The Blood Plasma Ascorbic Acid in Patients With Achlorhydria (Pernicious and Iron Deficiency Anemia)

Alt, Howard L.; Chinn, Herman I.; Farmer, Chester J.

doi:10.1097/00000441-193902000-00010

Cited by 17 publications

(11 citation statements)

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“…A possible explanation of this finding is that after vagotomy and pyloroplasty there is a relative malabsorption of ascorbic acid. The absorption of ascorbic acid is impaired by achlorhydria (Alt, Chinn, and Farmer, 1939), so it may be that the therapeutic hypochlorhydria achieved by complete vagotomy is responsible for the failure of a normal diet to correct completely the abnormal leucocyte ascorbic acid levels found in patients with duodenal ulcer.…”

Section: Discussionmentioning

confidence: 99%

Ascorbic acid nutrition in gastroduodenal disorders.

Cohen¹,

Duncan²

1967

BMJ

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Section: Discussionmentioning

confidence: 99%

Ascorbic acid nutrition in gastroduodenal disorders.

Cohen¹,

Duncan²

1967

BMJ

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“…The following year Alt et al compared the plasma ascorbic acid levels among 44 patients with achlorhydria associated with iron deficiency anemia or pernicious anemia with controls [34]. They stratified the results by the amount of ascorbic acid in their diets.…”

Section: Destruction Of Ascorbic Acid In the Gi Tractmentioning

confidence: 99%

“…The pernicious anemia group who had inadequate dietary ascorbic acid had plasma levels of 0.47 mg/dL compared to 0.64 mg/dL for controls. They also evaluated the effect of pH on ascorbic acid stability in vitro and incubation for 3 hours at pH 7.95 resulted in destruction of 65% of the ascorbic acid vs. only 14% at pH 1.45 [34]. More recent studies have suggested a similar method for destruction of ascorbic acid related to hypochlorhydria induced by potent acid suppression [29;35].…”

Section: Destruction Of Ascorbic Acid In the Gi Tractmentioning

confidence: 99%

Vitamin C, Gastritis, and Gastric Disease: A Historical Review and Update

Aditi

Graham

2012

Dig Dis Sci

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The discovery of Helicobacter pylori as the cause of gastritis and peptic ulcers ushered in the modern era of research into gastritis and into acid-peptic diseases and rekindled interest in the role of ascorbic acid in the pathophysiology and treatment of gastritis and peptic ulcer disease. Here, we review historic and modern studies on ascorbic acid and gastric diseases with an emphasis on H. pylori gastritis and its sequelae. The relationship of ascorbic acid and gastritis and peptic ulcer and its complications was extensively studied during the 1930’s through the 1950’s. Much of this extensive literature has been effectively “lost”. Ascorbic acid deficiency was associated with all forms of gastritis (e.g., autoimmune, chemical, and infectious) due in varying degrees to insufficient intake, increased metabolic requirements, and destruction within the GI tract. Importantly, gastritis-associated abnormalities in gastric ascorbic acid metabolism are reversed by H. pylori eradication and potentially worsened by proton pump inhibitor (PPI) therapy. Diets rich in naturally occuring ascorbic acid are associated with protection of the gastric corpus from atrophy and a reduction in the incidence of gastric cancer possibly through the ability of ascorbic acid to reduce oxidative damage to the gastric mucosa by scavenging carcinogenic N-nitroso compounds and free radicals and attenuating the H. pylori-induced inflammatory cascade. Ascorbic acid supplementation was possibly associated with a decreased incidence of bleeding from peptic ulcer disease. Pharmacologic doses of ascorbic acid also may improve the effectiveness of H. pylori eradication therapy. Occasionally, looking back can help plot the way forward.

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“…Achlorhydria may interfere with the absorption of ascorbic acid (Alt et al, 1939) and of thiamin (Melnick et al, 1941). In unexplained malnutrition, especially in patients over 40, achlorhydria should always be suspected.…”

Section: Interference With Ingestionmentioning

confidence: 99%

“…Alt et al (1939) have shown 65% destruction jf ascorbic acid in three hours at a pH of 7.95, and Melnick et al (1941) found that thiamin is stable in acid gastric juice (pH 1.5 to 8) during an incubation of 16 hours, but if antacids were added thiamin was completely destroyed. Bile and pancreatic juice also destroyed a considerable part of thiamin.…”

Section: Increased Destructionmentioning

confidence: 99%

Early Vitamin-deficiency States

Leitner¹

1948

BMJ

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The Blood Plasma Ascorbic Acid in Patients With Achlorhydria (Pernicious and Iron Deficiency Anemia)

Cited by 17 publications

References 0 publications

Ascorbic acid nutrition in gastroduodenal disorders.

Ascorbic acid nutrition in gastroduodenal disorders.

Vitamin C, Gastritis, and Gastric Disease: A Historical Review and Update

Early Vitamin-deficiency States

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