Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

Czaja, Mariusz; Szarszewski, Adam; Kamińska, Barbara; Bogotko-Szarszewska, Marta; Łuczak, Grazyna; Kozielska, E; Delińska-Galińska, Anna; Korzon, Maria

doi:10.1111/j.1742-1241.2007.01311.x

Cited by 6 publications

(10 citation statements)

References 23 publications

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“…found that the mean fasting serum gastrin level was higher in children with H. pylori ‐associated gastritis compared to H. pylori ‐negative cases, with or without gastritis. In contrast to earlier studies suggesting that a decrease in the number of somatostatin‐producing D cells with an unchanged number of gastrin‐producing G cells may lead to PUD, these authors found no difference in G‐cell density and D‐cell density, regardless of the presence or absence of gastritis or H. pylori infection [7].…”

Section: Pathogenesiscontrasting

confidence: 88%

Helicobacter pylori Infection in Pediatrics

Kindermann

Lopes

2009

Helicobacter

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his review summarizes the articles published on Helicobacter pylori infection in children between April 2008 and March 2009. Recent evidence highlights the decreasing prevalence trend of H. pylori infection and supports both intrafamilial and extrafamilial transmission. The association with various symptoms is still being debated. Interestingly, H. pylori infection seems inversely associated with allergic diseases. Monoclonal stool antigen tests are widely used and accurate for the diagnosis of H. pylori infection, but less accurate in young children. The new biprobe real-time PCR assay applied to stools showed a poor sensitivity in children. Using the urea hydrolysis rate next to the delta over baseline values, the (13)C-urea breath test provides excellent results for all age children, even for young children. Treatment of H. pylori infection remains a challenge, considering suboptimal efficacy of current therapy. Among emerging alternatives, sequential treatment appears promising. The adjunction of probiotics to conventional regimens, although eliciting great interest, has shown limited therapeutic benefit.

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Section: Pathogenesiscontrasting

confidence: 88%

Helicobacter pylori Infection in Pediatrics

Kindermann

Lopes

2009

Helicobacter

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“…It is also speculated that a decrease in somatostatin secretion, one of the factors inhibiting acid secretion, is the main cause of hyperacidity in H. pylori infection. A comparison of the G/D cell ratio between our study and that by Czaja et al [4] showed no increase in G cells but a decrease in D cells resulting in a high G/D ratio in our patient. Thus, a decrease in somatostatin secretion due to a reduction in D cell population might have induced hypergastrinemia in this case.…”

Section: Discussionsupporting

confidence: 61%

“…The specimen from the control patient showed 76 G cells, 62 D cells, and a G/D cell ratio of 1.22. In the Czaja report, the mean G cell count was 79, D cell count 45, and G/D cell ratio 1.79 in the normal controls [4]. The immunostaining study showed that the D cell count in this patient was lower than in controls, resulting in an increased G/D ratio.…”

Section: Case Reportmentioning

confidence: 78%

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A Five-Year-Old Boy with Marked Hypergastrinemia Associated with H. pylori Infection

Nakata

Tajiri

Etani

et al. 2010

Case Rep Gastroenterol

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A 5-year-old boy was referred to our department for persistent epigastric discomfort. Serum gastrin level was 635 pg/ml with a pepsinogen (PG) I level of 102.7 ng/ml and a PG I/II ratio of 23.2, indicating a hyperacidic state. Upper gastrointestinal endoscopy showed normal gastric mucosal folds and no abnormalities including no gastric mucosal atrophy. To investigate the cause of hypergastrinemia, a Ca injection test was performed and the patient showed no definitive response to a large load of Ca. Contrast-enhanced dynamic CT revealed no space-occupying lesions. The results from these two studies were not consistent with the presence of gastrinoma. A urea breath test showed 2.8‰, and a test for the fecal H. pylori antigen was positive. Since H. pylori infection was considered to be a possible cause of hypergastrinemia, eradication therapy was introduced. The therapy was shown to be successful by using a repeated urea breath test that showed a normalization to 0.6‰. 7 months after the therapy blood examination showed a gastrin level of 191 pg/ml, a PG I level of 36.7 ng/ml, and a PG I/II ratio of 7.3. An immunostaining study of the gastric mucosa suggested that a decrease in somatostatin secretion due to a reduction in D cell population might have induced hypergastrinemia in this case. In children with H. pylori infection showing marked hypergastrinemia, immunohistochemical examination and therapeutic diagnosis by eradication may be helpful in the differential diagnosis of gastrinoma.

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“…The details are presented in table 1. Also the changes in the number of D and G cells in atrophic gastritis were observed and several studies presented the therapy promoting the secretion of gastric acid and gastric pepsin and regulating the neuroendocrine mechanism in rats (Zhu et al, 2008;Wang et al, 2009;Czaja et al, 2008;Todorovic et al, 2008). However, as it was reported (Czaja et al, 2008), changes of serum gastrin concentration in gastric antrum in children with chronic gastritis are not statistically significantly connected with D and G cell densities.…”

Section: Diagnostic Influence Of Neuroendocrine Cell Morphometrymentioning

confidence: 51%