Tolerance to sterilised cow's milk in patients with eosinophilic oesophagitis triggered by milk.

BACKGROUND: Cow's milk protein is the main food trigger for eosinophilic oesophagitis (EoE) in children and adults and should be continuously avoided once identified as such. AIMS: To evaluate tolerance of sterilised cow's milk (boiled instead of UHT processing) with regard to maintenance of EoE remission, health-related quality of life (HRQoL), nutritional intake and allergic sensitisation in patients of all ages with milk-triggered EoE METHODS: We prospectively recruited patients in whom cow's milk was demonstrated to trigger EoE after an empirical food elimination diet-based study. They were given 200 ml of sterilised cow's milk twice daily for 8 weeks. Endoscopic assessment, peak eosinophil counts, oesophageal-related symptoms, HRQoL, blood eosinophils, eosinophil cationic protein (ECP), skin prick test and serum total and specific immunoglobulin E (IgE) to major milk proteins were monitored before and after sterilised milk intake. RESULTS: Eighteen patients (13 male) in EoE remission underwent a sterilised milk challenge. Twelve maintained EoE remission (<15 eos/hpf) while EoE recurred in the remainder. Endoscopic appearances deteriorated in non-tolerant patients. HRQoL scored well at baseline and was maintained among patients tolerant to sterilised milk, but deteriorated in reactive ones. No significant changes in blood eosinophil count, ECP, tryptase or total and milk-specific IgE serum levels were observed from baseline. However, cow's milk-specific IgE increased slightly in non-tolerant patients. Clinical and histological remission were maintained in patients who regularly consumed sterilised milk for 1 year. CONCLUSION: Sterilised milk did not trigger EoE in two-thirds of patients with documented milk-induced EoE, in either the short or long term.

Prevalence and incidence of microscopic colitis in patients with diarrhoea of unknown aetiology in a region in central Spain.

BACKGROUND: Often previously overlooked, microscopic colitis, including collagenous colitis and lymphocytic colitis, has now emerged as a common cause of chronic diarrhoea. AIMS: To evaluate the prevalence and incidence of microscopic colitis in patients with diarrhoea of unknown aetiology. METHODS: 271 consecutive patients who were referred to the General Hospital of Tomelloso from April 2008 to December 2010 for diarrhoea of unknown aetiology underwent a full colonoscopy to obtain biopsy samples to diagnose microscopic colitis on the basis of commonly accepted histological criteria. All patients were classified according to the Roma III criteria for diarrhoea-dominant irritable bowel syndrome. RESULTS: In 234/271 consecutive patients with normal endoscopic appearance we observed 32/234 patients with microscopic colitis (30 lymphocytic colitis and 2 collagenous colitis) with a prevalence of microscopic colitis of 48 cases/100,000 inhabitants (95%CI: 30-65) and mean annual standardised incidence of 18 cases/100,000 inhabitants (95%CI: 16.0-20.0). Analysing only the patients that met the Roma III criteria (84/271), we observed 10.7% microscopic colitis diagnosis, with higher risk in the presence of autoimmune disease, seronegative celiac disease and intake of non-steroidal anti-inflammatory drugs. CONCLUSIONS: Microscopic colitis was found in 13.7% of patients with chronic diarrhoea. Microscopic colitis is present in a relevant proportion of symptomatic patients meeting diagnostic criteria for irritable bowel syndrome (10.7%).

[Ulcerative colitis associated with Vogt-Koyanagi-Harada disease]. / Colitis ulcerosa asociada a enfermedad de Vogt-Koyanagi-Harada.

We report the case of a female patient who was diagnosed with Vogt-Koyanagi-Harada disease at the age of 14 years and who developed myelopathy, resulting in paraparesis. A cerebral magnetic resonance imaging scan revealed the presence of T2-hyperintense lesions in the periventricular white matter, suggesting demyelinization. Twelve years later, ulcerative colitis was diagnosed during workup for abdominal pain associated with bloody diarrhea. The association of these two diseases has previously been reported anecdotically. The management of the ulcerative colitis was complicated by the patient's neurological manifestations. Even though recent reports support the use of anti-TNF drugs in the management of Vogt-Koyanagi-Harada-associated uveitis, because of the lack of experience in patients with neurological symptoms, and the presence of apparently demyelinating lesions in our patient, we did not use these drugs in this case.

Colitis ulcerosa asociada a enfermedad de Vogt-Koyanagi-Harada / Ulcerative colitis associated with Vogt-Koyanagi-Harada disease

A continuación se presenta el caso de una paciente diagnosticada a los 14 años de enfermedad de Vogt-Koyanagi-Harada (VKH) en la que posteriormente se desarrolló paraparesia por mielopatía secundaria a esta enfermedad. Asimismo, se detectaron en la resonancia magnética craneal lesiones en la sustancia blanca periventricular, hiperintensas en secuencias ponderadas en T2, indicativas de desmielinización. Doce años después, la paciente se realizó un estudio debido a un cuadro de dolor abdominal asociado a diarrea con productos patológicos siendo diagnosticada de colitis ulcerosa (CU).La asociación de estas 2 enfermedades se ha comunicado con anterioridad de forma anecdótica.Las manifestaciones neurológicas de la paciente complicaron el tratamiento terapéutico de la CU, ya que, aunque publicaciones recientes avalan el tratamiento con anti-TNF (antitumor necrosis factor‘antifactor de necrosis tumoral’) en la uveítis propia de enfermedad de VKH, la falta de experiencia en casos asociados a focalidad neurológica y el desconocimiento de la verdadera patogénesis de las lesiones parenquimatosas indicativas de desmielinización desaconsejaron el uso de estos fármacos en este caso (AU)

We report the case of a female patient who was diagnosed with Vogt-Koyanagi-Harada disease at the age of 14 years and who developed myelopathy, resulting in paraparesis. A cerebral magnetic resonance imaging scan revealed the presence of T2-hyperintense lesions in the periventricular white matter, suggesting demyelinization. Twelve years later, ulcerative colitis was diagnosed during workup for abdominal pain associated with bloody diarrhea.The association of these two diseases has previously been reported anecdotically.The management of the ulcerative colitis was complicated by the patient's neurological manifestations. Even though recent reports support the use of anti-TNF drugs in the management of Vogt-Koyanagi-Harada-associated uveitis, because of the lack of experience in patients with neurological symptoms, and the presence of apparently demyelinating lesions in our patient, we did not use these drugs in this case (AU)

Síndrome constitucional asociado a hepatotoxicidad por metformina / Constitutional syndrome associated to metformin induced hepatotoxictyn

La metformina es un antidiabético oral frecuentemente utilizado en el tratamiento de la diabetes mellitus tipo 2. En un 5-20% de los pacientes provoca trastornos gastrointestinales inespecíficos. Son mucho más raros otros efectos secundarios de mayor envergadura, como la acidosis láctica. Se han documentado algunos casos aislados de hepatotoxicidad por este fármaco. Presentamos el caso de un paciente con síndrome constitucional y alteración de la bioquímica hepática atribuible a hepatotoxicidad por metformina, tras descartarse mediante múltiples estudios una etiología tumoral y observarse una resolución completa del cuadro con la suspensión del fármaco

Metformin is an oral antidiabetic agent frequently used to manage type II diabetes. This drug produces nonspecific gastrointestinal symptoms in 5-20% of patients and, more rarely, has also been associated with severe adverse effects such as lactic acidosis. Only a few isolated cases of hepatotoxicity due to this drug have been documented. We report the case of an 83-year-old man with constitutional syndrome and hepatic biochemical alterations, which were attributedto metformin after ruling out an oncologic etiology and observing complete clinical and biochemical resolution after withdrawal of the drug

Una causa infrecuente de obstrucción gástrica: síndrome de Bouveret / An uncommon cause of gastric outlet obstruction: Bouveret's syndrome

El síndrome de Bouveret (SB) es un tipo infrecuente de íleo biliar consistente en una obstrucción gastroduodenal secundaria al paso de cálculos desde la vesícula biliar al duodeno, a través de una fístula colecisto o coledocogastroduodenal. La primera descripción de este síndrome la realizó en 1896 León Bouveret. Desde esta época se han descrito en la literatura médica poco más de 200 casos. Si bien la mortalidad del cuadro se establece en un 25%, el pronóstico viene determinado por la comorbilidad, la edad avanzada y el retraso en el diagnóstico. Para llegar al diagnóstico suelen precisarse tanto técnicas radiológicas (radiografía simple, ecografía, tomografía computarizada o resonancia magnética) como endoscópicas. Se debe intentar siempre el tratamiento endoscópico, aunque es muy frecuente que éste sea fallido y sea preciso recurrir al tratamiento quirúrgico. Presentamos el caso de un paciente que consultó por la aparición de vómitos pospandriales y epigastralgia. A continuación discutimos el manejo diagnóstico y terapéutico de esta infrecuente causa de obstrucción gástrica

Bouveret’s syndrome is a rare type of gallstone ileus inwhich a gallstone enters the intestinal tract via a cholecystoenteric fistula and is lodged in the duodenum or the stomach. Since the first description by León Bouveret in 1896, fewer than 200 cases have been described in the worldwide literature. Mortality is high, at 25%, but may be related to the advanced age of the typical patient and comorbidities, aswell as diagnostic delay. Diagnosis may be made with radiological (abdominal X-ray, ultrasound, computed tomography or magnetic resonance imaging) and endoscopictechniques. Endoscopy is preferred as the first therapeutic option but is frequently unsuccessful and surgery is often required. We present the case of a patient admitted to hospital with a history of vomiting after eating and epigastric pain. The management of this rare cause of gastric outlet obstruction is discussed (AU)

[Constitutional syndrome associated to metformin induced hepatotoxicity]. / Síndrome constitucional asociado a hepatotoxicidad por metformina.

Metformin is an oral antidiabetic agent frequently used to manage type II diabetes. This drug produces nonspecific gastrointestinal symptoms in 5-20% of patients and, more rarely, has also been associated with severe adverse effects such as lactic acidosis. Only a few isolated cases of hepatotoxicity due to this drug have been documented. We report the case of an 83-year-old man with constitutional syndrome and hepatic biochemical alterations, which were attributed to metformin after ruling out an oncologic etiology and observing complete clinical and biochemical resolution after withdrawal of the drug.

[A rare cause of gastric outlet obstruction: Bouveret's syndrome]. / Una causa infrecuente de obstrucción gástrica: síndrome de Bouveret.

Bouveret's syndrome is a rare type of gallstone ileus in which a gallstone enters the intestinal tract via a cholecystoenteric fistula and is lodged in the duodenum or the stomach. Since the first description by León Bouveret in 1896, fewer than 200 cases have been described in the worldwide literature. Mortality is high, at 25%, but may be related to the advanced age of the typical patient and comorbidities, as well as diagnostic delay. Diagnosis may be made with radiological (abdominal X-ray, ultrasound, computed tomography or magnetic resonance imaging) and endoscopic techniques. Endoscopy is preferred as the first therapeutic option but is frequently unsuccessful and surgery is often required. We present the case of a patient admitted to hospital with a history of vomiting after eating and epigastric pain. The management of this rare cause of gastric outlet obstruction is discussed.