In autoimmune gastritis , the immune system attacks the parietal cells leading to hypochlorhydria (low stomach acid secretion). This results in an elevated gastrin level in an attempt to compensate for increased pH in the stomach. Eventually, all the parietal cells are lost and achlorhydria results leading to a loss of negative feedback on gastrin secretion. Plasma gastrin concentration is elevated in virtually all individuals with mucolipidosis type IV (mean 1507 pg/mL; range 400-4100 pg/mL) (normal 0-200 pg/mL) secondary to a constitutive achlorhydria. This finding facilitates the diagnosis of patients with this neurogenetic disorder.  Additionally, elevated gastrin levels may be present in chronic gastritis resulting from H pylori infection. 
As its name implies, the main effect of thyrotropin-releasing hormone is to stimulate the release of thyrotropin (also known as thyroid stimulating hormone) from the pituitary gland. Thyrotropin-releasing hormone is the master regulator of thyroid gland growth and function (including the secretion of the thyroid hormones thyroxine and triiodothyronine ). These hormones control the body’s metabolic rate , heat generation, neuromuscular function and heart rate, among other things. If there is insufficient thyroid hormone available for the brain, this will be detected by the hypothalamus and thyrotropin-releasing hormone will be released into the blood supplying the pituitary gland. The effect of thyrotropin-releasing hormone on the pituitary gland is to trigger thyroid stimulating hormone release, which stimulates the thyroid gland to make more thyroid hormone. In summary, thyrotropin-releasing hormone is really the brain’s first messenger signal in the many actions controlling thyroid hormone secretions.