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)
• gastric acid is important in carnivores¹⁾²⁾ in particular as it:
  • helps kill microbes in foods and prevent colonization of the intestines by these pathogens (particularly important in animals who are obligate scavengers but also in most carnivores)
    • will not kill microbes with adaptations to survive gastric acid include resistant cell walls, spore-forming capabilities or other traits that confer tolerance to high acidities and rapid changes in pH conditions
    • high gastric acid in humans also increases the difficulty of recolonization by beneficial microbes
    • in contrast, herbivores need more gut microbes to digest plant material such as cellulose and lignin
  • secretion of pepsinogen and its activation to pepsis in the stomach is modulated by an acid pH (2–4) and pepsin is needed to digest meat proteins
• humans, uniquely among the primates, appear to have stomach pH of 1.5 more akin to those of carrion feeders than to those of most carnivores and omnivores, presumably as early humans relied upon raw fermenting meats for survival and there are a high number of faecal-oral pathogens that can infect and kill humans ³⁾
  • premature infants have less acidic stomachs (pH > 4) and are more susceptible to enteric infections
  • the elderly show relatively low stomach acidity with one study showing 80% had pH > 6.6 and are also more prone to stomach and gut infections
  • in gastric bypass weight loss surgery, ~60% of teh stomach is removed and results in gastric pH levels that range from 5.7 to 6.8

• 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)
• reduced activity of pepsin
  • pepsin is responsible for roughly 10–15% of total protein hydrolysis, and needs an acidic environment to be created from pepsinogen and needs an acidic environment to hydrolyse proteins into amino acids
  • pepsin’s proteolytic activity, along with acid, helps limit survival of some ingested microbes
• 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)