The anatomy of the pelvic plexus in female cadavers: implications for retroperitoneal nerve-sparing surgery.

Background: The inferior hypogastric plexus (IHP) is a crucial structure for female continence and sexual function. A nerve-sparing approach should be pursued to reduce the risk of pelvic plexus damage during retroperitoneal pelvic surgery. Objectives: To analyse the relationship between the female IHP and several pelvic anatomical landmarks. Materials and Methods: Standardised cadaveric dissection was performed on 5 nulliparous female cadavers. The relationships of the IHP and the mid-cervical plane (MCP), the mid-sagittal plane (MSP), and the uterosacral ligament (USL) were investigated. Main outcome measures: Distance between IHP and MCP, MSP, and USL. Results: Distances between the right IHP and the right MSP (mean distance: 16.3 mm; range: 10.0-22.5 mm) and the right USL (mean distance: 4.8 mm; range: 0-15.0 mm) were shorter than those between the left IHP and ipsilateral landmarks (left MSP distance: 23.5 mm; range 18.0-30.0 mm; left USL distance: 5.0 mm; range: 0-20.0 mm). Although the MCP was 3.3 mm (range: 2.5-4.0 mm) left and lateral to the midsagittal line, the right IHP was closer to the MCP (mean distance: 19.6 mm; range: 13.0-25.0 mm) than the left one (mean distance: 20.2 mm; range: 15.0-26.0 mm). Conclusions: Distances between the right IHP and the MSP, MCP, and ipsilateral USL, are shorter compared to these associated to the left IHP. What is new?: Right autonomic pelvic plexus is closer to the midline planes and the ipsilateral USL. These anatomical relationships may be greatly helpful for pelvic surgeon while facing retroperitoneal pelvic surgery and looking for a nerve-sparing approach.

Salivary specific IgG is a sensitive indicator of the humoral immune response to Helicobacter pylori.

In humans, salivary antibodies are secreted during humoral immune response. Helicobacter pylori infection is associated with systemic humoral immune response reflected by raised serum levels of specific IgG. The present study was aimed at exploring whether salivary concentrations of specific H. pylori IgG are a reliable indicator of H. pylori infection. Serum and salivary samples were obtained from 291 subjects attending the GI clinic and tested for H. pylori-specific IgG by a direct ELISA (94% sensitivity, 95% specificity for serum determinations) using a crude H. pylori sonicate as antigen. Data are given as optical density (mean +/- S.D.). Levels of salivary H. pylori IgG paralleled those of circulating specific IgG in the 291 subjects studied (0.981 +/- 0.431 vs. 0.777 +/- 0.682, respectively). A significant positive correlation was found between specific H. pylori IgG in sera and saliva samples (r = 0.981, P < 0.0001). An overall concordance between circulating and salivary H. pylori IgG was observed in 238 out of the 291 (81.7%) subjects. Salivary H. pylori IgG represent a sensitive marker of specific humoral immune response and they may substitute circulating H. pylori IgG measurement when sera samples are not available.

Isotypic analysis of specific antibody response in serum, saliva, gastric and rectal homogenates of Helicobacter pylori-infected patients.

The relationship between systemic and local humoral immune response to Helicobacter pylori is poorly understood. To further address this issue we measured, using ELISA, H. pylori-specific IgG and IgA antibodies in serum, saliva, gastric and rectal homogenates of H. pylori-infected patients. A total of 107 patients who underwent upper GI endoscopy and/or sigmoidoscopy were studied. The isotypic pattern of H. pylori-specific antibodies appeared to differ at the serum, salivary, gastric and rectal mucosa level. Serum H. pylori IgG titers were higher than those of the serum-specific IgA. On the contrary, in saliva samples H. pylori IgA titers were higher than specific IgG titers. In gastric homogenates, specific IgG and IgA titers were similar. H. pylori-specific IgG were detectable in rectal homogenates but no or very low H. pylori-specific IgA were found in the same material. Furthermore, no difference was found in H. pylori IgG and IgA in serum, saliva and gastric homogenates between duodenal ulcer and non-ulcer dyspepsia patients. Data of the present study indicate that, in H. pylori-infected patients, the specific immune response is as follows: (1) it involves the secretory immune system; (2) it is paralleled by the specific salivary IgA; (3) it does not differentiate duodenal ulcer from non-ulcer dyspepsia patients; and (4) it does not take place in the large bowel.

Changes in the mucosal expression of interleukin 15 in Helicobacter pylori-associated gastritis.

Transcripts for interleukin (IL) 15 were detected in the gastric mucosal samples of 5/5 (100%) patients with no evidence of Helicobacter pylori infection and in 4/14 (28%) H. pylori-infected patients (P< 0.05). Both IL-15 mRNA and IL-15 protein were detected in 1/6 (17%) patients who successfully underwent H. pylori eradication therapy, before treatment and in 5/6 (83%) cases after eradication. Even though a parallel significant (P < 0.03) improvement of gastritis score occurred after eradication, the severity of gastritis did not differ according to the mucosal IL-15 expression among H. pylori-infected patients, irrespective of the CagA serology. This study demonstrates, for the first time, that transcripts for IL-15 are expressed in the human gastric mucosa. Changes occurring during H. pylori colonisation and after eradication raise the hypothesis that H. pylori may down-regulate IL-15 expression in the gastric mucosa.

Evidence against an increased risk of Helicobacter pylori infection in dentists: a serological and salivary study.

BACKGROUND: An oral-to-oral route of transmission of Helicobacter pylori infection has been postulated, which is supported by the observation that H. pylori is present in the saliva and in dental plaque. On the basis of this assumption, an increased risk of H. pylori infection among dentists was postulated. METHOD: Serum and salivary H. pylori immunoglobulin (lg)G antibodies were measured in a group of practising dentists. For comparison we also studied a group of controls from the same urban area matched for age, sex, smoking habits, alcohol and non-steroidal anti-inflammatory drug consumption, and history of dyspepsia. RESULTS: There was no significant difference in serum H. pylori lgG antibodies titres between dentists and controls [optical density (OD) 0.991 +/- 0.588 versus 1.025 +/- 0.591, respectively]. Salivary H. pylori lgG were 0.693 +/- 0.726 and 0.661 +/- 0.614 OD in the dentists and control groups, respectively. The frequency of H. pylori-seropositive subjects did not differ between the two groups [22 out of 39 (56%) versus 46 out of 71 (64%)]. A positive saliva assay was found in 23 out of 39 (59%) dentists and in 44 out of 71 (62%) controls. The odds ratio for a dentist being H. pylori-positive was 0.7 (95% confidence interval 0.3-1.7) by serology and 0.9 (95% confidence interval 0.4-2.1) by salivary antibody assay. CONCLUSION: The data of this study do not support the concept that dentists are a high-risk group for H. pylori infection.

Salivary-specific immunoglobulin G in the diagnosis of Helicobacter pylori infection in dyspeptic patients.

OBJECTIVES: Helicobacter pylori infection is arguably the most common chronic bacterial infection in humans. The high prevalence and the association with peptic ulceration and gastric cancer indicate that simple, noninvasive methods for diagnosis of the infection are needed. In this study, the accuracy of salivary diagnosis for H. pylori infection was assessed. METHODS: Saliva and serum samples of 152 dyspeptic patients were tested for H. pylori IgG and IgA by an in-house ELISA. All patients underwent gastroscopy with biopsy. RESULTS: One hundred thirty-one patients (86%) were found to be H. pylori positive on histology. Duodenal ulcer was found in 67 patients; 85 had no macroscopic lesion. Salivary and serum H. pylori IgG as well as serum H. pylori IgA titers were significantly higher in H. pylori-positive than in H. pylori-negative patients. The sensitivity and specificity of salivary H. pylori IgG were 82% and 71%, respectively; the positive and negative predictive values were 95% and 40%, respectively; and the accuracy 81%. The corresponding figures for serum H. pylori IgG were 97% and 91%; 98% and 83%; and 96%. Those for serum H. pylori IgA were 80% and 52%; 91% and 30%; and 76%. The sensitivity of salivary H. pylori IgG in detecting duodenal ulcer was 83% (56/67) that of serum H. pylori IgG was 97% (65/67) (odds ratio = 0.15; confidence interval = 0.02-0.8; p = 0.02). CONCLUSIONS: Salivary H. pylori IgG was a fairly sensitive and accurate indicator of gastric H. pylori colonization, with a high positive predictive value in our population. Data, however, suggest that salivary H. pylori IgG measurements do not compare favorably with serology.

Mucosal and systemic antibody levels against Helicobacter pylori do not parallel gastric inflammatory changes.

BACKGROUND AND AIMS: Mucosal and systemic antibodies against Helicobacter pylori have been detected but their role in the natural history of Helicobacter pylori-related diseases is unclear. In this study, the levels of Helicobacter pylori IgG and IgA were related to the grade of gastritis. PATIENTS AND METHODS: A series of 152 dyspeptic patients underwent gastroscopy with biopsies. Helicobacter pylori was detected in 131 (86%) patients. Samples of serum and unstimulated saliva were collected. Helicobacter pylori IgG and IgA were measured in homogenised gastric biopsies, saliva and serum by an in-house enzyme linked immunosorbent assay. RESULTS: Levels of gastric mucosa, salivary and serum Helicobacter pylori IgG were higher (p < or = 0.01) in Helicobacter pylori positive than negative patients. Likewise, levels of gastric mucosa and serum Helicobacter pylori IgA were higher (p < 0.01) in Helicobacter pylori positive patients. Gastric mucosa, saliva and serum Helicobacter pylori antibody levels did not differ between superficial and atrophic, active and inactive Helicobacter pylori positive gastritis. CONCLUSIONS: These data indicate that gastric inflammatory changes may not necessarily be related to the antibody response against Helicobacter pylori.

Evidence against colonic mucosa colonisation by Helicobacter pylori. Lack of a specific antibody response in homogenates of rectal endoscopic biopsies.

Aim of this study is to provide indirect evidence that human colonic mucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopic biopsies from 26 patients and in rectal samples of a further 36. All had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810 +/- 0.668 optical density vs 0.329 +/- 0.509 optical density for IgG, p = 0.007 and 0.660 +/- 0.477 vs 0.116 +/- 0.229 for IgA, p < 0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p = 0.16) different between Helicobacter pylori positive (48/62, 77%, 0.243 +/- 0.388 optical density) and negative (14/62, 23%; 0.095 +/- 0.088) patients. In same material, levels of Helicobacter pylori IgA were very low and undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.

Circulating D dimer in inflammatory bowel disease.

An activated thrombogenesis has been reported in inflammatory bowel disease (IBD). In this study we evaluated whether a fibrin degradation product, the D dimer, is increased in patients with IBD. D dimer plasma levels were evaluated by sandwich ELISA in patients with Crohn's disease (24), ulcerative colitis (25), gastrointestinal (GI) disease controls (10), hospital controls (13) and healthy subjects (14). Circulating D dimer was significantly higher in ulcerative colitis (median 651; 95% CI 89-1275 ng/ml) than in healthy subjects (median 412; 95% CI 112-672 ng/ml; p = 0.002), Crohn's disease (median 466; 95% CI 6-931 ng/ml; p = 0.005) and GI disease controls (median 446; 95% CI 196-688 ng/ml; p = 0.023). In ulcerative colitis, plasma D dimer was related to inflammatory parameters such as C-reactive protein (p < 0.01) and seromucoids (p < 0.001). Circulating D dimer was age-related in all groups (p < 0.05). Fibrin degradation, as reflected by plasma D dimer, is detected in patients with ulcerative colitis exhibiting a marked acute phase response.

Suggestion against an oral-oral route of transmission for Helicobacter pylori infection: a seroepidemiological study in a rural area.

In this study the seroepidemiology of H. pylori and Epstein-Barr virus was compared in the same setting. A sample of 705 subjects completed a structured questionnaire. A serum sample was drawn from each subject and assayed for H. pylori IgG. Antibodies to Epstein-Barr virus were determined in a subgroup of 466 subjects. Cross-tabulation of data showed that 274 (58.8%) subjects were seropositive and 20 (4.3%) were seronegative for both infections, 17 (3.6%) were seropositive for H. pylori, and 155 (33.3%) were seropositive for Epstein-Barr virus (odds ratio=2.08, 95% confidence interval: 1.008-4.3). Nevertheless, the agreement between H. pylori and Epstein-Barr virus seropositivity was no better than chance (kappa=0.067) and the age-related seroprevalence curve of Epstein-Barr virus was similar in H. pylori seropositive and seronegative subjects. Furthermore, multiple logistic regression analysis did not show any risk factor shared by both infections. The findings of this study do not support the hypothesis that H. pylori and Epstein-Barr virus share a common mode of transmission. It can be speculated that the oral cavity may not be an important reservoir for H. pylori.

Helicobacter pylori-specific IgG in chronic haemodialysis patients: relationship of hypergastrinaemia to positive serology.

BACKGROUND: Chronic haemodialysis (HD) patients frequently suffer from dyspeptic symptoms and hypergastrinaemia is a common finding in these patients. Helicobacter pylori (H. pylori) infection is associated with dyspepsia and hypergastrinaemia. METHODS: The aim of this study was to determine whether H. pylori is frequently found in HD patients and to explore the relationship of H. pylori with dyspeptic symptoms and/or hypergastrinaemia in these patients. Serum H. pylori specific IgG were measured by an in-house enzyme-linked immunosorbent assay (sensitivity and specificity is 97% and 91% respectively) in 103 chronic HD patients. The patients (53 M, 50 F, mean age f60 +/- 13 years) completed a questionnaire exploring the type, frequency and intensity of dyspeptic symptoms. Fasting plasma gastrin levels were also measured. Serum and plasma samples from 103 hospital patients matched for age, sex and dyspepsia were use as controls. RESULTS: There was no significant difference in terms of serum H. pylori IgG between HD patients and controls (0.977 +/- 0.295 vs 1.046 +/- 0.306 OD respectively). The prevalence of subjects with positive serology was relatively high in both groups, but did not differ between HD patients (73%) and controls (78%). Dyspepsia was reported in 72 (70%) cases. There was no relationship between presence (and grading) of dyspepsia or type of dyspeptic symptoms and H. pylori serology. In the HD group, patients seropositive for H pylori had a significantly higher gastrinaemia than those who were seronegative: 598 +/- 413 ng/ml vs 309 +/- 252 ng/ml (P < 0.0001). The relationship between seropositivity for H. pylori and hypergastrinaemia was significant (P = 0.00038), after adjustment by multiple regression analysis for sex, age, smoking, alcohol, months on dialysis, renal function, drugs, and dyspepsia. CONCLUSIONS: Data of this study suggest that H. pylori may play a role in contributing to hypergastrinaemia of HD patients.

Salivary immunoglobulin G assay to diagnose Helicobacter pylori infection in children.

An in-house enzyme-linked immunosorbent assay (ELISA) for measurement of Helicobacter pylori-specific immunoglobulin G (IgG) and IgA in saliva was evaluated by comparison with histopathologic (Giemsa staining) and biochemical (urease quick test) examination of gastric biopsy specimens obtained from 112 children referred for diagnostic gastroscopy. Serum H. pylori IgG was also measured in a subgroup of 50 children by the same ELISA. Salivary H. pylori IgG levels were significantly higher in H. pylori-positive (n = 57) than in H. pylori-negative (n = 55) children (P < 0.001). The sensitivity and specificity of the salivary IgG test were 93 and 82%, respectively; the positive and negative predictive values were 84 and 92%, respectively; and the accuracy was 87.5%. Salivary H. pylori IgA did not distinguish H. pylori-positive from H. pylori-negative children. The performance of serum H. pylori IgG was slightly (3 to 6%) better than that of salivary H. pylori IgG. The salivary IgG test can be considered a useful tool for the screening of H. pylori infection in children.

Seroepidemiology of Helicobacter pylori infection and hepatitis A in a rural area: evidence against a common mode of transmission.

BACKGROUND AND AIMS: Recent studies have shown that the age-specific seroprevalence of H pylori infection parallels hepatitis A (HAV), suggesting similar modes of transmission. The aim of this study was to investigate the seroepidemiology of H pylori and HAV in the same setting. PATIENTS: A sample of 705 resident subjects (273 men, age range 1-87 years, median 50) who attended the outpatient medical centre of the rural town of Cirò, Southern Italy (11,000 inhabitants) for blood testing were recruited. METHODS: All subjects completed a structured questionnaire. A serum sample was drawn from each subject and assayed for H pylori IgG by a validated in house enzyme linked immunosorbent assay. Antibodies to HAV were determined in 466 subjects (163 men, age range 1-87 years, median 49). A measure of agreement between H pylori and HAV seropositivity, the kappa statistic, was used. RESULTS: Overall, 446 (63%) subjects were seropositive for H pylori. Of the 466 subjects screened for both H pylori and HAV, 291 (62%) were seropositive for H pylori and 407 (87%) for HAV. Cross-tabulation of these data showed that 275 (59%) were seropositive and 43 (9%) seronegative for both H pylori and HAV, 16 (3%) were seropositive for H pylori, and 132 (28%) were seropositive for HAV (OR = 5.6, CI 3 to 10). There was a parallel, weakly correlated (r = 0.287) rise in the seroprevalence of the two infections with increasing age. However, the agreement between H pylori and HAV seropositivity was little better than chance (kappa = 0.21) and in those aged less than 20 years it was worse than chance (kappa = -0.064). Furthermore, multiple logistic regression analysis did not show any risk factor shared by both infections. CONCLUSIONS: The correlation between H pylori and HAV reflects the age-specific seroprevalence of both infections rather than a true association. This study provides evidence against a common mode of transmission of H pylori and HAV.