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Long-term use of antacids (AA) and acid-control (AC) medicines as a risk factor for various adverse manifestations

Long-term use of antacids (AA) and acid-control (AC) medicines as a risk factor for various adverse manifestations

Editor: Dr. Praful B. Godkar (Ph.D)
Eminent Author, Medical Biochemist and Scientist, Technical Education consultant.
AGD Biomedicals (Pvt) LTD. Andheri East, Mumbai.

AA and AC medicines are among the highest sold medicines in India. The use of long-term antacids (AA) and acid-control (AC) therapy could be avoided; if primary cause of hyperacidity related to microbial infection is diagnosed by fourth and fifth generation IVD laboratory tests(1) and treated appropriately (Refer Case study). Helicobacter pylori (HP) infection is responsible for a large number of hyperacidity and gastritis cases(4,5). Antibiotic therapy and regular use of probiotics could be useful to treat HP infection and prevent long-term use of AA and AC medicines(6,7).

A considerable data regarding the long-term use of AA and AC medicines and associated risk factors are documented(2,3). Hyperacidity caused by various other factors could be treated satisfactorily by controlling related various factors such as anxiety, smoking, excessive alcohol intake, specific medicines, deprivation of sleep, very spicy foods and irregular food habits(4). Adverse drug events are an increasingly relevant issue for healthcare systems(8). These are associated with poorer health outcomes and avoidable misuse of medicines. Various studies suggest the economic impact of undesired medicinal effects, which are substantial and could be avoided(8).

Q1. What are antacids (AA) and acid control (AC) medicines?

ANS: Antacids (AA) are a combination of various salts of magnesium, aluminium and calcium. These salts neutralize excess hydrochloric acid produced in the stomach and provide symptomatic relief from hyperacidity. Acid-control (AC) medicines are H2 blockers (histamine H2-receptor antagonists) and proton-pump inhibitors. These medicines decrease quantity of acid secreted by the stomach. H2 blockers bind to acid producing stomach cells and prevent histamine binding to the cells. Histamine is strong activator of gastric acid, released by the action of gastrin hormone. Gastrin is released, when food enters stomach. Proton-inhibitors bind to hydrogen-potassium ATP pump, responsible to produce hydrochloric acid, and prevent excess acid secretion by the parietal cells of the stomach.

Q2. What are the effects of long-term use of AA and AC medicines?

ANS: The long-term use of AA and AC medicines can lead to increase in gastric pH (more towards alkaline side), hypochlorhydria (low acid content in the stomach) and in some cases to achlorhydria (complete absence of acid in the stomach). Low hydrochloric acid content in the gastric secretions leads to deficiencies of vitamin C, vitamin B12, iron, calcium and magnesium. The long-term acid suppression by antacids also can lead to increased risk to intestinal (enteric), respiratory and urinary tract infections.
 
Note
 
(1) Normal fasting stomach content (gastric content) pH is 1.5-2.5 and following food it increases according to the pH of food and fluid contents.
 
(2) Normal gastric pH is necessary to activate pepsin enzyme, which acts on proteins to initiate protein digestion.
 
(3) Normal gastric pH is necessary for the absorption of vitamin C and B12 in the gastrointestinal tract and also minerals such as iron, calcium and magnesium.
 
(4) Normal gastric pH inhibits bacterial growth in the stomach.
 
(5) Long-term decrease in hydrochloric acid and increase in gastric pH may lead to bacterial infections, which may affect small intestine, liver and kidneys.

CASE STUDY

A 31-year-old female reported with symptoms of gastritis: Malaise, loss of appetite, loss of weight, arthralgia, hyperacidity and pain in the stomach.  She was treated with combination of antacids (AA) and acid-control(AC) drugs for a prolonged period. She suffered from continuous pain in the bones and joints. The following laboratory tests were advised: Complete hemogram, routine urine and feces examination. Significant findings of the laboratory report were as follows:
PARAMETER VALUE REFERENCE RANGE (NORMAL RANGE)
Blood hemoglobin 9.5 g/dl 12-16 g/dl
Feces occult blood Present, + Feces occult blood absent
The following additional tests were advised, since she suffered from long-term hyperacidity and gastritis:
(1) Serum IgG antibodies to Helicobacter pyrori: IgG antibodies to Helicobacter pyrori: Present
(2) Examination of Mucosa collected from the antrum part of the stomach for smear and culture characters of bacteria.
Microbiology laboratory findings were as follows:
(1) Presence of Gram negative bacteria.
(2) Biochemical reactions: Organism showed positive reactions to urease, catalase and oxidase. Diagnosis: Infection of Helicobacter pyrori
Note:
(1) Contamination of Helicobacter pyrori (HP) is through polluted water and foods. Mode of transmission of HP is by fecal-oral or oro-oral route (dental plaque, saliva)(4).
(2) Around 50 per cent of world’s population harbours HP in the upper gastrointestinal (GI) tract(5), but the prevalence of this infection varies worldwide. It is as low as 10 per cent in developed Western nations to as high as 80 per cent in developing countries including India (4,5). Clinical manifestations occur only in approximately 20 percent cases.
(3) Less interactive strains of H. pylori (such as cag−, s2 vacA, iceA2) colonise in lower numbers and with populations preferentially distributed towards the lumen of the stomach. These populations are also in equilibrium with the host, and with less serious pathophysiological consequences. Hosts may carry both populations simultaneously.
(4) Helicobacter pylori survives in the mucosa of antrum, which is a non-acid secreting region of the stomach. By the action of urease, HP tries to neutralize the gastric hydrochloric acid. Urease enzyme secreted by HP acts on urea to form ammonium carbonate, which neutralizes gastric hydrochloric acid. This leads to increase in the level of gastrin hormone and further increase in acid secretion in the stomach.
(5) Gastric disorders have a negative impact on quality of life and can cause work impairment and higher health-related costs(8). GI disorders may also lead to social withdrawal in some patients due to fear of recurrence of symptoms.

Q3. What is the importance of complete hemogram (CBC) test in the diagnosis of hyperacidity related to Helicobacter pylori infection?

ANS: Complete hemogram gives the following information about hyperacidity leading to gastritis: Low blood hemoglobin level. One of the reason for significantly low blood hemoglobin value indicates loss of blood due to peptic ulcers leading to gastritis.

Q4. What is the importance of POCT dipstick examination of feces in the detection of Helicobacter pylori infection?

ANS: POCT dip-sticks can detect occult blood in feces in one minute, which gives idea about gastro-intestinal bleeding due to gastric and duodenal ulcers caused by hyperacidity.

Q5. What are the latest innovations in IVD clinical laboratory tests that could significantly impact the monitoring and management of gastric function tests?

ANS: Latest Fifth-generation Rapid Immunographic Test (ICT) cards can detect antibodies to specific bacteria in serum in 2-3 minutes at patient bedside(1) (Refer to case study).

Q6. How does timely detection of IVD impact patient outcomes and overall healthcare costs?

ANS: Globally, healthcare expenditure for GI disorders was estimated to be approximately $135.9 billion and that for acid suppressing drugs was found to be $60 billion in the last five years. Timely detection of the cause for gastritis by IVD laboratory tests is useful to cure the patient early and also for prevention of misuse of AA and AC medicines.

References

(1) Godkar PB, Godkar DP. Text book of Medical laboratory technology (4th edition, 2024), Bhlani Publishers, Mumbai. India.

(2) Arun Koyyada. Long-term use of proton pump inhibitors as a risk factor for various adverse manifestations, Pharmacovigilance. GITAM Institute of Pharmacy, GITAM University, Rushikonda, Visakhapatnam, 530045 Andhra Pradesh, India. Received 5 June 2020, Accepted 16 June 2020, Available online 9 July 2020, Version of Record 29 January 2021.

(3) Llorente C, Jepsen P, Inamine T, Wang L, Bluemel S, Wang HJ, Loomba R, Bajaj JS, Schubert ML, Sikaroodi M, Gillevet PM, Xu J, Kisseleva T, Ho SB, DePew J, Du X, Sørensen HT, Vilstrup H, Nelson KE, Brenner DA, Fouts DE, Schnabl B. Gastric acid suppression promotes alcoholic liver disease by inducing overgrowth of intestinal Enterococcus. Nat Commun. 2017 Oct 16;8(1):837. doi: 10.1038/s41467-017-00796-x. PMID: 29038503.

(4) Li Y, Choi H, Leung K, Jiang F, Graham DY, Leung WK (19 April 2023). “Global prevalence of Helicobacter pylori infection between 1980 and 2022: a systematic review and meta-analysis”. The Lancet Gastroenterology & Hepatology. 8 (6): 553–564. doi:10.1016/S2468-1253(23)00070-5. PMID 37086739. S2CID 258272798.

(5) Hooi JK, Lai WY, Ng WK, Suen MM, Underwood FE, Tanyingoh D, et al. (August 2017). “Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis”. Gastroenterology. 153 (2): 420–429. doi:10.1053/j.gastro.2017.04.022. PMID 28456631.

(6) Koga Y (December 2022). “Microbiota in the stomach and application of probiotics to gastroduodenal diseases”. World J Gastroenterol. 28 (47): 6702–6715. doi:10.3748/wjg.v28.i47.6702. PMC 9813937. PMID 36620346.

(7) Ruggiero P (November 2014). “Use of probiotics in the fight against Helicobacter pylori”. World J Gastrointest Pathophysiol. 5 (4): 384–91. doi:10.4291/wjgp.v5.i4.384. PMC 4231502. PMID 25400981.

(8) Carlos Chiatti, Silvia Bustacchini, Gianluca Furneri, Lorenzo Mantovani, Marco Cristiani, Clementina Misuraca, Fabrizia Lattanzio. The economic burden of inappropriate drug prescribing, lack of adherence and compliance, adverse drug events in older people: a systematic review. Drug Saf, 2012 Jan:35 Suppl 1:73-87. doi: 10.1007/BF03319105.

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