INTRODUCCIÓNLas alteraciones hepáticas en los pacientes con enfermedad celíaca (EC) fueron descritas por primera vez por Pollock en 1977 (1), revisando las biopsias hepáticas de 19 pacientes con malabsorción, en su mayor parte secundaria a EC. En tres casos el diagnóstico fue de hepatitis crónica, en uno de cirrosis y en otro de carcinoma hepatocelular, siendo los otros casos diagnosticados de cambios mínimos asociados a veces con fibrosis o inflamación periportal. Desde entonces la EC ha sido implicada en diferentes patologías hepáticas (2-4) incluyendo hepatopatías autoinmunes (5,6) e hipertransaminasemia criptogénica (7-10). Además, numerosos estudios han asociado la EC RESUMENla enfermedad celiaca (EC) es una causa importante de elevación de transaminasas: entre un 5 y un 10% de los pacientes con elevación crónica, criptogénica, de las transaminasas presentan EC y, al contrario, la EC puede estar asociada a diferentes enfermedades hepáticas. En efecto, un amplio abanico de patología hepática puede asociarse a EC, tanto en niños como en adultos, que pueden resumirse en: a) daño hepático mínimo caracterizado por la ausencia de síntomas o signos clínicos asociables a una enfermedad hepática cró-nica y con cambios histológicos no específicos que desaparecen después de la introducción de una dieta sin gluten; b) hepatopatías de etiología autoinmune, incluyendo la hepatitis autoinmune, la colangitis esclerosante primaria y la cirrosis biliar primaria, en las que la respectiva evolución no está influenciada por la introducción de dieta sin gluten; y c) insuficiencia hepática grave y cirrosis hepática criptogéni-ca descompensada, potencialmente tratables con la dieta sin gluten.Todas estas patologías están condicionadas por diferentes factores individuales y por una predisposición genética. La progresión y la reversibilidad del daño hepático en los diferentes cuadros patológicos, pueden estar condicionadas por la exposición al gluten y la edad, precoz o tardía, en la cual ha sido introducido en la dieta. Hay suficiente evidencia clínica para recomendar un atento cribado cruzado tanto para el diagnóstico del daño hepático asintomático en los pacientes con EC como para el diagnóstico de la EC en los pacientes con daño hepático criptogénico.Palabras clave: Enfermedad celiaca. Hepatopatía. Anti-tTG. Transaminasas. ABSTRACTCeliac disease (CD) is an important cause of serum aminotransferase elevation: between 5 and 10% of patients with persistent and cryptogenetic transaminase elevation may have CD. In fact, a wide spectrum of liver injuries in children and adults may be related to CD, particularly: a) mild parenchymal damage characterized by absence of any clinical signs or symptoms suggesting chronic liver disease, and by non-specific histological changes reversible on a gluten-free diet; b) chronic liver damage with autoimmune etiology, including autoimmune hepatitis, primary sclerosing cholangitis, and primary biliary cirrhosis, which may be associated with CD but are generally unaffected by gluten withdrawal; and c)...
A 77-year-old-male (Case R) who had had a previous diagnosis of mild COVID-19 episode, was hospitalized 35 days later. On Day 23 post-admission, he developed a second COVID-19 episode, now severe, and finally died. Initially, Case R COVID-19 recurrence was interpreted as a reinfection due to the exposure to a SARS-CoV-2 RT-PCR-positive room-mate. However, whole-genome-sequencing indicated that case R recurrence corresponded to a reactivation of the strain involved in his first episode. Case R reactivation had major consequences, leading to a more severe episode, and causing a subsequent transmission to another two hospitalized patients, one of them with fatal outcome.
The objective of this study was to quantify the magnitude of iron deficiency in the postoperative period after open aortic surgery. This was a prospective observational study in 55 consecutive patients. Blood samples were obtained on postoperative days 1, 2, 4, 30, and 45, and the parameters determined were the following: iron, transferrin, transferrin saturation index, transferrin-soluble receptor, ferritin, red cell count, hemoglobin, hematocrit, serum C-reactive protein, fibrinogen, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, and number of blood units transfused. We performed statistical ANOVA test for repetitive measurements (lower bound) in regard to its basal level. Iron deficiency and its parameters reached the maximum at 48 hours postoperatively (iron: 18.92 g/dL and transferrin saturation index: 11.1%) (P <.05). There was not a complete recovery after 45 days (iron: 51.23 g/dL and transferrin saturation index: 18.0%) (P <.05). A similar evolution was observed in the other measured parameters (red cell count: 3.5 x 106/L.; hemoglobin: 10.4 g/dL; hematocrit: 30.7%) (P <.005), none affecting the values of concentration or volume (P <.05). Transferrin-soluble receptors, normal at first, were increased at postoperative days 30 and 45 (2.7 and 2.4 mg/dL respectively, P <.005). After open aortic surgery there is an important acute-phase reaction, a dramatic iron deficiency, and a lack of its transporters until the 45th analyzed day. The elevation of transferrin-soluble receptors in the 4th and 6th weeks denotes a necessity of iron supplementation for a correct development of the immature hematic cells since blood parameters do not reach normal levels in the 6th postoperative week.
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