gastric hypochlorhydria / achlorhydria

see also:

• Helicobacter pylori infection
• proton pump inhibitors (PPIs)
• atrophic_gastritis
• hyperchlorhydria

• hypochlorhydria is a reduction in the ability of the parietal cells of the stomach to secrete hydrochloric acid which is a critical component of gastro-intestinal function
• in humans, the normal gastric pH is around 1 to 3, which varies throughout the day.
  • the highest basal secretion levels are in the late evening (around midnight to 3am)

• uncommon before 50yrs age (2-5%) and increases markedly with each decade after
• said to be present in 2.5% of those aged under 60yrs and in 5% of those over 60yrs, increasing to 12% of those over 80yrs
• HOWEVER, this is dependent upon how it is defined and what population is being studied, the prevalence of long term prescribing of proton pump inhibitors (PPIs) and of Helicobacter pylori infection

• proton pump inhibitors (PPIs), antacids, H2-type antihistamines
• Helicobacter pylori infection
  • infection can cause hypochlorhydria which can persist > 8months after infection & can remain chronically leading to atrophic_gastritis
• atrophic_gastritis
  • Helicobacter pylori infection
  • auto-immune gastritis (Pernicious anaemia)
• partial gastrectomy
  • gastric sleeve surgery
• gastric bypass procedures
• hypothyroidism
• stomach cancer
• deficiency of chloride, sodium, potassium, zinc, and/or iodine, as these elements are needed to produce adequate levels of stomach acid (HCl)
• other much less common causes

• small intestinal bacterial overgrowth (SIBO)
  • elevation of serum folate is suggestive of small bowel bacterial overgrowth as bacterial folate can be absorbed into the circulation
  • a hydrogen breath test can check for bacterial overgrowth
• intestinal metaplasia
• iron deficiency anaemia
  • acidic pH facilitates iron absorption
• vitamin B12 (cobalamin) deficiency due to:
  • GIT bacterial overgrowth
  • stomach acid is required to chemically detach vitamin B12 from the food proteins you eat, without enough acid, the B12 remains locked in the food and cannot be processed.
  • concurrent loss of intrinsic factor
• nutritional deficiencies through decreased absorption of basic electrolytes (magnesium, zinc, etc.) and vitamins (including vitamin C, vitamin K, and the B complex of vitamins)
• higher risk of certain pathogens causing disease as stomach acid normally would kill them
  • Vibrio vulnificus (commonly from seafood)
  • cholera
  • Salmonella
  • Salmonella typhi (typhoid enteric fever)
  • some parasites
• risk of development of gastric adenocarcinoma or gastric carcinoid tumor

• a consistently high gastric pH (>3.5), i.e. functionally achlorhydric/hypochlorhydric in the basal state
• “failure to acidify after maximal stimulation (pentagastrin/histamine)”
• endoscopic Congo red (no color change = no acid)
• 24hr oesophageal pH monitoring study
• Heidelberg test - swallow electronic device which measures pH
• non‑invasive quininium resin test to infer gastric acidity
• extremely low levels of pepsinogen A (PgA) (< 17 µg/L) in blood serum
• high serum gastrin levels (> 500–1000 pg/mL)