Iron deficiency anaemia    
Iron Guidelines Now Available Ibrahim Parvanta 21.04.98
Anaemia responsive to iron without low ferritin? Renuka Jayatissa 20.08.98
Re: Anaemia responsive to iron without low ferritin? Fernando E. Viteri 20.08.98
Re: Anaemia responsive to iron without low ferritin Pattanee Winichagoon 20.08.98
Re: Anaemia responsive to iron without low ferritin? David Brewster 21.08.98
Re: Anaemia responsive to iron without low ferritin? George Fuchs 21.08.98
Re: Anaemia responsive to iron John B. Tomaro 21.08.98
Re: iron deficiency anaemia Nevin Scrimshaw 21.08.98
iron deficiency anaemia Patrick Kolsteren 21.08.98
Supplementation in adolescent girls Paul Amuna 22.08.98
Re: supplementation in adolescent girls Fernando Viteri 25.08.98
Re: Anaemia responsive to iron without low ferritin? Harsha De Silva 28.08.98
Re: Anaemia responsive to iron without low ferritin? Fernando E. Viteri 30.08.98


From: "Parvanta, Ibrahim" <ixp1atcdc.gov>

Subject: Iron Guidelines Now Available

Date: Tue, 21 Apr 1998 16:49:18 -0400

 

GUIDELINES FOR THE USE OF IRON SUPPLEMENTS TO PREVENT AND TREAT IRON

DEFICIENCY ANEMIA prepared by Dr. Rebecca Stoltzfus and Ms. Michele

Dreyfuss, The Johns Hopkins University, for the International

Nutritional Anemia Consultative Group (INACG) is now available. The

purpose of these guidelines is to provide practical, scientifically

sound guidance to those responsible for planning and implementing

anemia control programs.

 

If you would like to download Guidelines for the Use of Iron

Supplements to Prevent and Treat Iron Deficiency Anemia free of

charge, visit our web site at:

 

http://www.ilsi.org/inacg.html

 

or contact the INACG at:

 

INACG Secretariat, ILSI Human Nutrition Institute

1126 Sixteenth Street, NW, Washington, DC 20036-4810, USA

Tel: 202-659-9024, Fax: 202-659-3617, E-mail: OMNIatdc.ilsi.org


From: amalateureka.lk, Dr.Renuka Jayatissa

Anaemia responsive to iron without low ferritin?

Date: 8/21/98 12:32 AM

 

I have carried out a research project on iron supplementation on Adolesence schoolgirls to detect the effect of daily Vs weekly doses of iron in this age group. Because the anaemia prevalence among adolescence is 36% in Sri Lanka.On the basis of the result, 21% were anaemic (n=659). The ferritin value was done in a sub sample (n=88). Only 2 participants had ferritin values below 20ug/l and none were below 12ug/l. After 2 months supplementation anaemia prevalence was reduced to 9%. It seems that either ferritin is not a good marker of iron deficiency anaemia or some other factor caused the fall in anaemia prevalence - neither of which seems probably: could anyone explain these data?

Dr.Renuka Jayatissa (MBBS, MSc, MD)

NUTRITION Department, Medical Research Institute

Baseline Road, Colombo 08, Sri Lanka

Email- amalateureka.lk


From: viteriatnature.berkeley.edu

Date: Thu, 20 Aug 1998 10:48:09 -0800

Subject: Re: Ngonut: Anaemia responsive to iron without low ferritin?

 

Dear Dr. Jayatissa:

 

There are now several trials on daily or weekly iron

supplementation to school girls (Malaysia,Indonesia, Guatemala, Panama,

India) all showing a positive effect on improving iron status manifested by

reductions of anemia prevalence and increments in ferritin levels by both

methods if the trial is of several months duration and with proper doses.

In the short term, daily iron has slight therapeutic advantages, as would

be expected unless weekly iron was absorbed 7 times more than daily (highly

improbable!). One of these trials is published and two or three are already

sent for publication.

 

I would like to ask, first , if infection is prevalent in your

sample, if ferritin levels are subjected to standardized controls and if

you have ferritin distributions in different age-sex groups. How often do

you see ferritin levels below 10 in infants 6 - 18 months old ? It could

be that for the method you use and for your population, a cut off of 30

would be appropriate, as suggested by Skikney in populations where

infection is highly prevavent. Did you measured ferritin after your

short-term trial ?. A response to iron administration on various measures

of iron status is the best proof that iron deficiency existed (your case in

point). Lastly, vitamin A or folate deficiencies can fictitiously elevate

ferritin values.

 

The idea I have been proposing is that weekly iron supplementation

should be a LONG-TERM, PREVENTIVE MEASURE, IDEALLY COMMUNITY BASED (e. g.

school setting, factories, religious and mother groups, etc.) AND UNDER THE

GUIDANCE OF THE HEALTH SECTOR. Therefore, the long-term effect among

adolescent girls would be to increase their iron reserves. However, when

daily or weekly doses are administered for a short period of time to anemic

subjects and Hb response is the only parameter followed it seems to me that

what is being sought is a therapeutic response. Under those circumstances

daily doses are more efficacious in treating anemic girls in a shorter

period of time but at greater risk of undesirable side effects and it

appears that the effect is only short term (a paper on this matter has been

submitted). Long term weekly doses will also correct anemia at somewhat

slower pase but with the advantages that the side effects are much less and

there are less signs of oxidative stress compared to daily doses (recent

studies).

 

I think that because of all of the above, it is a mistake to

"detect the effect of daily Vs weekly doses of iron". The purposes of each

scheme should be different: daily for short term (and temporary) therapy.

Weekly for long term prevention of development of iron deficiency and for

improving iron stores in women prone to become pregtnant.

 

Fernando E. Viteri, MD., ScD., Professor, Nutritional Sciences

University of California, Berkeley, CA 94720-3104

Phone: (510) 642 6900, FAX: (510) 642 0535

Email: viteriatnature.berkeley.edu


Date: Thu, 20 Aug 1998 14:59:07 +0100

From: Pattanee Winichagoon <nupwnatmahidol.ac.th>

Subject: Re: Ngonut: Anaemia responsive to iron without low ferritin?

Dear Em-orn and Dr. Jayatissa:

Thanks for forwarding and sharing the message below.

I did have a similar observation, though not to the same extent that you found. My first speculation is whether infection can cause such a high level of ferritin, such that even the cutoff 20 is still too low to pick up those who really are iron def. Have you look at the ferritin distribution of those who responded to iron supplement? I think we need to have a better way to look at ferritin results more than just look at a specific cutoff, as this may be too arbitrary.

My other interest now is to look at the ferritin profile in those subjects having hemoglobinopathy (non-diseased form) and see if they differ from normal hemoglobin. I feel that we need to also understand this profile in a population with a mix of abnormal hemoglobin in order to properly interpret the results.

With best regards.

Sincerely,

 

Dr. Pattanee Winichagoon, Associate Professor

Head, Community Nutrition Division

Institute of Nutrition, Mahidol University (INMU) Salaya, Nakhon Pathom 73170, Thailand.

Tel: (66-2)-889-2168, 441-9037 to 441-9038, 889-3820, 889-3920 Fax: (66-2)-441-9344, 441-9345

e-mail: nupwnatmahidol.ac.th


From: David.BrewsteratCASRDH.HEALTH.nt.gov.au Date:

Fri, 21 Aug 1998 08:33:01 +0930

Subject: Ngonut: Re: Anaemia responsive to iron without low ferritin?

 

In fact there is considerable evidence that both are probable, that is

that ferritin is not a good marker of iron deficiency and some other

factor may have caused the fall in haemoglobin.

Ferritin is an acute phase reactant, so rises with infection (even

viral infections in children) giving false negative results in iron

deficiency anaemia. This is well known and was discussed in one of the

original ferritin article by Lipschitz. There is a laboratory

solution, but it may not be easy for you to do due to expense. The

plasma transferrin receptor (Fleming et al) is not affected by

infection and is a reliable indicator of iron deficiency.

We have just completed a similar study in children from an Australian

Aboriginal community in which 40% are iron deficient, and found that

even in community children, ferritin is falsely elevated in nearly

all. But we also found that even in iron-repleted children, there was

a drop in haemoglobin despite continued iron therapy from 6-12 weeks

in about half, especially in those with haemoglobins around the

105-110 g/L range. This is the anaemia due to infection/inflammation,

which may be partly iron responsive. This may have been a factor in

your subjects.

 

Professor David Brewster

Northern Territory Clinical School

Darwin, Australia

References:

1 Fleming D, Wood RJ. Plasma transferrin receptor helps to predict iron deficiency in the anemia of chronic disease. Nutr.Rev. 1995; 53: 167-169.

2 Yip R, Dallman PR. The roles of inflammation and iron deficiency as causes of anemia. Am.J.Clin.Nutr. 1988; 48 : 1295-1300.

3 Reeves JD, Yip R, Kiley VA, Dallman PR. Iron deficiency in infants: the influence of mild antecedent infection. J.Pediatr. 1984; 105: 874-879.

4 Lipschitz DA, Cook JD , Finch CA. A clinical evaluation of serum ferritin as an index of iron stores. N.Engl.J.Med. 1974; 290: 1213-1216.


Date: Fri, 21 Aug 1998 10:51:07 +0600

From: George Fuchs <gfuchsatcitechco.net>

Subject: Re: Ngonut: Anaemia responsive to iron without low ferritin?

 

Dear Dr. Jayatissa,

 

Regarding other causes of anemia in Southeast Asia, you might take a look

at some observations we stumbled upon in Thailand. I'm fairly sure that

Sri Lanka is in the "hemoglobinopathy belt". A certain few individuals

with a hemoglobinopathy trait will also have some degree of iron deficiency

and may exhibit a partial response to iron therapy.

 

Linprisarn S, Tienboon P, Promtet N, Putsyainunt P, Santawanpat S, and

Fuchs GJ: Iron deficiency and anemia in children with a high prevalence of

hemoglobinopathies: implications for screening. Int J Epidemiol

1996;25:1262-66.

 

George Fuchs

ICDDR,B: Centre for Health and Population Research, Dhaka


Date: 21 Aug 98 07:04 EST

From: "TOMARO JOHN B." <TomaroatATGE.AUTOMAIL.COM>

Subject: Re: Ngonut: Anaemia responsive to iron wi

 

I read your brief comment with great interest. Would you be able to provide

results of the weekly vs daily administration of iron.

The Aga Khan University, Department of Community Health Sciences has a

similar study under way in some poor areas near Karachi. It would be

intersting to have your complete results.

Thanks for your kind assistance.

Sincerely,

John B. Tomaro, Director of Health Programme

Aga Khan Foundation, Geneva


Date: Fri, 21 Aug 1998 16:41:17 +0100

From: "Dr. Nevin Scrimshaw" <nevinatcyberportal.net>

Subject: Re: Ngonut: iron deficiency anaemia

I note that in your subject message you refer to intermittent iron supplementation of mild to moderate anemia as treatment. In common with Viteri and others, we are not recommending intermittent supplementation as TREATMENT. It is intended for PREVENTION although of course when given to a population with mild to moderate anemia it will take two to three months for anemia to disappear as a public health problem. Daily supplementation is more costly, more logistically difficult, has more side effects and is usually not significantly more effective.

There has never been any doubt that severe anemia, when identified, should always be treated and that this should be with daily iron.

Nevin Scrimshaw


Date: Fri, 21 Aug 1998 08:26:48 +0100

From: "Patrick Kolsteren" <pkolsterenatitg.be>

Subject: Ngonut: iron deficiency anaemia

 

Dear ngonutters,

I have followed with great interest the iron deficiency anaemia debate and would like to add some comments to the discussion.

It is not a surprise to hear the results of the supplementation in Sri Lanka.

A number of recent studies have indeed queried the appropriateness of the cut-off levels of ferritin. If one takes in an anaemic group of patients, the bone marrow staining as the golden standard for iron reserve depletion and calculates the sensitivity and specificity one finds that a low cut-off of ferritin is specific but not very sensitive. Medical doctors when making a diagnosis (on an individual basis) want a test with a high positive Likelihood ratio so that the probability of a patient with a positive test having the disease is high. This is why the cut-off for ferritin is taken so low. In prevalence studies we want actually a very sensitive test first. Later we can add to that a more specific test to eliminate the false positives.

On the basis of these test characteristics and in comparison with bone marrow studies, a cut-off of 40g/L has the highest efficiency (best trade-off between sensitivity and specificity) when patients are not suspected of having an inflammatory process. If inflammation is suspected the cut-off can be increased to 70 g/L. Another alternative is to take a response to treatment as the golden standard of iron deficiency. Those who increase their haemoglobin or iron reserves (taking the effect of regression to the mean in consideration) are the true deficients. This gives an idea on the prevalence. Transferrin receptor measurements are less prone to inflammatory influence and are promising. The ration transferrin receptor/ log ferritin is an excellent indicator for iron deficiency with a ROC curve of near 1.

Intermittend iron treatment. There is no doubt that, certainly for mild and moderate anaemia intermittent iron supplementation is as effective as daily treatment with less side effects and at a lower cost. Studies by Viteri on rats showed that this can be explained a saturation phenomenon of the mucosal receptors for iron.

A large dose saturates the receptors and subsequent dosages are poorly absorbed. The absorption is most effective in the rats when it falls in synchrony with the turnover of the intestinal mucosa, which is 3 days.

I hope this was of some interest.

Cheers

Patrick

 

Here are some references which might be of interest:

1. Dujardin et al. Likelihood ratios: A real improvement for clinical decision making? Eur. J. Epidemiol. 1994; 10: 29-36.

2. Punnonen K et al. Serum transferrin receptor and its ration to serum ferritin in the diagnosis of iron deficiency. Blood. 1989: 1052-1057.

3. Gordon H et al. Laboratory diagnosis of iron deficiency. J. Gen.

Int.Med. 1992; 7: 145-153.

4. Viteri F. Iron supplementation for the control of iron deficiency in populations at risk. Nutr. Rev. 197;6: 195-209.

 

Dr.P.Kolsteren

Nutrition Unit

Institute of Tropical Medicine Antwerp

NAtionalestraat 155, 2000 Antwerpen, Belgium tel 32-3-2476389 Fax 32-3-2476543


Date: Sat, 22 Aug 1998 18:00:49 +0100

From: paul.amunaatsbu.ac.uk (Paul Amuna)

Subject: Ngonut: Dr Viteri's response to Dr Jayatissa's mail on supplementation in adolescent girls

 

Dear Dr Viteri,

I wish to contribute to the interesting debate on the subject of daily vs.

weekly supplementation of iron in adolescent girls.

Clearly, biochemical indices, particularly multiple indices have consistently indicated a high incidence and prevalence of iron deficiency anaemia (IDA) in both developing and western industrialised countries. The multifactorial aetiological factors are also very well documented.

Approaches to primary prevention however still remain a contentious issue and it is interesting to see the attempts various workers are making particularly towards primary (and indeed secondary) prevention among vulnerable groups e.g. adolescent girls and in areas of high prevalence such as the example presented by Dr Jayatissa in Sri Lanka.

I fully agree with you that daily supplementation should be used for therapeutic purposes rather than medium or longer term prevention, particularly when we consider the dangers of oxidative stress and possible worsening of otherwise subclinical infectious states. It might also be unhelpful in environments where IDA and haemoglobinopathies e.g.

thalassaemia and sickle cell disease tend to be common.

Your suggestion of a weekly supplementation for high risk adolescent girls is an interesting one and I believe many other members will have views on this. As a medium term approach to primary prevention of IDA, I would go along with that provided there are enough trials to prove its efficacy ( we await your paper on the subject). For long term solutions to the IDA problem however, I do not believe that the solution lies in that direction.

Yes, the side effects may not be a very big problem but I am sure logistics would be; storage of Fe tablets particularly in developing country homes may be a big problem. Moreover, people may not be prepared to take "tablets" weekly for the "rest of their lives" and some may say that they are not ill to be taking such supplements anyway.

Hallberg, Nelson and other workers have shown that IDA is quite common and worrying, even in Europe. We have been studying the relationship between food choice, total energy intake and iron nutrition among adolescent school children in some London boroughs. Our results (yet to be published) show a very strong and significant positive correlation between total energy intake and iron nutrition among both adolescent boys and girls, but with a much lower iron intake among girls.

Some people used to think that IDA was not such a big problem in industrialised countries and that the aetiological factors are more rife in developing countries. We believe that the causes of IDA in developing countries are first and foremost related to food security and calorie intake!!!. This is made worse by other factors such as infections, malaria, haemoglobinopathies etc. In industrialised nations, we believe the major cause of IDA may be related to FOOD CHOICE among both boys and girls. We found that our sample (over 150) were choosing certain food groups and certain types of meals. This is corroborated by other studies in other parts of the UK we have reviewed. Our paper is in preparation so watch this space.

My approach to a long term primary preventive programme therefore would center on the key question of household and community food security. This means tackling all the issues, both socio-economic, political and otherwise, affecting food security in developing countries, as well as dealing with the parasites which afflict people living in these communities. At the same time, deal with acute IDA therapeutically. In industrialised nations, food security may be the major problem in some inner city areas but the overriding factor in our view is that of food choice among the young and adolescent population. Nutrition education and health promotion aimed at behavior modification will be key to finding solutions in this case and there may be policy implications as well.

I await your comments on this and any other views and suggestions.

Thanks to all and let's continue this healthy debate

Dr Paul Amuna MB, ChB, MMed Sc. FRSH

Nutrition Research Centre,

South Bank University, London UK


Date: Tue, 25 Aug 1998 16:39:22 +0100

From: viteriatnature.berkeley.edu

Subject: Re: Ngonut: Dr. Viteri's response to Dr. Jayatissa's mail on

supplementation in adolescent girls

 

Dear Dr. Amuna:

Thank you for your interesting comments. I think that it is important for all to clarify things. I am truly grateful for your willingness to discuss the issue of weekly iron supplementation.

I comment your comments:

You state that "approaches to primary prevention however still remain a contentious issue". I think there is consensus being formed that makes different and complementary approaches feasible in different situations. These include from perinatal practices to iron supplementation schemes and parasite control where appropriate. Everybody agrees that the ideal approach should be food and public health-based (foods and their combinations in meals, iron fortification, etc.). We have worked and continue to work in these areas.

Nutrition education, food safety and policies, preventing and correcting poverty, assuring proper "true food availability", etc. should be a center of our general efforts. However, in rural areas and in poor slums of developing countries (where the problem is more acute) these "food-based interventions" are going to take many years to be effective.

Examples: It took more than 40 years for Costa Rica to achieve relative food security, even though the whole policy of the country was geared in that direction. Still, vulnerable groups have high prevalences of iron deficiency (similar to the situation in many industrialized countries).

Chile, with an outstanding nutritional and health policy, has not been able to implement iron fortification of milk distributed by the national health service, even though its effectiveness was demonstrated nearly 30 years ago.

In brief, to be realistic, unfortunately it will take many years for the rural and urban poor in the developing world to achieve primary prevention of iron deficiency through proper access to food. AGAIN, WE MUST CONTINUE TO STRUGGLE TO ACHIEVE IT. The question is what to do in the meantime ?

Considering that according to WHO 47 % of the rural population in developing countries lack access to health care, to base primary prevention on the health system is far from effective. Yes, we should continue to invest in increasing effective coverage. Still, daily iron supplementation for therapeutic purposes does not address the primary prevention issue. I understand you agree with this. Moreover, in order to treat only the anemics, first, they must be identified (currently an impossible task in most developing country areas, for many reasons). Then, for every anemic subject there is one or more iron deficient individual in the vulnerable groups. We can predict that where anemia prevalence is about 20 % (a conservative figure for vulnerable groups in developing areas), about 50 % of these groups will be iron deficient. This should be our main target population. Lastly, a large proportion of subjects treated for anemia under these conditions recur until they move to a less vulnerable group or are able to improve their food bioavailable iron.

I am sure that you also agree that therapy for iron deficiency anemia is rarely an emergency that requires a "rapid" increment of Hb.

Quoting Dr. Crosby; "Iron deficiency is rarely a threat to life and speed in its repair is unimportant". Therefore, large therapeutic doses of iron as advocated by many, and that have the risk of side effects (and rejection of therapy) and of "oxidative stress" is rarely justified.

I thank you for considering weekly iron supplementation "as a medium term approach to primary prevention of IDA .. for high risk adolescent girls .. . provided there are enough trials to prove its efficacy ( we await your paper on the subject)". As you are aware, the idea of weekly preventive iron (plus folate) supplementation is new and several efficacy trials among vulnerable groups have been finished recently (some are published, others have been submitted for publication and others are still in progress). Specifically, a trial in Indonesia among adolescent girls has been published, one in Malaysia and three others, one in Guatemala, another in India and another in Berkeley have been submitted.

Hopefully these will be published soon. I can anticipate to you that all are positive.

Ideally, I agree with you that "For long term solutions to the IDA problem however, I do not believe that the solution lies in that direction", as discussed above. However, there may be exceptions: based on the present situation, iron supplementation during pregnancy (the earlier the better); fertile age women planning to become pregnant or at "risk" of pregnancy (e. g. Teenagers) who even in the industrial world, as you point out, have a prevalence of 20 % or more of iron deficiency and possibly, infants and toddlers. I can add that over 50 % of women enter pregnancy without adequate iron reserves and that these largely determine the iron nutrition throughout pregnancy even when iron supplements are prescribed (?). I see preventive supplementation as a surrogate to targeted fortification to these vulnerable groups.

I do not necessarily agree with your statement that "" people may not be prepared to take "tablets" weekly for the "rest of their lives" and some may say that they are not ill to be taking such supplements anyway."" for the following reasons: 1) There are successful commnunity-based,long-term malaria prevention programs based on weekly intake of a tablet. 2) Intensive involvement of community organizations (e. g. schools, religious organizations, enterprises paying women weekly or by-weekly, etc.) together with education and motivational techniques must be tried to insure compliance with tablet intakes. In Panama, Guatemala and Thailand teachers are enthusiastically giving weekly iron tablets with significant success (various national reports are available and some are being submitted for publication). They see a significant benefit to the children and in Panama the teachers have already pushed for national programs. 3) Governmental and other organizations can remind people to take their tablets weekly (e. g. in Ecuador, all radio and TV stations pass frequent spots in "iron intake days"). 4) The supply of iron tablets in a convenient form must be explored (e. g. blisters containing 50 tablets would be good for 1 year) and made available in neighborhood stores. In other words, the DEMEDICALIZATION of iron deficiency prevention programs and the use of techniques to insure adherence is a must. 5) Preventive supplementation should be used only with vulnerable groups and these subjects would not have to take weekly iron the "rest of their lives".

Having said that, to try to "prevent iron deficiency" by supplementation only during pregnancy is very inefficient. To insure adequate iron nutrition of women in areas where they are vulnerable and other approaches are not available now, iron supplementation should be considered throughout reproductive cycles, including pre- and post-pregnancy periods. Once they move out of being "vulnerable" by age, low probability of a new pregnancy, or effective birth control, they should no longer take weekly iron unless they are at risk of iron deficiency for other reasons. Also, if food-based and parasite control measures are in place and are proven successful, preventive iron supplementation could be discontinued.

I FULLY AGREE that the ideal for the solution of all nutritional problems is what you state: " household and community food security" plus adequate food choices and healthy life styles, equitable distribution of portunities, fair trade, etc. These are more amenable in well informed, educated and economically stable and equitable societies, living in a civil political and socioeconomic environment, with socially-minded political structures. Even there iron deficiency of vulnerable groups persist in a substantial proportion of the population, as you have stated. My question is: WHAT TO DO IN THE MEANTIME, PARTICULARLY WHERE THESE CONDITIONS DO NOT EXIST AND WILL TAKE A LONG TIME TO IMPLEMENT ?

In essence we must think differently to what has been the practice for "prevention of iron deficiency" and proven ineffective in the developing world for the last 50 years. I hope that preventive supplementation programs are only short-term and remedial while our ideals materialize. I am afraid this will take longer than what I still have to live. I apologize for such a lengthy response.

I look forward to your reply and to a continuous and fruitful dialog.

Sincerely,

Fernando


Date: Fri, 28 Aug 1998 15:12:33 +0100

From: "Dr.Harsha De Silva" <amalateureka.lk>

Subject: Re: Ngonut: Anaemia responsive to iron without low ferritin?

 

Dear Dr. Viteri,

Thank you very much for your comment. At the beginning ofthe study the ferritin value range was 18.5-150 ug/l with mean of 58.1(58.3) and the prevalence of anaemia was 14.3% (n=42). After 2 months supplementation ferritin became 16.0-185.0 with the mean of 80.8(38.9) and the anaemia prevalence came down to 2.3%. After this fruitful Email discussion I took the cut off as 30 and looked at my data. Now it correctly tally with the result.

The number of participants With ferritin value below 30 before and after the treatment was 9 and 4 respectively. The number of adolescents with anaemia was 6 and 1 respectively.

Thank you so much for everybody who help me on this topic.

Renuka.

 

Dear Dr. Jayatissa:

> There are now several trials on daily or weekly iron

>supplementation to school girls (Malaysia,Indonesia, Guatemala, Panama,

>India) all showing a positive effect on improving iron status manifested by

>reductions of anemia prevalence and increments in ferritin levels by both

>methods if the trial is of several months duration and with proper doses.

>In the short term, daily iron has slight therapeutic advantages, as would

>be expected unless weekly iron was absorbed 7 times more than daily (highly

>improbable!). One of these trials is published and two or three are already

>sent for publication.

> I would like to ask, first , if infection is prevalent in your

>sample, if ferritin levels are subjected to standardized controls and if

>you have ferritin distributions in different age-sex groups. How often do

>you see ferritin levels below 10 in infants 6 - 18 months old ? It could

>be that for the method you use and for your population, a cut off of 30

>would be appropriate, as suggested by Skikney in populations where

>infection is highly prevavent. Did you measured ferritin after your

>short-term trial ?. A response to iron administration on various measures

>of iron status is the best proof that iron deficiency existed (your case in

>point). Lastly, vitamin A or folate deficiencies can fictitiously elevate

>ferritin values.

> The idea I have been proposing is that weekly iron supplementation

>should be a LONG-TERM, PREVENTIVE MEASURE, IDEALLY COMMUNITY BASED (e. g.

>school setting, factories, religious and mother groups, etc.) AND UNDER THE

>GUIDANCE OF THE HEALTH SECTOR. Therefore, the long-term effect among

>adolescent girls would be to increase their iron reserves. However, when

>daily or weekly doses are administered for a short period of time to anemic

>subjects and Hb response is the only parameter followed it seems to me that

>what is being sought is a therapeutic response. Under those circumstances

>daily doses are more efficacious in treating anemic girls in a shorter

>period of time but at greater risk of undesirable side effects and it

>appears that the effect is only short term (a paper on this matter has been

>submitted). Long term weekly doses will also correct anemia at somewhat

>slower pase but with the advantages that the side effects are much less and

>there are less signs of oxidative stress compared to daily doses (recent

>studies).

> I think that because of all of the above, it is a mistake to

>"detect the effect of daily Vs weekly doses of iron". The purposes of each

>scheme should be different: daily for short term (and temporary) therapy.

>Weekly for long term prevention of development of iron deficiency and for

>improving iron stores in women prone to become pregtnant.


Date: Sun, 30 Aug 1998 17:33:01 +0100

From: viteriatnature.berkeley.edu

Subject: Re: Ngonut: Anaemia responsive to iron without low ferritin?

 

Dear Dr. Jayatissa

I hope your ferritin means are geometric. I would also urge you to look at the prevalence of ferritins above 70 and above 85. Contrary to what many people think, we maintain that high ferritins are undesirable. In a pilot study to see if we could determine oxidative stress in a group of non-pregnant women receiving 120 mg Fe daily and whose geometric ferritin mean was 25 g/l at the start, ferritins above 60 may indicated risk of oxidative stress as indicated by a proportion of them also exhaling high levels of ethane and showing elevated MDA in plasma. These did not happen when women received 120 mg of iron weekly. Ferritin levels above 70 are uncommon in US fertile-age women in the US (Cook et al. 1986) and may suggest some degree of iron overload. In your population of adolescents who already have high ferritins, maybe due to infection (an oxidative stress condition) I would not like to see high ferritin values as a consquence of supplementation. I have suggested ferritins of 75 and 85 g/l in your population considering the initially high ferritins, the origin of which remain a mistery to me.

Basically, what I am saying is be cautious in interpreting rapid rises in ferritin. It would be better to have a slow progressive increment in iron reserves with long-term preventive supplementation. In effect, this is what happens !!

Fernando E. Viteri, MD., ScD., Professor, Nutritional Sciences

University of California

Berkeley, CA 94720-3104

Phone: (510) 642 6900

FAX: (510) 642 0535

Email: viteriatnature.berkeley.edu