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Author Topic: Iron deficiency again??  (Read 6642 times)
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« on: April 29, 2010, 02:52:34 PM »

My cbc labs and some thoughts... (while i'm slightly frustrated)

hgb               9.4

total rbc         4.94    (4.2-5.4)

pcv/hct          30.6     (38-47)

mcv                61.9    (82-92)

mch                19       (27-31)

mchc              30.7     (32-36)

total wbc         7.39     (4.5 - 11)


My hgb manages to go upto 10.5 sometimes, thats when i'm at my energetic best.  But mostly it is between 9 and 9.5.

Iron deficiency at play - due to the IBS/celiac/malabsorption.

I read somewhere...

Normal blood iron levels dont necessarily means enough iron in the body.

Iron studies keep changing depending on one's diet when the tests are done, and whether supplements/iron foods are being eaten in the past few days.

Low ferritin tells whether one needs iron supplementation. (mine is always 10-20)

Earlier I was always on iron pills, and my ferritin and hgb never showed any improvement, so it was assumed I dont have iron deficiency. And a lot of other health problems I had seemed to indicate iron oveload. 

Later i was suggested iron drops as an alternative when required. I read here on forums about others trying it too.

Probably I have to stick with the drops for a long time, and keep tracking ferritin. It is also said that for iron overload symptoms to occur, ferritin MUST BE HIGH.  Mine has never gone above 20.

Does this mean it may be a better idea for me to stick to iron drops TILL my ferritin and hgb are better?

Is it possible I overload on iron ONLY when I take the pills (that time my iron studies indicate overload), and when I stop the pills my problems solve themselves, but then the iron deficiency shows.

We keep doing the same hgb, ferritin, iron studies over and over again, and each time each doctor has conflicting views!  i'm losing patience here!

Does it even make sense that when  my iron studies show iron staturation above normal/iron overloading,  but ferritin still at 10-20 Huh?

Also is the mentzers index reliable at telling us if anemia is due to iron def or due to thal? 

Sorry i'm rambling today, i'm tired and fed up.

For me....

For all of you,

Symptomatic Beta Thal Minor.
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« Reply #1 on: May 10, 2010, 03:51:17 AM »


I think you should keep taking iron drops,if they don't rouble your stomach or something,because i don't think with that low ferritin you are heading towards iron over load.


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« Reply #2 on: May 10, 2010, 04:49:30 AM »

Hi Preety
Ferritin is only a rough estimate and may actually not reflect actual Iron overload. If Iron is not helping you to raise your hb you should try B- complex and folic acid. My cousin also has IBS and she is also a thal minor. Her hb is around 8 and even drops to 7. In less than a year her weight had dropped from a healthy 58 to a skinny 40. She too was on Iron supplements as both her ferritin and iron saturation was low, but it worsened her IBS and she had to stop it. B-COMPLEX has helped her a lot.

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« Reply #3 on: May 14, 2010, 04:12:39 PM »

Thanks Zaini and Maha,

We decided to do a trial of iron drops for few weeks and see if ferritin goes up even a bit. Right now its 20, and hgb is 9.4.   If the drops do get absorbed, I may have my answers.   :-)

Iron pills worsen the IBS so i totally avoid them. I'm 40 kilos now, max i can touch is 42 kilos. :-(

Yes I have been taking folic acid since long, started B complex now since a month. :-)

I also started a protein powder to help my nutrition levels, as my IBS keeps my appetite low too.

Keeping my hopes up!

Symptomatic Beta Thal Minor.
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« Reply #4 on: July 23, 2010, 07:15:10 AM »

I just read an article that lays a connection between IBS and vitamin D deficiency. I thought it was something for you, Preety.

Here is it:

Amid the Murk of 'Gut Flora,' Vitamin D Receptor Emerges as a Key Player

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Monday, July 12, 2010

Within the human digestive tract is a teeming mass of hundreds of types of bacteria, a potpourri of microbes numbering in the trillions that help us digest food and keep bad bacteria in check.

Now scientists have found that the vitamin D receptor is a key player amid the gut bacteria – what scientists refer to matter-of-factly as the “gut flora” – helping to govern their activity, responding to their cues, and sometimes countering their presence. The work was published online recently in the American Journal of Pathology.

The findings deliver a new lead to scientists investigating how bacteria might play a role in the development of inflammatory bowel diseases such as Crohn’s disease or ulceractive colitis. The work complements studies suggesting that Salmonella infection can increase the risk of inflammatory bowel disease.

“Vitamin D deficiency is a known factor in the pathology of inflammatory bowel disease and colon cancer,” said microbiologist Jun Sun, Ph.D., of the University of Rochester Medical Center, “but there have been very few reports about how bacteria might play a role by targeting the vitamin D receptor. Our work suggests one possible mechanism, by working through the vitamin D receptor, a sensor and regulator for the majority of functions of vitamin D.”

Sun specializes in the actions of bacteria in the body and how their interactions within the body contribute to disease. She has shown that bacteria often found in the human intestine affect molecular signals known to contribute to inflammatory response and cell growth.

Her work with the vitamin D receptor takes place at a time when the molecule is coming under increasing scrutiny. Scientists have associated vitamin D and the receptor with many types of cancer, as well as osteoporosis, heart disease, diabetes, inflammatory bowel disease, and infection.

Sun’s team took a close look at the vitamin D receptor in mice and its interactions with bacteria in the colon. The team studied normal mice; mice in which the vitamin D receptor had been knocked out; and mice that were completely free of any germs. Scientists observed how the mice responded to infection with either a harmless strain of E. coli or a pathogenic strain of Salmonella typhimurium.

The team found that Salmonella is able to regulate the vitamin D receptor, increasing its activity and determining where in the colon the receptor is active. In the presence of Salmonella, the receptor was more prevalent than usual deep within folded intestinal structures known as crypts.

Sun’s team also discovered that the vitamin D receptor plays a key role in defending the body from assault by Salmonella and squelching inflammation. The receptor stops a molecule known as NF-Kappa B, a well-known master player in the world of inflammation, by binding to it and preventing it from activating other inflammatory molecules. While scientists have known that the receptor interacts with NF-Kappa B, details of the interaction modulated by bacteria in the colon are new.

The scientists found that Salmonella was much more virulent and aggressive in mice in which the vitamin D receptor had been turned off. These mice showed higher levels of activity of inflammatory molecules, and they lost weight more quickly and were much more likely to die in response to infection.

“We live together in a mutually beneficial state with most of the bacteria in our gut,” said Sun, assistant professor in the Gastroenterology and Hepatology Division of the Department of Medicine. “They help us digest foods like fruits and vegetables, and we provide them a place to live and thrive. We co-exist peacefully – most of the time.

“But we aren’t able to culture most of these bacteria in the laboratory, and we don’t know what most of them are doing. We need to understand our gut flora much more than we do. This is particularly important for understanding how we might manipulate the natural gut flora to stop an invader like Salmonella,” added Sun, who also has appointments in the James P. Wilmot Cancer Center and the Department of Microbiology and Immunology.

In addition to Sun, authors of the study from Rochester include the first author, post-doctoral associate Shaoping Wu, Ph.D., of the Gastroenterology and Hepatology Division; Jian-Dong Li, M.D., Ph.D., of the Department of Microbiology and Immunology; former technician Anne P. Liao; and former research assistant Yinglin Xia, Ph.D.

Other authors include Yan Chun Li, Ph.D., of the University of Chicago, who supplied the vitamin D receptor “knockout” mice, and R. Balfour Sartor, M.D., of the University of North Carolina at Chapel Hill, who supplied the specialized germ-free mice through the Center for Gastrointestinal Biology and Diseases Gnotobiotic Core Facility and the National Gnotobiotic Rodent Resource Center.

This work was funded by the National Institute of Diabetes and Digestive and Kidney Diseases.
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Source: University of Rochester Medical Center
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« Reply #5 on: July 23, 2010, 03:44:32 PM »

Ah, a nice study done at my local university. By the way, the name thalassemia was coined at this same center back in the 1950's.

About 2/3 of those tested are testing deficient for vitamin D, and this is even with the low end level set too low (25). Most now agree that the low end acceptable level for vitamin D should be 30. I can't think of any circumstances in which anyone with a blood disorder should not be tested for D levels. Get tested and if you are low, take a supplement daily. I take 5000 IU daily except during summer when I can get plenty of sunshine.


All we are saying is give thals a chance.
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« Reply #6 on: July 26, 2010, 02:18:20 PM »

Thanks Dori,

Yeah I have to avoid the sun completely as it gives me migraines and discomfort. I do take vitamin D regularly.

Now my IBS confuses me even more - it gets triggered randomly. I can have some plain wheat products and some spices now, but not refined flours, other grains or fats.

I'm still on the iron drops, will get tested after few months only.   


Symptomatic Beta Thal Minor.
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