Luis Téllez Villajos

Epistaxis en el paciente cirrótico: una complicación a tener en cuenta

INTRODUCTION Epistaxis in cirrhotic patients is a common issue. However, the literature published to date is very scarce. MATERIAL AND METHODS Retrospective case series of patients with cirrhosis who presented with a significant epistaxis, between 2006 and 2016. RESULTS Data were collected from 39 cirrhotic patients with a mean age of 61.4 (±14) years, 75% of which were males. The main comorbidities were hypertension (33%) and diabetes mellitus (26%). Seven (18%) patients were taking antiplatelet drugs and 3 (8%) anticoagulants. One third of patients had a previous history of epistaxis and 6 had a previous ENT pathology. The main aetiological factor of cirrhosis was alcohol in 46% of cases, with 15 (38%) patients presenting with Child A, 12 (31%) Child B and 12 (31%) Child C class. The median MELD score upon admission was 16 [12-21]. Thirty-five (97%) patients had portal hypertension. At admission, the median platelet count was 89,000 [60,000-163,000] and mean INR was 1.52 (±0.37). Clinically, epistaxis presented as haematemesis or melaena in 8 (21%) patients, simulating gastrointestinal bleeding due to swallowing of blood. In 10 (26%) patients, epistaxis was considered as the probable trigger of an episode of hepatic encephalopathy. Two patients required ICU admission due to bleeding and 8 (21%) died during hospitalisation due to causes not directly related to epistaxis. CONCLUSIONS Epistaxis is a complication to be taken into account in cirrhotic patients, as it can act as an encephalopathy trigger or simulate an episode of gastrointestinal bleeding.

Pancreatitis aguda necrótica y aparición súbita de una masa abdominal: una complicación infrecuente

Las complicaciones hemorrágicas de la pancreatitis aguda (PA) son infrecuentes y se asocian con una alta morbimortalidad. Asimismo el desequilibrio del sistema de la coagulación en la PA grave, favorece la aparición de eventos trombóticos a nivel esplácnico. Presentamos el caso de una complicación no descrita hasta la fecha que refleja este fenómeno y la complejidad del manejo de estos pacientes. Varón de 42 años, fumador y bebedor de 120 g de alcohol/ día, que ingresó en nuestro servicio por un cuadro de 48 h de evolución de dolor abdominal epigástrico y continuo, compatible con el diagnóstico de PA. En la analítica al ingreso destacaba una bilirrubina total de 2,96 mg/dl (normal: < 1,2 mg/dl), GGT 500 U/l (normal: 7-30 U/l), LDH 346 U/l (normal: 140-240 U/l), amilasa 144 U/l (normal: 42141 U/l), lipasa 355 UI/l (normal: 42-111 U/L), PCR 147 mg/l (normal: < 5 mg/l) y leucocitosis de 21.700/ l (normal: < 10.500/ l). Las transaminasas, fosfatasa alcalina, urea y hematocrito eran normales. La ecografía abdominal al ingreso no mostró hallazgos relevantes. Ante la persistencia del dolor al tercer día y el incremento de la PCR hasta 234 mg/dl, se realizó una TC abdominal en la que se objetivó una necrosis de la cabeza pancreática (2530% del parénquima) y una trombosis del 50% de la vena mesentérica superior (VMS). Se decidió iniciar tratamiento anticoagulante con heparina de bajo peso molecular a dosis de 1 mg/kg/12 h. El paciente evolucionó favorablemente hasta que en el séptimo día, de forma brusca, presentó dolor intenso en hemiabdomen inferior, deterioro del estado general y anemización hasta 5 g/dl de hemoglobina. En la exploración destacaba la aparición repentina de una masa de 8 cm de diámetro en flanco derecho. Se realizó una angio-TC urgente que constató la presencia de un hematoma de 8 × 15 × 9 cm en la pared del colon dere-

Enteropatía por olmesartán

cteriano, infecciones (por ejemplo, giardiasis, enfermedad de hipple, tuberculosis), linfoma intestinal, esprue colágeno, fermedad de Crohn, esprue tropical y fármacos. Tras el análisis de los casos reportados hasta la fecha, la mayorı́a los pacientes habı́an sido diagnosticados previamente de fermedad celiaca sin respuesta a la dieta libre de gluten o fermedad celiaca refractaria. No se ha descrito relación entre tiempo de exposición a olmesartán y el desarrollo de la teropatı́a. El daño del epitelio intestinal podrı́a estar en relación n la respuesta celular inmunomediada secundaria a un sequilibrio entre factores antiinflamatorios y proinflamatorios. linked to blood pressure medicine olmesartan medoxomil. 2013 [consultado 1 Mar 2014]. Disponible en: http://www.fda.gov/Drugs/DrugSafety/ucm359477. htm 2. Théophile H, David XR, Miremont-Salamé G, Haramburu F. Five cases of spruelike enteropathy in patients treated by olmesartan. Dig Liver Dis. 2014;46:465–9, http://dx.doi.org/10.1016/j.dld.2013.12.014 3. Stanich PP, Yearsley M, Meyer MM. Olmesartan-associated sprue-like enteropathy. J Clin Gastroenterol. 2013;47:894–5. 4. Rubio-Tapia A, Herman ML, Ludvigsson JF, Kelly DG, Mangan TF, Wu TT, et al. Severe spruelike enteropathy associated with olmesartan. Mayo Clin Proc. 2012;87:732–8. 5. Nielsen JA, Steephen A, Lewin M. Angiotensin-II inhibitor (olmesartan)-induced collagenous sprue with resolution following discontinuation of drug. World J Gastroenterol. 2013;19:6928–30. 6.

Atrofia vellositaria sin enfermedad celíaca: ¿un nuevo síndrome o más confusión?

It is not unusual for clinicians, particularly for those working in gastroenterology, to find intestinal villus atrophy (IVA) in duodenum biopsies from patients treated with chronic diarrhoea. In most cases, this finding rules out the existence of coeliac disease (CD)1. CD is an autoimmune disease that mostly develops in genetically predisposed subjects carrying HLA-DQ2/DQ82. To obtain a definitive diagnosis of CD, it is necessary not just to have compatible clinical data, but also to assess other findings, among them: the presence of positive serology, mainly through the detection of IgA or IgG anti-transglutaminase antibodies, or, in cases with negative serology or border levels, the presence of antiendomysial IgA antibodies; a compatible histology, standardised by means of the MARSH Classification3; and a clinical response to a glutenfree diet2. The new immunohistochemistry and flow cytometry techniques that make it possible to characterise the predominant lymphocyte subpopulations located in the intestinal lamina propria have not been available for that long. Thanks to these techniques, we have been able to establish how the increase of TCR gammadelta lymphocytes and the decrease of NK CD3+/CD7lymphocytes are findings specifically associated with CD4, thus facilitating the differential diagnosis of other diseases. These techniques are not available for every medical centre. In spite of the aforesaid, CD diagnosis is not always easy to obtain, since there is a small group of patients who have IVA and are responsive to a gluten-free diet but whose antibodies are negative, resulting in the creation of the increasingly widespread seronegative CD concept. Even though CD is the most frequent cause of IVA1, there are other less frequent processes that may trigger it (table 1), widening a range of diagnostic possibilities before this histological finding

¿Es posible suspender el tratamiento con antivirales orales en los pacientes con hepatitis crónica B antígeno e negativa? Experiencia y nuevas expectativas

BACKGROUND Treatment of HBeAg-negative chronic hepatitis B (CHB) with nucleos(t)ide analogues (NA) is usually indefinite, since the loss of HBsAg, as a criterion for its discontinuation, is a rare event. Recent evidence suggests that discontinuing NA therapy may be feasible in selected patients. OBJECTIVES To analyze the rate of virological relapse in patients with HBeAg-negative CHB who discontinued treatment with NAs. METHODS We performed a single-center observational study that included 140 patients with HBsAg-negative CHB. Twenty-two patients, who received only NAs, discontinued treatment for different reasons and were subsequently monitored. All had normal ALT and AST, undetectable DNA and absence of cirrhosis or significant comorbidities before stopping treatment. RESULTS Twelve patients showed virologic relapse (54.54%). The mean interval between discontinuation and relapse was 6.38 months (± 1.9) (75% relapsed during the first 12 months after discontinuation). Five received adefovir, 1 lamivudine and adefovir, 1 tenofovir and 5 lamivudine alone. The mean treatment duration in this group was 38.5 months (± 4.5). The sustained response group had a higher mean age and longer treatment duration than patients with virologic relapse but these differences were not statistically significant. CONCLUSIONS The results suggest that NA treatment can be stopped in selected patients with CHB as long as they are not cirrhotic, have completed a minimum period of treatment, have normal ALT and sustained undetectable DNA. These patients should be closely monitored during the first year and then indefinitely.