Changes in adipokine levels and metabolic profiles following bariatric surgery.

BACKGROUND: Bariatric surgery is considered to be the most effective treatment option for weight reduction in obese patients. Abdominal obesity is frequently accompanied by metabolic syndrome (MS). Adipokines are cell signaling proteins that have direct impact upon the metabolic homeostasis. The purpose of this analysis was to evaluate the effect of bariatric surgery, including laparoscopic sleeve gastrectomy (LSG) and laparoscopic gastric bypass (LRYGB) on the adipokine levels and metabolic profile as well as MS and status of type 2 diabetes (T2D). METHODS: We analyzed anthropometric parameters, blood levels of adipokines, vitamins, lipids and inflammatory markers in 30 bariatric surgery patients with obesity of class II or III 1 month before and 1 year after surgery as well as in 60 obese patients from general practice (GP) and 15 patients with normal body mass (control). RESULTS: The BMI was significantly higher among patients before surgery and GP patients in comparison to control and post-surgery patients. The levels of glucose, cholesterol and LDL-cholesterol, triglyceride and hs-CRP were the highest in patients before surgery but decreased significantly after surgery, while the level of HDL-cholesterol increased after surgery. The levels of adiponectin increased and that of leptin decreased after surgery. The significant difference in the concentration of resistin was revealed between LSG and LRYGB methods. The relationship between resistin and vitamin D was also found. The patients with MS and T2D displayed significantly greater reduction in lipid markers and adipokine levels than the rest of patients. CONCLUSION: Remarkable changes in levels of adipokines after bariatric surgery appear like increase in adiponectin and decrease in leptin levels. Significant improvement in anthropometric parameters, metabolic and inflammatory markers occurs, suggesting high potential for reduction of metabolic syndrome and risk for type 2 diabetes. We have shown for the first time ever that level of vitamin D may be involved in resistin regulation.

GastroPanel® Biomarker Assay: The Most Comprehensive Test for Helicobacter pylori Infection and Its Clinical Sequelae. A Critical Review.

BACKGROUND/AIM: Several clinical conditions seriously hamper the diagnostic accuracy of the commonly used tests for Helicobacter pylori (Hp), 13C-urea breath test (UBT) and stool antigen test (SAT). The present communication is a critical review of the potential limitations of UBT and SAT, and describes the approach on how these can be avoided. Drawbacks of the Hp tests: False-negative results are most often due to low bacterial load in the stomach due to: i) use of proton pump inhibitor medication; ii) use of antibiotics; iii) presence of atrophic gastritis and hypoacid stomach; iv); bleeding peptic ulcer; v) gastric cancer (GC) and vi) mucosal-associated lymphatic tissue lymphoma. The UBT also gives false-positive results when urease-producing bacterial species, other than Hp colonize an acid-free stomach. Importantly, neither UBT nor SAT are capable of diagnosing atrophic gastritis, thus missing the patients at highest risk for GC. GastroPanel® (Biohit Oyj, Finland) circumvents these shortcomings with a serological test consisting of a panel of stomach-specific biomarkers: pepsinogen I, pepsinogen II, gastrin-17 and Hp antibodies. GastroPanel® is a tool for non-invasive examination of i) dyspeptic patients for exclusion or diagnosis of Hp or atrophic gastritis, also disclosing the status of gastric acid output; ii) for screening of asymptomatic individuals at risk of GC; and iii) for comprehensive diagnosis of Hp infection. GastroSoft® application integrates the biomarker profile with the patient's medical information, accurately classifying the biomarker profiles into eight diagnostic categories. CONCLUSION: Given that Hp is the single most important risk factor of GC, the non-invasive diagnosis and screening of Hp should be based on more accurate and more comprehensive testing than UBT or SAT alone. The GastroPanel® is such test, being completely devoid of the known serious shortcomings of UBT and SAT.

Serological biomarker testing helps avoiding unnecessary endoscopies in obese patients before bariatric surgery.

BACKGROUND: To assess the value of serological biomarker testing as a substitute for esophagogastroduodenoscopy (EGDS) in pre-operative assessment of patients referred for bariatric surgery. METHODS: Sixty-five obese patients with a mean age of 43 years (range: 21-65) and a mean body mass index (BMI) of 44 (range: 36-59) were studied. The patients were tested with a four-biomarker panel: pepsinogen I and II, gastrin-17 (basal and stimulated), and Helicobacter pylori (HP) antibodies (GastroPanel®, Biohit Oyj, Finland). On the basis of the biomarker test, the patients were classified into the HS (healthy stomach) group (n = 22) with the normal biomarker profile and the NHS (non-healthy stomach) group (n = 43). The classification of patients into HS and NHS was evaluated against the gold standard, i.e. EGDS with biopsies. RESULTS: The concordance (Cohen's kappa) between the biomarker test and gastric histology was 0.68; 95% CI 0.504-0.854, with an overall agreement of 84.6% (95% CI 73.9-91.4%). In the NHS group, all 43 patients had biopsy-confirmed chronic gastritis: 39 non-atrophic HP-gastritis, 4 atrophic antrum gastritis (AGA) of moderate severity.In the HS group only 6 patients had mild superficial H.pylori negative gastritis. Of the 22 HS subjects with the normal biomarker profile, 20 (31% of all 65) had no complaints either, while the remaining two had reflux symptoms with esophagitis. In the NHS group 10 patients had esophagitis and 8 had also reflux symptoms. CONCLUSIONS: The normal biomarker profile is an excellent surrogate for healthy stomach, implicating that pre-operative EGDS could have been avoided in 31% of our asymptomatic bariatric surgery patients who had the normal biomarker profile.

The Prevalence of Helicobacter pylori in Estonian Bariatric Surgery Patients.

Helicobacter pylori (Hp) is one of the most important human pathogens that can cause duodenal and gastric ulcers, gastritis and stomach cancer. Hp infection is considered to be a cause of limiting access to bariatric surgery. The aim of this study was to determine the prevalence of Hp in patients with obesity going into bariatric surgery and to reveal the relationship between Hp and clinical data. The study group was formed of 68 preoperative bariatric surgery patients (body mass index (BMI) 44.7 ± 4.8). Gastric biopsies (antrum and corpus) were used for histological and molecular (caqA and glmM genes) examinations. The PCR method revealed Hp infection in 64.7% of obese patients that is higher in comparison with histological analysis (55.9%). The prevalence of cagA and glmM genes in antrum mucosa was 45.6% and 47.0% while in the corpus it was 41.2% and 38.3%, respectively. The coincidence of both cagA and glmM virulence genes in the antrum and corpus mucosa was 33.8% and 22.1%, respectively. Either of the genes was found in 58.8% of antrum and 57.3% of corpus mucosa. Presence of caqA and glmM genes was in association with active and atrophic chronic gastritis. In conclusion, our study demonstrated that two thirds of morbidly obese patients undergoing bariatric surgery are infected with Hp and have a high prevalence of cagA and glmM virulence genes that points out the necessity for diagnostics and treatment of this infection before surgery.

Plasma levels of gastric biomarkers in patients after bariatric surgery: biomarkers after bariatric surgery.

BACKGROUND/AIMS: To investigate the profile of stomach specific biomarkers in blood plasma after bariatric surgery. METHODOLOGY: The study included 20 laparoscopic gastric bypass (LGBP) and 20 laparoscopic gastric sleeve (LGS) patients operated on average 22 months earlier. The biomarkers were fasting plasma level of pepsinogen I (PGI), pepsinogen II (PGII), PGI/PGII ratio, fasting and stimulated levels of amidated gastrin-17 (G17), and Helicobacter pylori antibodies (IgG). RESULTS: The prevalence of cases with abnormally low PGI (levels < 30 microg/L, seen typically in advanced atrophy of the gastric corpus mucosa, were 80 % and 40% in LGS and the LGBP groups, respectively (p = 0.013). Mean fasting G17 was normal, 3.1 +/- 4.3 pmol/L, in the LGBP patients but high, 13.9 +/- 17.2 pmol/L, in the LGS patients (p = 0.01), the levels exceeding the upper normal cut-off limit (7 pmol/L) in 40% of the LGS patients. The stimulated levels of G17 were normal (> 3 pmol/L after a protein rich drink) in all LGS patients, suggesting that the antral G cells functioned normally. CONCLUSIONS: Plasma PGI tends to be low in patients after bariatric surgery, in particular after LGS. "Sleeve" resection results in impairments in the secretory functions of the gastric corpus and fundus butleaves the antral functions intact.

Persistence of Helicobacter pylori infection in patients with peptic ulcer perforation.

OBJECTIVE: In patients with perforated peptic ulcer (PPU) the convergence between the high eradication rate of Helicobacter pylori infection and low rates of ulcer relapse after treatment has been associated with reinfection by non-virulent strains. The objective of this study was to evaluate the persistence of infection by virulent H. pylori strains and ulcer recurrence in 33 patients with PPU one year after surgery and antimicrobial treatment. MATERIAL AND METHODS: The histological evaluation and molecular detection of H. pylori cagA and ureA genes, vacA allelic types and the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses of the glmM gene products from antral mucosa specimens were performed initially, 2-5 months and 1 year after therapy. RESULTS: The density of H. pylori colonization was temporarily decreased (p<0.05) 2-5 months after therapy. After one year, complete eradication was achieved in only 7 patients (23%) at histological examination and recurrent ulcers were found in 3/33 (9%) patients. The vacA s1a allelic type of cagA-positive strains persisted in 19/33 (58%) PPU patients with identical PCR-RFLP fingerprints in 8/9 (89%) of the patients. CONCLUSIONS: In PPU patients with a low eradication rate of H. pylori infection after surgical and antimicrobial treatment, the frequent recrudescence of the infection is mostly caused by the persisting virulent strains of the cagA and vacA s1a subtypes. In the 1-year follow-up period the recurrent ulceration can be postponed just by the lowered colonization density of H. pylori after eradicative therapy.

Association of cagA and vacA genotypes of Helicobacter pylori with gastric diseases in Estonia.

Gastric biopsy specimens from 156 adult patients from southern Estonia suffering from chronic gastritis, peptic ulcer disease, and perforated peptic ulcer were analyzed by PCR. The cagA gene was evenly distributed throughout 87% of the specimens from the patients with the different gastric diseases. The presence of the cagA gene correlated with that of vacA signal sequence type s1a (99%). However, no clear differences were found in the distribution of cagA and vacA genotypes among patients in Estonia with severe perforated peptic ulcer, uncomplicated peptic ulcer, or chronic gastritis.