So yesterday V Sir spoke about Gastritis [and a lot of other things such as how women give themselves Peptic Ulcer by excessive use of NSAIDS when all they have is problems with their better half, MIL, FIL and kids whereas the Doctor who prescribed the NSAID (When there was no need for it) is not to blame because he (unlike women) has a LOT of things on his mind.] As usual, there were his jokes and regular insults “Jackasses!”
After discussing Gastritis (which is a histological diagnosis; you need to do a biopsy before you declare that the patient has gastritis), he showed us this picture of two men sharing a drink. *Neurons fire and connections are made*
Robin Warren and Barry Marshall after winning the Nobel Prize in 2005
Robin Warren and Barry Marshall are the two men who changed the history of Peptic Ulcers with their discovery that Helicobacter pylori can cause the ulcers. They were awarded the Nobel Prize for Medicine in 2005.
Since time immemorial, scientists considered that gastritis could be due to:
- · Heavy use of NSAIDS
- · Alcohol Overdose
- · Stress (Trauma, emotional, surgical)
- · Suicide Attempts
- · Uraemia
- · Heavy smoking
- · Nasogastric Intubation
But nobody considered the possibility of a bacterial infection causing the symptoms.
Why? Well, because how would the Bacteria survive under such high acidity?
I'd read about this when read micro:)
The treatment for this evolved from gastrectomy to vagotomy to several other variants but none of them provided a permanent distress-free solution because the procedures left the patients with many more difficulties.
At this point, Barry Marshall and Robin Warren began working together to study about the Peptic Ulcers in greater detail.
Merely isolating the bacteria cultured from the gastric contents was not indicative since they could always be contaminated species from the environment.In order to consider a species as the causative agent for a disease it must satisfy Koch’s Postulates:
Isolate the infectious agent from the individual. (blood, aspirated contents)
Culture the agent and inoculate them into a healthy individual.
There must be an infection when the agent was introduced in the healthy individual.
It must be possible to isolate the causative agent again from the second individual.
H.pylori doesn't grow in mice or pigs so it was essential to test the Postulates on humans. But this was declined for numerous reasons. The only ethically acceptable person for testing this crazy idea was Barry himself so he collected the fluid and swallowed the broth. Sure enough, the classical symptoms developed and he was sick for a week.10 days later a gastric biopsy confirmed the culprit and this made the gastroenterologists and pharmaceutical companies sit up and take note. Of course, surgeons weren’t happy with this discovery because it meant that they didn’t have to go around doing gastrectomy and other surgeries that claimed to cure Peptic Ulcers.. Slowly, things began to change and today, Peptic ulcers are almost never treated surgically but with antibiotics.
This is a great example of challenging the accepted what we all take for granted. Someone said that ulcers can’t be caused by bacteria so that thought persisted for decades. Progress comes when we question “Why?” at the end of every statement. In this age of cutting edge technology and advanced molecular biology it’s possible to test a lot of theories that we take for granted. Some of the answers to important questions lie right before us, it takes a trained mind to see.
As they say, The eyes cannot see what the mind does not know..
- Wikipedia: To avoid the acidic environment of the interior of
the stomach (lumen), H. pylori uses its flagella to burrow into the mucus
lining of the stomach to reach the epithelial cells underneath, where the pH is
more neutral. H. pylori is able to sense the pH gradient in the mucus and move
towards the less acidic region (chemotaxis). This also keeps the bacteria from
being swept away into the lumen with the bacteria’s mucus environment, which is
constantly moving from its site of creation at the epithelium to its dissolution
at the lumen interface.
H. pylori is found in the mucus, on the inner surface of the epithelium, and occasionally inside the epithelial cells themselves. It adheres to the epithelial cells by producing adhesins, which bind to lipids and carbohydrates in the epithelial cell membrane. One such adhesion, BabA, binds to the Lewis b antigen displayed on the surface of stomach epithelial cells. Another such adhesion, SabA, binds to increased levels of sialyl-Lewis x antigen expressed on gastric mucosa.
In addition to using chemotaxis to avoid areas of low pH, H. pylori also neutralizes the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. The ammonia, which is basic, then neutralizes stomach acid.