MediUnite Journal Monthly Magasine "Vital" - March 2024
MediUnite Journal Monthly Magasine "Vital" - March 2024
MediUnite Journal Monthly Magasine "Vital" - March 2024
MEDICAL
AWARENESS, HOW
WE’RE CHANGING
GLOBAL WELLBEING
Pg 2. Alzheimer's Brain Changes,
Read the article on Pathophysiology
for Alzheimer's disease
Pg 4. Nerve Cell Vulnerability?
Read the article on RSV’s Impact
Pg 5. What’s the Rationale? Read
the article on PPIs in H. pylori
treatment
Pg 7. Feed Your Gut, Feed Your
Mind, Read the article on gut health
Pg 8. What is the battle against
antibiotics? Read the article on
antiobiotic immunity
Pg 9. Radiant Skin or Dire
Consequences? Read the article on
Retinol’s Dermatological Useage
Pg 11. Should We Be Worried?
Read the article on pharmaceuticals
research points to NFTs and AB as the two 1. Perspective chapter: Alzheimer - A complex genetic
key pathological players in the development background. (2021, December 28). IntechOpen - Open Science
Open Minds | IntechOpen.
of AD by impairing neuron function and https://www.intechopen.com/chapters/79831
2. Real-time imaging of mitochondrial redox reveals increased
synapses which cause extensive cell death. mitochondrial oxidative stress associated with amyloid β
With enough neuronal death, the cortex aggregates in vivo in a mouse model of Alzheimer’s disease.
(2024, January 18). BioMed Central.
starts to atrophy which leads to impairments 3. PubMed. (n.d.). Imaging beta amyloid aggregation and iron
in functions the atrophic area is involved in. accumulation in Alzheimer's disease using quantitative
susceptibility mapping MRI.
https://pubmed.ncbi.nlm.nih.gov/30739060/
Current research is focused on discovering 4. https://molecularneurodegeneration.biomedcentral.com/article
s/10.1186/s13024-024-00702-2
the mechanisms that link NFTs and AB with 5. Wang, Y. (2016). Tau in physiology and pathology. PubMed.
OS and necrosis in the brain. https://pubmed.ncbi.nlm.nih.gov/26631930/
PPIs tend to have a direct and in‐direct effect on H. pylori eradication (2‐4).
Direct effects:
1. PPIs have a weak antibacterial effect. Acid converted metabolites of PPIs have been shown to
have a more potent antibacterial effect than parent PPIs.
2. They also bind and deactivate the urease and ATPase enzymes of H. pylori, which are important
for its survival. It has been doubtful that these direct effects alone are responsible for the significant
increase in eradication rates, as it has been shown in the GU‐ MACH2 study that omeprazole alone
had an eradication rate of 4% only. Therefore, it has been suggested that PPIs contribution to a higher
eradication rate comes from its synergistic or in‐direct effects to Amoxicillin + Clarithromycin OR
Metronidazole + Clarithromycin.
Indirect effects:
1. PPIs inhibit acid secretion and increases intragastric pH levels. Several papers have showed that
the minimum inhibitor concentration (MIC) of these antibiotics is pH dependent. Amoxicillin and
Clarithromycin antibacterial activity against H. pylori is increased by 8 and 20 times, respectively after
PPI administration. However, metronidazole’s activity is no pH dependent.
2. As a result of acid inhibition, antibiotics concentration within the stomach is increased
providing a stronger action.
3. H. Pylori replicates/grows at neutral pH of 6‐7, and it turns into the coccoid form that is
resistant to antibiotics. The coccoid form is non‐replicative and non‐growing (6). Therefore, it is
important to maintain a neutral pH to allow the bacteria to turn back into its replicative form, a
form that is resistant to antibiotics, unlike the resistant coccoid form.
As stated earlier, it is very important to have a neutral or high pH levels as soon as possible to
synergize the antibiotics effect. The time that a PPI require to inhibit acid secretion is critical to a
successful therapy. The usual duration for an eradication therapy is 7 days. If acid suppression is
achieved within 3 days of taking PPI, then the actual effective duration of the antibiotics is only 4
days. Saitoh and colleagues conducted research that examined the time (in days) needed to inhibit
acid secretion by omeprazole, lansoprazole and rabeprazole. As shown in (figure 2), Rabeprazole
acid suppression is achieved after 1 day and are faster than lansoprazole and omeprazole that took 3
days to provide acid suppression. Therefore, Rabeprazole is recommended over the latter.
Hunfield examined the difference between esomeprazole and rabeprazole. He found that within the
first 24hour the intragastric pH were significantly higher with esomeprazole than with rabeprazole.
Therefore, Esomeprazole is superior to rabeprazole in terms of time needed to maintain a high pH
levels for optimum eradication therapy.
References
1. Lind T, Megraud F, Unge P, et al: The MACH2 study: role of
omeprazole in eradication of Helicobacter pylori with 1-week triple
therapies. Gastroenterology 1999;116:248–253.
2. Nagata K, Satoh H, Iwahi T, et al: Proton inhibitory action of the
gastric proton pump inhibitor lansoprazole against urease activity
of Helicobacter pylori: unique action selective for H. pylori cells.
Antimicrob Agents Chemother 1993;37:769–774. 19
3. Mauch F, Bode G, Malfertheiner P: Identification and
characterization of an ATPase system of Helicobacter pylori and
effect of proton pump inhibitors. Am J Gastroenterol 1993;88:1801–
1802. 20
4. Grayson ML, Elipoulos GM, Ferraro MJ, et al: Effect of varying pH
on the susceptibility of Campylobacter pylori to antimicrobial
agents. Eur J Clin Microbiol Infect Dis 1989;8:888–889.
5. McNulty CA, Dent JC, Ford GA, et al: Inhibitory antimicrobial
concentrations against Campylobacter pylori in gastric mucosa. J
Antimicrob Chemother 1988;22:729–738.
6. Ierardi E, Losurdo G, Fortezza RF, Principi M, Barone M, Leo AD.
Optimizing proton pump inhibitors in Helicobacter pylori
treatment: Old and new tricks to improve effectiveness. World J
Gastroenterol. 2019 Sep 14;25(34):5097-5104. doi:
10.3748/wjg.v25.i34.5097. PMID: 31558859; PMCID: PMC6747288.
7. Hunfeld, N.G. et al. (2012) “A comparison of the acid-inhibitory
effects of ESOMEPRAZOLE and rabeprazole in relation to
pharmacokinetics and CYP2C19 polymorphism,” Alimentary
Pharmacology & Therapeutics, 35(7), pp. 810–818. Available at:
https://doi.org/10.1111/j.1365- 2036.2012.05014.x.