Talk:Sickle-cell disease

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February 12, 2005 Peer review Reviewed
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older entries[edit]

Just as a comment for further discussion, I did hemoglobin research for about 4 and a half years. I recall a conversation (ca 1993 or 1994) with Professor Gary Ackers (at the time, chair of biochemistry and molecular biophysics at Washington University in St Louis Medical School, and one of the leading experts on hemoglobin cooperativity) about a paper, in which they mapped the site of action of the digestive enzyme the malaria parasite used on hemoglobins (as Hb is what they eat). It turns out that in the process of polymerization (HB S now, the sickle cell Hb), the polymerization caps the site of digestion, making Hb a poor meal for the parasite. That, to my understanding, was the way that in heterozygous individuals the mutation had selective pressure against the parasite. It slowed the rate of growth, because they couldn't feed as effectively on heterozygous individuals. Inter-cell death seems to be a poor mechanism for selective pressure, as few cells are sickled in heterozygous individuals. dwmyers

Simple test for sickle cell carriers[edit]

I read this in a test on genetics in GCSE Biology. If a sample of a carrier's blood is kept in low oxygen conditions, a few cells with become sickle shaped. This is roughly what the test said:

A couple are worried that they might pass on sickle cell anaemia to their children, so they had blood samples taken for a test. The father's sample developed sickle cells in low oxygen conditions whereas the mother's didn't. What does this mean?

Of course, it meant that the couple's children would a half chance of becoming a carrier, but won't develop the disease. But since I can't obtain the paper, I can't prove that it was there, but I doubt that it's a lie.

Cerebral vasculopathy[edit]

doi:10.1111/bjh.12300 Br J Haem 14:54, 25 April 2013 (UTC)

More treatment, vicar?[edit]

doi:10.1111/bjh.12413 JFW | T@lk 19:28, 17 June 2013 (UTC)

Vaso-occlusion[edit]

doi:10.1182/blood-2013-05-498311 - review in Blood. JFW | T@lk 16:08, 8 December 2013 (UTC)

Transition of care[edit]

Children become adults doi:10.1111/bjh.12700 JFW | T@lk 16:13, 24 December 2013 (UTC)

Another: doi:10.1097/MPH.0b013e3182847483 JFW | T@lk 17:12, 14 September 2014 (UTC)

Eurocentrism![edit]

Why are sickle type red blood cells "abnormal", and disc type red blood cells "normal"?

is the evolutionary immunity to plague and smallpox abnormal?

grabba 68.98.131.130 (talk) 07:49, 17 January 2014 (UTC)

I don't see where Eurocentrism comes into play, but if you read any of the article you'd see that infarcts to vital organs, severe pain, a shortened lifespan, and the fact that most people in the world do not have sickling cells would likely be the reason sickle cells are considered abnormal.MartinezMD (talk) 23:05, 17 January 2014 (UTC)

Guidelines[edit]

... in JAMA: doi:10.1001/jama.2014.10517 JFW | T@lk 21:33, 9 September 2014 (UTC)

And NICE: National Institute for Health and Clinical Excellence. Clinical guideline 143: Sickle cell acute painful episode. London, 2012. JFW | T@lk 08:54, 14 September 2014 (UTC)

Some other recent secondary sources (MESH "Anemia, Sickle Cell"[MAJR] with "Review"):

For the epidemiology and the management in resource-poor settings we might need to refer to the WHO literature.

There's plenty more, so any expansion will have to be selective. Subarticles may be required. JFW | T@lk 11:08, 14 September 2014 (UTC)

doi:10.1586/ehm.12.20 is about the research into histone deacetylase inhibition, for the "research" section. JFW | T@lk 22:21, 28 October 2014 (UTC)

Updating[edit]

Having identified some sources (previous section) I am planning to update this article and bring it to GA status reasonably soon. It gets the basics right but there's a fair number of sources that don't meet WP:MEDRS and at places it is difficult to understand for the lay reader. Some other WP:MEDMOS problems were also present. There's a total of 29 Cochrane reviews (link), but we're only citing four Cochrane reviews currently.

My views for each section:

  • Signs and symptoms: currently a little bit chaotic and doesn't separate acute from chronic problems
  • Genetics: a fair bit of jargon needs "opening up"
  • Pathophysiology: should be maximally up to date according to current understanding (needs 2-3 solid sources)
  • Diagnosis: screening/case finding should be separated from diagnostics in the setting of complications (e.g. stroke) and surveillance; we need to talk about neuroimaging and echocardiography
  • Prevention: there is currently no section that discusses prevention strategies; I haven't yet seen sources that discuss premarital screening and counseling in the same way Cyprus attempts to reduce unions that might lead to thalassaemia major
  • Management: again we need to separate prophylaxis, acute care, and long-term disease management
  • Prognosis: this needs strong sources to be reliable for the average reader
  • Epidemiology: good sources needed, perhaps less on a country-by-country basis
  • History: the current section needs consolidating with a better secondary source as support
  • Research directions: needs to be written

As always, assistance would always be appreciated. JFW | T@lk 16:50, 14 September 2014 (UTC)

As far as the history section, the most recent dates are from the 1940's-50's. I'm sure something has happened or been discovered about sickle-cell disease since then. Wulf.174 (talk) 00:04, 2 October 2014 (UTC)
OK, but what? JFW | T@lk 23:13, 6 October 2014 (UTC)

Suggestion for Prognosis Section[edit]

In this article, it states that "the estimated mean survival for sickle-cell patients was 53 years old for men and 58 years old for women with homozygous SCD." Throughout the entire article it also talks about much lower life expectancies are for individuals that have SCD. My question is, should this life expectancy be compared to the typical European/American life expectancies (which would be relatively high) or the life expectancy of people living in areas where SCD is much more common? These areas are typically much more impoverished and likely have much lower life expectancies as it is. In this case, 53 years of age for men and 58 years of age for women does not seem like it would be too far removed from the life expectancies of the people living in these traditionally malaria-stricken countries. Their average life expectancy at least be given in order to have a good reference point for how people with SCD compare. — Preceding unsigned comment added by Haynes.239 (talkcontribs) 03:32, 1 October 2014 (UTC)

Sources are needed. JFW | T@lk 23:13, 6 October 2014 (UTC)

I will get back to you on this one.

Haynes.239 (talk) 01:11, 15 October 2014 (UTC)

Origin of SCD[edit]

In the article, it says that "Sickle-cell gene mutation probably arose spontaneously in different geographic areas, as suggested by restriction endonuclease analysis. These variants are known as Cameroon, Senegal, Benin, Bantu and Saudi-Asian." A study done in 1988 only traces the origins of mutation back to three places, namely Benin, Senegal, and Central African Republic (Nigon, 1988). This is information appears to be inconsistent with what is known about the origin of SCD. — Preceding unsigned comment added by Haynes.239 (talkcontribs) 03:44, 1 October 2014 (UTC)

Can you point us to a source? JFW | T@lk 23:13, 6 October 2014 (UTC)

Yes. Nigon, V. "Structural Analysis of the 5 Prime Flanking Region of The. Beta. Globin Gene in African Sickle Cell Anemia Patients: Further Evidence for Three Origins of the Sickle Cell Mutation in Africa." (1988). Print. Haynes.239 (talk) 01:09, 15 October 2014 (UTC)

Print where? A journal? A book? Looks like a primary source too. JFW | T@lk 17:01, 19 October 2014 (UTC)
PMID 2898142 is definitely a primary source. JFW | T@lk 21:52, 19 October 2014 (UTC)

Sicklemic Belt[edit]

The name of the area that has the highest frequency of persons infected with SCD is called the "Sicklemic Belt" (Lehman and Huntsman, 1974). I think this needs to be mentioned, as the particular region does have a more specific name. — Preceding unsigned comment added by Haynes.239 (talkcontribs) 03:51, 1 October 2014 (UTC)

Never heard of the term, and I don't think we need to mention it. JFW | T@lk 23:13, 6 October 2014 (UTC)

Sickle-cell disease's relation to malaria[edit]

There should be more ties to how sickle-cell disease is shaping certain African populations, and how these populations no longer have a high rate of malaria like they previously did. There are only brief areas on the page that mention how malaria and sickle-cell disease relate to each other, but I believe there should be a bigger section that ties it together. Wulf.174 (talk) 23:48, 1 October 2014 (UTC)

Point us to a source that looks into this, and we can have that conversation. JFW | T@lk 23:13, 6 October 2014 (UTC)

No access[edit]

The following source was temporarily removed:

Malowany JI, Butany J (February 2012). "Pathology of sickle cell disease". Seminars in Diagnostic Pathology 29 (1): 49–55. doi:10.1053/j.semdp.2011.07.005. PMID 22372205. 

It looks very useful, but I had no access and it was being used for a statement that could be backed up with other sources as well. JFW | T@lk 22:05, 28 October 2014 (UTC)

History section[edit]

I have removed the content that I could not trace to secondary sources. It is reproduced here for reference:

It can be reintroduced if secondary sources can be found. JFW | T@lk 23:41, 28 October 2014 (UTC)

References

Addition about evolution[edit]

Haynes.239 made an addition about the evolutionary aspects of sickle cell disease.[1] The main problem is that it is based on primary sources (see WP:PSTS). JFW | T@lk 06:58, 18 November 2014 (UTC)

Reproductive issues[edit]

doi:10.1182/blood-2014-07-577619 - from Blood JFW | T@lk 22:24, 4 December 2014 (UTC)