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P Clavé

Publications and source records attributed to P Clavé.

15 recordsLinked to original sources
PubMed2001

Esophageal pH monitoring: are you sure that the electrode is properly placed?

OBJECTIVE: A crucial methodological aspect of ambulatory 24-h esophageal pH monitoring is electrode placement. Lower esophageal sphincter (LES) location is recommended for standard electrode positioning. The aim of the present study was to evaluate prospectively whether LES manometric location and intragastric pH acid confirmation suffice to guarantee that the pH electrode is properly placed. METHODS: We evaluated data from 402 consecutive patients undergoing esophageal pH monitoring. LES location was determined by manometry, and the pH electrode was introduced until a pH recording <3 was obtained. Subsequently, it was positioned 5 cm above the proximal LES border. Thereafter, adequate catheter placement and absence of bends or loops were checked by fluoroscopy. Patients with bent or rolled catheters were instructed to have breakfast immediately, and catheter placement was checked again by fluoroscopy. RESULTS: When checked by fluoroscopy, the catheter was properly placed in 383 patients (95.3%). In the other 19 (4.7%), it was not located in the distal part of the esophagus owing to bending or rolling: 14 in the esophagus and five in the pharynx. After breakfast, 14 of the 19 malpositioned catheters were properly positioned whereas five remained bent or rolled. Those bent in the esophagus were more prone to unbending (12 of 14) than those bent or rolled in the pharynx (two of five). CONCLUSIONS: After LES location by manometry and demonstration of acid pH during the pH step-up technique, the pH electrode was properly placed in more than 95% of cases. Nevertheless, it cannot be completely guaranteed that the pH catheter will not bend or roll, and the pH electrode will not be malpositioned. Eating immediately after electrode placement resolves this problem in the majority (75%) of cases. Therefore, we recommend that patients undergoing esophageal pH-metric studies be instructed to eat as soon as possible after electrode placement to minimize these possible pitfalls.

Adolescent↗
PubMed2000

Pharmacological and molecular characterization of muscular cholecystokinin receptors in the human lower oesophageal sphincter.

In vitro cholecystokinin (CCK) contracts the human lower oesophageal sphincter by stimulating muscular receptors. The aim of this study was to characterize the muscular CCK receptor subtypes in the human lower oesophageal sphincter. Twenty-five circular strips from six patients were studied. RNA was extracted, reverse transcribed, and cDNAs were amplified with primers for human CCK-A and B receptors. The potency of the contraction induced by CCK-8, desulphated CCK-8, and gastrin-I, and the effect of the CCK-A (loxiglumide and SR 27897) and the CCK-B (YM022 and L-365 260) specific receptor antagonists were compared. Both CCK-A and CCK-B receptor mRNAs were found in functional lower oesophageal sphincter strips. The potency of the CCK-8 concentration-dependent contraction was two and three orders of magnitude higher than that of desulphated CCK-8 and gastrin-I, respectively. The CCK-8-induced contraction was blocked by the CCK-A receptor antagonists loxiglumide (IC50 11 micromol L-1) and SR 27897 (IC50 74 nmol L-1) but not by CCK-B receptor antagonists (1 micromol L-1). Our data suggest that, although the human lower oesophageal sphincter expresses both CCK-A and CCK-B receptors, the contractile effect of CCK-8 on the circular muscle is mainly due to the activation of CCK-A receptors.

Adult↗
PubMed1998

Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors.

BACKGROUND & AIMS: Exogenous cholecystokinin (CCK) decreases lower esophageal sphincter (LES) pressure and increases transient LES relaxations (TLESRs) in humans. The aims of this study were to determine whether endogenous CCK increases gastroesophageal reflux in humans and whether this is a direct effect on the LES. METHODS: Esophageal pH, LES pressure, and gallbladder volume were measured in 8 healthy volunteers after ingestion of a 181-kcal meal alone or adding 12 g cholestyramine to increase endogenous CCK release. In 7 additional volunteers, the effect of cholestyramine was studied during intravenous perfusion of saline or the CCK-A receptor antagonist loxiglumide. In circular LES strips from 9 transplant donors, we measured the effect of CCK-8 (10(-11) to 3 x 10(-8) mol/L) on basal tension and on electrical field-induced relaxation. RESULTS: Cholestyramine increased gallbladder emptying, reflux episodes, TLESRs, and time of esophageal pH of <4. Loxiglumide inhibited postprandial gallbladder emptying, reflux episodes, TLESRs, and time of pH of <4 and prevented the decrease in LES pressure induced by cholestyramine. In vitro, CCK-8 contracted LES strips through a tetrodotoxin-insensitive pathway but did not modify electrical field-induced LES relaxations. CONCLUSIONS: Endogenous CCK enhances postprandial gastroesophageal reflux in humans by increasing the rate of TLESRs and reduces postprandial LES pressure. These actions seem mediated by extrasphincteric CCK-A receptors that override a direct contractile effect of CCK on the LES muscle.

Adult↗
PubMed1998

[The use of anorectal manometry and dynamic proctography in patients for diagnosis of solitary rectal ulcer syndrome].

BACKGROUND: Solitary rectal ulcer syndrome is caused by rectal prolapse and/or anismus. The diagnosis by physical examination, or using endoscopy or radiology alone is difficult. AIM: To evaluate the diagnostic utility of videoproctography and anorectal manometry in solitary rectal ulcer syndrome. PATIENTS AND METHODS: We studied six patients (5 women/1 man; 21-66 years) with rectal lesions suggestive of solitary rectal ulcer. By videoproctography, we measured the changes in the anorectal angle and the shape of the rectal wall during voiding. By manometry, we measured the resting pressure of the anal canal, and the pressure during maximal voluntary contraction and during straining. RESULTS: Proctography showed a rectal prolapse in 5 patients (non-exteriorized in 4). Both manometry and proctography demonstrated the normal relaxation of puborectalis and external sphincter during straining in 4 patients, manometry found sphincteric weakness in two of these patients. Both manometry and proctography evidenced anismus in a patient with rectal prolapse. CONCLUSION: The high prevalence of rectal prolapse in our patients allows us to recommend proctography in patients with morphological lesions suggestive of solitary rectal ulcer. The manometric examination identifies patients at risk of developing incontinence. Both techniques contribute to ascertain the presence of anismus and are indispensable in the selection of the adequate treatment for patients with solitary rectal ulcer.

Adult↗
PubMed1997

Chloroquine stabilizes pancreatic lysosomes and improves survival of mice with diet-induced acute pancreatitis.

Activation of digestive zymogens by lysosomal enzymes has been suggested as a triggering event in acute pancreatitis (AP). chloroquine (CQ), a weak base that accumulates in the lysosomes and increases their pH, can inhibit the activity of lysosomal enzymes. In the present study, we examined the effect of CQ on choline-deficient, ethionine-supplemented (CDE) diet-induced AP. CQ-diphosphate (15-50 mg.kg-1) or vehicle was given intraperitoneally at 0, 24, and 48 h to female CD1 mice that were fed with either normal diet or CDE diet. For mortality studies, animals were observed for 168 h. Serum and pancreas samples were collected from animals sacrificed 56 h after the start of the CDE diet. Treatment with CQ at 50 mg.kg-1 significantly (p < 0.05) improved the survival of mice with CDE diet-induced AP. In the normal pancreas, CQ decreased the specific activity of lysosomal enzymes cathepsin B1, beta-hexosaminidase, beta-glucuronidase, and acid phosphatase. In the pancreas with AP, CQ did not modify the activity of cathepsin B1, whereas it increased the latency of all enzymes. In conclusion, our results confirm the beneficial effect of CQ on survival of mice with CDE diet-induced AP and suggest that this effect of CQ may be due to its stabilizing action on lysosomes.

Acid Phosphatase↗
PubMed1996

[Activity and subcellular distribution of lysosomal enzymes in acute pancreatitis induced by CDE diet in mice].

The aim of the present study was to analyze the activity and subcellular distribution of the lisosomal enzymes and the stability of the lisosomes in acute pancreatitis induced by CDE diet in mice. The activity and the latency of the catepsin-B1 enzymes, acid phosphatase, beta-hexosaminidase and beta-glucuronidase in normal pancreas and in pancreatitis induced by CDE diet were determined. The distribution of the acid phosphatase lisosomal marker was determined in subcellular fractions obtained by differential centrifugation. The activity of the catepsin-B1 enzyme increased 47% in the pancreas of mice with pancreatitis induced by CDE diet. The acid phosphatase activity was not modified and the beta-hexosaminidase and beta-glucuronidase was decreased. The specific activity of the acid phosphatase lisosomal marker also increased in the subcellular fraction containing the zimogene granules and decreased the latency (parameter indicative of lisosome stability) of all the lisosomal enzymes analyzed in the pancreatic homogenate. These results suggest that the lisosomal enzymes, specially the catepsin-B1, and the decrease in the stability of the lisosomes may play a role in the pathogenesis of acute pancreatitis.

Acid Phosphatase↗
PubMed1995

Gastric emptying of two radiolabelled antacids with simultaneous monitoring of gastric pH.

The aim of this study was to assess the gastric emptying rate of two antacids using an scintigraphic technique and simultaneous monitoring of gastric pH in 16 healthy male volunteers. Ten ml of Talcid (hydrotalcite 1 g) and Maalox (Mg-Al-hydroxide), with a similar neutralization capacity, were labelled with technetium-99m using a pyrophosphate bridge. Labelled antacids were given on separate days (within 2 weeks), 1 h after a standard meal. Intragastric pH was measured for at least 4 h, using ambulatory pH-metry with a dual-crystant antimony catheter. Continuous monitoring was started 1 h prior to the meal (baseline) and lasted 3 h (post-prandial, post-antacid and final periods). The antacid capacity of labelled and unlabelled antacids was similar. The mean percentages of antacids retained in the stomach fitted a linear model. The mean half-emptying time of Talcid was 63.9 +/- 27.9 min, while that of Maalox was 57.3 +/- 23.9 min (P = NS). The recordings of gastric pH (mean values of pH for each period) showed a similar profile for both antacids. The mean pH (Maalox vs Talcid) was 1.69 vs 2.07 in the baseline period, 1.95 vs 1.93 in the post-prandial period, 1.79 vs 1.15 in the post-antacid period (P = NS) and 0.4 vs 0.52 in the final period (P < 0.05 vs prior periods). In conclusion, the gastric emptying of Talcid and Maalox was similar and pH profiles were parallel and remained unchanged for the two antacids within the first hour of intake. A significant decrease in pH was observed 1 h after intake of the antacids, suggesting a possible rebound effect.

Adult↗
PubMed1995

Amylase, lipase, pancreatic isoamylase, and phospholipase A in diagnosis of acute pancreatitis.

To determine the utility of serum amylase (AMY), lipase (Lp), pancreatic isoamylase (isoA), phospholipase A (PLA), and urine AMY in the diagnosis of acute pancreatitis, samples of serum and urine were obtained on admission and every day thereafter for 5 days from 384 patients with acute abdominal pain. Diagnostic accuracy, determined as the area under the receiver operating characteristic curve, was > 0.975 for serum AMY, Lp, isoA, and urine AMY. For each of these enzymes, a threshold value (twice to sixfold the upper limit of the reference values) offering diagnostic efficiency > 95% could be determined. In contrast, accuracy and efficiency of serum PLA were low. The profiles of these enzymes in acute pancreatitis decreased in a parallel fashion over 5 days except for PLA. We conclude that diagnostic utilities are similar for serum AMY, Lp, isoA, and urine AMY for acute pancreatitis, provided that an appropriate threshold is established.

Acute Disease↗
PubMed1992

[Rebound hyperglycemia and peroperative normalization of insulinemia. Complete excision of insulinoma?].

Clinical usefulness of the hyperglycemic rebound and the normalization of plasma insulin level as intraoperative markers of complete removal of insulinoma was assessed. Surgical removal was curative (no clinical or biological recurrence) in six patients harboring a single adenoma (mean follow-up = 32.2 months). In these patients plasma glucose increased an average of 32 mg/dl 30 minutes after resection, 68 mg/dl after 60 minutes, and 91 mg/dl after 90 minutes. Sensitivity of hyperglycemic rebound (defined as a plasma glucose increment of at least 30 mg/dl after tumor removal) as a marker of complete resection of the insulinoma was 40% at 30 min and 83% at 60 minutes after resection. Preresectional values of plasma immunoreactive insulin were elevated in 3 out of 4 patients with adenoma. All postresectional values were within normal ranges. Two patients operated on because of malignant insulinoma, underwent partial tumor resection; hyperglycemic rebound was also present, and high preresectional insulin values became normal 30 minutes after partial tumor removal. We conclude that information provided by intraoperative monitoring of both plasma glucose and insulin cannot be used as the only markers of complete resection of all insulinomas. Only long term clinical and biological follow-up can guarantee the complete resection of an insulinoma.

Blood Glucose↗
PubMed1992

Splenic hematoma in acute pancreatitis. Role of coagulation disorders.

Splenic hematomas are infrequent complications of acute pancreatitis. In some cases, local factors that may play a role in the pathogenesis of the hematoma (thrombosis of the splenic artery or veins, intrasplenic pseudocysts, perisplenic adhesions, enzymatic digestion) are found. In the absence of local factors, the etiology of splenic hemorrhage remains unknown. We report two cases of splenic hematoma occurring during an acute necro-hemorrhagic pancreatitis associated with renal failure that required renal replacement therapy (hemodialysis and continuous arteriovenous hemodialysis). In both cases, more than half of splenic parenchyma was affected by multiple infarctions. No local factors responsible for the splenic abnormalities were detected in either case. Thrombosis of the splenic arterial microcirculation and a coagulation disorder consistent with disseminated intravascular coagulation was detected in one patient. In the second patient, coagulation disorders secondary to either liver disease, pancreatitis and its septic complications, or extracorporeal circuit heparinization for renal replacement therapy were present. Coagulation disorders should be considered whenever a splenic hematoma is found in a patient with acute pancreatitis. Disseminated intravascular coagulation may be the etiology of a splenic hematoma in acute pancreatitis.

Acute Disease↗
PubMed1992

[The treatment of a simple pancreatic pseudoaneurysm or one associated with hemosuccus pancreaticus].

When a permanent communication occurs between an artery and a pancreatic pseudocyst, the pseudocyst becomes a pseudoaneurysm. Pancreatic pseudoaneurysms are primarily found in patients with alcoholic chronic pancreatitis. Fistulization of a pseudoaneurysm into the main pancreatic duct results in ductal hemorrhage. From 1980 to 1990, 43 cases of pancreatic pseudoaneurysm and 24 cases of ductal hemorrhage (15 of these secondary to pancreatic pseudoaneurysm) have been published. Pancreatectomy, ligation of the affected vessel (alone or in combination with a drainage procedure), or intraarterial embolization have all been used to treat pancreatic pseudoaneurysms. We herein describe two patients with alcoholic chronic pancreatitis and pancreatic pseudoaneurysm; one patient presented with ductal hemorrhage. The inferior pancreatico-duodenal artery was the affected vessel. Both patients were treated with suture-ligation; an internal drainage was added to the patient presenting with ductal hemorrhage.

Alcoholism↗
PubMedDate not supplied

[Accuracy of imaging techniques and tumor markers in the diagnosis of pancreatic cancer].

OBJECTIVE: The aim of this study was to evaluate the diagnostic accuracy of: a) three imaging techniques: ultrasonography (US), computed tomography (CT) and endoscopic retrograde cholangiopancreatography (ERCP), and b) the serum tumor markers CEA, CA 19-9 and CA 125, in the diagnosis of pancreatic cancer. PATIENTS AND METHODS: A total of 137 patients were prospectively evaluated. Pancreatic cancer was diagnosed in 25 patients; chronic pancreatitis in 24; acute pancreatitis in 22; extrapancreatic malignancies in 24, and benign digestive disease in 42. The reference interval for each marker was determined in 36 healthy volunteers. Diagnostic accuracy was determined using receiver operating characteristic (ROC) curves. Each diagnostic test was used in order: a) to diagnose pancreatic cancer when the disease was clinically suspected, and b) to differentiate between pancreatic cancer and chronic pancreatitis. RESULTS: CT (0.976-0.888) and US (0.857) diagnostic accuracy resulted greater than the best serum tumor marker CA 19-9 (0.755-0.786) (p = NS), in both diagnostic conditions. To obtain a diagnostic specificity of 90% in pancreatic cancer, the CA 19-9 cutoff level should increase up to 3 and 7.5 folds being in this case better than CEA and CA 125 (p < 0.05). CONCLUSIONS: CT scan offers the greatest accuracy in the diagnosis of PC. Among the tumor markers, CA 19-9 offers the best accuracy in the diagnosis of pancreatic cancer.

Acute Disease↗