Talk:Glucose-6-phosphate dehydrogenase deficiency

I

I moved this from "Glucose-6-Phosphate Dehydrogenase deficiency"; the capitals were making it hard to find the page. It was an attempt to seperate the name of the enzyme affected from the deficiency, but IMHO that's contrary to policy. JFW | T@lk 09:57, 27 Apr 2004 (UTC)

Hemolysis in DKA

I found conflicting reports as to haemolysis in the context of DKA. PMID 8887143 seems to suggest it is the drop in glucose that precipitates the haemolysis. PMID 4623682 suggests the DKA caused the haemolysis. There is actually very little published literature on the subject. JFW | T@lk 17:36, 23 March 2006 (UTC)

epid

thalasemias could also be added in their relationship to preventing malaria. and linked.

This page is pretty useless to readers without a background in medicine, and thus as a general information encyclopedia article. Recommend a summary be written in lay-english, without all the medical jargon.

DRUGS AND FOODSTUFF TO AVOID FOR PERSONS WITH LACK OF G6PD (FAVISM)

It is vital for the people with the FIVISM (G6PD Deficient) persons to know that they should avoid some drugs, chemicals and foodstuffs. The list of the DRUGS AND FOODSTUFF TO AVOID for the G6PD deficient (FAVISM) persons are stated in the "G6PD Deficiency - FAVISM Association" at the following link: link title

There is already a link to g6pd.org - Wikipedia has no duty in warning people against foods or drugs. That is the job of their healthcare provider. JFW | T@lk 19:48, 28 October 2007 (UTC)

http://g6pddeficiency.org/ says to avoid ALL legumes, not just fava beans. Kortoso (talk) 22:09, 15 January 2016 (UTC)

Favism?

An anonymous editor from the 70.108 range has now twice left the following note in the article:

This page needs to be edited. Favism is a medical disorder, resulting from eating broad beans. G6PD deficient is a biochemical imbalance. They are often linked but not always. For instance see here: http://www.kfshrc.edu.sa/annals/166/95-371.html This article needs to be edited to reflect this, and Favism should have its own separate article.

I don't find the URL provided very informative. As far as I can gather (and support with the Mehta reference), favism is the syndrome that develops when people with marked erythrocyte G6PD deficiency consume beans with high levels of vicine, divicine, convicine and isouramil. People with normal or low-normal G6PD levels do not develop this syndrome - I have never heard of favism in a patient with normal G6PD levels. Furthermore, Wikipedia articles occasionally cover multiple related topics in one article when it is thought this makes things easier to explain. JFW | T@lk 19:48, 28 October 2007 (UTC)

Sorry for the guerilla editing, but there seems to be a big problem with commonly equating G6PD with favism when this is simply not the case. G6PD deficieny is much more common than favism, and equating the two is being needlessly alarmist. The Al-Ali article (HTML version) is only used as a specific example, not a authoritative reference. It describes a small study of over 757 Saudi men. Over 42% of them tested positive for G6PD deficiency, but none of them reported symptoms of favism. The abstract of the Mehta review states, "Although most affected individuals are asymptomatic," indicating clearly that most G6PD deficient individuals do not show favism. The Beutler review states the relationship between favism and G6PD deficiency clearly, "Patients with favism are always G6PD deficient, but not all G6PD-deficient individuals develop hemolysis when they ingest fava beans. Thus, G6PD deficiency is a necessary but not sufficient cause of favism. Presumably some other factor, probably also genetic and very likely related to metabolism of the active ingredients in the beans, is involved." It is reasonable that this one Wikipedia article should treat both G6PD and favism, but it should be clear about the difference, rather than simply equating the two. I understand that "best practice" might be to err on the side of caution and presume that a patient presenting with G6PD also has favism, and I think the wikipedia article has an obligation to state this advice (perhaps in a separate "best practices" section). However, the article should also give the facts, up front, that among individuals who test positive for G6PD deficiency, the precise odds for having favism or other specific food/drug sensitivities are mostly unknown. For the general case of sensitivity to fava beans (favism), the odds are known to be low. Factors that might affect these odds include G6PD variant and age. —Preceding unsigned comment added by 70.108.59.224 (talk) 01:41, 29 October 2007 (UTC)

That's not guerilla editing, especially now you have simply made the correction you thought was necessary. Still, if you were a haematologist treating G6PD, would you allow people with mild deficiency to eat broad beans? I think one would still be erring on the side of caution. JFW | T@lk 06:33, 29 October 2007 (UTC)

Beutler

On the occasion of the ASH fiftieth anniversary, Ernest Beutler has again reviewed G6PD deficiency: doi:10.1182/blood-2007-04-077412 JFW | T@lk 16:27, 23 December 2007 (UTC)

MCOTW

contradictions

The section on chemicals that should be avoided should be avoided, it seems to be a guide and doesn't make good reading, is there a common link or should it be mentioned that a number of substances produce reactions and a few examples of each class? LeeVJ (talk) 22:26, 13 August 2008 (UTC)

I agree. The list should be sourced, prosaified and hopefully classed in some way or another. JFW | T@lk 06:55, 15 August 2008 (UTC)

I wouldn't agree with removal of the list as it forms an important component of pathogenesis/precipitation of the disease. —KetanPanchal^taLK 04:26, 16 August 2008 (UTC)

Twenty questions for this article

Most of these are rhetorical questions meant to spur development of the article, some are simply things that I believe a reader of the article would be interested in, and others are just things I'm personally curious about. There are some obvious issues with accessibility and overlisting and the article should have in-line citations.

• 1. The relationship between Favism and GSPD deficiency is unclear: Is it not well understood, or is it just not clear in the article?
• 2. The article lists 400m as affected, which is surprising given that I've never heard of it before. Is it underdiagnosed and usually asymptomatic?
• 3. Is it more prevalent in certain ethnic groups the way Sickle cell anemia is?
• 4. How common are the various forms?
• 5. What are the criteria for the various forms?
• 6. How severe are the symptoms of the disease? (Hemolytic crisis means very little to your average encyclopedia reader)
• 7. How frequent are the symptoms of the disease? (i.e. do sufferers always react to a stimulus, and do all react to the same stimuli?)
• 8. What is the overall social impact of the disease? (i.e. cultural dietary restrictions, lost productivity, mortality, etc...)
• 9. When was Favism first described as an illness? (i.e. when did they link it to the beans?)
• 10. When was G6PD deficiency first described?
• 11. What are the signs of the disease in lay terms? (In other words, how can your average hypochondriac know that this must be the disease that causes all of their problems?)
• 12. Is it a recessive (maybe codominant?) X-linked genetic disorder? What chromosome is it on? Is it a single gene, multiple genes that affect a single pathway, or multiple genes that affect multiple pathways?
• 13. In diagnosis the disease, what else must be ruled out that causes similar symptoms?
• 14. Is the deficiency usually undiagnosed in people without active disease and is there any implication to this?
• 15. Are there any screening tests for carriers?
• 16. Are the available treatments for the disease effective?
• 17. Are the treatments for the disease available to those who are most affected?
• 18. Given that the gene is apparently quite common (again, the 400m), how often do homozygous females develop CGD, which is apparently quite rare?
• 19. CGD appears to affect granulocytes. Does G6PD cause any problems for cells other than erythrocytes?
• 20. Purely random question that I'm sure almost no one else cares about: is G6PD associated with any human blood group system?

Just some ideas to kick around for anyone working on the article. SDY (talk) 22:29, 13 August 2008 (UTC)

Wow, nice list. I'll get to work on some of these Friday, perhaps Saturday, next few days are very important and I probably won't be on Wikipedia much. —Cyclonenim^T@lk? 22:34, 13 August 2008 (UTC)

One other thing that needs to be mentioned is the supposed protective effect against malaria. --WS (talk) 23:05, 13 August 2008 (UTC)

The Lancet review is very recent (Jan 2008). That sounds like it could well be a useful source for much of the content. JFW | T@lk 06:56, 15 August 2008 (UTC)

Thank you. I'd like to double up on the request for percentage in the population in various countries. That would put the point on its importance or lack thereof. Kortoso (talk) 22:17, 15 January 2016 (UTC)

Here's a start: http://cs.stanford.edu/people/emmap1/visualizations/map_subset/g6pd_any_map_2.html Kortoso (talk) 22:22, 15 January 2016 (UTC)

Shifting of section

For a better known disease like G6PD-deficiency, the manual of style recommends that common signs and symptoms be mentioned first, and then pathogenesis. But, I felt that if pathogenesis is explained first, it would be possible to discuss the basis for precipitation of the condition by the mentioned drugs and conditions. What do others feel about this? BTW, thanks and congratulations (yet, again) to SDY for such a comprehensive review. —KetanPanchal^taLK 04:32, 16 August 2008 (UTC)

I've got to say I kind of support this idea, regardless of what MEDMOS says. In diseases such as G6PDD it's essential to know first how the disease affects the sufferer in terms of pathogenesis. Then we can cover the signs and symptoms of the disease and continue in the normal order. —Cyclonenim^T@lk? 12:36, 16 August 2008 (UTC)

That's why the pathogenesis needs to be explained in simple terms in the introduction. JFW | T@lk 21:28, 19 August 2008 (UTC)

PMID 8639919

Naylor CE, Rowland P, Basak AK, Gover S, Mason PJ, Bautista JM, Vulliamy TJ, Luzzatto L, Adams MJ study on 'Glucose 6-phosphate dehydrogenase mutations causing enzyme deficiency in a model of the tertiary structure of the human enzyme'. Luzzatoo, Vulliamy and Mason are some of the most prominent in G6PD papers, might be worth a look. The paper is free, too. —[[:Cyclonenim (talk · contribs) 14:40, 20 August 2008 (UTC)

Possible sources

• PMID 16225031 – nice clinically-focused review in Am Fam Physician, pretty recent (2005)
• PMID 7949118 – Beutler's 1994 review, practically a standalone textbook, seems to have been cited by every article on G6PD since
• PMID 18177777 – most recent review

First two are free (yay!) Fvasconcellos (t·c) 14:30, 23 August 2008 (UTC)

blood donations?

(my first time adding a topic in a discussion page. correct me if I do it wrong, thanks.)

I don't think I found anything relating to donating blood to Red Cross here. Other sites said that Red Cross does not accept G6PD blood, maybe that should be added in, so people who want to donate blood would know. --Combine 108 (talk) 01:19, 14 October 2008 (UTC)

http://www.redcross.org/ "Your search for "G6PD" did not match any documents" Kortoso (talk) 22:18, 15 January 2016 (UTC)

Article review

My first observation is with the term "disease". G6PD Deficiency is a genetic disorder and no more a disease than blond hair or brown eyes. You can not "catch" it from another person other than through conception.

The article is well done and better than most I've seen. I received a letter from a Dr in India recently who believes G6PDD to be much more common than currently thought. He also stated that, although not at first logical, older patients were dying unnecessarily from reactions due to undiagnosed G6PDD. I personally would like to see a lot more medical research on this disorder. I speak to a lot of individuals with it and I believe it affects us much more dramatically than is currently believed. Especially in its more severe forms.

Thank you for your efforts.

Drbaker48 (talk) 05:43, 20 May 2009 (UTC)

Treatment

I suggest adding more research results to this section. In a particular study, N-Acetyl cysteine, L-cysteine, and β-mercaptoethanol increased Se-GSH-Px activity in G6PD-deficient human erythrocytes, indicating that other reducing agents can be utilized to complement Se-GSH-Px activity in G6PD deficiency .

Thanks, Mfarshada (talk) 21:57, 11 June 2013 (UTC)

doi:10.1007/s10238-004-0038-z is a primary laboratory study. Needs a secondary source. JFW | T@lk 11:45, 31 December 2013 (UTC)

References

Review

Br J Haem - emphasis on pharmacogenetics. doi:10.1111/bjh.12665. JFW | T@lk 11:45, 31 December 2013 (UTC)

possible confusion with Glucose-6-phosphatASE deficiency

I suggest adding explicit warning of possible confusion with Glucose-6-phosphatASE deficiency, which is completely unrelated to this disorder. When searching this topic on google the link leads here. — Preceding unsigned comment added by 195.113.62.191 (talk) 16:12, 7 January 2014 (UTC)

Davidlwinkler's edits

Davidlwinkler made a number of edits, mainly to the introduction, supported by some URL references. In general, there is no need to add references to the introduction, because it only summarises what the rest of the article is saying. Specifically, references in medical articles should be WP:MEDRS-compatible. That is, using high-quality secondary sources such as review articles or textbooks. I have pointed out a number of good resources on this talk page.

I have rewritten the introduction for now, and there is an ongoing need for the rest of the article to be updated to WP:MEDMOS and WP:MEDRS standards. JFW | T@lk 09:11, 25 August 2014 (UTC)

jfdwolff, very well put, and I will continue to search for support for my claim. — Preceding unsigned comment added by Davidlwinkler (talk • contribs) 18:05, 25 August 2014‎

Davidlwinkler I really wish you would look at WP:MEDRS because it is the key guideline here. There is no shortage of sources. doi:10.1111/bjh.12665 is a very recent free review from the British Journal of Haematology (it makes a very passing allusion to acute renal impairment). There are other good sources, such as doi:10.2165/11536520-000000000-00000 (medications that can provoke haemolysis) and doi:10.1016/S0140-6736(08)60073-2 is a Lancet review from 2008. JFW | T@lk 21:00, 25 August 2014 (UTC)

{{ul|Jfdwolff|JFW]] Thank you for the great suggestions. I've used NIH for the majority of my references, but as for the others I know that I need to use more credible references, and I will definitely utilize these and use them in the future. David

Error in pathway image

In the image in the section on pathophysiology there is an error. G6PD does bring NADP to NADPH, however, glutathione reductase with the help of NADPH yields GSH (reduced form) from GSSG (oxidized form). Then, GSH is oxidized by glutathione peroxidase to GSSG while bringing peroxide to water. This error is also on the G6PD page. 72.177.214.193 (talk) 00:49, 13 May 2015 (UTC)

Deaths

The statistics refer to a global population or just New Jersey? Kortoso (talk) 22:03, 15 January 2016 (UTC)

Guideline

On laboratory diagnosis: doi:10.1111/bjh.16366 JFW | T@lk 13:46, 4 February 2020 (UTC)

Text

"In connection with the Covid19 pandemic, various medical publications explicitly indicated complications with the drug hydroxychloroquine. This could lead to hemolysis and microembolism , and thus death."

We need proper sources. Chloroquine is already mentioned in the body of the text. Will also added hydroxychloroquine. Not every article on Wikipedia needs to be directly tied to COVID19 Doc James (talk · contribs · email) 06:37, 9 May 2020 (UTC)

References

Recent Edits

Can we have an explanation on why mentions of Iraq, Sephardi Jews and Mizrahi Jews have been repeatedly removed from this article? First by 62.219.247.113 on 08/04/2024 and then, after I reverted that change, again by user Elgv18483. I have gone through the cited sources. The article was factual and accurate as it was, and no editing was necessary. I want to assume good faith here, but 62.219.247.113 has been warned about this already back in January - yet they keep doing it - and neither user has offered an edit summary.

@62.219.247.113:
@Elgv18483: What's going on?
139.133.148.19 (talk) 20:14, 13 April 2024 (GMT)

Seeing as no reply has been forthcoming, and it has been a whole week, I'm going ahead with reverting the latest changes to the article.--139.133.148.19 (talk) 17:46, 20 April 2024 (UTC)