Zmiany w błonie śluzowej żołądka u dorosłych chorych na celiakię

Wstęp: Celiakia jest przewlekłą chorobą zapalną przewodu pokarmowego o podłożu autoimmunologicznym, występującą u osób predysponowanych genetycznie. Znaczenie zmian patologicznych w błonie śluzowej żołądka u chorych na celiakię i ich wpływ na przebieg kliniczny tej choroby nie zostały dotąd w pełni poznane. Cel: Ocena częstości występowania zmian histopatologicznych w błonie śluzowej żołądka u dorosłych osób z celiakią oraz wpływu tych zmian na obraz kliniczny choroby. Materiał i metody: Do badań włączono 90 pacjentów, w tym 35 chorych na celiakię i 55 osób z objawami dyspeptycznymi (grupa kontrolna). Obejmowały one wywiad chorobowy, badanie przedmiotowe, badania krwi oraz panendoskopię. Wycinki z błony śluzowej żołądka i części pozaopuszkowej dwunastnicy barwiono hematoksyliną i eozyną. Oceniano nasilenie zmian zapalnych oraz liczbę limfocytów śródnabłonkowych (intraepithelial lymphocytes - IEL). Za pomocą badania immunohistochemicznego z zastosowaniem przeciwciał monoklonalnych anty-CD3+ identyfikowano limfocyty CD3+. Ocenę bioptatów z dwunastnicy w kierunku celiakii wykonano zgodnie z klasyfikacją Marsha. Wyniki: U chorych na celiakię, zarówno nieleczonych, jak i leczonych dietą bezglutenową, obserwowano wzrost IEL, jednak ich liczba była znamiennie większa u chorych niestosujących diety bezglutenowej. Limfocytarne zapalenie żołądka rozpoznano u 8,6% chorych na celiakię. Osoby te podawały nasilone dolegliwości dyspeptyczne. W badaniu immunohistochemicznym wykazano obecność nacieków limfocytów T CD3+ zarówno w bioptatach błony śluzowej żołądka, jak i części pozaopuszkowej dwunastnicy.Introduction: Coeliac disease is a chronic inflammatory disorder of the gastrointestinal tract, of autoimmune etiology, in genetically predisposed persons. The role of the gastric lesions and their influence on the clinical course of that disease have not been explained. Aim: To evaluate the frequency of morphological lesions in the gastric mucosa in adults with coeliac disease and their effect on the clinical picture of gluten enteropathy. Material and methods: Ninety patients, including 35 patients with coeliac disease and 55 with dyspeptic symptoms (control group) were examined. Clinical studies comprised history of disease, physical examination, blood tests and gastroscopies. Biopsies from the gastric and distal part of the duodenal mucosa were stained with haematoxylin-eosin, for estimation of the intensity of mucosal changes and a count of the intraepithelial lymphocytes (IEL). Immunohistochemical studies with anti-CD3 antibodies were performed for the identification of CD3+ lymphocytes. Results: An increased number of IEL was observed in coeliac patients treated as well as not treated with gluten, compared with the control group. Lymphocytic gastritis (LG) was observed in 8.6% of coeliac patients. Patients with coeliac disease and LG presented intense dyspeptic symptoms. Presence of CD3+ T lymphocytes was revealed in the gastric and duodenal mucosa with immunohistochemical staining. Conclusions: Morphological lesions in the gastric mucosa belong to gastroenteropathy in the course of coeliac disease and may induce dyspeptic symptoms. Taking biopsies from the distal part of the duodenum in patients with dyspeptic symptoms should be considered

Alterations in serum levels of selected markers of oxidative imbalance in adult celiac patients with extraintestinal manifestations : pilot study

Oxidative stress is considered to be one of the mechanisms responsible for gluten toxicity, but its role in celiac disease (CD) remains unclear. The aim of the study was to evaluate oxidative imbalance in the pathomechanism of CD by determining the concentrations of nitric oxide (NO) and selected antioxidant parameters. The study involved 197 adult patients: 53 patients with untreated active CD, 92 celiac patients on gluten‑free diet (GFD), and 52 controls. The serum levels of antioxidants (uric acid, bilirubin, ferritin, albumin), celiac antibodies, NO, glutathione peroxidase 3 (GPx3), and vitamin E were measured. A histopathological study of duodenal biopsy was performed. Celiac patients had higher uric acid concentrations than controls (P <0.001). NO levels were higher in patients with active CD than in controls (P <0.01) and were correlated with the degree of mucosal damage ($r^{2}$ = 0.04; P = 0.01). Vitamin E levels were decreased in celiac patients (P <0.01), and GPx3 activity was reduced in patients with active CD compared with controls (P <0.001)

Effect of long-term proton pump inhibitor therapy on complete blood count parameters and selected trace elements : a pilot study

Introduction: Proton pump inhibitors (PPIs) are widely prescribed for several gastrointestinal conditions, often as long-term therapy. The effects of long-term PPI use have not been fully elucidated. Objectives: We aimed to determine the association between long-term PPI use and complete blood count parameters, particularly red blood cell (RBC) count, white blood cell (WBC) count, and hemoglobin concentrations, as well as serum levels of selected micronutrients such as selenium (Se), iron (Fe), copper (Cu), and zinc (Zn). Patients and methods: We enrolled 37 patients on long-term PPI therapy (mean [SD] age, 57.1 [15.4] years) and 30 healthy controls (mean [SD] age, 39.3 [11.8] years). In each group, complete blood count, and serum Fe levels were performed, and serum Cu, Zn, and Se levels were measured using atomic absorption spectrometry. Results: Red blood cell and WBC counts were lower in the PPI group compared with controls (mean [SD], 4.24 [0.55]×106/μl vs 4.7 [0.4]×106/μl; P <0.001 and 6.13 [1.44]×103/μl vs 7.3 [1.28]×103/μl; P <0.001, respectively). Hemoglobin and serum Fe concentrations were also lower in the PPI group (mean [SD], 12.5 [1.8] g/dl vs 14.3 [0.8] g/dl; P <0.001 and 16.3 [5.4] μmol/l vs 23.4 [2.7] μmol/l; P <0.001, respectively). Serum Zn and Cu concentrations were higher in PPI users than in controls. Conclusions: Long-term PPI therapy may reduce RBC and WBC counts as well as hemoglobin levels, leading to iron deficiency. It may also affect concentrations of some micronutrients, although the underlying mechanism of this association is not fully clear

Postprandial effect of gastrointestinal hormones and gastric activity in patients with irritable bowel syndrome

Abstract Altered gut regulation, including motor and secretory mechanisms, is characteristic of irritable bowel syndrome (IBS). The severity of postprandial symptoms in IBS patients is associated with discomfort and pain; gas-related symptoms such as bloating and abdominal distension; and abnormal colonic motility. The aim of this study was to assess the postprandial response, i.e., gut peptide secretion and gastric myoelectric activity, in patients with constipation-predominant IBS. The study was conducted on 42 IBS patients (14 males, 28 females, mean age 45.1 ± 15.3 years) and 42 healthy participants (16 males, 26 females, mean age 41.1 ± 8.7 years). The study assessed plasma gut peptide levels (gastrin, CCK—Cholecystokinin, VIP—Vasoactive Intestinal Peptide, ghrelin, insulin) and gastric myoelectric activity obtained from electrogastrography (EGG) in the preprandial and postprandial period (meal–oral nutritional supplement 300 kcal/300 ml). Mean preprandial gastrin and insulin levels were significantly elevated in IBS patients compared to the control group (gastrin: 72.27 ± 26.89 vs. 12.27 ± 4.91 pg/ml; p < 0.00001 and insulin: 15.31 ± 12.92 vs. 8.04 ± 3.21 IU/ml; p = 0.0001), while VIP and ghrelin levels were decreased in IBS patients (VIP: 6.69 ± 4.68 vs. 27.26 ± 21.51 ng/ml; p = 0.0001 and ghrelin: 176.01 ± 88.47 vs. 250.24 ± 84.55 pg/ml; p < 0.0001). A nonsignificant change in the CCK level was observed. IBS patients showed significant changes in postprandial hormone levels compared to the preprandial state—specifically, there were increases in gastrin (p = 0.000), CCK (p < 0.0001), VIP (p < 0.0001), ghrelin (p = 0.000) and insulin (p < 0.0001). Patients with IBS showed reduced preprandial and postprandial normogastria (59.8 ± 22.0 vs. 66.3 ± 20.2%) compared to control values (83.19 ± 16.7%; p < 0.0001 vs. 86.1 ± 9.4%; p < 0.0001). In response to the meal, we did not observe an increase in the percentage of normogastria or the average percentage slow-wave coupling (APSWC) in IBS patients. The postprandial to preprandial power ratio (PR) indicates alterations in gastric contractions; in controls, PR = 2.7, whereas in IBS patients, PR = 1.7, which was significantly lower (p = 0.00009). This ratio reflects a decrease in gastric contractility. Disturbances in the postprandial concentration of gut peptides (gastrin, insulin and ghrelin) in plasma may contribute to abnormal gastric function and consequently intestinal motility, which are manifested in the intensification of clinical symptoms, such as visceral hypersensitivity or irregular bowel movements in IBS patients