C. Martin De Argila

Helicobacter pylori infection and insulin-dependent diabetes mellitus

Helicobacter pylori is associated with different diseases: duodenal ulcer, rosacea, ischaemic heart disease and gastric cancer. Given the abnormal immunological response and the high prevalence of gastrointestinal symptoms in diabetic patients, we conducted a study on H. pylori prevalence among these patients. We designed a case control study of a population-based cohort. Eighty insulin-dependent diabetes mellitus (IDDM) patients with an average age (24.05 +/- 8.3 years), and 100 control subjects (25 +/- 7.1 years) were selected to verify the seroprevalence of Helicobacter pylori in these populations. One serum sample was obtained from each subject for evaluation of antibodies against Helicobacter pylori, parietal cells (APA) and pancreatic islets cells (ICA). The seroprevalence of H. pylori among IDDM patients aged less than 24 years was significantly higher than among control subjects; the corresponding rate among IDDM aged greater than 24 years was significantly lower than among control subjects. Antibodies against parietal cells (APA) and islet cells (ICA) among H. pylori positive diabetic patients were significantly higher than among H. pylori negative diabetic patients. IDDM patients were subdivided on the basis of the evolutive course of diabetes. Seroprevalence of H. pylori as well as prevalence of ICAs decreased with IDDM duration. Nevertheless, no variation in the prevalence of APAs during the course of diabetes was observed. We observed an association between the seroprevalence of Helicobacter pylori and the duration of IDDM. The seroprevalence of H. pylori and ICA decreased with the evolutive course of diabetes mellitus among IDDM. The prevalence of ICA and APA in IDDM H. pylori positive subjects was higher than among controls.

Training model for teaching endoscopic submucosal dissection of gastric tumors

INTRODUCTION The elevated risk of complications and technical complexity of endoscopic submucosal dissection (ESD) has limited its implementation in our medical system. OBJECTIVE To design and evaluate a training program for learning the ESD technique. METHODS Four endoscopists with no experience with ESD underwent a 4-step training program: 1) review of the existing literature, didactic material, and theoretical aspects of ESD; 2) ESD training in an ex-vivo animal model; 3) ESD training in an in-vivo animal model (supervised by ESD expert); and 4) ESD performance in a patient. A standard gastroscope and an ESD knife (IT, Flex or Hook-knife Olympus) were employed. The classical ESD technique was performed: rising of the lesion, circumferential incision, and submucosal dissection. RESULTS Ex-vivo animal model: 6 x swine stomach/esophagus -cost < 100 euro; 6 x ESD: antrum (n = 2), body (n = 3) and fundus/cardia (n = 1)-; size of resected specimen: 4-10 cm; ESD duration: 105-240 minutes; therapeutic success: 100%; complications: perforation (1/6: 16%) sealed with clips. In-vivo animal model: 6 ESD (antrum/body of stomach: 4; esophagus: 2); size: 2-5 cm; duration: 40-165 minutes; success: 100%; complications: 0%. PATIENT ESD of a gastric lesion located in the antrum/body; size: 3 cm; duration 210 minutes; a complete resection was achieved; no complications. CONCLUSIONS The results of the present study support the usefulness of this model for learning ESD in our system.

Basal and stimulated gastrin levels and gastric acid output five months after therapy for Helicobacter pylori eradication in duodenal ulcer patients

The aim of our study was to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated serum gastrin levels and gastric acid output 5 months after therapy of patients with duodenal ulcer. Thirty-two patients (24 men and eight women with a mean age of 45 years) who had had endoscopy and were diagnosed as having duodenal ulcer entered the study. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body, and fundus. These specimens were then sent for microbiological and histological examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 and 5 months after therapy, and biopsy specimens were again taken from the gastric antrum and body. Before treatment, serum samples were taken to measure basal and stimulated (90 min) gastrin levels after ingestion of two beef cubes, and basal and stimulated acid outputs (after pentagastrin) were studied. Measurements of gastrin and gastric acid output were repeated 5 months after therapy. H. pylori was eradicated in 26 patients (81.3%). Basal gastrin levels (mean +/- SD) at diagnosis and after eradication were 44 +/- 12 and 35.8 +/- 2 pg/ml, respectively (p < 0.05). Similarly, stimulated gastrin levels (integrated values) decreased from 5,303 +/- 1,526 pg/ml/min before therapy to 3,779 +/- 1,204 pg/ml/min after eradication (p < 0.001). However, basal (4.9 +/- 4mEq/h) and stimulated (28.5 +/- 10mEq/h) acid output did not vary after eradication (3.9 +/- 4 mEq/h and 26.2 +/- 12 mEq/h, respectively). We conclude that basal and stimulated gastric acid output are not changed by H. pylori eradication in duodenal ulcer patients 5 months after therapy, in spite of its association with a significant decrease in basal and stimulated gastrin levels.

Improvement in lipid and haemostasis patterns afterHelicobacter pylori infection eradication in type 1 diabetic patients

Helicobacter pylori has been implicated in the cardiovascular risk of diabetic patients. The aim of our study was to investigate whether the Helicobacter pylori infection plays a role in the lipid and haemostasis patterns of type 1 diabetic patients. Twenty nine patients with type 1 diabetes mellitus and H. pylori infection were enrolled (Chlamydia pneumoniae negative). The H. pylori infection status was assessed by serology and urease breath test. In all patients levels of total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol, lipoprotein (a) (Lpa) C reactive protein (CRP), fibrinogen, thrombin/antithrombin III complex (TAT), plasminogen activator inhibitor type 1(PAI-1), tissue plasminogen activator (t-PA) and von Willebrand antigen were measured. All patients were evaluated before and after H. pylori eradicating treatment with amoxicillin, clarithromycin and omeprazole. Twenty two patients were eradicated and seven remained infected. In H. pylori eradicated patients, HDL cholesterol increased (59.7+/-18.9 mg/dl vs 65.2+/-15. 9 mg/dl, P << 0.05), after treatment. After H. pylori eradication, the levels of CRP and TAT decreased (48+/-0.7 ng/l vs 3.3+/-0.4 ng/l;P << 0.05), (27.7+/-44.7 microg/ml vs 2.1+/-1.4 microg/ml, P << 0.05), respectively. The decrease in TAT was higher in the group of H. pylori (+) patients with higher levels of TAT (TAT >> 20 ng/ml, 92.8+/-41.6 ng/ml vs 1.9+/-2.0 ng/ml, P << 0.005; TAT 4Eth 20 ng/ml; 10.1+/-5.2 ng/ml vs 2.2+/-0.6 ng/ml, P << 0.05). These changes did not occur in patients without H. pylori eradication. Eradication of H. pylori infection in type 1 diabetic patients modifies some parameters of lipid and haemostasis patterns, (increase of HDL-cholesterol, reduction of Lpa and decrease of CRP and TAT) and so contributes to improvement of cardiovascular risk factors in these patients.

Verification of decreased basal and stimulated serum pepsinogen-I levels is a useful non-invasive method for determining the success of eradication therapy for Helicobacter pylori.

BACKGROUND We wanted to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated pepsinogen-I levels in duodenal ulcer patients and to verify whether modification of such levels is a useful method for determining the success of eradication therapy. METHODS Thirty-two patients (24 men; mean age, 45 years) with active duodenal ulcer were studied. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body and fundus for microbiologic and histologic examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 month after completing therapy, and biopsy specimens were again taken from the gastric antrum and body. Serum samples were taken at initial and repeat endoscopies, to measure basal and stimulated (120 min) pepsinogen-I levels after injection of pentagastrin. RESULTS H. pylori was eradicated in 26 patients (81%). Significant histologic improvement, in both the antrum and body, was observed (p < 0.001). Basal pepsinogen-I levels (mean and 95% confidence interval) at diagnosis and after eradication were 106 (92-119) and 87 (74-100) ng/ml, respectively (P < 0.001). Similarly, stimulated pepsinogen-I levels (integrated values) decreased from 4790 (4199-5381) before therapy to 3970 (3383-4557) ng/ml.min after eradication (P < 0.001). Pepsinogen I levels did not change in patients in whom H. pylori was not eradicated. The area under the receiver operating characteristic curve for decreased basal and stimulated pepsinogen-I levels was 0.77 (SE, 0.09) and 0.79 (SE, 0.1), respectively. CONCLUSION H. pylori eradication in duodenal ulcer patients was associated with a significant decrease in basal and stimulated pepsinogen-I levels. Measurement of these levels could determine how successful response to therapy has been in both the eradication and resolution of associated gastritis. Other advantages of this procedure are that it has low cost and results are evident at an early stage.

A case of spontaneous peritonitis caused by Weeksella virosa

A case of spontaneous peritonitis caused by Weeksella virosa is reported. This Flavobacterium has never been reported as a cause of spontaneous bacterial peritonitis. The patient responded to antimicrobial therapy. Clinical and therapeutic implications are discussed.

Tumor estromal colónico de características atípicas

Resumen Presentamos el caso de una paciente con un tumor de la estroma gastrointestinal cuyo interes reside en sus caracteristicas atipicas: se trataba de una mujer joven, con una lesion localizada en el colon que se manifesto inicialmente como una perforacion silente, y que presentaba una tipificacion inmunohistoquimica poco habitual. Revisamos los aspectos clinicos, diagnosticos y terapeuticos de este raro grupo de neoplasias digestivas.

Estudio de prevalencia de Helicobacter pylori y Chlamydia pneumoniae en placas de ateroma de pacientes diabéticos y no diabéticos con arteriosclerosis

Fundamento La arteriosclerosis se comporta como un proceso inflamatorio cronico. Algunos estudios han sugerido que Chlamydia pneumoniae y Helicobacter pylori pueden representar un papel en la patogenia de la arteriosclerosis en pacientes diabeticos y no diabeticos. EL objetivo del estudio fue determinar mediante cultivo y reaccion en cadena de la polimerasa (PCR), la presencia de C. pneumoniae y H. pylori en arterias de pacientes con arteriosclerosis. Metodos y resultados El estudio presenta un diseno transversal, con 40 pacientes (22 diabeticos y 18 no diabeticos) sometidos a una intervencion de revascularizacion. Se recogieron muestras de ateroma y se utilizaron los siguientes metodos de deteccion de la infeccion: PCR y cultivo de las placas de ateroma para detectar C. pneumoniae y H. pylori. Se utilizo la serologia para determinar el contacto previo del paciente con el germen. En el grupo total, 29 pacientes (72,5%) presentaban serologia positiva a H. pylori y 20 (50%) a C. pneumoniae (p Conclusion En este estudio se demuestra la nula presencia de H. pylori y escasa de C. pneumoniae en placas de ateroma. La relacion entre arteriosclerosis e infeccion por C. pneumoniae, pero no por H. pylori, podria explicarse por infeccion directa de la pared arterial.

Increased Incidence of Helicobacter pylori in Gastric Cancer, as Shown by the Rapid Urease Test

Nowadays it is widely accepted that Helicobacter pylori infection is the main etiologic factor in chronic gastritis type B (CGB). However, its contribution to the developement of gastric ulcer remains controversial. In vivo studies on gnotobiotic piglets [1,2] and healthy humans [3, 4] have shown that a typical CGB picture can be reproduced by the ingestion of this microorganism. A further point supporting a relationship between H. pylori and CGB is the possibility of inducing a partial or complete histologic recovery of the disease after the clearance of bacteria by bismuth salts or antibiotics [5–8].

Helicobacter pylori in Subtotal Gastrectomies

Surgery has long been the cornerstone in the management of peptic ulcer disease (PUD) refractory to medical treatment. Although the number of elective interventions has substantially decreased after the marketing of H2 receptor antagonists, the surgical approach maintains its full validity in the management of complicated PUD.