What is Hypergastrinemia?
Hypergastrinemia refers to an elevated level of the hormone
gastrin in the blood. Gastrin is primarily produced by G-cells in the antrum of the stomach and stimulates the secretion of gastric acid by the parietal cells. Elevated levels of gastrin can lead to various gastrointestinal disorders.
Histological Features of Hypergastrinemia
In the context of histology, hypergastrinemia can lead to several changes in the
gastrointestinal tract. The most notable changes occur in the stomach and include hyperplasia of the parietal cells, an increase in the number of ECL (enterochromaffin-like) cells, and hypertrophy of the gastric mucosa.
Role of Parietal Cells
Parietal cells are responsible for the secretion of hydrochloric acid (HCl) in the stomach. Hypergastrinemia often results in the hyperplasia of these cells, meaning there is an increased number of parietal cells. This can be observed histologically as an increase in the thickness of the gastric mucosa, particularly in the fundus and body of the stomach.Enterochromaffin-like (ECL) Cells
Hypergastrinemia also stimulates the proliferation of ECL cells, which are found in the gastric mucosa. ECL cells secrete histamine, which in turn stimulates parietal cells to produce more acid. Histologically, an increased number of ECL cells can be observed, and in some cases, this can lead to the formation of
neuroendocrine tumors or ECL-cell hyperplasia.
Hypertrophy of Gastric Mucosa
Another histological feature associated with hypergastrinemia is the hypertrophy of the gastric mucosa. This means that the mucosal layer of the stomach becomes thicker due to the increased cellular activity and proliferation. This thickening can be observed in histological sections stained with hematoxylin and eosin (H&E).Causes of Hypergastrinemia
Several conditions can lead to hypergastrinemia. The most common include
Zollinger-Ellison Syndrome, chronic atrophic gastritis, and prolonged use of proton pump inhibitors (PPIs). Each of these conditions has distinct histological features that can be observed under a microscope.
Zollinger-Ellison Syndrome
Zollinger-Ellison Syndrome is caused by gastrin-secreting tumors called gastrinomas, usually located in the pancreas or duodenum. In this condition, histological examination often reveals hyperplasia of parietal cells and an increased number of ECL cells. The presence of
gastrinomas can also be confirmed through histological staining techniques.
Chronic Atrophic Gastritis
Chronic atrophic gastritis is characterized by the loss of gastric glandular cells, leading to reduced acid secretion and compensatory hypergastrinemia. Histologically, this condition presents as a thinning of the gastric mucosa, loss of parietal cells, and infiltration of inflammatory cells. The remaining G-cells may appear hyperplastic as they compensate for the loss of other cells.Proton Pump Inhibitors (PPIs)
Prolonged use of PPIs can lead to hypergastrinemia due to the feedback mechanism that increases gastrin production to compensate for reduced acid secretion. Histologically, this condition may show mild hyperplasia of G-cells and parietal cells. The gastric mucosa may also appear slightly thickened.Diagnostic Approaches
Diagnosing hypergastrinemia involves a combination of clinical, biochemical, and histological approaches. Biochemical tests measure serum gastrin levels, while histological examination of gastric biopsies can reveal changes in the gastric mucosa, parietal cells, and ECL cells. Special staining techniques, such as immunohistochemistry, can help identify specific cell types and their proliferation status.Treatment and Prognosis
Treatment of hypergastrinemia depends on the underlying cause. For instance, gastrinomas in Zollinger-Ellison Syndrome may require surgical removal, while chronic atrophic gastritis might be managed with vitamin B12 supplementation and eradication of H. pylori infection. Monitoring and reducing PPI usage can help manage drug-induced hypergastrinemia. The prognosis varies based on the underlying condition and the effectiveness of the treatment.
