Superoxide dismutase activity in Helicobacter pylori-positive antral gastritis in children

Reactive oxygen metabolites have been implicated in gastric mucosal injuries. Superoxide dismutase, a scavenger of superoxide radical, is a key enzyme in gastric mucosal protection against several damaging factors. This study was aimed at investigating the relationship of superoxide dismutase activity to Helicobacter pylori-induced antral gastritis in children. Two groups of 11 children each, one positive and the other negative for Helicobacter pylori, were studied. Biopsies from the antrum and corpus were obtained for evaluation of Helicobacter pylori by CLOtest and histology as well as for superoxide dismutase activity (cytochrome c method). Erythrocytic and serum superoxide dismutase levels were determined as well. Superoxide dismutase activity was significantly higher only in the antrum of children with Helicobacter pylori-induced antral gastritis. There was no significant difference in superoxide dismutase activity in the corpus, erythrocytes, or serum of both groups. These findings may suggest a pathogenic relationship between the presence of Helicobacter pylori and oxygen radicals in inducing antral mucosal injury.     

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.     

The morphological diagnosis of Helicobacter pylori in the gastric mucosa in chronic gastritis]

JC virus (JCV), a human polyomavirus, is the agent of the demyelinating disease progressive multifocal leukoencephalopathy (PML). JCV exists in four main genotypes in the USA. Type 1, including subtypes Type 1A and Type 1B, makes up about 64% of strains in the USA and is thought to be of European origin. Type 2 is found in Asia, and Type 3 in Africa. A fourth type is found only in the USA. In general, these genotypes differ in 1-2.5% of their DNA sequence. Thirty MS patients and 30 paired controls from Budapest were studied. The clinical course of MS was mainly secondary progressive, and patients were stable at the time of testing. Most of the controls were relatives of the probands: a spouse, parent, or child. Overall, 25 of 60 (42%) of the urines tested positive for JCV by PCR. These included 13 of 30 MS patients, and 12 of 30 controls. Genotyping in the VPI gene showed all 25 JCV strains to be Type 1. Among the MS patients, seven were Type 1A and six were Type 1B. Among the controls, nine were Type 1A and three were Type 1B. In five pairs of MS patients and controls, both were positive for JCV by PCR. Two of these were husband/wife pairs of which one pair was matched for subtype (both Type 1A), and the other was not. Two of them were mother/daughter pairs, and both were matched for subtype (both Type 1B). These findings demonstrate that JCV Type 1 predominates among Hungarians, and suggest that parent/child pairs can be used to trace JCV transmission within the MS family.     

Collagenous gastritis revealed by severe anemia in a child

Non-traumatic duodenocaval fistulae are rare, but may be the source of massive gastrointestional bleeding with associated fever and sepsis. These fistulae result from penetrating duodenal peptic ulcers or right nephrectomy and subsequent radiation to the upper abdomen. The outcome depends on early diagnosis and surgery before a potentially fatal hemorrhage occurs. The therapy of choice includes closure of the fistula and repair of the duodenum and inferior vena cava. We describe the seventh case with radiogenic duodenal ulcer. Gastrointestinal bleeding occurred 10 years after radical nephrectomy and radiation (60 Gy). The patient survived following partial pancreatoduodenectomy (Whipple).     

Altered expression of membrane inhibitors of complement in human gastric epithelium during Helicobacter-associated gastritis

Tramadol hydrochloride is a novel, centrally acting analgesic with two complementary mechanisms of action: opioid and aminergic. Relative to codeine, tramadol has similar analgesic properties but may have fewer constipating, euphoric, and respiratory depressant effects. A two-center randomized double-blind controlled clinical trial was performed to assess the analgesic efficacy and reported side effects of tramadol 100 mg, tramadol 50 mg, codeine 60 mg, aspirin (ASA) 650 mg with codeine 60 mg, and placebo. Using a third molar extraction pain model, 200 healthy subjects were enrolled in a 6-hour evaluation after a single dose of drug. Of the 200 patients enrolled, seven provided incomplete efficacy data or discontinued prematurely and one was lost to follow-up. Using standard measures of analgesia, including total pain relief score (TOTPAR), maximum pain relief score (MaxPAR), sum of pain intensity difference scores (SPID), peak pain intensity difference (Peak PID), remedication, and global evaluations, all active treatments were found to be numerically superior to placebo. ASA/codeine was found to be statistically superior to placebo for all measures of efficacy. Tramadol 100 mg was statistically superior to placebo for TOTPAR, SPID, and time of remedication, whereas tramadol 50 mg was statistically superior to placebo onlyfor remedication time. Codeine was not found to be statistically superior to placebo for any efficacy measure. A greater TOTPAR response compared with all other active measures was seen for ASA/codeine during the first 3 hours of study. The 6-hour TOTPAR scores for the tramadol groups and ASA/ codeine group were not significantly different. Gastrointestinal side effects (nausea, dysphagia, vomiting) were reported more frequently with tramadol 100 mg, ASA/ codeine, and codeine 60 mg than with placebo.     

Influence of bacterial CagA status on gastritis, gastric function indices, and pattern of symptoms in H. pylori-positive dyspeptic patients

OBJECTIVE: To date, little is known about a possible relationship between H. pylori-related disturbances of gastric function and the bacterial virulence. The aim of this study was to assess whether certain gastric function indices as well as the pattern of symptoms in nonulcer dyspepsia (NUD) are related to CagA status. METHODS: A total of 56 consecutive patients with NUD (38 H. pylori-positive and 18 H. pylori-negative) were studied. Dyspeptic symptoms were categorized according to the predominant complaints and scored for severity and frequency. In all subjects, basal and pentagastrin-stimulated acid secretion, fasting and meal-induced gastrin release, fasting serum pepsinogen I (PG I) levels, and gastric emptying of solids were determined. CagA status was determined by assaying serum CagA IgG antibodies by western blotting. RESULTS: Eighteen of 38 (47%) H. pylori-positive dyspeptics were CagA seropositive. Type and severity of dyspeptic symptoms did not significantly differ between CagA-positive and CagA-negative dyspeptics nor between H. pylori-positive and negative patients. Among the gastric function indices studied, only meal-stimulated gastrin was significantly influenced by CagA status (peak gastrin 129.9 [44.1] vs 99.1 [48.6] pg/ml in CagA-positive and negative NUD, respectively), but this was not accompanied by any significant modification of basal or stimulated acid secretion or gastric emptying of solids. The activities of both antral and corpus gastritis in NUD harboring CagA-positive strains were significantly higher than those of CagA-negative NUD. Accordingly, serum PG I levels were significantly higher in CagA-positive than CagA-negative or H. pylori-negative dyspeptics. CONCLUSIONS: These findings support a role for CagA status in influencing the activity and perhaps the distribution of gastritis in NUD, as well as the degree of gastrin response to a meal; however, this is not accompanied by disturbances of acid secretion or gastric emptying or by differences in the type and severity of symptoms.     

Experimental Helicobacter pylori infection induces antral gastritis and gastric mucosa-associated lymphoid tissue in guinea pigs

Humans infected with Helicobacter pylori have abnormally low levels of the antioxidant vitamin C, which protects against the formation of carcinogenic nitrosamines, in gastric juice. Guinea pigs, like humans and nonhuman primates, have a dietary requirement for vitamin C. As such, these species have gastrointestinal vitamin C transport systems not found in other animals. We have developed and characterized a guinea pig model of chronic gastric H. pylori infection with the rodent-adapted Sydney strain of H. pylori. At 4 weeks postinfection, five of six animals of the infected group and zero of two animals of the control group were positive for H. pylori as determined by culture or PCR. At 15 weeks, six of six animals of the infected group and zero of two animals of the control group were positive. H. pylori-specific seroconversion was observed among infected animals. There were no histologic abnormalities in the gastric antra or fundi of control guinea pigs. In contrast, there was multifocal, mild to moderate lymphohistiocytic antral gastritis and formation of antral lymphoid follicles in H. pylori-infected animals. The lesion distribution in the gastric antra paralleled that observed in H. pylori-infected humans. The H. pylori-infected guinea pig should prove useful in modeling the interaction of helicobacter and vitamin C in gastric carcinogenesis.     

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

BACKGROUND: Cancer of the skin may be difficult to diagnose clinically if there are minimal skin findings on examination. OBJECTIVE: To remind physicians that the symptoms of squamous cell carcinoma (SCC) may precede physical signs of the tumor. METHODS: Perineural invasion of SCC was confirmed by histologic examination of surgical specimens. RESULTS: We present two patients whose initial presentation of SCC was facial pain due to extensive perineural invasion. Their diagnoses were delayed until skin lesions eventually became evident months later. CONCLUSION: Early detection can be lifesaving, thus emphasizing the importance of including skin cancer in the differential for facial pain or paresthesia.     

Pathological changes in the formation of Helicobacter pylori-induced gastric lesions in Mongolian gerbils

OBJECTIVES: We investigated the expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and their genes in the hearts of patients with cardiac amyloidosis and those with isolated atrial amyloidosis. BACKGROUND: The expression of ANP and BNP is augmented in the ventricles of failing or hypertrophied hearts, or both. The expression of ANP and BNP in the ventricles of hearts with cardiac amyloidosis, which is hemodynamically similar to restrictive cardiomyopathy, is not yet known. ANP is the precursor protein of isolated atrial amyloid. METHODS: We analyzed the immunohistocytochemical localizations of ANP and BNP as well as the expression of their mRNAs by in situ hybridization in the myocardium and measured the plasma levels of ANP and BNP in patients with cardiac amyloidosis. RESULTS: Four of the five right and all six left ventricular endomyocardial biopsy specimens obtained from six patients with cardiac amyloidosis were immunohistochemically positive for both ANP and BNP; none of the biopsy specimens from eight normal subjects were positive for ANP or BNP. All four of the right atria obtained at operation showed positive immunoreactions for both peptides. Electron microscopy identified specific secretory granules in ventricular myocytes of the patients with cardiac amyloidosis, but not in ventricular myocytes from the normal control subjects. Double immunocytochemical analysis revealed the co-localization of ANP and BNP in the same granules and that isolated atrial amyloid fibrils were immunoreactive for ANP and BNP, whereas ventricular amyloid fibrils were negative for both peptides. Both ANP mRNA and BNP mRNA were expressed in the ventricles of the patients with cardiac amyloidosis but not in the normal ventricles. The autopsy study of four patients with cardiac amyloidosis revealed an almost transmural distribution of ANP and BNP, with predominance in the endocardial side. Plasma BNP levels in the patients were markedly elevated ([mean +/- SD] 1,165.1+/-561.2 pg/ml) compared with those in the control subjects (8.9+/-6.0 pg/ml, p < 0.05). CONCLUSIONS: Expression of ANP and BNP and their genes was augmented in the ventricular myocytes of the patients with cardiac amyloidosis. Both regional mechanical stress by amyloid deposits and hemodynamic stress by diastolic dysfunction may be responsible for the expression of the peptides in patients with cardiac amyloidosis.     

Alterations of the enteric nervous system in neonatal necrotizing enterocolitis revealed by whole-mount immunohistochemistry

We report the results of a comprehensive search of Drosophila melanogaster DNA sequences in GenBank for di-, tri-, and tetranucleotide repeats of more than four repeat units, and a DNA library screen for dinucleotide repeats. Dinucleotide repeats are more abundant (66%) than tri- (30%) or tetranucleotide (4%) repeats. We estimate that 1917 dinucleotide repeats with 10 or more repeat units are present in the euchromatic D. melanogaster genome and, on average, they occur once every 60 kb. Relative to many other animals, dinucleotide repeats in D. melanogaster are short. Tri- and tetranucleotide repeats have even fewer repeat units on average than dinucleotide repeats. Our WorldWide Web site (http://www.bio.cornell.edu/genetics/aquadro/+ ++aquadro.html) posts the complete list of 1298 microsatellites (> or = five repeat units) identified from the GenBank search. We also summarize assay conditions for 70 D. melanogaster microsatellites characterized in previous studies and an additional 56 newly characterized markers.     

Helicobacter pylori inhibits the secretory activity of gastric parietal cells in patients with chronic gastritis. An ultrastructural study

BACKGROUND: Previous in vitro studies suggested that Helicobacter pylori may inhibit the acid secretion of gastric parietal cells. The aim of this study was to investigate ultrastructurally the influence of H. pylori infection on the gastric parietal cell function in vivo. METHODS: This study comprised 28 patients with chronic gastritis. Biopsy specimens were taken from the gastric body in all cases and examined by electron microscopy. Gastric parietal cells were counted in each ultrathin section and classified into secretory and non-secretory types. The pH of the gastric juice was also measured in all patients. RESULTS: The number of parietal cells in the secretory phase was significantly lower in H. pylori-infected (n = 16) patients than in those (n = 12) without H. pylori infection. The intragastric pH was significantly higher in patients with H. pylori-associated gastritis than in those without H. pylori infection. Parietal cells in secretory phase tended to decrease in proportion to the activity of the gastric mucosal inflammation. CONCLUSIONS: The results of this investigation suggests that H. pylori-associated gastritis is related to a decreased secretory activity of the gastric parietal cells.     

Cure of autoimmune gastritis by Helicobacter pylori eradication in a 21-year-old male

BACKGROUND: More recent investigations have shown that in some patients Helicobacter pylori (Hp) antibodies can act as antigastric antibodies and lead to atrophic autoimmune gastritis of the oxyntic mucosa. The question thus arises as to whether this form of autoimmune gastritis can be healed by eradicating Hp. METHODS: Case history of a 21-year-old man with active autoimmune gastritis of the oxyntic mucosa with lymphocytic infiltration of the entire lamina propria, foci of lymphocytic destruction of a number of glands, and hypertrophy of the preserved parietal cells, but no signs of Hp in the Warthin Starry stain. The search for parietal cell antibodies and intrinsic factor antibodies proved negative, while the level of the gastrin in the serum was slightly elevated. Since the presence of Hp IgG antibodies (243 U/ml) was confirmed. Hp eradication therapy was carried out. RESULTS: 15 months after Hp treatment the Hp IgG antibody titre had decreased to 11 U/ml. The autoimmune gastritis had healed, and autoaggressive inflammatory infiltrates with focal destruction of corpus glands and hypertrophy of the parietal cells were no longer detectable. CONCLUSIONS: Autoimmune gastritis induced by Hp may possibly be cured with Hp eradication treatment; to confirm this, further controlled prospective studies are needed.     

Structural organization of lymphatics in the monkey esophagus as revealed by enzyme-histochemistry

The fine structure and distribution of lymphatic vessels in the monkey esophageal wall were studied by light and electron microscopy using an enzyme-histochemical method. Identification of lymphatics was made by 5'-nucleotidase staining, whereas blood vessels were visualized by alkaline phosphatase staining. This technique revealed intramural lymphatic networks in the mucosa, submucosa, and myenteric layer of the esophagus. The organization of lymphatics in the esophagus basically conformed to that of the small intestine, although they showed certain distribution patterns peculiar to the esophagus. The lamina propria mucosae exhibited a double-layered lymphatic network, and lymphatic capillaries extended into its papillae. Despite their forming blind ends and being closed by endothelial cells, the lymphatics in the mucosal papillae were found to contain lymphocytes in their lumen. This suggests that free cells might penetrate the endothelium to enter these initial portions of the lymphatics.     

Positive result by serology indicates active Helicobacter pylori infection in patients with atrophic gastritis

Patients with atrophic corpus gastritis and elevated Helicobacter pylori antibody titers but 13C-urea breath test (13C-UBT) and histology results negative for H. pylori were randomized into eradication therapy or follow-up only. Antibody levels decreased significantly in six out of seven patients in the eradication group, while in the follow-up group, the titers declined in only one out of eight patients. In patients with atrophic corpus gastritis, positive serology results may indicate an ongoing infection in spite of negative 13C-UBT and histology results.     

Polyamine profile in human gastric mucosa infected by Helicobacter pylori

Septicemia is a frequent cause of death in HIV-infected adults in developing countries. Additional prospective studies are needed to determine the etiology of bloodstream infections (BSI) in febrile HIV-infected adults and guide initial evaluation and treatment in this setting. We assessed the prevalence and etiology of community-acquired BSI among 299 consecutive febrile adult medical admissions to Mulago Hospital, Kampala, Uganda, over a 4-month period in 1997. The median age of our patients was 30 years, 159 (53%) were male, and 227 (76%) HIV-1-seropositive. Overall, prevalence of bacteremia or fungemia (1 patient) was 24%. Bacteremia was more frequent in HIV-infected than in uninfected patients (27% versus 15%, respectively; p = .04). Mycobacterium tuberculosis (n = 28), Streptococcus pneumoniae (n = 15) and Salmonella species (n = 13) were the most frequent isolates. All Salmonella and mycobacterial isolates were recovered from HIV-infected patients. Pneumococcal bacteremia was not associated with HIV seropositivity. M. avium complex and M. simiae were isolated from two HIV-infected patients. The rate of mycobacteremia among febrile HIV-infected adults presenting for hospitalization was 13%. Bacteremia and disseminated tuberculosis are frequent causes of morbidity in febrile HIV-infected Ugandan adults. Initial empiric antibiotic coverage in this setting should be targeted toward the pneumococcus and gram-negative enteric bacilli, especially nontyphi Salmonella species. All patients presenting with chronic cough should be evaluated for tuberculosis.     

Are duodenal ulcer seasonal fluctuations paralleled by seasonal changes in 24-hour gastric acidity and Helicobacter pylori infection?

Short-term cultures from two histologically benign chemodectomas, one from the carotid body and one from the vagal nerve, were analyzed cytogenetically. The former had a small abnormal clone with the karyotype 46,XX,t(3;19)(q21;q13),t(12;15) (p13;q12-14), whereas the majority of the cells from the latter tumor displayed two related abnormal clones: 46,XY,i(I)(q10)/ 46,iderm,add(2)(q37). The findings add to the evidence that chemodectomas are heterogeneous neoplasms and suggest that the heterogeneity may possibly be associated with the site of origin.     

Regulation of differentiation and keratin 10 expression by all-trans retinoic acid during the estrous cycle in the rat vaginal epithelium

In rodents, the vaginal epithelium shows cyclic changes with an alternating pattern of keratinization under estrogen control and mucification under progesterone control. Retinoids are powerful regulators of cell differentiation, an excess of retinoids suppressing the keratinizing differentiation of keratinocytes. Here, we have examined the vaginal epithelium during the estrous cycle and compare the effects of retinoids on both types of hormonally induced differentiation, i.e. keratinization and mucification. All-trans retinoic acid was administered either by daily injections during the estrous cycle or by a single injection before the estrogen rise; these two protocols gave similar results. Retinoic acid suppressed estrogen-induced vaginal keratinization and cytokeratin K10 expression (a biochemical marker of terminal differentiation). Progesterone-induced mucification was not impaired; however, retinoic acid impeded mucous cell desquamation, suggesting an effect of retinoic acid on cell adhesiveness. Retinoic acid induced the appearance of apoptotic-like cells, as revealed by immunocytochemical staining of DNA fragmentation.     

Structural organization of the intact bacterial cellulosome as revealed by electron microscopy

The architecture of the intact cellulosome of Clostridium thermocellum, a huge extracellular multi-polypetide bacterial enzyme complex engaged in degradation of cellulose, was investigated by electron microscopy. This was done because former electron microscopic studies aimed at elucidation of the structure of polycellulosomes and cellulosomes were restricted by the fact that data on macromolecular details could only be derived from deformed or disrupted enzyme complexes, or by application of cryo preparation and imaging techniques yielding insufficient resolution. The shape of well-preserved cellulosomes was more or less spherical, often similar to that of an olive fruit with a cavity. Therein, multiple fibrillar structures could be visualized, interpreted to be the proximal stretches of copies of the fibrillar protein Cip A ('scaffoldin'), the nonenzymatic scaffolding protein known to function as attachment site for the enzymatic subunits, as well as fibrillar parts of anchoring proteins. The enzymatic subunits were depicted to be attached, in a repetitive fashion, to the distal stretches of the Cip A proteins. The enzymatic subunits were seen, in the intact cellulosome, to form a shell-like complex substructure surrounding the cavity. Obviously, this kind of architecture makes sure that the catalytic domains of the enzymatic subunits are exposed to the environment, and, hence, to the substrate, the cellulose fibrils. Attempts were made to demonstrate the alternating occurrence of coiled domains and fibrillar stretches along the elongated protein Cip A previously characterized by sequencing, X-ray, and NMR studies. To this end, Cip A molecules, with adhering enzymatic subunits, were partially removed from their native location within the cellulosome, "stretched" by hydromechanical forces directly on the electron microscopic support film, negatively stained, and depicted by electron microscopy. The alternating occurrence of presumed coiled domains and fibrillar stretches along Cip A could be visualized, together with detached enzymatic subunits found on the support film.     

p21 expression and mutation in gastric carcinoma: analysis by immunohistochemistry and PCR-SSCP

The biopsy of the temporal artery is a necessary procedure in order to gain a certain diagnosis of temporal arteritis. Is an easy method and customarily sure, but needing a knowledge of the clinical picture of this arteritis and of it surgical anatomy. The AA. explain the technique they follow.