV infection.

Methods: Prospective, multicentre, national registry that includes naïve and treatment-experienced patients with HCV genotype 1 infection, who had bridging fibrosis or cirrhosis and were treated with triple therapy (peginterferon alfa-2a or alfa-2b, ribavirin and boceprevir) as compassionate use, and in accordance with the Summary of Product Characteristics.

Results: Most of the patients (68.

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Hepatitis C virus (HCV) infection affects about 170 million people worldwide and it is a major cause of liver cirrhosis and hepatocellular carcinoma. HCV is a hepatotropic non-cytopathic virus able to persist in a great percentage of infected hosts due to its ability to escape from the immune control. Liver damage and disease progression during HCV infection are driven by both viral and host factors.

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Article Synopsis
  • Virus-specific T cells are important for fighting off liver infections, but in chronic cases, they stop working effectively against the virus.
  • Hepatitis B and C viruses trick the immune system into ignoring them by destroying these virus-fighting T cells through a process called apoptosis.
  • A protein called Bim plays a key role in this cell death, helping the viruses survive in the body by keeping the immune response quiet.
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PD-1 molecule promotes anergy and IL-7 receptor (CD127) induces an anti-apoptotic effect on T cells. Correlation between PD-1/CD127 phenotype and hepatitis C virus (HCV)-specific CD8(+) cell reactivity in resolved infection (RI) after treatment and persistent HCV-infection (PI) was analysed. Directly ex vivo, PD-1 and CD127 expression on HCV-specific CD8(+) cells displayed a positive and negative correlation, respectively with viraemia.

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Article Synopsis
  • Chemokines made in the liver during hepatitis C help move special immune cells called T cells to fight off the virus.
  • These chemokines work mostly with a type of T cell response called Th1/Tc1, and they get released more during chronic hepatitis C.
  • Researchers think controlling how these chemokines and their receptors work could help treat liver damage and improve immune responses against the virus.
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Context: Mast cells (MCs) have been implicated in fibrogenesis, angiogenesis, and immunity against bacteria. These 3 mechanisms participate in the peritoneal pathology secondary to peritoneal dialysis (PD) treatment. Despite their potential relevance to PD-related pathology, few studies have focused on MCs.

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