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Serum nitric oxide levels before and after eradication of Helicobacter pylori infection- A prospective study
April 1995
Esophageal, Gastric, and Duodenal Disorders
• NITRIC OXIDE LEVELS IN GASTRIC JUICE OF PATIENTS WITH HELICOBACTER PYLORI INFECTION. R_J. Maliakkal, J.L.Achord, A.A. Mihas. Division of Gastroenterology, VA Medical Center, University of Mississippi School of Medicine, Jackson MS. We have previously reported that patients with Helicobacter pylori (HP) infection have significantly lower levels of nitric oxide (NO) in their sera than those without. The aim of the present study was to determine the level of NO in the gastric juice of patients with HP infection. Gastric juice was collected from patients undergoing upper gastrointestinal endoscopy following which antral biopsies were obtained. Nitrite (NO2) and nitrate (NO3) levels (stable end products of NO) in gastric juice were measured by methods previouslydescribed. HP infection was conlh-medby histology using the giemsa stain. The results are shown in table: GROUP
n [
GASTRIC JUICE ( N O 2 + NO3) ng/ml
HP - POSITIVE
6
50.2 :~ 5.13
HP - NEGATIVE
5
122.8 :~ 27.0
SERUM MALONYL DIALDEHYDE LEVELS IN PATIENTS BEFORE AND AFTER HELICOBACTER PYLORI ERADICATION. R.J. Maliakkal, V.K. Kanji, A.A. Mihas. Division of Gastroenterology, VA Medical Center, University of Mississippi, Jackson, MS. The mechanisms involved in the pathogenesis of peptic ulcer disease (PUD) have not been fully elucidated. An imbalance between aggressive and protective factors offers an attractive hypothesis, Injury to mucosal cell membranes secondary to lipid peruxidation and the resultant alteration in prostaglandin level is a plausible mechanism. Serum malonyl dialdehyde (MDA) levels reflect tissue injury secondary to lipid peroxidation. While a large body of evidence supports the role ofHelicobacter pylori (HP) in gastroduodenal mucosal injury, the mechanisms involved in the pathogensis need further clarification. We prospectively evaluated serum MDA levels in patients with PUD in whom HP infection was confirmed by histology (giemsa stain) and serology (IgG). Serum MDA levels were measured spectrophotometrically by standardized methods previously described. After triple therapy, HI' eradication was assessed with gastric antral biopsies and serum MDA levels were repeated. The results (m ± SEM' are shown in the table: PRE-TREATMENT HP- POSITIVE
The levels of NO2 + NO3 in gastric juice of patients with HP infection was significantly lower than those without. In conclusion: These findings in the gastric juice of liP infected patients are consistent with the hypothesis that NO may modulate HP-induced gastroduodenal mucosal injury. Furthermore it concurs with the serological observations made in HP infected patients in our laboratory.
• SERUM NITRIC OXIDE LEVELS BEFORE AND AFrER ERADICATION OF HELICOBACTER PYLORI INFECTION- A PROSPECTIVE STUDY. R.J. Maliakkal J.L. Achord, A.A. Mihas. Division of Gastroenterology, VA Medical Center, University of Mississippi School of Medicine, Jackson MS. We have previously reported that patients with HI' infection have a significantly lower level of NO in their sera. The aim of the present study was to d~ermine the effect of liP eradication on serum NO levels. For this purpose, the levels of nitrite (NO2) and nitrate (NO3), the stable end products of NO, were measured in the sera of 11 patients with peptic ulcer disease. In all patients HP infection was documented by histology (giemsa stain) and serology (IgO). One month after triple therapy, eradication was assessed by histological examination of gastric antral biopsies. The serum NO levels were measured. Results (m ± SEM) are shown below: PRE-TREATMENT
SERUM NO2 +NO3 (ng/ml)
POST- TREATMENT
(n=ll) HP- POSITIVE
(n=5) HP- NEGATIVE
133.4 4-9.7
198.8 a: 22.3*
150.6 4-5.3
(n=6) HP-POSITIVE
164.5 4-5.2
Eradication of I-IP, resulted in a statistically significant increase in the serum NOz + NO3 levels (*P = 0.0016). Patients who failed HP eradication had similar serum NO2 + NO3 levels pre- and post treatment. In conclusion: Eradication of I-IP infection is associated with a significant increase in serum NO level. Thus NO may play a crucial role in HP-induced damage to gastroduodenal mucosa.
A157
n= II
POST TREATMENT HP-POSITIVE HP-NEGATIVE n=6
n=5
SERUM 26.2 4-2.2 19.9 ± 2.5* MDA nmoles/ml 23.5 ± 2.3 21.9 4- 1.5'* *P = .0.003.; **P = 0.176 Serum MDA levels are significantly greater in patients infected with HI?. Eradication of liP resulted in a significant redtiction of serum MDA levels. In conclusion : Elevated MDA levels in PIP infected patients suggests that the HP- associated mucosal injury may be secondary to lipid peroxidation.
• HIGH INTRASUB/ECT VARIABILITY IN THE MEASUREMENT OF POSTPRANDIAL REFLUX:
IS AMBULATORY pH MONITORING RELIABLE? A. G. Maniatis, C. B. Dalton, S. R. Brazer. Div of Gastroenterology, Dept of Medicine, Duke University Medical Center, Durham, NC. Postprandial reflux has been increasingly employed as an independent index of GERD and constitutes a significant component of overall acid contact as determined by pH monitoring. METHODS: Patients with abnormal supine GER (SACT >5%) as determined by ambulatory pH testing within the previous 2 years were hospitalized on the Clinical Research Unit. They were instructed to discontinue all anti-reflux medication except antacids for 48 hours (omeprazole for 5 days) prior to testing. A pH probe was placed 5 cm above the manometrically defined LES. After a refluxogenic meal of 1,000 kcal (50% fat), patients were monitored for 3 hours in the upright position. The procedure was repeated on 3 occasions under identical circumstances for a total of 4 p H determinations per patient. RESULTS: 18 patients (ii women, 14 caucasian, imedian age 51.5 years (IQR: 42-60)) were studied. The m e a n postprandial ACT was 10.8%, with a mean standard deviation of 5.1%. The median intra-subject range was 1 1 . 4 % (IQR: 4.3-17.8).
CONCLUSIONS: i. Tremendous intra-subject variability exists in the m e a s u r e m e n t of postprandial reflux despite optimally controlled conditions. 2. Postprandial reflux is not a reliable index of GERD. 3. These data call into question the reliability of p r o l o n g e d pH monitoring in the assessment of GERD. Fuad¢4~ M 0 1 - ~ 4 ~ NCRR, G C R ~ . NIn.
Esophageal, Gastric, and Duodenal Disorders
• NITRIC OXIDE LEVELS IN GASTRIC JUICE OF PATIENTS WITH HELICOBACTER PYLORI INFECTION. R_J. Maliakkal, J.L.Achord, A.A. Mihas. Division of Gastroenterology, VA Medical Center, University of Mississippi School of Medicine, Jackson MS. We have previously reported that patients with Helicobacter pylori (HP) infection have significantly lower levels of nitric oxide (NO) in their sera than those without. The aim of the present study was to determine the level of NO in the gastric juice of patients with HP infection. Gastric juice was collected from patients undergoing upper gastrointestinal endoscopy following which antral biopsies were obtained. Nitrite (NO2) and nitrate (NO3) levels (stable end products of NO) in gastric juice were measured by methods previouslydescribed. HP infection was conlh-medby histology using the giemsa stain. The results are shown in table: GROUP
n [
GASTRIC JUICE ( N O 2 + NO3) ng/ml
HP - POSITIVE
6
50.2 :~ 5.13
HP - NEGATIVE
5
122.8 :~ 27.0
SERUM MALONYL DIALDEHYDE LEVELS IN PATIENTS BEFORE AND AFTER HELICOBACTER PYLORI ERADICATION. R.J. Maliakkal, V.K. Kanji, A.A. Mihas. Division of Gastroenterology, VA Medical Center, University of Mississippi, Jackson, MS. The mechanisms involved in the pathogenesis of peptic ulcer disease (PUD) have not been fully elucidated. An imbalance between aggressive and protective factors offers an attractive hypothesis, Injury to mucosal cell membranes secondary to lipid peruxidation and the resultant alteration in prostaglandin level is a plausible mechanism. Serum malonyl dialdehyde (MDA) levels reflect tissue injury secondary to lipid peroxidation. While a large body of evidence supports the role ofHelicobacter pylori (HP) in gastroduodenal mucosal injury, the mechanisms involved in the pathogensis need further clarification. We prospectively evaluated serum MDA levels in patients with PUD in whom HP infection was confirmed by histology (giemsa stain) and serology (IgG). Serum MDA levels were measured spectrophotometrically by standardized methods previously described. After triple therapy, HI' eradication was assessed with gastric antral biopsies and serum MDA levels were repeated. The results (m ± SEM' are shown in the table: PRE-TREATMENT HP- POSITIVE
The levels of NO2 + NO3 in gastric juice of patients with HP infection was significantly lower than those without. In conclusion: These findings in the gastric juice of liP infected patients are consistent with the hypothesis that NO may modulate HP-induced gastroduodenal mucosal injury. Furthermore it concurs with the serological observations made in HP infected patients in our laboratory.
• SERUM NITRIC OXIDE LEVELS BEFORE AND AFrER ERADICATION OF HELICOBACTER PYLORI INFECTION- A PROSPECTIVE STUDY. R.J. Maliakkal J.L. Achord, A.A. Mihas. Division of Gastroenterology, VA Medical Center, University of Mississippi School of Medicine, Jackson MS. We have previously reported that patients with HI' infection have a significantly lower level of NO in their sera. The aim of the present study was to d~ermine the effect of liP eradication on serum NO levels. For this purpose, the levels of nitrite (NO2) and nitrate (NO3), the stable end products of NO, were measured in the sera of 11 patients with peptic ulcer disease. In all patients HP infection was documented by histology (giemsa stain) and serology (IgO). One month after triple therapy, eradication was assessed by histological examination of gastric antral biopsies. The serum NO levels were measured. Results (m ± SEM) are shown below: PRE-TREATMENT
SERUM NO2 +NO3 (ng/ml)
POST- TREATMENT
(n=ll) HP- POSITIVE
(n=5) HP- NEGATIVE
133.4 4-9.7
198.8 a: 22.3*
150.6 4-5.3
(n=6) HP-POSITIVE
164.5 4-5.2
Eradication of I-IP, resulted in a statistically significant increase in the serum NOz + NO3 levels (*P = 0.0016). Patients who failed HP eradication had similar serum NO2 + NO3 levels pre- and post treatment. In conclusion: Eradication of I-IP infection is associated with a significant increase in serum NO level. Thus NO may play a crucial role in HP-induced damage to gastroduodenal mucosa.
A157
n= II
POST TREATMENT HP-POSITIVE HP-NEGATIVE n=6
n=5
SERUM 26.2 4-2.2 19.9 ± 2.5* MDA nmoles/ml 23.5 ± 2.3 21.9 4- 1.5'* *P = .0.003.; **P = 0.176 Serum MDA levels are significantly greater in patients infected with HI?. Eradication of liP resulted in a significant redtiction of serum MDA levels. In conclusion : Elevated MDA levels in PIP infected patients suggests that the HP- associated mucosal injury may be secondary to lipid peroxidation.
• HIGH INTRASUB/ECT VARIABILITY IN THE MEASUREMENT OF POSTPRANDIAL REFLUX:
IS AMBULATORY pH MONITORING RELIABLE? A. G. Maniatis, C. B. Dalton, S. R. Brazer. Div of Gastroenterology, Dept of Medicine, Duke University Medical Center, Durham, NC. Postprandial reflux has been increasingly employed as an independent index of GERD and constitutes a significant component of overall acid contact as determined by pH monitoring. METHODS: Patients with abnormal supine GER (SACT >5%) as determined by ambulatory pH testing within the previous 2 years were hospitalized on the Clinical Research Unit. They were instructed to discontinue all anti-reflux medication except antacids for 48 hours (omeprazole for 5 days) prior to testing. A pH probe was placed 5 cm above the manometrically defined LES. After a refluxogenic meal of 1,000 kcal (50% fat), patients were monitored for 3 hours in the upright position. The procedure was repeated on 3 occasions under identical circumstances for a total of 4 p H determinations per patient. RESULTS: 18 patients (ii women, 14 caucasian, imedian age 51.5 years (IQR: 42-60)) were studied. The m e a n postprandial ACT was 10.8%, with a mean standard deviation of 5.1%. The median intra-subject range was 1 1 . 4 % (IQR: 4.3-17.8).
CONCLUSIONS: i. Tremendous intra-subject variability exists in the m e a s u r e m e n t of postprandial reflux despite optimally controlled conditions. 2. Postprandial reflux is not a reliable index of GERD. 3. These data call into question the reliability of p r o l o n g e d pH monitoring in the assessment of GERD. Fuad¢4~ M 0 1 - ~ 4 ~ NCRR, G C R ~ . NIn.