Gastroenterologie Clinique Et Biologique最新文献

Abdominal tuberculosis involving the portal vasculature is a rare phenomenon. We retrospectively reviewed the imaging findings of 183 cases of abdominal tuberculosis at our institution from 2002 to 2010 and found thrombosis of the splenoportal axis associated with abdominal lymphadenopathy in seven patients. However, there was no relationship between the lymph nodal size and development of thrombosis. Reversibility was noted in one patient, who had near complete recanalisation of portal vein. Mechanisms, other than direct mass effect on the splenoportal axis, may be involved, like contiguous spread of inflammation or granulomas in the vessel wall.

Background

Capsule endoscopy (CE) is an effective method for investigating the small bowel, especially in cases of obscure gastrointestinal bleeding (OGIB), although the long-term outcome of patients with a negative CE is generally not known.

Patients and methods

For 49 patients with OGIB and a negative CE, their referring physicians filled out a follow-up questionnaire to assess bleeding recurrence and any repeat investigations after negative video capsule endoscopy (VCE).

Results

A minimum follow-up duration of one year (median: 15.9 months) was available for 35 patients with an overall rebleeding rate of 23% (n = 8). Of these eight patients, four women presented with recurrence prior to new investigations. In the four remaining patients, repeat endoscopy work-ups after negative CE were performed and revealed previously missed lesions with bleeding potential, mainly in the stomach. Overall, 13 patients, with or without rebleeding, had repeat endoscopy work-ups after a negative CE, leading to a definitive diagnosis in nine patients, with lesions located in the stomach and colon in eight of them.

Conclusion

Patients with OGIB and a negative CE had a low rate of rebleeding. This study highlights the importance of the initial endoscopy work-up, and suggests that CE be proposed after a minimum of two gastroscopies and one complete colonoscopy.

We report the case of a patient diagnosed with a villous adenoma of the duodenum showing high degree dysplasia who developed a nephrotic syndrome (NS) due to a membranous nephropathy (MN), demonstrated by renal biopsy. Only the endoscopic resection of the duodenal adenoma could control the NS. The first manifestation of a MN is often the development of a NS. Up to 20% of patients older than 65 years who develop a MN have cancer. Tumours most often identified are those of lung, prostate and digestive tract. A renal biopsy is required to identify this type of nephropathy. If a diagnosis of MN is made, an associated tumour should be looked for.

Nous rapportons le cas d’une patiente, porteuse d’un adénome tubulovilleux du duodénum avec une dysplasie de haut grade, qui a développé un syndrome néphrotique sur une glomérulonéphrite extra-membraneuse (GNEM), démontrée par biopsie rénale. Celui-ci n’a pu être contrôlé que par la résection endoscopique de l’adénome duodénal. La première manifestation d’une GNEM est souvent l’apparition d’un syndrome néphrotique. Jusqu’à 20 % des patients âgés de plus de 65 ans qui développent GNEM sont atteints d’un cancer. Les tumeurs les plus fréquemment retrouvées sont celles du poumon, de la prostate et du tractus digestif. Il est donc indispensable de réaliser une biopsie rénale en cas de syndrome néphrotique pour identifier le type d’atteinte glomérulaire. Si le diagnostic de GNEM est posé par la biopsie rénale, une recherche de néoplasie associée doit être entreprise.

Introduction

In severe attacks of ulcerative colitis (UC) treated with intravenous corticosteroids, a fulminant colitis index (FCI) greater or equal to 8 has been associated with a greater likelihood of colectomy (72 vs 16% with an FCI < 8). This retrospective study aimed to assess the accuracy of such an association in infliximab-treated patients with moderate-to-severe bouts of UC.

Patients and methods

The study was based on the medical files of 43 patients who had received at least one infusion of infliximab to treat moderate-to-severe UC (partial Mayo Clinic score). Remission and clinical response were also assessed using the partial Mayo score. The accuracy of an FCI greater or equal to 8 to predict the likelihood of colectomy was assessed by calculating the sensitivity, specificity, positive and negative predictive values, Yule's Q coefficient, Youden's index and statistical significance (Chi² test).

Results

After treatment with infliximab, 10 patients were in remission (23.3%), 21 (48.8%) had a clinical response, four (9.3%) had treatment failure (without, however, requiring colectomy) and eight (18.6%) had a colectomy. Calculation of the above-mentioned indicators revealed that an FCI greater or equal to 8 was not an indicator of the risk of colectomy in this patient population, and found that only an FCI greater or equal to 16 was statistically significant. However, low values for sensitivity, positive predictive value and Youden's index preclude the clinical application of this latter result.

Conclusion

In patients treated with infliximab for moderate-to-severe UC attacks, the FCI is not a predictor of colectomy. In such patients, the factors predictive of a response to treatment or likelihood of colectomy, currently acknowledged with corticosteroid treatment, need to be further assessed for infliximab treatment.

Background and aims

An association between Budd-Chiari syndrome (BCS) and celiac disease (CD) is uncommon. The aims of our study were to investigate the etiology of BCS and to search for a particular HLA Ag pattern among patients.

Patients and methods

BCS diagnosis was based on Doppler ultrasound and CD diagnosis on duodenal biopsy, transglutaminase (TGAb) and gliadin antibodies (GAb). Patients were screened for prothrombotic disorders and seven had a PCR-SSO test for HLA genotypes. Patients were treated with anticoagulants and gluten-free diet.

Results

Nine patients were included; mean age 27 years (20–42); sex ratio (F/M) 2; mean follow-up duration 31 months (6–54). All patients had endoscopic and histological features of CD. GAb/TGAb were found in 78 % (n = 7). Ag HLA found were HLA DQβ1^*02 (n = 6) and DQβ1^*03 (n = 3). Prothrombotic conditions identified were latent myeloproliferative disorder (n = 1), protein C deficiency (n = 1), probable factor V Leiden (n = 1) and oral contraceptive use (n = 1). No prothrombotic state could be identified in the five other patients.

Conclusion

The BCS–CD association is relatively frequent in our country. Underlying prothrombotic conditions were absent in more than 50 % of cases, suggesting CD plays a role in the occurrence of thrombosis. HLA alleles found are strongly associated with CD, without any particular pattern for the BCS–CD association.

Background & aims

End-stage chronic liver disease is associated with vitamin D deficiency but the prevalence across a broad-spectrum of liver disease is unknown. This study prospectively examines prevalence of vitamin D deficiency and response to replacement in chronic liver disease.

Methods

One hundred and fifty-eight outpatients with chronic liver disease were enrolled. Serum 25-hydroxyvitamin D (25[OH]D) levels were classified as: severely deficient less than 25 nmol/l, deficient 25–54 nmol/l or replete greater than 54 nmol/l. Sixty-five of 158 (41%) had cirrhosis.

Results

25[OH]D was suboptimal in 101/158 (64%), including severe deficiency in 24 patients (15%). Vitamin D deficiency occurred in liver disease of all aetiologies, including patients with only mild liver disease. 25[OH]D increased by 60.0% (19.11 ± 13.20 nmol/l) in patients with deficiency after vitamin D replacement and decreased by 25.2% (-18.33 ± 12.02 nmol/l) in non-treated initially replete patients over a median of 4 months.

Conclusions

Vitamin D deficiency improves with oral vitamin D supplementation and levels fall without supplementation. Chronic liver disease patients are at very high risk of vitamin D deficiency regardless of etiology or severity.