Peer-to-Peer Sessions in Primary Care to Improve the Hepatitis B Detection Rate in Seville, Spain.

INTRODUCTION AND AIM: The detection of hepatitis B virus (HBV) depends on primary care center activity. The present study aims to investigate the impact of peer-to-peer sessions with hepatologists on hepatitis B screening efficacy in primary care centers. MATERIAL AND METHODS: Peer-to-peer one-hour sessions were scheduled to improve the screening program for HBV in Seville, Spain. The sessions were focused on who should be tested for HBV and how positive cases should be referred. Fourteen out of 26 health care centers were selected to participate in peer-to-peer sessions. The centers were classified according to how many sessions they held (no sessions, one session or more than one session). RESULTS: Over a five-year period, HBV screening was performed in 32 203 people. In Seville, the prevalence of HBsAg was 0.87% (283/32 203). The detection rates for new HBsAg-positive cases were 7.1, 16.9 and 21.3 cases/105 population/year in non-session, one-time session and more than one session centers, respectively (p < 0.05). The rate of patients who effectively visited centers as outpatients was significantly higher after peer-to-peer sessions-86/94 (91%) for one session and 81/89 (91%) for two session centers vs. 16/27 (67%) for non-session centers (p = 0.002). The only independent predictor of patient referral was peer-to-peer sessions (OR, 1.925 [95% CI, 1.002-3.699]; p < 0.05). CONCLUSIONS: Peer-to-peer sessions in primary care centers increased HBV detection and visitation rates.

LPAC syndrome associated with deletion of the full exon 4 in a ABCB4 genetic mutation in a patient with hepatitis C.

Low-phospholipid-associated cholelithiasis syndrome (LPAC) is associated with ABCB4 genetic mutation. ABCB4 encodes MDR3 protein, involved in biliary phosphatidylcholine excretion.Higher prevalence in women, biliary symptoms in young adults and ursodesoxycholic acid (UDCA) response are the main features. We report the case of a 48-year-old man with hepatitis C, genotype 1b, fibrosis F3, null responder to Peg-IFN-alpha-2b/ribavirin and nephritic colic. In 2011 he developed jaundice, pruritus and epigastric pain.He showed increased serum levels of AST, ALT, GGT, bilirubin and alpha-fetoprotein, and viral load (14,600,000 IU/mL). Pancreatic- CT, endoscopic ultrasonography and echo-Doppler showed noncirrhotic chronic liver disease. The episode resolved spontaneously and one year later he suffered a similar episode. UDCA was started with excellent response. An immunohistochemistry study and sequencing of ABCB4 did not find alteration. MLPA® technique detected heterozygous deletion of the full exon 4 confirming LPAC syndrome diagnosis.

Síndrome LPAC secundario a deleción del exón 4 del gen ABCB4 en un paciente con hepatitis C / LPAC syndrome associated with deletion of the full exon 4 in a ABCB4 genetic mutation in a patient with hepatitis C

El síndrome LPAC (low-phospholipid-associated cholelithiasis syndrome) está asociado a mutaciones del gen ABCB4, que codifica la proteína MDR3, esencial en la secreción de fosfatidilcolina en las sales biliares. Este síndrome se caracteriza por una mayor prevalencia en mujeres, síntomas biliares en adultos jóvenes y excelente respuesta al ácido ursodesoxicólico (AUDC). Presentamos el caso de un hombre de 48 años con hepatitis C, genotipo 1b, fibrosis F3, nula respuesta Peg-IFN-α-2b/ribavirina y cólicos nefríticos de repetición. En 2011 desarrolló ictericia, prurito y dolor cólico epigástrico acompañado de aumento sérico de AST, ALT, GGT, bilirrubina y alfafetoproteína, y carga viral (14.600.000 UI/ml). La endoscopia oral, la ecoendoscopia, la angio-TAC y la ecografía-doppler evidenciaron hepatopatía crónica no cirrótica. El cuadro se autolimitó y un año después sufrió un episodio similar. Iniciamos tratamiento con AUDC, con excelente respuesta clínica. El estudio inmunohistoquímico y la secuenciación completa del gen ABCB4 no mostraron alteraciones. La técnica MLPA® detectó deleción heterocigota del exón 4 completo y confirmó la sospecha de síndrome LPAC (AU)

Low-phospholipid-associated cholelithiasis syndrome (LPAC) is associated with ABCB4 genetic mutation. ABCB4 encodes MDR3 protein, involved in biliary phosphatidylcholine excretion. Higher prevalence in women, biliary symptoms in young adults and ursodesoxycholic acid (UDCA) response are the main features. We report the case of a 48-year-old man with hepatitis C, genotype 1b, fibrosis F3, null responder to Peg-IFNα2b/ribavirin and nephritic colic. In 2011 he developed jaundice, pruritus and epigastric pain. He showed increased serum levels of AST, ALT, GGT, bilirubin and alpha-fetoprotein, and viral load (14,600,000IU/mL). Pancreatic- CT, endoscopic ultrasonography and echo-Doppler showed noncirrhotic chronic liver disease. The episode resolved spontaneously and one year later he suffered a similar episode. UDCA was started with excellent response. An immunohistochemistry study and sequencing of ABCB4 did not find alteration. MLPA® technique detected heterozygous deletion of the full exon 4 confirming LPAC (AU)