Iron Deficiency Without Anemia – Common, Important, Neglected

Buy Lab Tests Online

madman

Super Moderator
Iron Deficiency Without Anemia – Common, Important, Neglected (2019)

Esa Soppi* Department of internal medicine, Eira Hospital, Laivurinkatu 29, FI-00150 Helsinki, Finland








Abstract
A serum ferritin concentration of <30 µg/L is the most sensitive and specific test for the identification of iron deficiency in patients with or without anemia.
However, patients may be iron deficient at much higher concentrations of ferritin. Iron deficiency without anemia and with normal red blood count is a clinical challenge, and many patients have been diagnosed with a multitude of conditions ranging from hypothyroidism to depression to chronic fatigue syndrome over the years when they have sought help for their often debilitating symptoms. The keys to a correct diagnosis are assessment of the serum ferritin concentration and a meticulous medical history focusing on the possibility of life-long blood losses and diseases such as celiac disease. Differential diagnostic causes for the symptoms must be sought for. The mainstay of therapy is oral iron in sufficient doses for at least 6 to 9 moths together with serum ferritin monitoring. Some patients who do not respond to oral iron treatment may need intravenous iron. The longer the iron deficiency has lasted, the more challenging the therapy may be. Some iron deficient patients without anemia may have had the condition for over a decade, and may not fully recover. The amount of human suffering, the loss of quality of life and the indirect costs to society caused by iron deficiency are huge.






Introduction
Iron deficiency is the most common nutritional deficiency. Several studies in Western countries have shown that 3–9% of children have iron deficiency before puberty. Some 11–33% of young women have iron deficiency after menarche, and 3.5–13% of males are iron deficient after having passed the growth spurt in adolescence. The prevalence of iron deficiency is constantly high, at 9–22%, among menstruating women, but among adult males the prevalence settles to around 1–2%. After menopause, the prevalence of iron deficiency among females approaches the prevalence of males and is 1.4–4% [1-3]. It has been estimated that 25–40% of females have iron deficiency anemia at some stage in their life [3,4]. Still, iron deficiency without anemia is much more common than iron deficiency anemia.

Excluding major blood loss, iron deficiency ensues as the end result of a long period of negative iron balance, i.e., when iron losses exceed iron intake or there are increased demands [5,6]. First, iron stores are gradually and progressively depleted and only then anemia may develop. Clinical data is emerging and showing that many patients may remain in prelatent or latent stages of iron deficiency without progressing to anemia [2,3,7-9].

During my 30-year carrier as a consulting internist I have met hundreds of patients, mainly menstruating females, who have sought medical advice for prolonged (1–35 years) fatigue, brain fog, muscle and joint pains, weight gain, headache, dyspnea, palpitations (sometimes associated with sleep disturbances), arrhythmia, lump in the throat or difficulty in swallowing or restless legs. Over time, the patients have often received a spectrum of diagnoses and corresponding treatments: subclinical hypothyroidism, fibromyalgia, burnout, overtraining, asthma, somber mood extending from melancholy to severe therapyresistant depression, chronic fatigue syndrome and chronic Lyme disease. It is important to include iron deficiency without anemia as a differential diagnostic possibility, because this type of iron deficiency is very often associated with symptoms that severely impair the patient’s performance and quality of life and may even hinder the patient from overcoming the ordinary challenges of everyday life and may cause permanent disability.






Differential diagnosis
The symptoms experienced by persons with iron deficiency are not pathognomonic, although the saying that “usual diseases are common” fits very well. It is important that the physician considers the etiology: What causes the iron deficiency in the patient (Table 2)? Among the common causes for iron deficiency are heavy menstrual bleedings and hemorrhages in connection with pregnancy and delivery among females and multiple blood donations, celiac disease and ulcerative colitis in both genders.

There are several conditions and illnesses with symptoms mimicking iron deficiency. Examples are hypothyroidism, profound vitamin D deficiency, vitamin B12 deficiency, celiac disease, testosterone deficiency, abnormal calcium metabolism, sleep apnea, heavy smoking and even occult malignancy [3,17]. Adequate differential diagnostic consideration is, of course, needed. There are innumerable patients with iron deficiency who have been put on thyroid hormone medication despite normal thyroid function. This is due to the fact that the symptoms of hypothyroidism and iron deficiency are very similar, and the serum thyrotropin activity tends to increase in iron deficiency [22,25]. In this setting, increased TSH-values are due to the enzyme thyroid peroxidase, a hormone that contributes to thyroid hormone synthesis. Thyroid peroxidase contains an iron moiety and in iron deficiency the function of the enzyme is disturbed. The symptoms may abate transiently when the patient takes thyroid hormone, but the iron deficiency must be corrected as soon as possible, during which time the need of thyroxin often decreases. Patients with iron deficiency tend to tolerate thyroid hormones poorly. Once the iron stores have been replenished, it is best to discontinue thyroid medication, if possible. Since both hypothyroidism and iron deficiency are common, it is by no means rare for a patient to have both conditions simultaneously, possibly even complemented with other comorbidities which further accentuate symptoms.












*Iron inhibits the absorption of thyroid hormones, and hence it is best to take the thyroxin tablet in the morning and the first iron pill around noon. Iron absorption is reduced by milk, calcium and magnesium products and by proton pump inhibitors. Also, coffee, tea and cereal products affect negatively the uptake of iron. At higher doses of iron intake, these diet restrictions have less importance. The impact of vitamin C as an uptake enhancer diminishes also when the iron dose increases. The role of the diet as a treatment modality of iron deficiency is generally modest, but once iron deficiency has been corrected, dietary iron is a significant iron homeostasis-maintaining factor.








Conclusion
Iron deficiency is very common and may be ranked among the most common public health concerns today. Diagnosing iron deficiency, especially if there is no iron deficiency anemia, is a challenge for the clinician. Iron deficiency without anemia seems to be an autonomous clinical condition which needs special attention, as has been suggested earlier [9].
Clearly, we have yet much to learn about iron deficiency and iron metabolism and how they relate to the spectrum of symptoms experienced by the patient. Iron deficiency is a real and harsh disease which may lead to severe symptoms and work incapacity. The longer the duration of iron deficiency, the more difficult it is to treat. The treatment of iron deficiency is often carried out with too small doses of iron and for too short a time. The treatment response must be followed up with assessments of the blood count and the serum ferritin concentration. Follow-up must continue for at least one year after normalization of the hemoglobin and ferritin concentrations.
 

Attachments

  • AUG18-IRON-CCRR-5-456 pdf.pdf
    802.4 KB · Views: 135
Last edited:
Defy Medical TRT clinic doctor

madman

Super Moderator
Table 1. Different stages of iron deficiency (*A significant part of these patients may never progress to overt anemia)
Screenshot (494).png
 

madman

Super Moderator
Figure 1. The hemoglobin value of a young man, age 35, had been about 165 g/l in numerous blood samples taken over several years before the consultation
Screenshot (495).png
 

madman

Super Moderator
Figure 2. The female patient, age 51, had had fatigue, reduced mental awareness and restless legs for several years before her appointment
Screenshot (496).png
 

madman

Super Moderator
Figure 3. A small dose of iron in a young female iron deficient patient without anemia causes a very modest increase in ferritin concentration (from 5 to 9 µg/L) but decreases the soluble transferrin receptor (sTfR) concentration to the normal range
Screenshot (497).png
 

madman

Super Moderator
Figure 4. Judging from the patient’s history and symptoms, her iron deficiency had prevailed for more than 20 years, although both the ferritin and the hemoglobin values were available only at 2 years before the patient's first office visit (time point -2)
Screenshot (501).png
 

madman

Super Moderator
Figure 5. Rise in ferritin level per 100 mg of infused ferric carboxymaltose in relation to the ferritin level before the first infusion. The figure shows that it is not possible – using the preinfusion serum ferritin value – to estimate with certainty how well the amount of storage iron will be corrected by infusion treatment
Screenshot (502).png
 

madman

Super Moderator
Pay attention to your ferritin level as it is more important to overall health than many may think.

*A serum ferritin concentration of <30 µg/L is the most sensitive and specific test for the identification of iron deficiency in patients with or without anemia. However, patients may be iron deficient at much higher concentrations of ferritin
 

Systemlord

Member
So what do you make of low ferritin 22 and high rbc 6.99 and high hemoglobin 18.9?

Leading up to my critical iron deficiency months prior I notice my hemoglobin declining (14.1) while the hormone panel showing levels at 450 ng/dL, as I had iron and ferritin below range, over time my MCH was decreasing and hemoglobin along with it.

My hemoglobin was always on the higher end before trouble started, now with testosterone 450 ng/dL hemoglobin was now below my pre-TRT levels, I have higher hemoglobin now (15.6) with a Total T of between 97-119 ng/dL than I did at 450 ng/dL.

In time the same will happen to you, it's called microcytic anemia.
 
Last edited:

Systemlord

Member
But my hemoglobin is increasing. Crazy high. I want to donate again ASAP. Last donation 3 months ago took my ferritin from 29 to 19.

You haven't reached the tipping point yet, eventually you'll get there. When I was at my worst, iron was 40 and ferritin was 24, this point where I experienced iron deficiency.
 

TorontoTRT

Active Member
But I want my hemoglobin to lower. I can’t find this answer anywhere though. How can ferritin be low, but hemoglobin, RBC and HCT insanely high?
Right now:
RBC 6.99
HG 18.9
HCT 56
FERRITIN 22
 

GreenMachineX

Well-Known Member
But I want my hemoglobin to lower. I can’t find this answer anywhere though. How can ferritin be low, but hemoglobin, RBC and HCT insanely high?
Right now:
RBC 6.99
HG 18.9
HCT 56
FERRITIN 22
Happened to several of us. For most of us the answer was to reduce our testosterone dosage. I’m now using 100mg per week and feel great at 600-700 total test with free T at 20. Chasing numbers near the 1000 isn’t worth it.
 

madman

Super Moderator
So what do you make of low ferritin 22 and high rbc 6.99 and high hemoglobin 18.9?



What is your trt protocol and where does your TT/FT levels sit?

What is your SHBG?

Do you suffer from sleep apnea as it can definitely contribute to/cause elevated rbc's/hemoglobin/hematocrit.

Being on trt and having sleep apnea would be a double whammy!

As you know use of exogenous testosterone will increase ones rbc's/hemoglobin/hematocrit levels within the 1st month of treatment and can continue to increase in the following months until levels peak at 9-12 months.

Not only are higher supra-physiological T levels thought to play a role but also higher TT/FT levels will have an impact.

Anytime one increases T dose an increase in rbc's/hemoglobin/hematocrit will follow.

In many cases most men on trt start donating blood well before this peak is reached to try
and maintain healthy levels but unfortunately many end up donating blood too frequently and end up crashing their ferritin which eventually will lead to iron deficiency.....top it off with the fact that many are already not taking in enough dietary or supplementary iron which eventually will become a recipe for disaster.

Even in cases where one is donating blood too often and at the same time taking in adequate iron whether through diet/supplementation they will still have issues with replenishing ferritin stores as it takes time to build them back up (3-6 months.....longer in some cases depending on severity of depletion).

Most men should not donate more than twice a year......some may be able to get away with 3 times/year max......otherwise you will end up crashing your ferritin and eventually develop iron deficiency.

The only ways to lower rbc's/hematocrit/hemoglobin when on trt is to lower T dose or donate.

The most sensible piece of advice would be to bring down your TT/FT levels into a descent range as many on trt are running higher levels than they truly need but at the same time you need to find the lowest TT/FT level you can run while reaping the positive benefits of T otherwise you will end up experiencing low-t symptoms again.

You definitely need to start supplementing iron to get your ferritin levels back in a healthy range so for you that would meant HALTING any further blood donations and seeing as your rbc's/hemoglobin/hematocrit are high you strongly need to consider lowering your T dose and looking into bringing down your TT/FT levels as it will bring down your rbc's/hemoglobin/hematocrit.....mind you I have no idea what dose of T you are on let alone where your TT/FT levels sit (so this may very well not be an option).





"The development of iron deficiency anemia is a gradual process. If your body is not taking in enough iron, your body first uses the iron that is stored in tissues (i.e., ferritin) and blood levels of ferritin will begin to decrease. If not corrected, the stored iron begins to be depleted as it is used in the production of red blood cells. In the early stages of iron-deficiency, blood levels of iron can be normal while stored iron, and therefore ferritin levels, will begin to decrease"
 
Last edited:

madman

Super Moderator
Critical point here

"The development of iron deficiency anemia is a gradual process. If your body is not taking in enough iron, your body first uses the iron that is stored in tissues (i.e., ferritin) and blood levels of ferritin will begin to decrease. If not corrected, the stored iron begins to be depleted as it is used in the production of red blood cells. In the early stages of iron-deficiency, blood levels of iron can be normal while stored iron, and therefore ferritin levels, will begin to decrease"
 

TorontoTRT

Active Member
My problem is HCT (56), HG (19) and RBCs (6.9) are the same no matter on the protocol.
I’ve done 100 mg once weekly, 40 mg every 3.5 days, 72 mg every 5 days, and currently:
70 mg every 4 days test cyp total weekly 122.5 mg
Numbers on trough below
TT 926
FT 23.2
E2 72 ( no high e2 sides )
SHBG 31

Numbers on trough much weaker on previous 72 mg every 5 days protocol
TT 600
FT 13.5
E2 35
SHBG 31

same blood numbers
 
Last edited:
Buy Lab Tests Online
Defy Medical TRT clinic

Sponsors

enclomiphene
nelson vergel coaching for men
Discounted Labs
TRT in UK Balance my hormones
Testosterone books nelson vergel
Register on ExcelMale.com
Trimix HCG Offer Excelmale
Thumos USA men's mentoring and coaching
Testosterone TRT HRT Doctor Near Me

Online statistics

Members online
5
Guests online
4
Total visitors
9

Latest posts

bodybuilder test discounted labs
Top