Presence of Gastric Autoantibodies Impairs Gastric Secretory Function in Patients with Helicobacter pylori-positive Duodenal Ulcer

Background: Although the association between Helicobacter pylori infection and gastric autoimmunity is now well established, to date little is known about the significance of anticanalicular autoantibodies in patients with duodenal ulcer (DU). We therefore investigated the prevalence of serum antiparietal cell autoreactivity in DU patients as well as the relationship between these autoantibodies, gastric histopathology and gastric secretory function in this setting. Methods: Forty-one consecutive patients with H. pylori-positive DU were initially recruited. In all patients, basal (BAO) and pentagastrin stimulated acid output (PAO), fasting and meal-induced serum gastrin levels, as well as serum pepsinogen I concentrations, were measured. Antral and body gastritis was evaluated according to the Sydney system. Serum anticanalicular autoreactivity was determined by the indirect immunoperoxidase technique. Results: Serum anticanalicular autoantibodies were found in 7 out of 34 patients (20%). The presence of these antibodies was associated with a significantly higher grade of body gastritis (activity: 1.9 versus 0.9) as well as with significantly higher fasting and meal stimulated gastrin levels (mean fasting gastrin, 76.4 (15.2) pg/ml versus 59.3 (20.5) pg/ml). In addition, PAO values were significantly lower in patients with gastric autoantibodies than in those without this autoreactivity (mean 0.35 (0.16) mmol kg^-1 h^-1 versus 0.49 (0.16) mmol kg^-1 h^-1). In contrast, no significant differences were found between patients with and without anticanalicular autoantibodies as regards fasting serum pepsinogen I concentrations. Conclusions: Serum anticanalicular autoantibodies can be detected in 20% of patients with DU and are associated with a more severe pattern of body gastritis, higher gastrin levels and decreased peak acid secretion values. Their presence could account for the normal or reduced acid output which can be seen in a subset of DU patients.     

Clinical aspects of the AIDS dementia complex in relation to histopathological and immunohistochemical variables

To correlate cerebral histopathological and immunohistochemical changes in the neuroclinical features of the AIDS dementia complex (ADC), autopsy results of 28 ADC patients were related, in a retrospective analysis, to scores on a standardised neurological examination performed at neurologic onset. From a histopathological point of view, the cases were classified as follows: 9 cases of HIV leucoencephalopathy (HIVL; diffuse myelin damage and rare microglial nodules), 7 cases of HIV encephalitis (HIVE; several microglial nodules and no myelin damage) and 12 cases of mixed HIVL and HIVE (HIVL-E). The groups differed significantly with respect to symptoms and CD4 count at neurologic onset, survival and neurological impairment. Immunohistochemically, the interstitial component (p24-positive cells scattered singly within the white matter) was significantly more prevalent in HIVL, and the micronodular component (p24-positive cells confined within microglial nodules) in HIVE. Neurological damage was worse in cases with a high prevalence of interstitial component or a low prevalence of micronodular component. HIVE, HIVL and HIVL-E are distinct clinical forms of ADC. Neurological impairment is related to white matter damage.     

Plasma Cholecystokinin Levels after Vertical Banded Gastroplasty: Effects of an Acidified Meal

Background: Although cholecystokinin (CCK) is involved in the short-term regulation of satiety, it has not been investigated in obese patients subjected to bariatric restrictive operations. Methods: 8 morbidly obese patients (BMI 49.1 ± 6.9), 7F and 1M, were investigated before and after vertical banded gastroplasty (VBG). 6 healthy lean volunteers served as the control group. CCK was determined (RIA) after an overnight fast and after the administration of an acidified (pH 3) liquid meal. Blood samples were taken 45 min before the meal, 5 min after it and then every 30 min for 3 hours. Results: There were no differences between groups in basal CCK levels. However, the peak of CCK after the meal was significantly higher (P <0.01) in obese patients after VBG (24.9 ± 18 pmol/l) than before VBG (9.8 ± 6.7 pmol/l) and when compared with the control group (8.0 ± 6.3 pmol/l).The time needed to reach the peak was longer in healthy volunteers (105 ± 24.9 min) than in obese patients before VBG (45 ± 40 min) and after VBG (7.5± 12 min) (P<0.01). Conclusions: VBG increases the peak of CCK secretion and shortens the time to reach it. These changes could contribute to the satiety effects of gastric restrictive operations.     

Effect of aerobic training quantity on the VO2 max of circumpubertal swimmers

Maximal oxygen uptake (VO2 max) was measured in 38 swimmers aged 10-14 years. Thirty of 38 boys participated in this study for at least 2 consecutive years. Group 1 consisted of 23 subjects (48 measures) who trained for 7 h/week while group 2 consisted of 15 subjects (27 measures) who trained for 14 h/week. In group 2, VO2 max normalized to body weight was significantly higher at 14 years of age than at 10, whereas the increase was nonsignificant during this period in group 1. The subjects of group 2 showed a large increase of VO2 max/kg body weight from the age of 13, which corresponded in this study to the age of peak height growth velocity. The differences between the two groups were statistically significant at both 13 (P less than 0.02) and 14 years of age (P less than 0.05). At 13 and 14, the most trained subjects also showed significantly higher (P less than 0.05) values of maximal oxygen pulse/kg body weight (VO2 max/kg/HR max). Maximal heart rate (HR max) was similar in the two groups between 10 and 14 years of age. Therefore, we conclude that an increase in a training program of the aerobic type induces a large increase in VO2 max from the age of peak height growth velocity. This is likely due to an increase in the stroke volume.     

Neuropathology of AIDS dementia. A review after 205 post mortem examinations

109 brains were selected after the exclusion of those affected by space occupying lesions or opportunistic infections. All brains with HIV specificity (nodules with multinucleated cells and, at times, two peculiar kinds of myelin involvement) were atrophic (62%); nevertheless dementia had been mentioned only in the 55% of the corresponding autopsy requests. In agreement with previous studies we conclude that HIV encephalopathy does not always give rise to neurological signs.     

Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6

Fetal loss in animals and humans is frequently associated with inflammatory conditions. D6 is a promiscuous chemokine receptor with decoy function, expressed in lymphatic endothelium, that recognizes and targets to degradation most inflammatory CC chemokines. Here, we report that D6 is expressed in placenta on invading extravillous trophoblasts and on the apical side of syncytiotrophoblast cells, at the very interface between maternal blood and fetus. Exposure of D6-/- pregnant mice to LPS or antiphospholipid autoantibodies results in higher levels of inflammatory CC chemokines and increased leukocyte infiltrate in placenta, causing an increased rate of fetal loss, which is prevented by blocking inflammatory chemokines. Thus, the promiscuous decoy receptor for inflammatory CC chemokines D6 plays a nonredundant role in the protection against fetal loss caused by systemic inflammation and antiphospholipid antibodies.