Letters to the Editor

Hyperammonaemia in cirrhosis and Helicobacter pylori infection

Helicobacter pylori infection could play a role in different clinical alterations observed in cirrhosis, from gastroduodenal lesions to hepatic encephalopathy. Although its prevalence in cirrhotics is similar to that in controls, H. pylori infection is responsible for the increased prevalence of peptic ulcer observed in these patients. The ammonia production by H. pylori urease does not seem to increase blood ammonia levels during cirrhosis, indicating that its role in hepatic encephalopathy could be marginalized in clinical practice. Dual and triple therapies have been shown to be equally effective for H. pylori eradication in these patients.

OBJECTIVES:

The cause of sudden infant death syndrome (SIDS) is unknown, but our previous hypothesis proposed that Helicobacter pylori could be a causative organism. In this study, we aimed to test this hypothesis by examining gastric and tracheal tissues from a prospective cohort of SIDS infants and re-examining previously studied paraffin-fixed tissues for H. pylori.

METHODS:

Fresh gastric antral and trachea specimens obtained at postmortem from nine consecutive new cases of SIDS in Perth, Western Australia were studied prospectively. Tissues were evaluated for H. pylori by rapid urease test (CLOtest), bacterial culture, histology (hematoxylin and eosin, Warthin-Starry Silver, and immmunoperoxidase staining), and polymerase chain reaction (PCR). The latter two tests were also used for the re-examination of paraffin-embedded specimens from infants who died from SIDS (n = 17) and other non-SIDS causes (n = 7) in Kansas City, Missouri.

RESULTS:

Specimens from nine consecutive SIDS infants in Western Australia showed no evidence of H. pylori by any analyses. In the paraffin-embedded gastric and trachea specimens from Missouri, rod and coccoid-shaped bacteria were seen histologically in 33.3% of the specimens, but these were not typical H. pylori. Upon analysis by PCR, “H. pylori DNA” was detected in 53% (9/17) of SIDS samples versus 57% (4/7) in non-SIDS samples. In all cases the immunoperoxidase stain was negative, suggesting that PCR either 1) gave false positive results in this type of potentially contaminated postmortem specimen or 2) H. pylori DNA was indeed present but not increased in prevalence in SIDS infants.

CONCLUSIONS:

H. pylori is unlikely to be an etiological agent in SIDS.

Background. Helicobacter pylori infection has been described as a risk factor for hepatic encephalopathy in patients with chronic liver disease although the topic remains controversial.

Aims. To determine whether Helicobacter pylori infection is an independent predictive factor for encephalopathy in patients with liver cirrhosis.

Methods. Clinical, epidemiological, analytical and nutritional parameters of 205 patients were collected. Helicobacter pylori infection was determined by serology. Encephalopathy (grade 11 or higher) was clinically assessed during follow-up. The relationship between each parameter and encephalopathy was analysed by Kaplan-Meier curves and the Log rank test. The most significant parameters underwent multivariate analysis by Cox regression.

Results. Twenty-five variables were related to encephalopathy in the bivariate analysis. Multivariate analysis selected five independent factors: previous bouts of encephalopathy (Odds ratio 3.79; 95% confidence interval 1.94–7.38), albumin (Odds ratio 0.86; 95% confidence interval 0.80–0.92), tricipital skin fold (Odds ratio 0.79; 95% confidence interval 0.66–0.95] chronic pulmonary disease (Odds ratio 2.78, 95% confidence interval; 1.31–5.92), and on-going alcoholism (Odds ratio 2.62; 95% confidence interval 1.16-5.88].

Conclusions. Helicobacter pylori is not an independent risk factor for hepatic encephalopathy.

Background/Aims: An involvement of Helicobacter pylori in the development of hepatic encephalopathy in cirrhotic patients has been proposed, but data confirming such an association are lacking. This prospective study aimed to assess whether ammonia levels and indicators of subclinical portosystemic encephalopathy were influenced by H. pylori status in a series of 62 cirrhotic patients. The effects of H. pylori eradication on such parameters were also investigated.

Methods: Fasting blood ammonia levels, mental state, number connection test, flapping tremor, and EEG tracings were recorded at baseline, and in H. pyloripositive patients (as diagnosed by rapid urease test and ¹⁴C-urea breath test) these parameters were reassessed 2 months following eradication therapy.

Results: In this series of non-advanced cirrhotic patients, the prevalence of H. pylori infection was 52%. No significant differences were observed between H. pylori+ and H. pylori− cases with respect to fasting venous blood ammonia concentration (47±24 vs 43±22 μmol/l) or to the remaining parameters assessing portosystemic encephalopathy. In addition, H. pylori eradication failed to induce any significant variation in either fasting blood ammonia levels (from 45±23 to 48±26 μmol/l) or neurologic disturbances.

Conclusion: These results indicate that H. pylori infection is not a major contributing factor to either fasting blood ammonia levels or parameters assessing subclinical portosystemic encephalopathy in patients with non-advanced liver cirrhosis.

Objective: Elevated blood ammonia is an important pathogenic factor of hepatic encephalopathy. Although colonic bacteria are considered the main source of ammonia, the stomach in subjects with urease-producing Helicobacter pylori (H. pylori) is an alternative site. The objective of this study was to determine whether H. pylori is associated with this complication. Methods: After assessing liver function and portal hypertension, 55 cirrhotics were evaluated for encephalopathy and H. pylori infection. Response to 2 weeks of amoxicillin (2 g/day) and omeprazole (40 mg/day) was then assessed in 17 (13 H. pylori-positive, four H. pylori-negative) encephalopathic subjects. Results: H. pylori infection was more common (67% vs 33%, p = 0.004) among encephalopathic patients. Additional factors associated with encephalopathy included older age (60.1 ± 1.5 vs 49.8 ± 2.4 yr, p = 0.001), lower albumin (3.17 ± 0.08 vs 3.69 ± 0.12 g/dl, p = 0.001), higher total bilirubin (2.24 ± 0.20 vs 1.53 ± 0.23 mg/dl, p = 0.034), greater ascites score (0.8 ± 0.1 vs 0.3 ± 0.1, p = 0.01), greater diuretic score (1.1 ± 0.1 vs 0.3 ± 0.1, p = 0.002), and greater modified Child score (6.7 ± 0.3 vs 5.1 ± 0.3, p = 0.001). When adjusted for severity of cirrhosis and age, H. pylori continued to demonstrate a statistical association (p = 0.039). After anti-H. pylori therapy, symptomatology in infected encephalopathic patients appeared to improve, whereas noninfected subjects were unaffected. Conclusion: In cirrhotic patients, H. pylori infection is associated with hepatic encephalopathy, especially in younger patients with decompensated liver disease.