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S Grandjouan

Publications and source records attributed to S Grandjouan.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Intestinal motility in patients with small bowel diverticulosis].

It has been demonstrated that motility disorders may be responsible for esophageal and colon diverticulosis. Recently anatomic alterations of both small bowel muscular layers and myenteric plexus have been described in patients with small bowel diverticulosis. Such pathological features could be responsible for motility disorders and small bowel diverticulosis formation. The aim of this work was to study the small bowel motility in patients with small bowel diverticulosis. Ten patients (mean age: 69.2 +/- 6 years mean +/- SEM) with more than 3 diverticula in the jejunum or the ileum (excepting duodenal diverticulum) were studied. After an overnight fast, a 4 lumen probe (side holes 10 cm apart) was used to record duodeno-jejunal motility for 4 hours. Esophageal manometry was also performed in 8 patients. The mean number of phase 3 of the migrating motor complex (mean +/- SEM) during 4 hours was significantly lower in patients with small bowel diverticulosis (0.15 +/- 0.05/hours; mean +/- SEM) than in 10 normal volunteers (0.52 +/- 0.07/hours; mean +/- SEM) (P less than 0.01); 5 patients had zero phase 3 during the 4 hours of recording; one patient displayed intestinal hypomotility associated with aberrant phase 3 like activity; 4 patients showed simultaneous minute-rhythm during more than 80 percent of the phase 2 of the migrating motor complex. Esophageal manometry was also disturbed in 6 patients (low amplitude contractions less than 30 cm H2O in the distal esophagus). Bacterial overgrowth was investigated in 8 patients by means of a glucose breath-test and was found in 6 cases. In conclusion, duodeno jejunal motility is altered in patients with small bowel diverticulosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Detection of minority point mutations by modified PCR technique: a new approach for a sensitive diagnosis of tumor-progression markers.

The detection of point mutations correlated with diseases, in enzymatically amplified DNA sequences (Polymerase Chain Reaction), is currently performed by digestion of PCR products when an existing restriction site disappears at least in one allele of the amplified mutated sequence or by allele specific radiolabeled probes in all other cases. These methods are the most sensitive but they cannot detect a mutation if it is present in less than 5% of the studied cells. We describe here a method based on the introduction of an artificial restriction site, using a modified primer during the PCR, which creates a RFLP indicative of the studied mutation. This RFLP is detected by a radiolabeled oligonucleotide probe which is not related to the mutation. Our approach multiplies the sensitivity by a factor of 1000 and it is practical for use in screening purposes and the detection, after treatment, of the residual disease in human malignancies. Using this method we detected 20% more mutations at codon 12 in the Ki ras oncogene in DNA from colorectal cancers that were undetectable with all the previous methods.

Base Sequence↗
PubMed1989

[Effects of trimebutine on motility of the small intestine in humans].

Trimebutine maleate induces a specific motor response in the human proximal small bowel: except for the few minutes lapse following the occurrence of a spontaneous phase 3, an intravenous injection of 100 mg trimebutine systematically produces, in fed or fasted state, a systemic propagated activity analogous to the spontaneous phase 3 of the migrating motor complex. In lower doses, this effect is not observed. The intraduodenal administration of a high dose (600 mg) induces a similar response to that observed after intravenous injection. Trimebutine possibly acts as a stimulator of peripheral receptors of the enkephalinergic nervous system. Theoretically, these results may result in recommending the therapeutic use of trimebutine in intestinal motility disorders where disappearance or depletion of phase 3 are observed. However, information is still lacking about the relationship between therapeutic activity and the effects on intestinal motility in pathological states.

Benzoates↗
PubMed1989

Tumor-specific loss of 11p15.5 alleles in del11p13 Wilms tumor and in familial adrenocortical carcinoma.

We have compared constitutional and tumor genotypes in nine cases of hereditary Wilms tumor (WT) and in three unrelated cases of familial adrenocortical carcinoma (ADCC). Since susceptibility to these tumors can be observed in malformation syndromes associated with a constitutional deletion of band 11p13 (WT) and with a constitutional duplication of band 11p15.5 (WT, ADCC), we investigated these two candidate regions by using 11p polymorphic markers. As expected, somatic chromosomal events, resulting in a loss of heterozygosity limited to region 11p15.5, were observed in the tumor of two familial cases of adrenocortical carcinoma. Surprisingly, however, analysis of the WT of two patients with a constitutional deletion of band 11p13, associated with aniridia, genitourinary abnormalities, and mental retardation (WAGR syndrome), revealed a loss of heterozygosity limited to region 11p15.5. These data therefore suggest that observation of a specific loss of heterozygosity may not necessarily point to the site of the initial germinal mutation. Together with previous similar observations of a loss of heterozygosity limited to 11p15.5 in breast cancer and in rhabdomyosarcoma, our data suggest that region 11p15.5 may carry a non-tissue-specific gene that could be involved in genetic predisposition, in tumor progression, or in both.

Adrenal Cortex Neoplasms↗
PubMed1989

A comparison of metoclopramide and trimebutine on small bowel motility in humans.

Trimebutine meleate and metoclopramide increase small bowel motility. The present manometric study of the human normal interdigestive duodeno-jejunal motility demonstrated two different pharmacological effects in 15 healthy volunteers. Trimebutine constantly induced a premature phase 3 activity (0.81 +/- 0.4 min after a 100-mg intravenous injection) with patterns similar to spontaneous phase 3. Metoclopramide increased the motility index (contractile activity) during phase 2 without inducing a premature phase 3. No significant variations in plasma motilin concentration were noticed after either trimebutine or metoclopramide. The pancreatic polypeptide concentration rose significantly after metoclopramide injection.

Adult↗
PubMed1989

Mitotic deletions of 11p15.5 in two different tumors indicate that the CALCA locus is distal to the PTH locus.

We have compared the constitutional and tumor genotypes in two patients with Wilms tumor and adrenocortical carcinoma. The allelic distribution of chromosome 11-specific markers spanning chromosome 11 from pter to qter (HRAS1-HBB-[CALCA/PTH]-FSHB-CAT-APOA1) and an approach combining RFLP analysis and gene copy number determination showed that a mitotic deletion had occurred in both tumors. The loss of one copy of the gene for alpha-calcitonin-gene-related polypeptide (CALCA), together with that of a more distal marker (HRAS1 or HBB), indicates that CALCA is distal to the gene for parathyroid hormone (PTH), which was not deleted in either tumor. These results suggest that mitotic deletion mapping may be as useful as meiotic deletion or recombination mapping in ordering closely linked markers, such as CALCA and PTH, for which other approaches, including physical mapping and multipoint linkage analysis, have failed to accurately identify the gene order.

Adrenal Cortex Neoplasms↗
PubMed1989

[Neoadjuvant chemotherapy in locally advanced gastric adenocarcinoma. Preliminary results].

Gastric adenocarcinoma locally advanced or located at the cardia, or of large size or with local lymphadenopathies are of bad prognosis. To improve the surgical results we have tested the feasibility and tumoral efficacity of pre-operative (neoadjuvant) chemotherapy. Twenty patients have been included between 6/87 and 12/88. Median age was 63 years (36-74); all patients were in good general condition (OMS 0-1). The tumors were located at the cardia in 50%. The tumor median size was 10 cm (6-19), pathological lymph nodes were seem at CAT. Scan in 10/20. The neoadjuvant chemotherapy was continuous IV, 5 FU 1 g/m2/day for 5 days + CDDP 100 mg/m2, day 1. The cycles were repeated every 4 weeks. The median number of cycles prior surgery was 2 (1-4) and depended of tolerance and efficacy. We have observed (WHO criteria). 1 CR, 12 PR (Responsible rate: 65%). 6 MR or S. One patient was non evaluable because coronary insufficiency complicating the first cycle. The neoadjuvant chemotherapy toxicity was mainly hematological. The surgical procedure was curative in 15/20 patients; palliative 4 and non feasible for progression 1. Normal rate of post-operative complications was encountered: 2 subphrenic abscess, 1 pneumopathy, 1 stercoral peritonitis. At this date 3/20 patients died (17 patients are still alive, among them 14 are NED (the overall median survival is more than 10 months). This study demonstrated the feasibility and high response rate of neoadjuvant chemotherapy in patients with locally advanced gastric carcinomas. A randomized trial is warranted to demonstrate the survival benefit.

Adenocarcinoma↗
PubMed1989

[Anatomo-pathologic study of hepatic toxicity in intra-arterial hepatic chemotherapy].

Intra-arterial hepatic chemotherapy is effective in the treatment of colorectal or endocrine carcinomas liver metastasis. However it is potentially toxic for the healthy liver. To check this, we studied non tumoral liver specimens in 14 patients treated by intra-arterial chemotherapy with 5 fluorouracil, 5 fluoro-2 deoxyuridine and an association of 5 fluorouracil and streptozotocin. The main hepatic lesions observed were: sclerosing cholangitis, central vein (dilatation and fibrosis) and moderate hepatocellular necrosis or cholestasis in the centrolobular area. Thus intra-arterial hepatic chemotherapy has important toxic effects on healthy liver, even if clinical and biological liver disturbances are minimal in most cases. Caution must be exercised in using this method.

Adult↗
PubMed1988

[Comparative study of the effects of metoclopramide and metopimazine on the duodenojejunal motility during the interdigestive period: a manometric study in healthy subjects].

The objective of this paper was to compare the effects of metoclopramide (MTC) and of metopimazine (MTP) on intestinal motility in normal subjects in the period between digestion by injecting these two agents at a well-defined time of the migrating motor complex (MMC). Duodenojejunal motility was recorded by manometry (four microperfused catheters; study segment: 30 cm) during the period between phases of digestion (fasting greater than 12 hrs), for 4.6 hrs on average (3, 4, 6 hrs). 14 normal volunteer subjects (6 males, and 8 females 19 to 49 years of age) were randomly assigned to 2 study groups and were given MTC (10 mg) or MTP (10 mg) in slow IV injection (5 mins.) at a controlled rate, performed 25 mins after onset of a phase 3 (P3) in the study segment. As a reference, results obtained in a control group of seven subjects recorded under the same conditions are reported, in addition. Changes in MMC were evaluated in each group by the mean number of P3 hourly and the percent of subjects presenting a P3 within the two hours following injection of the test drug. Variations in phase 2 type motility (P2) were measured using motility indices (MI): the sum of the amplitudes, number of waves, per 5 minute interval. The number of hourly P3 was 0.40 for MTC vs 0.28 for MTP (control 0.47); 90 minutes after an injection, the first P3 appeared in 71% of patients in the MTC groups vs. 14% in the MTP group (control 57%). P3 recorded following injection were not different from the preceding in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Intrahepatic collections of fluid of pancreatic origin. A case].

A case of intrahepatic liquid collections of pancreatic origin is reported. A search in the literature yielded 8 cases of pancreatic pseudocysts which developed in the liver left lobe. The present case was original owing to its localization in the right hepatic lobe, to the large volume of the intrahepatic effusions and to the scarcity of underlying pancreatic symptoms. Ultrasonography and computerized axial tomography were useful aids to the diagnosis as well as to the therapeutic procedures. Surgery, which usually is a matter of discussion in chronic pancreatitis, was necessary to obtain the favourable outcome expected in such diseases.

Humans↗
PubMed1987

Induction of phase 3 of the migrating motor complex in human small intestine by trimebutine.

The effects of trimebutine, a drug used in the treatment of various gastrointestinal motility disorders, have been investigated fed and fasted healthy subjects. Duodenojejunal motility was recorded manometrically with a 4-lumen probe. Trimebutine 50 or 100 mg was injected i.v. 3 or 25 min after observing a spontaneous Phase 3 complex in the fasted state. Other experiments were done in the postprandial state and after intravenous naloxone 0.8 mg. In the fasted state, trimebutine 100 mg, injected 25 min after a spontaneous Phase 3 complex consistently induced a premature Phase 3 complex. The mean duration of the migrating motor complex cycle decreased from 86.4 +/- 10.8 min to 32.5 +/- 1.0 min. Trimebutine 50 mg injected 3 and 25 min after a spontaneous Phase 3 complex did not significantly modify the periodicity of the migrating motor complex. Trimebutine 100 mg initiated Phase 3-like activity in the post-prandial state. Previous intravenous administration of naloxone 0.8 mg (Narcan) suppressed the stimulatory action of TMB. Thus, trimebutine is able to modify the motility pattern in the small intestine of man, possibly by acting at opioid receptors.

Adult↗
PubMed1987

[Effect of trimebutine on the motility of the normal human small intestines: mechanism of action].

The effects of intravenous trimebutine (TMB) on duodenojejunal motility were investigated in normal subjects in fed and fasted states. The motility was recorded manometrically. In the fasting state TMB 100 mg, 25 min after a spontaneous phase 3 (P3) constantly induced a premature P3. The mean period (means +/- SE) of the migrating motor complex (MMC) cycle decreased from 84 +/- 10.9 to 32.5 +/- 1.0 min. TMB 50 mg, 3 and 25 min after a spontaneous P3 did not significantly modify the periodicity of MMC. TMB 100 mg initiated P3-like activity in post-prandial state. Previous administration of a low dose of naloxone suppressed the stimulating action of TMB. After a TMB injection the motilin plasma level did not vary; a brief increated of PP plasma level was observed. It may be concluded that in the human small intestine TMB included a typical modification of the motility pattern. Opiate receptors might be involved.

Adult↗
PubMedDate not supplied

[Muir-Torre syndrome and familial colorectal cancer: 2 families with molecular genetic analysis].

INTRODUCTION: The Muir-Torre Syndrome is a rare genodermatosis, defined by the occurrence of cutaneous tumors (such as sebaceous adenomas, epitheliomas, or carcinomas, and/or keratoacanthomas), and internal malignancies. Recently, molecular analysis in hereditary non polyposis colorectal cancer demonstrated a common genetic basis, linking these two disorders, with the observation of germline mutations in the hMSH2 gene (one of the DNA mismatch repair system genes) in both syndromes. Such molecular demonstration of a single nosological entity should be clinically used to improve the indications of molecular testings in oncogenetics, still restricted to highly stringent criteria for hereditary non polyposis colorectal cancer. CLINICAL CASES: We identified three patients from two different families, who fulfilled the criteria for both Muir-Torre Syndrome and hereditary non polyposis colorectal cancer. The search of a germline mutation of the hMSH2 gene was performed on an affected member from each family, and their relatives with their informed consent. Within each family, all individuals with colorectal cancer were carriers of the same mutation. In the first family, this mutation was a pathogenic microinsertion, usable for predictive testing. In the second family, a missense mutation was identified, requesting further demonstration of its pathogenicity before its use in a predictive purpose. CONCLUSIONS: The diagnosis of cutaneous tumors compatible with Muir-Torre syndrome should lead the dermatologist to suspect an hereditary non polyposis colorectal cancer that should bring to an oncogenetic approach: personnal and familial history of colorectal cancer, molecular analysis, recommendations for colonoscopic screening in at-risk relatives. In the case of a colorectal cancer at a young age, or in the case of familial cases, the gastroenterologist should screen for cutaneous lesions of Muir-Torre syndrome, which could add a criteria for an hereditary syndrome, and lead to molecular oncogenetic analysis.

Adenoma↗