PubMed Health⌕ Search

Biomedical subjects

R Guimbaud

Publications and source records attributed to R Guimbaud.

At least 19 recordsLinked to original sources

Characterization of promoter regulatory elements involved in downexpression of the DNA polymerase kappa in colorectal cancer.

The low-fidelity DNA polymerases thought to be specialized in DNA damage processing are frequently misregulated in cancers. We show here that DNA polymerase kappa (polkappa), prone to replicate across oxidative and aromatic adducts and known to function in nucleotide excision repair (NER), is downregulated in colorectal tumour biopsies. Contrary to the replicative poldelta and polalpha, for which only activating domains were described, we identified an upstream 465-bp-long repressor region in the promoter of POLK. We also found an activating 237-bp region that includes stimulating protein-1 (SP1) and cyclic AMP-responsive element (CRE)-binding sites. Mutations at one CRE-binding site led to a dramatic 80% decrease in promoter activity. Alterations of the SP1-binding site also affected, to a lesser extent, the transcription. Gel shift assays confirmed the role played by CRE/SP1 recognition sequences. Moreover, ectopic expression of SP1 or CRE-binding protein (CREB) protein favoured polkappa transcription. Finally, we found that polkappa downexpression in colorectal biopsies correlated with a decreased level of CREB and SP1 transcripts. This work shows that the promoter of POLK is cis-controlled and suggests that silencing of CREB and SP1 proteins could contribute to downregulation of this repair polymerase in colorectal tumours.

Acetylation↗

A phase I clinical and pharmacokinetic study of capecitabine (Xeloda) and irinotecan combination therapy (XELIRI) in patients with metastatic gastrointestinal tumours.

Capecitabine is a highly active oral fluoropyrimidine that is an attractive alternative to 5-fluorouracil in colorectal cancer treatment. The current study, undertaken in 27 patients with gastrointestinal tumours, aimed to assess the toxicity and potential for significant pharmacokinetic interactions of a combination regimen incorporating capecitabine with 3-weekly irinotecan (XELIRI). Irinotecan (200 and 250 mg m(-2)) was administered as a 90-min infusion on day 1 in combination with escalating capecitabine doses (700-1250 mg m(-2) twice daily) administered on days 2-15 of a 3-week treatment cycle. Pharmacokinetics were characterised on days 1 and 2 of the first two cycles. A total of 103 treatment cycles were administered. The principal dose-limiting toxicities were diarrhoea and neutropenia. Capecitabine 1150 mg m(-2) twice daily with irinotecan 250 mg m(-2) was identified as the maximum-tolerated dose and capecitabine 1000 mg m(-2) with irinotecan 250 mg m(-2) was identified as the recommended dose for further study. Analyses confirmed that there were no significant pharmacokinetic interactions between the two agents. The combination was clinically active, with complete and partial responses achieved in heavily pretreated patients. This study indicates that XELIRI is a potentially feasible and clinically active regimen in patients with advanced gastrointestinal cancer.

Adult↗

Multimodal therapy with intravenous biweekly leucovorin, 5-fluorouracil and irinotecan combined with hepatic arterial infusion pirarubicin in non-resectable hepatic metastases from colorectal cancer (a European Association for Research in Oncology trial).

BACKGROUND: The purpose of this study was to evaluate the tolerance and efficacy of combining i.v. irinotecan, 5-fluorouracil (5-FU) and leucovorin (LV) with hepatic arterial infusion (HAI) of pirarubicin in non-resectable liver metastases from colorectal cancer. PATIENTS AND METHODS: Thirty-one patients were included in a phase II trial with i.v. irinotecan/5-FU/LV administered every 2 weeks, combined with HAI pirarubicin 60 mg/m(2) on day 1 every 4 weeks. In most cases HAI was administered via a percutaneous catheter. RESULTS: The main grade 3/4 toxicity was neutropenia, encountered in 78% of the patients. When all patients were considered in the analysis, tumour response rate was 15 out of 31 [48%; 95% confidence interval (CI) 32% to 65%]. Liver resection was made possible in 11 patients (35%; 95% CI 21% to 53%). There were no toxic death. Median overall survival was 20.5 months, and median progression-free survival was 9.1 months. In patients with completely resected metastases, median overall survival was not reached and median progression-free survival was 20.2 months. CONCLUSION: The multimodality approach used in the present study was well-tolerated and yielded dramatic responses. An aggressive approach combining i.v. and HAI chemotherapy deserves further investigation.

Adult↗

[Leiomyosarcoma of the inferior vena cava].

Leiomyosarcoma of the inferior vena cava is a rare tumor of mesenchymal origin most commonly found in women. Clinical signs are non-specific. Imagery with ultrasound, CT, or MRI may strongly suggest the diagnosis, but it can only be confirmed by histologic examination of tissue obtained pre or intra-operatively. The tumor is slow growing but nonetheless carries a bad prognosis; it may grow to a large size before directly invading adjacent structures. Systemic spread is a late occurrence. Radical surgical resection is the only treatment which offers any hope for prolonged survival. Standard vascular surgical techniques are usually sufficient. Progress in the techniques of hepatectomy and liver transplantation have allowed the experienced surgeon to undertake the removal of retrohepatic lesions once considered unresectable. High-lying lesions adjacent to the hepatic veins or with thrombus extending into the proximal vena cava may require extracorporeal circulation with or without profound hypothermic circulatory arrest. The efficacy of chemotherapy, whether pre-operative for inaccessible tumors or post-operative for incompletely resected or recurrent tumor, is poorly defined and very limited.

Aged↗

[Detection of hereditary non-polyposis colon cancer (HNPCC)].

Hereditary Non-Polyposis Colon Cancer (HNPCC) or Lynch's Syndrome remains an underappreciated clinical entity-perhaps due to the restrictiveness of the diagnostic criteria. Even though HNPCC makes up only a small fraction (2-3%) of Colorectal Cancer (CRC) compared with sporadic CRC, it is important to make the diagnosis to allow for targeted management of the patients and their kindreds and thus to reduce morbidity and mortality. Better knowledge of tumor characteristics including RER phenotype may allow for the application of less restrictive diagnostic criteria; but these characteristics are not specific to HNPCC and also occur in 15% of sporadic CRC. Nevertheless, a screening strategy combining a broader clinical selection (less strict than the Amsterdam criteria) with a study of tumoral phenotype may allow the identification of more cases of HNPCC. The physician caring for cases of CRC must be aware of these screening strategies and relevant clinical and biological clues which might indicate a more complete genetic investigation.

Colorectal Neoplasms, Hereditary Nonpolyposis↗

Long-term outcome of patients with gastrointestinal bleeding of obscure origin explored by push enteroscopy.

BACKGROUND AND STUDY AIMS: Little is known of the long-term outcome in patients with gastrointestinal bleeding of obscure origin, who undergo investigation by means of push enteroscopy. The aim of this study was to assess the rate of recurrent bleeding and its predictive factors in patients with gastrointestinal bleeding of obscure origin, after exploration by push enteroscopy. PATIENTS AND METHODS: 105 patients with gastrointestinal bleeding of obscure origin (iron-deficiency anemia: n = 56; overt bleeding: n = 49) underwent exploration by push enteroscopy from December 1994 to December 1998. They were classified into three groups according to enteroscopy findings: no lesion found (group A; 56 patients), arteriovenous malformations (group B; 18 patients), and other gastrointestinal lesions (group C; 31 patients). Actuarial rates of rebleeding during follow-up were calculated and factors associated with rebleeding were assessed by means of univariate and multivariate analysis. RESULTS: Follow-up data were obtained for 101 patients (96 %). The mean follow-up was 29 months (6 - 54 months). The 2-year actuarial rate of rebleeding was 31 % in the overall population, and 27.6 %, 56 % and 24 % in groups A, B, and C, respectively (P = 0.13). The number of previous bleeding episodes and the number of packed red cell units transfused were two independent factors predictive of recurrent bleeding. The modality of recurrent bleeding (anemia or overt bleeding) was similar to that of the initial episode in 94 % of cases. In group A, a gastrointestinal lesion was found after rebleeding in one of the 12 patients with iron-deficiency anemia, and in four of the five patients with overt bleeding. CONCLUSION: Recurrent bleeding occurs in about one-third of patients who undergo investigation by push enteroscopy for gastrointestinal bleeding of obscure origin, with a trend towards more frequent rebleeding in patients with arteriovenous malformations. Frequent previous bleeding episodes and transfusion requirements are predictive of recurrent bleeding.

Adolescent↗

Dihydropyrimidine dehydrogenase activity in normal, inflammatory and tumour tissues of colon and liver in humans.

BACKGROUND/PURPOSE: Dihydropyridmidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5FU). Although this catabolism is likely to occur in the liver in humans, there may be a local inactivation in tumours, modifying the efficacy of 5FU. The aim of this study was to examine the DPD activity in normal, inflammatory and malignant tissues from both the colon and the liver to assess the modifications of DPD activity in the process of tumourigenesis. METHODS: DPD activity was evaluated in 107 patients, corresponding to 194 samples (70 colorectal tumour and normal colon, nine metastases secondary to a colon cancer, ten inflammatory colon, 20 samples of normal liver, seven from primary liver cancer, and eight from inflammatory liver). DPD activity was determined using an enzymatic reaction followed by analysis of 5FU and its catabolite dihydro-5FU by high-performance liquid chromatograph. Results were expressed as pmol of 5FU catabolized/min x mg protein. RESULTS: DPD was highly variable in tumour and normal tissues, both from colon and liver. In colon, the correlation between DPD activity in tumour and normal mucosa was weak, even if it was statistically significant due to the higher number of samples. In inflammatory colon tissue (ulcerative colitis or Crohn's disease), DPD activity was significantly higher than in normal tissue (P = 0.006). In liver metastases from colon cancer, DPD activity was not significantly different from that observed in primary colon tumour (P = 0.32). In liver, DPD activity was significantly lower in primary liver tumour than in uninvolved liver specimens (P = 0.001). In inflammatory liver tissue (hepatitis), DPD activity ranged between normal and tumour tissues, and did not differ significantly either from normal tissue or primary liver cancer. CONCLUSIONS: DPD activity was modified in colon and in liver during a pathological process and the dysregulation of DPD increased from a benign to a malignant tissue.

Adolescent↗

Inducible nitric oxide synthase activity in colon biopsies from inflammatory areas: correlation with inflammation intensity in patients with ulcerative colitis but not with Crohn's disease.

Nitric oxide synthase (NOS) activities are responsible for the enzymatic conversion of L-arginine into NO and L-citrulline. Relatively low amounts of NO are produced in intestinal epithelial cells or are released from nerve endings. The effects of NO production are related to the maintenance of epithelial integrity and permeability. A pathological role of an increased NO production has been suggested to play a role in models of experimental colitis. In humans, NOS activity in colon mucosa from patients with ulcerative colitis is clearly increased when compared with the activity of the control group. In contrast, an increase of NOS activity in the colon mucosa from patients with Crohn's disease remains controversial. In the present work, we have measured NOS activity in colon biopsies originating from the control group (n = 16), from patients with ulcerative colitis (n = 23) and Crohn's disease (n = 17) using the radiochemical method of the conversion of L-[guanido-14C] arginine into radioactive L-citrulline. In the control group, NOS activity was mainly of the inducible type (88% of total NOS activity) since it was characterised by its insensibility to the absence of calcium in the assay medium. In colon biopsies originating from patients with ulcerative colitis, inducible NOS activity was increased 3 fold (p < 0.005) and in patients with Crohn's disease, inducible NOS activity was increased 5 fold (p < 0.005). Correlations between NOS activity in colon biopsies and the intensity parameters of the disease i.e. Truelove index, endoscopic score and histological parameters were evidenced in patients with ulcerative colitis. In contrast, in patients with Crohn's disease, the high inducible NOS activity was not correlated with any intensity parameters of the disease. From these data, we concluded that although inducible NOS activity was increased several fold in colon biopsies originating from patients with both ulcerative colitis and Crohn's disease, a correlation between this activity and the severity of bowel inflammation was not found in either cases.

Adult↗

Dose and time dependencies of 5-fluorouracil pharmacokinetics.

OBJECTIVES: The purpose of this study was to examine the interpatient and intrapatient variability of the Michaelis-Menten plasma parameters of 5-fluorouracil administered according to a schedule combining a bolus of 400 mg/m2 followed by 22-hour infusion of 600 mg/m2 for 2 consecutive days. PATIENTS: A pharmacokinetic population approach was used to analyze the data from 21 patients with colorectal cancer. RESULTS: The 5-fluorouracil plasma concentrations versus time were best described by a two-compartment model with nonlinear elimination from the central compartment. The relationships between the pharmacokinetic parameters and patient characteristics were tested. On day 1 the mean values (with interindividual variability as expressed by the coefficient of variation) were 1390 mg x h(-1) (20%), and 5.57 mg x L(-1) (22%) for the maximum rate of elimination, and the half-saturating plasma concentration. The maximum rate of elimination was positively correlated to the body surface area and the percentage of liver involvement by metastatic disease determined by tomodensitometric examination. The model was successfully tested with independent data sets corresponding to other schedules. The analysis of this intrapatient variability showed that the half-saturating plasma concentration increased from day 1 to day 2, especially in the patients with low lymphocyte cell dihydropyrimidine dehydrogenase activity. CONCLUSION: The pharmacokinetic parameters obtained in this study would be useful to predict the 5-fluorouracil plasma concentrations following other schedules of administration of 5-fluorouracil and to study the possible pharmacokinetic interactions between 5-fluorouracil and other drugs.

Adult↗

Role of tumour necrosis factor-alpha and inducible nitric oxide synthase in the prevention of nitro-flurbiprofen small intestine toxicity.

The present study compares the intestinal toxicity of nitro-flurbiprofen and flurbiprofen in order to determine their differential properties on tumour necrosis factor-alpha production and inducible nitric oxide synthase induction. Rats received one s.c. injection of flurbiprofen, nitro-flurbiprofen at equimolar dose of solvent. Twenty-four hours later, the rats were sacrificed and small intestine tissue was taken up for macroscopical quantification of ulceration, ex vivo production of tumour necrosis factor-alpha and nitrites, and determination of tissue inducible nitric oxide synthase and myeloperoxidase activities. Anti-inflammatory activity was examined in the carrageenan-induced paw edema model. We demonstrated that flurbiprofen induced dose-dependently small intestine production of tumour necrosis factor-alpha, nitrites, myeloperoxidase and inducible nitric oxide synthase activities. On the other hand, nitro-flurbiprofen did neither induce tumour necrosis factor-alpha nor nitrite production. Concurrently, no small intestine ulceration was observed with nitro-flurbiprofen whereas flurbiprofen induced dose-dependent ulceration. Nitro-flurbiprofen is devoid of intestinal toxicity despite inhibiting cyclooxygenase activity. This is associated with the absence of tumour necrosis factor-alpha and inducible nitric oxide synthase induction in normal rats. Nitro-flurbiprofen is an anti-inflammatory drug with a much more favorable gastro-intestinal toxicity profile than flurbiprofen.

Animals↗

Technetium Tc 99m hexamethyl propylene amine oxine leukocyte scintigraphy in patients with ulcerative colitis: correlation with clinical, biologic, endoscopic, and pathologic intensity, and local release of interleukin 8.

BACKGROUND: Technetium Tc 99m hexamethyl propylene amine oxine (99mTc-HMPAO) has been used to radiolabel leukocytes with promising results for its clinical use in inflammatory bowel disease. During active ulcerative colitis, colonoscopy is indicated to determine the extent and the intensity of the disease for proper management. The aim of this prospective study was to determine whether 99mTc-HMPAO-labeled leukocyte scintigraphy can give information similar to that obtained with colonoscopy during acute attacks of ulcerative colitis. METHODS: Thirty-three consecutive patients with 50 acute episodes of ulcerative colitis underwent 99mTc-HMPAO scintigraphy and colonoscopy with biopsies. Scintigraphic determination of disease extent and intensity were compared with those obtained by colonoscopy with biopsies and clinicobiologic markers. RESULTS: The scintigraphic index of disease intensity was correlated with endoscopic index, Truelove index, biologic markers, and local release of interleukin-8. The extent measured by scintigraphy was well correlated to the endoscopic and histologic extent. CONCLUSIONS: 99mTc-HMPAO scintigraphy accurately determines the extent and the intensity of acute ulcerative colitis lesions. This noninvasive method can specify the extent and the intensity of an acute attack in patients with previously known ulcerative colitis.

Adult↗

Increase in tumor necrosis factor-alpha production linked to the toxicity of indomethacin for the rat small intestine.

1. The toxic effects of nonsteroidal anti-inflammatory drugs for the lower gastrointestinal tract share certain features with inflammatory processes, suggesting that the release of inflammation cytokines such as TNF-alpha may damage the intestine. 2. Rats received a s.c. injection of indomethacin. Then, jejunum-ileum was taken up for the quantification of ulcerations, production of TNF-alpha, nitrites and PGE2 ex vivo and activity of calcium-independent NO synthase and myeloperoxydase. Activation of NO metabolism and myeloperoxydase were measured as potential effectors of TNF-alpha. 3. Jejunum-ileum from rats having received indomethacin (10 mg kg(-1)) produced TNF-alpha ex vivo. Cytokine production was associated with the onset of macroscopic ulcerations of the small intestine, and preceded nitrite production and tissue activity of myeloperoxidase. 4. Similar intestinal ulcerations and upregulation of TNF-alpha were obtained with flurbiprofen (30 mg kg(-1)), chemically unrelated to indomethacin. 5. TNF-alpha production was proportional to the indomethacin dose (from 3-20 mg kg(-1)) and correlated with the surface area of ulcerations and nitrite production, 24 h after indomethacin administration. 6. Pretreatment of rats with RO 20-1724, a type-IV phosphodiesterase inhibitor which inhibits TNF-alpha synthesis, substantially reduced jejunum-ileum ulcerations, TNF-alpha and nitrite production and tissue enzyme activities. 7. These findings provide evidence that TNF-alpha is increased in indomethacin-induced intestinal ulcerations and support suggestions that TNF-alpha is involved at an early stage of nonsteroidal anti-inflammatory drug toxicity for the small intestine.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗

Network of inflammatory cytokines and correlation with disease activity in ulcerative colitis.

OBJECTIVE: The inflammatory component of most human inflammatory chronic diseases implicates the production of proinflammatory cytokines. Tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) seem to play an important role in ulcerative colitis (UC) in relevant experimental models. Moreover, antiTNF therapy seems promising experimentally and clinically. However, these cytokines, and TNFalpha more particularly, are hardly seen in vivo in such patients. The mediators of choice, correlated with disease activities or drug efficacy, remain unclear. To characterize in vivo the network of colonic cytokines in patients with UC, and the contribution of the various cytokines to disease activity we performed this study, using the colonic perfusion method. METHODS: A 20-cm colon length was perfused. Perfusate samples were collected for cytokine determination by enzyme-linked immnoassays. Nineteen perfusions were performed in mild to moderate UC, including two successive perfusions in four patients. Six healthy control patients and four having Crohn's disease (CD) with rectal involvement were studied. Endoscopic score, leukocyte scintigraphy, and systemic markers of inflammation were simultaneously quantified. RESULTS: Large amounts of IL1beta, TNFalpha, IL6, and IL8 were produced in UC patients with a highly significant correlation between TNFalpha, IL1beta and IL8 two by two. Multivariate factorial analysis indicated that IL1beta showed the best correlation with disease activity. Locally produced IL6 was strongly associated with circulating platelet counts. Moreover, production of inflammatory cytokines was associated with similar variations of disease activity in the four patients with two successive perfusions performed. The level of inflammatory cytokines in CD was lower than in UC; TNFalpha, IL1beta, and IL6 were not found in any control patients. CONCLUSION: UC appears to be a chronic inflammatory disease characterized by high production of all four proinflammatory cytokines (IL1beta, TNFalpha, IL6, and IL8). These results suggest that colonic perfusion may be a suitable method to evaluate the local anticytokine properties of new drugs, in correlation with disease activity and systemic markers of inflammation.

Adult↗

Diagnostic yield of push-type enteroscopy in relation to indication.

BACKGROUND: Push-type enteroscopy, a recent method for investigating the small intestine, is currently undergoing assessment. Its diagnostic yield varies in the studies reported to date. AIM: To assess the diagnostic value of push-type enteroscopy according to indication. PATIENTS AND METHODS: From January 1994 to September 1995, 152 consecutive patients (mean age 34 years) underwent push-type enteroscopy (jejunoscopy, n = 93; retrograde ileoscopy, n = 17; and double way enteroscopy, n = 42). The indications were: unexplained iron deficiency anaemia or macroscopic gastrointestinal bleeding (n = 76), radiological abnormalities of the small intestine (n = 23), chronic diarrhoea and/or malabsorption syndrome (n = 18), abdominal pain (n = 12), and miscellaneous (n = 23). All patients had undergone previous negative aetiological investigations. RESULTS: The jejunum and ileum were explored through 120 cm (30-160 cm) and 60 cm (20-120 cm). Digestive bleeding: lesions of the small bowel were found in 6% of the patients with isolated iron deficiency anaemia and 20% of patients with patent digestive haemorrhage. Radiological abnormalities of the small intestine: push-type enteroscopy provided a diagnosis or modified the interpretation of radiological findings in 18/23 cases (78%). Chronic diarrhoea and/or malabsorption: push-type enteroscopy yielded explanatory findings in four cases (22%). Abdominal pain: push-type enteroscopy provided no diagnosis. CONCLUSION: In this series, push-type enteroscopy was of particular value in investigating patients with radiological abnormalities of the small intestine. It was of some value in the exploration of patent digestive haemorrhage or chronic diarrhoea, but not of abdominal pain. Its value was limited in the exploration of iron deficiency anaemia.

Adult↗

Effects of murine recombinant interleukin-10 on the inflammatory disease of rats transgenic for HLA-B27 and human beta 2-microglobulin.

Rats transgenic for HLA-B27 and human beta 2-microglobulin develop a spontaneous, multisystem, inflammatory disease that resembles human B27-associated disease and that involves the gut mucosa. This model predominantly affects the colon and is characterized by an extensive infiltration of the mucosa by inflammatory cells, largely composed of mononuclear cells. In addition, an increased plasma level of nitric oxide (NO)-derived metabolites was described in this model. Deficiency in the anti-inflammatory cytokine, interleukin-10 (IL-10), leads to the development of colitis in IL-10 knockout mice, suggesting that IL-10 plays a major role in the control of gut inflammation. The objectives of this work were to study the mechanisms of the inflammatory bowel disease (IBD) in HLA-B27 rats and to determine the effects of treatment with IL-10. The 33-3 line of HLA-B27 recombinant rats with established disease was treated in two consecutive experiments with murine recombinant IL-10 for five weeks. Assessment of the effect of this treatment was performed, based on clinical, histological and biological (myeloperoxidase and inducible NO synthase activities; tumor necrosis factor-alpha, interferon-delta, CD3, iNOS and beta-actin mRNA expression. In 33-3 rats with established disease, mesenteric lymph nodes were hyperplastic, and colonic cellularity and MPO and iNOS activities in the colonic mucosa were increased without any detectable effects of IL-10 administration. IFN-gamma and iNOS mRNA were only detected in the colon of transgenic rats. Despite a lack of effect on disease expression, IL-10 strikingly reduced the level of IFN-gamma mRNA in gut mucosa. Up-regulation of IFN-gamma mRNA suggests that the IBD of HLA-B27 rats is mediated by T-helper 1 lymphocytes. Sustained administration of IL-10, in HLA-B27 rats with established disease, efficiently inhibited IFN-gamma mRNA expression but did not influence disease expression: these results indicate that IFN-gamma may exert a critical role at an earlier stage of the disease rather in the maintenance of the lesions.

Animals↗

[Comparison of push-type endoscopy and barium transit study of the small intestine in digestive bleeding and unexplained iron-deficiency anemia].

OBJECTIVES: A radiological examination of the small bowel is often performed in case of gastrointestinal bleeding of obscure origin. More recently, push-type enteroscopy has been reported as a valuable tool in this indication. The purpose of this study was to compare the diagnosis efficiency of these two procedures. METHODS: From February 1994 to February 1996, 40 patients (mean age: 52 years) with obscure gastrointestinal bleeding (iron-deficiency anemia without obvious cause of blood loss or malabsorption: n = 17; macroscopic gastrointestinal bleeding: n = 23) were examined by small bowel follow-through and push-type enteroscopy (jejunoscopy n = 19; double way examination n = 21). Each patient had negative upper and lower gastrointestinal tract endoscopies prior to small bowel examinations. RESULTS: Small bowel follow-through revealed only one lesion potentially responsible for blood loss (2.5%), corresponding to a jejunal leiomyoma. Push-type enteroscopy detected small bowel lesions potentially responsible for blood loss in 6 patients (15%). The lesions were located in the jejunum in 5 cases (arteriovenous malformations: n = 3; metastasis: n = 1; leiomyoma: n = 1), in the ileum in 1 case (leiomyoma). The efficiency of push-type enteroscopy for the detection of a small bowel lesion was of 22% in case of macroscopic bleeding and of 6% in case of iron-deficiency anemia. Push-type enteroscopy also revealed lesions previously undetected by gastroscopy or colonoscopy in 8 patients (20%). CONCLUSION: Push-type enteroscopy was more effective than small bowel follow-through to detect the origin of obscure gastrointestinal bleeding. Push-type enteroscopy revealed a cause of bleeding in 35% of patients, located in the small bowel in only 15% of the patients.

Adult↗