Analytic basis of both gastrointestinal & bile duct way transit incordination link to DM & metabolic acidosis could be of help to further explain your view of this issue.

I have no view of my own on this issue, I just asked a question hoping that someone else does.

However, thank you for the piece of advice!

By the way, is the duodenal ulcer disease of any importance in Sao Paulo? How much is its prevalence, complications rate, and things like these?

I am afraid that I did not understand correctly: the azygo-portal disconnection procedure is used to treat the duodenal peptic ulcer disease? How does it work in cases like a duodenal ulcer?

Unfortunately, I did not read anything about a procedure like this. Would you give some referrals? What I know on this matter, are just routine truncal with inner drainage and the selective proximal vagotomies. More or less...

A-ha, I see now! The most gentle procedure to perform, I like it.

Though Johnson, one of those Founding Fathers who coined it, wrote that this kind of operation is just for elective surgery, I performed it occasionally even in cases of the perforated duodenal or pyloric ulcers - not frequently, in those cases only when the hole is not more than 3 mm in its diameter, inflammational alterations of the minor omentum are not severe and allow to distinguish the vagus branches, Latarjet, etc, and if it occurs before 6 hours from the beginning of the perforation. And when the condition of the patient permits to work with pleasure and without all these harry-ups (and the latter is usually depended on the size of perforation directly).

Diabetic patients have a delayed gastric empting, often the performance of gastric upper endoscopy requires 24 hours and more of food astension. Moreover, mucosal microcirculation is a process necessary for the integrity of mucosal barrier and it is strongly worsened in diabetic patients. These condition predispose more to gastric than duodenal ulcer. However, diabetes is associated to an increase of H. pylori infection and the bacterium strict relationship to duodenal ulcer is well-known.

Have you got any populational data on both these matters (diabetes and ulcer; diabetes and Hp-colonization relationships)?

A meta-analysis involving 20000 patients about the association diabetes-H. pylori has been recently published (Scand J Infect Dis. 2013 Dec;45(12):930-8)

It is very impressive data you have collected! I shall try to obtain this article.

Although, DM patients are expected to have stasis of enteral transit, but yet constant gastrointestinal mal-absortion due to diffuse visceral micro angiopathy complex leading to neuronal disfuncion, therefore favouring low insidence of duodenal ulcer.

So they are. However, who have ever seen the DM patient with the chronic duodenal ulcer?

Here you will find attached a recent study that does not find any difference in acid related gastric and esophageal disorders between dianetic and non-diabetic patients.

Thank you for providing this link for all the participants!

However, the authors of the article (J.Holub et al, 2010) do not distinguish between duodenal and gasric ulcers, not speaking of further classification. I understand that the lower oesophagus-stomach-duodenum is the deeply integrated unity and should be considered as a whole to a certain way.

On the other hand, I've got used to sort out: erosions from ulcers; acute ulcers from chronic; duodenal from gastric; distal, or 'acid' ulcers from mediogastral, or atrophic, and so on. They are different entities in terms of patients' age, the disease duration, condition of the gastric and duodenal walls, indications and contraindications for surgical treatment, and outcomes of both conservative and surgical therapies, etc.

So, the DM patients might have had higher GERD or/and gastric ulcer a prevalence vs non-DM who might had duodenal ulcers more frequently, or might had not. From a point of view of the Hp eradication, this detail may be of no importance, but from a more complex point of view, namely, from position of understanding of the pathophysiological mechanisms, it does matter.

As for 'meta-analysis involving 20,000 participants', it devoted to the diabetic nephropathy which was find to occur in Hp-infected individuals more frequently as compared with non-infected.

What evil a bacterium it is, indeed! It was found almost everwhere including cariouse teeth, liver, and gallbladder, and who knows where else. Why should not eradicate it in all the mankind at once?

I think that some conditions strongly suggest the eradication but only in evidence based related disorders. All other speculations are fascinating hypotheses but show still many obscure aspects. The strategy "test and treat" for the whole human race is an appropriate provocation for some aspects of the "maniacal" research. However, it ia not reliable because a therapeutic strategy with a 100% outcome is not available. I wonder if the vaccine may be the final solution.

Dr.Enzo,

Thank you for this really profound (and wise) explanation.

And what about the preventive Hp eradication in an epidemic hotbed, for example, in the patient's family if its members are simptom-free?

By the way, it just has come into my mind: Are there some evidence that the mammalians, aves, or fish, for example, may suffer from the 'peptic ulcer' in a natural way too?

If the subjects are symptom free, there is no need to detect Hp. However, if a member of the family is carrier of the bacterium, it should be investigated in all the family members and, obviously, treated. This for two reasons: a) 20% of infected patients are asymptomatic, b) the familiar condition of promiscuity favor the contagion. Some animal Helicobacters (see H. Heilmanii, a species frequently found in pets) may provoke gastric and duodenal ulcer in humans. I know that Prof. Dino Vaira from Bologna endoscoped infected dolphins and found ulcers in the stomach, but I do not know any more details. You can ask this author, whose profile is on Research Gate.

There exists a common misunderstanding repeated again and again in popular literature on Gastroenterology, namely, about a shift of the peptic ulcer development mechanism occuring from Hp-associated disease to NSAIDs-associated one.

The peptic ulcer disease (one can put an adjective 'peptic' between inverted commas, so to say), so...

The ulcer disease is not a living being to change its pathogenetic mechanisms or evolve from one form to another one, more sophisticated.

(By the way, about the Hp and NSAID-ulcers: If it is right that the ulcer will 'die' after its perforation, would it not more profitable for anyone to have Hp ulcer in the age of thirty than NSAIDs ulcer in the age of seventy?

Nor the Helicobacter, neither NSAIDs cannot produce the ulcer disease by themselves, it is as evident as 2+2=4, because they are almost evenly distributed factors acting on the whole surface of the stomach and duodenum. It is a matter of paralogism, not of data deficiency. Of this absurd contradiction between diffuse factors and its putative local action, not only R.Virchow wrote [Historisches, Kritisches und Positives zur Lehre der Unterleibsaffektionen / Virch Arch 1853; 5: S.362], but Palmer, and W.Rau [Funktionelle Anatomie der Magestrombahn: lokalisierende Faktoren in der Pathogenese des Magengeschwuers / Langenbecks Arch Chir 1986; 367: 129-138], and even A.Soll and David Graham in the beginning of a chapter 'Peptic ulcer disease' [Textbook of Gastroenterology, 5th ed, ed.by T.Yamada, Blackwell, 2009].

Is there any difference between diffuse and local factors of pathogenesis? Just imagine the result if one has sat down on a chair with a single pin protruded, and another person has lunched onto another seat, with a hedgehog curled on it. Would be results the same?

Besides, a pin and a hedgehog need quite different an approach to deal with, as anyone interested may read in Lewis Carroll's books.

I would like to accent that the difference is not just a curious gap in academic knowledge. More and more frequently the ulcer starts its course as complicated with bleeding or perforation, so that post factum Hp eradication just missed its main goal to prevent the ulcer development.

On another hand, to the best of my knowledge at any rate, nobody has made still a simpliest experiment with the main supposed pathogens. If Cag A or/and ammonium are the main factors of the ulcerogenesis indeed, why not to perform a direct injection of one or both media into the animal stomach wall for the ulcer to develop (or not), so that to put a dot on 'i'.