Angioedema intestinal aislado inducido por enalapril / Isolated intestinal angioedema induced by enalapril

El angioedema inducido por inhibidores de la enzima convertidora de angiotensina es una entidad poco frecuente caracterizada por edema en piel y mucosas, debido al aumento de la permeabilidad vascular provocada por la inhibición de la enzima convertidora y el subsiguiente aumento de la bradiquinina. De manera frecuente cursa con compromiso facial y de mucosas, siendo infrecuente el compromiso intestinal o de vía aérea. El angioedema intestinal puede presentarse asociado a angioedema facial o aislado, siendo este último excepcional. Cursa con episodios recurrentes de dolor, distensión abdominal y diarrea acuosa con recuperación completa en dos o tres días. Si bien es una entidad poco frecuente, el hecho de que esté asociada a fármacos utilizados con frecuencia nos hace incluirla en el diagnóstico diferencial del dolor abdominal recurrente. Presentamos un caso de angioedema intestinal aislado, asociado al uso de enalapril.

Angioedema induced by angiotensin converting enzyme inhibitors is a rare entity characterized by skin and mucosal edema, due to increased vascular permeability caused by inhibition of the converting enzyme and subsequent increase in bradykinin. It frequently presents with facial and mucosal involvement, being uncommon the intestinal or airway compromise. Intestinal angioedema may be associated with facial or isolated angioedema, the latter being exceptional. It is associated with recurrent episodes of pain, abdominal distention and watery diarrhea which complete recovery in two or three days. Although it is a rare entity, the fact that it is associated with frequently used drugs makes us include it in the differential diagnosis of recurrent abdominal pain. We report a case of isolated intestinal angioedema associated with the use of enalapril.

Long-Term Outcomes of NSAID-Induced Small Intestinal Injury Assessed by Capsule Endoscopy in Korea: A Nationwide Multicenter Retrospective Study

BACKGROUND/AIMS: We evaluated the long-term outcome and clinical course of patients of nonsteroidal anti-inflammatory drug (NSAID)-induced small intestinal injury by performing capsule endoscopy (CE). METHODS: A multicenter retrospective study was conducted using data collected from the CE nationwide database registry, which has been established since 2002. RESULTS: A total of 140 patients (87 males; mean age, 60.6+/-14.8 years) from the CE nationwide database registry (n=2,885) were diagnosed with NSAID-induced small intestinal injury and enrolled in our study. Forty-nine patients (35.0%) presented with a history of aspirin use and an additional 49 (35.0%) were taking NSAIDs without aspirin. The most prominent findings after performing CE were multiple ulcerations (n=82, 58.6%) and erosions or aphthae (n=32, 22.9%). During the follow-up period (mean, 15.9+/-19.0 months; range, 0 to 106 months), NSAID-induced small intestinal injury only recurred in six patients (4.3%). Older age and hypertension were positive predictive factors for recurrence. CONCLUSIONS: These results suggest that the recurrence of NSAID-induced small bowel injury was not frequent in the presence of conservative treatment. Therefore, the initial diagnosis using CE and the medication history are important.

Diclofenac sodium and Imipenem action on rat intestinal mucosa: a biomechanical and histological study / Ação do Diclofenaco de sódio e Imipenem na mucosa intestinal do rato: estudo biomecânico e histológico

PURPOSE: To study diclofenac sodium induced histological and mechanical alterations and their prevention with Imipenem in rat intestine. METHODS: Male Wistar rats (n=240) were randomly assigned to four experimental groups: GI: n=60 treated with 0.9 percent saline IM; GII: n=60 treated with 6mg/kg body weight diclofenac sodium IM for four days; GIII: n=60 treated with 30mg/kg body weight Imipenem IM for four days, and GIV n=60 treated with diclofenac sodium plus Imipenem at the above doses IM for 4 days. Each group was further divided into 4 subgroups of 15 rats each and sacrificed at 4, 7, 14, and 21 days of follow-up, respectively. Abdominal cavity macroscopy and histology, and small bowel breaking strength were analyzed at each sacrifice moment. RESULTS: There were no histological or mechanical alterations in normal control rats throughout the study. Ulcerated lesions in intestinal mucosa were observed and breaking strength decreased in all diclofenac sodium treated rats. Ulcerated lesions in intestinal mucosa were prevented by Imipenem in all rats. CONCLUSION: Diclofenac sodium induced ulcerated lesions in rat intestinal mucosa can be prevented by Imipenem treatment.

OBJETIVO: Avaliar as alterações histológicas e biomecânicas do diclofenaco de sódio na mucosa intestinal do rato e a associação com o uso de Imipenem. MÉTODOS: Foram estudados 240 ratos Wistar distribuídos aleatoriamente em quatro grupos experimentais: GI: 60 ratos tratados com injeção IM de soro fisiológico 0,9 por cento; GII: 60 ratos tratados com injeção IM de diclofenaco de sódio na dose de 6mg/kg de peso por 4 dias; GIII: 60 ratos tratados com injeção IM de Imipenem na dose de 30 mg/kg de peso por 4 dias; GIV: 60 ratos tratados com injeção IM de soro fisiológico e diclofenaco de sódio nas doses acima. Em cada grupo os animais foram posteriormente divididos em 4 momentos de 15 animais em cada um para sacrifício, respectivamente, no 4º, 7º, 14º e 21º dias após o início do tratamento. As alterações da cavidade abdominal, assim como as características histológicas e de força de ruptura do intestino delgado foram analisadas em cada momento, em cada grupo. RESULTADOS: Não foram encontradas alterações histológicas e biomecânicas nos animais do Grupo I nesse estudo. Lesões ulceradas na mucosa do intestino delgado foram observadas nos animais tratados com diclofenaco de sódio, assim como diminuição da força de ruptura. As lesões ulceradas encontradas foram prevenidas pelo uso de Imipenem. CONCLUSÃO: O diclofenaco de sódio induz lesões ulceradas na mucosa intestinal do rato que podem ser prevenidas pelo uso de Imipenem.

Curso de Reumatologia: aula 5: anti-inflamatórios não hormonais e alterações intestinais / Course of Rheumatology: class 5: nonsteroidal anti-inflammatory drugs and intestinal alterations

A enteropatia relacionada aos anti-inflamatórios não hormonais (ou não esteroides) é um processo gradual que envolve efeito tóxico direto à mucosa, lesão mitocondrial, quebra da integridade intercelular, recirculação êntero-hepática do anti-inflamatório e ativação neutrofílica pelo conteúdo intraluminal, inclusive por bactérias. A mediação pela cicloxigenase provavelmente é menos importante do que no trato gastrointestinal superior. Estudos com a nova modalidade endoscópica, como a que se utiliza de cápsula endoscópica, demonstram anormalidades relacionadas aos anti-inflamatórios não esteroides (AINEs), que incluem inflamação, erosões, fibrose, estenoses, lesões enantemáticas, erosões patequiais, perfurações e formação de membranas diafragmáticas no jejuno, íleo e colon.

Nonsteroidal anti-inflammatory drug enteropathy is a stepwise process involving direct mucosal toxity, mitochondrial damage, breakdown of intercellular integrity enterohepatic recirculation and neutrophil activation by liminal contents including bacteria. Unlike upper gastrointestinal toxity, cyclooxygenase-mediated mechanisms are probably less important. Newer imaging modalities such as capsule endoscopy studies demonstrate nonsteroidal anti-inflammatory drug-induced abonormalities that include inflammation, erosion, fibrosis, stricture, red spots, petechiae erosions, perforation, and formation of mucosal diaphragms in the jejunum, ileum and colon.

NSAID-induced Gastroenteropathy / 대한소화기학회지

Non-steroidal anti-inflammatory drugs (NSAIDs) are used for the management of various conditions, such as pain, fever, inflammation, cancer, or cardiovascular diseases. These drugs may induce injury throughout the gastrointestinal tract. NSAIDs are associated with diverse upper gastrointestinal adverse effects, including dyspepsia, erosions, peptic ulcer diseases and complications such as bleeding perforation. Established risk factors for these adverse effects include age, prior ulcer, types, doses and duration of NSAIDs, concurrent other NSAIDs administration, and the concomitant uses of corticosteroids or anticoagulants. Misoprostol, proton pump inhibitors, and cyclooxygenase-2 selective inhibitors have been used to reduce the risk of NSAID-associated upper gastrointestinal events. NSAID-induced enteropathy is more common than complications of the stomach and duodenum and is usually manifested by occult blood loss or hypoalbuminemia. Furthermore, NSAIDs induce small intestinal injuries causing gut barrier damage, and bacterial translocation that have been proposed to be associated with the burden of illness in decompensated chronic heart failure. However, the risk factors for NSAID-induced enteropathy and bacterial translocation, as well as its preventive measures, are not well documented.

Prevention of mercuric chloride induced histopathological changes in the small intestine of mice with LIV-52.

Mercuric chloride was administered in drinking water to mice at 1 mM and 5 mM for 100 and 30 days respectively. Lower concentration caused mild pathological changes in the small intestine while higher concentration caused severe pathological changes. Pathological symptoms were less pronounced when Liv52 was administered along with 5 mM mercuric chloric and Hg-induced changes were totally absent when drug was used along with 1 mM HgCl2 solution. After Hg-exposure at both concentrations mice were allowed to recover naturally or with drug (Post-therapy). Again, use of drug appeared useful. At least under laboratory conditions this herbal drug seems to reduce Hg-induced pathological changes in small intestine of mice.