Archived Bulletin Board
Tests and Drugs
Weight Loss Experiment
Nutrients and Toxics
Table of Contents ||
ANEMIA--TYPES AND CAUSES
Many disease conditions are associated with thyroid
diseases, but of all these diseases, the one with the highest association is
anemia. I read one study which indicated that about one half of all
hyperthyroids had clinically diagnosed anemia. It's possible, and to me
quite likely, that the other half were also anemic but not diagnosed because
they had copper-deficiency anemia and not iron-deficiency anemia.
Anemia is usually caused by a deficiency of hemoglobin
which is the oxygen carrying molecule in the red blood cell. While many
minerals are important in the body's manufacture of hemoglobin, iron and copper
are the most important. A deficiency of either iron or copper will result
in anemia, either iron-deficiency anemia or copper-deficiency anemia.
Anemia is often medically diagnosed by determining blood
levels of iron and the iron-carrying protein ferritin. This test
will determine anemia if the anemia is due to iron deficiency. However,
this test will not show if the person has copper-deficiency anemia.
It seems that many doctors are unaware of copper-deficiency
anemia and will try to correct all cases of anemia by prescribing very large
doses of iron. Since the majority of cases of anemia are probably the
result of iron deficiency, then this procedure usually works. However, in
copper-deficiency anemia, taking excess amounts of iron will further deplete
copper and cause the anemia to worsen. This exact scenario has happened to
more than one person in our group.
SYMPTOMS OF ANEMIA
The symptoms of anemia are: rapid heart beat, dizziness
upon standing, reduced capacity to exercise, reduced endurance, elevated heart
rate when exercising and failure of the heart to return to a normal rate in a
reasonable time upon exercise cessation, low physical energy, low mental energy
("brain fog"), feeling of unease which is alleviated by a period of
breathing deeply, inability to fall asleep or to sleep well (insomnia), waking
up gasping for breath, and an increase of all these symptoms when traveling to a
higher altitude (vacationing in the mountains).
All of these symptoms are related to a reduced amount of
oxygen getting to the cells. The most serious of these symptoms is the increase in heart
rate. Because each red blood cell carries less oxygen to the cells, the
heart rate increases to increase the blood flow so that the cells will not be
CONNECTION BETWEEN ANEMIA AND THYROID DISEASE
Keep in mind that there is no clear-cut proof of this, but
I believe that the mineral deficiencies which lead to hypothyroidism and
hyperthyroidism bear remarkable similarity to the mineral deficiencies which
lead to the two main types of anemia.
Iron-deficiency anemia and hypothyroidism are similar in
that in both iron is more deficient than copper.
Copper-deficiency anemia and hyperthyroidism are similar in that in both copper
is more deficient than iron.
It is an easy step to postulate that anemia is the single
most important pre-existing and causative condition in the etiology of
hypothyroidism and hyperthyroidism. Hypothyroidism may be the result of
iron-deficiency anemia and hyperthyroidism may be the result of
Since iron is needed by the body in amounts approximately
five times that of copper, then iron deficiency probably occurs more often than
copper deficiency. I've read that one-fifth of the world's population
suffers from iron deficiency. This may be one of the reasons that
hypothyroidism is more common than hyperthyroidism.
WHO GETS ANEMIA AND THYROID DISEASE
Women in their child-bearing years need more iron and
copper than women at other ages and men at any age because of the monthly
blood loss during menstruation. Pregnancy, child-birth, and nursing place
additional mineral drains on this group of women. This age group of women is the
same group that is 8-10 times more likely to get thyroid diseases and autoimmune
When a otherwise healthy teenage girl gets hyperthyroidism
right after beginning her period, then it has to be the result of a deficiency
of minerals that are depleted by the blood loss. What other explanation
could there be? When a woman develops hyperthyroidism during pregnancy or
breast feeding, it also indicates a deficiency.
Who else gets anemic and gets thyroid disease? People
who exercise excessively like Olympic athletes and they often get anemia and
hyperthyroidism. Older men and women, especially if they don't eat much
red meat (iron) or drink much beer (copper). Also, people with poor
digestion such as those with celiac disease.
WHAT ARE THE MAJOR DEFICIENCIES INVOLVED IN ANEMIA?
Following is a study from the US Dept of Agriculture, which
seems to be doing some of the best nutritional research in the country.
The study clearly states that copper deficiency causes anemia and serious
Cardiovascular effects of dietary copper deficiency.
Saari JT, Schuschke DA
US Department of Agriculture, Agricultural Research Service, Grand Forks
Human Nutrition Research Center, ND 58202-9034, USA.
Dietary copper deficiency may impair cardiovascular health by contributing
to high blood pressure, enhancement of inflammation, anemia, reduced blood
clotting and arteriosclerosis. The purpose of this review is to compile
information on the numerous changes of the heart, blood and blood vessels
that may contribute to these cardiovascular defects. These alterations
include weakened structural integrity of the heart and blood vessels,
impairment of the use of energy by the heart, reduced ability of the heart
to contract, altered ability of blood vessels to control their diameter and
to grow, and altered structure and function of circulating blood cells. The
fundamental causes of these changes rest largely on reduced effectiveness of
enzymes that depend on copper for their activity.
- Zinc is essential for normal iron metabolism and prevention of anemia,
but high levels of zinc can depress iron and lead to anemia.
|J Am Coll Nutr 1998 Jun;17(3):291-5
Zinc status relates to hematological deficits in middle-aged women.
Nishiyama S, Irisa K, Matsubasa T, Higashi A, Matsuda I
Department of Pediatrics, Kumamoto University, School of Medicine, Japan.
OBJECTIVE: The objective of our study was to investigate zinc (Zn) status
and the effects of Zn supplementation in relation to iron deficiency anemia
in middle-aged women. It is important to define the role of Zn in
hematologic abnormalities and to determine the frequency of Zn deficiency.
METHODS: Fifty-two Japanese women, selected from a health examination survey
on 6200 women, had hemoglobin concentrations below 12.0 g/dl, total iron
binding capacity (TIBC) below 390 micrograms/dl and fairly normocytemia.
These 52 were divided into three groups and we then compared the
hematological status before and after iron (group A) or Zn (group B) or iron
plus Zn (group C) supplementation. RESULTS: After treatment, concentrations
of hemoglobin (Hb) increased slightly in groups A and B, but not
statistically significant. In group C, Hb levels were significantly
increased from 10.8 +/- 1.1 to 12.8 +/- 1.1 g/dl. Furthermore, numbers of
RBC and reticulocytes, and concentrations of albumin were also increased
significantly. Increased values over 1.0 g/dl of hemoglobin levels were
noted in four women (26.6%) in group A, three women (14.2%) in group B and
13 women (81.2%) in group C. CONCLUSION: Zn status to some extent can
account for hematological abnormalities in middle-aged women. At least 5.0%
of middle-aged Japanese women may have Zn deficiency. Normocytic anemia with
low TIBC levels may serve as a good indicator of a marginal Zn deficiency.
- This study of a hyena which ingested high-zinc coins
shows that excessive zinc can cause anemia
|J Zoo Wildl Med 1999 Sep;30(3):431-4
Zinc toxicosis in a captive striped hyena (Hyaena hyaena).
Agnew DW, Barbiers RB, Poppenga RH, Watson GL
Detroit Zoological Institute, Royal Oak, Michigan 48068, USA.
An 11-yr-old captive-born female striped hyena (Hyaena hyaena) acutely
developed lameness and swelling of the left front foot with anorexia,
depression, and lethargy. Hematologic evaluation revealed regenerative
anemia, azotemia, and other mild serum electrolyte and mineral
abnormalities. Twenty radiographically visible coins and 10 coin fragments
were removed by laparotomy and gastrotomy following unsuccessful medical
therapy. The animal died during anesthetic recovery. Zinc serum levels were
41.0 ppm at first presentation and 36.0 ppm at the time of surgery, compared
with concentrations of 1.78 ppm and 2.82 ppm for serum taken from this
female and a male hyena 3 mo previously. Zinc toxicosis was diagnosed based
on the similarity of clinical signs to those described in dogs, presence in
the stomach of pennies minted after 1982 (when the zinc content of U.S.
pennies was increased substantially), necropsy findings, and elevated serum
and liver zinc values. The case highlights the risk posed by penny ingestion
for subsequent zinc toxicosis in captive omnivores.
WHAT OTHER FACTORS MAY CAUSE ANEMIA?
We have seen that certain minerals like cadmium, aluminum, and
mercury are involved in thyroid disease because they deplete copper, iron, zinc, and
selenium. Are they also involved in anemia?
Smokers get hyperthyroidism at a higher rate than
nonsmokers and the reason is probably the high levels of cadmium in tobacco
which depletes copper. Do smokers have a higher rate of anemia than
nonsmokers? There are not a lot of studies which directly address this
issue, but some that look at it indirectly. The following study suggests that this
hypothesis may be true:
|Epidemiology 2000 May;11(3):285-91
Smoking and myelodysplastic syndromes.
Bjork J, Albin M, Mauritzson N, Stromberg U, Johansson B, Hagmar L
Department of Occupational and Environmental Medicine, Lund University
[Medline record in process]
The purpose of this case-control study was to investigate tobacco smoking as
a risk factor for myelodysplastic syndromes, emphasizing karyotypic
aberrations as markers for exposure and risk differentiation with respect to
morphology. We obtained smoking history by interview of 330 cytogenetically
investigated adult myelodysplastic syndrome cases and 337 controls, matched
with respect to sex, year of birth, and county of living. Smoking for at
least 1 year at some time 20 years or less before diagnosis was associated
with an elevated relative risk (RR) for primary myelodysplastic syndromes
(odds ratio (OR) 1.8; 95% confidence interval (CI) = 1.2-2.7). The results
indicated a relation with intensity and duration of smoking as well as a
decrease in risk a few years after cessation of smoking. Smoking was
associated with an increased RR for primary myelodysplastic syndromes with
chromosome 7 abnormalities (OR 5.0; 95% CI = 1.1-23). Elevated RRs were
also seen for refractory anemia (OR 2.5; 95% CI = 1.2-5.6) and for
refractory anemia with ringed sideroblasts (OR 3.2; 95% CI = 0.88-12). The
findings suggest that smoking is a risk factor for myelodysplastic
PMID: 10784245, UI: 20244831
Following is a very good review which states that cadmium and lead
toxicity causes anemia. Extremely interesting is the comment that "
Quoting the study, "Hg++ accumulation in the brains of
suckling rats is approx. 10 times higher than in grown animals. Milk increases
the bioavailability of Hg++." Does this "10 times" strike a
bell for you as it does for me? This is the factor by which women (high in
estrogen) are more likely to get hyperthyroidism than men. The evidence is
clearly pointing to heavy metal toxicity from cadmium and mercury which is
accelerated by estrogen as the causative factor for hyperthyroidism and
|Z Ernahrungswiss 1990 Mar;29(1):54-73
[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in
food for infants and small children].
[Article in German]
Walther-Straub-Institut fur Pharmakologie und Toxikologie der Ludwig-Maximilians-Universitat,
There are differences between young and adult organisms regarding toxokinetic
aspects and clinical manifestations of heavy metal intoxications. Chronically,
toxic Cd intake causes a microcytotic hypochromic anemia in young rats at
lower exposure levels and after shorter exposure periods than in adult
animals. Cd absorption is increased by co-administration of milk and in
conjunction with iron deficiency. After long exposure periods toxic Cd
concentrations accumulate in the kidney cortex; this process starts very early
in life. In 3-year-old children Cd concentrations in the kidney can reach up
to one-third of those found in adults. Hg++ and methyl-Hg can cause Hg
encephalopathia, and frequently cause mental retardation in adults. Correspondingly,
Hg++ accumulation in the brains of suckling rats is approx. 10 times higher
than in grown animals. Milk increases the bioavailability of Hg++. In
suckling rats Hg is bound to a greater extent to ligands in the erythrocytes.
Methyl-Hg concentrations in breast milk reach 5% of those in maternal plasma
and that is a severe hazard for breastfed children of exposed mothers. Toxic
Pb concentrations can lead to Pb encephalopathia. A high percentage of
surviving children have seizures and show signs of mental retardation. Anemia
and reduced intelligence scores were recently observed in children after
exposure to very low levels of Pb. Pb absorption is increased in children
and after co-administration of milk. There are no definite proofs for
carcinogenesis or mutagenesis after oral exposure to Cd, Hg, and Pb in man.
Heavy metal concentrations were found in the same order of magnitude in
commercial infant formulas and in breast milk. When infant formulas are
reconstituted with contaminated tap water, however, Pb and Cd concentrations
can be much higher. The average heavy metal uptake from such diets exceeds the
provisional tolerable weekly intake levels set by the WHO for adults,
calculated on the basis of an average food intake and a downscaled body
weight. These considerations do not even provide for differences in absorption
and distribution or for the increased sensitivity of children to heavy metal
exposure. However, dilution effects for essential heavy metals were observed
in fast-growing young children; this effect might be extrapolated to toxic
metals. These theoretical considerations are compared with epidemiological
evidence. A health statistic from Baltimore shows a decline of Pb
intoxications in infants. This observation correlates with a simultaneous
decline in exposure to Pb which was due, for example, to decreased use of lead
dyes in house paints and the abolition of tin cans for infant food.
What about aluminum? Does high aluminum intake cause
anemia? The following study shows that aluminum can interfere with iron
absorption and metabolism and contribute to anemia.
|Toxicology 2000 Jan 3;142(2):97-109
Effect of dietary aluminum on tissue nonheme iron and ferritin levels in
Han J, Han J, Dunn MA
Department of Food Science and Human Nutrition, University of Hawaii,
Honolulu 96822, USA.
Aluminum toxicity is well documented but the mechanism of action is poorly
understood. In renal failure patients with aluminum overload,
disturbances in iron metabolism leading to anemia are apparent. Few
animal models, however, have been used to study the effects of dietary
aluminum on iron metabolism. The purpose of this study was to determine if
dietary aluminum exposure alters tissue iron and ferritin concentrations in
the chick, as has been found in cultured human cells exposed to aluminum.
Groups of day-old chicks were fed purified diets containing one of two
levels of iron (control or high iron), and one of three levels of aluminum
chloride in a 2 x 3 factorial design. Diets were consumed ad libitum for 1
week, then pair-feeding was initiated for 2 more weeks. A seventh group
consumed a low iron diet ad libitum for comparative purposes. After the
3-week feeding period, samples of kidney, liver, and intestinal mucosa were
analyzed for nonheme iron and ferritin concentrations by a colorimetric
assay and SDS-PAGE, respectively. Results showed that dietary aluminum
intake reduced iron stores in liver and intestine, but had no effect on
nonheme iron levels in the kidney. Ferritin levels were reduced by aluminum
intake in all tissues studied. The decreases in tissue ferritin levels were
proportionately more than the decreases in tissue nonheme iron levels. This
resulted in increased nonheme iron to ferritin ratios that amounted to as
much as 140 and 525% in kidney and intestine, respectively. These
findings are consistent with the interpretation that, in the growing chick,
dietary aluminum can inhibit iron absorption, disrupt the regulation of
tissue ferritin levels by iron, and potentially alter the
compartmentalization and protective sequestration of iron within cells.
PMID: 10685509, UI: 20147936
- The following study shows that aluminum inhibits iron
metabolism, red blood cell production (
|Acta Physiol Pharmacol Bulg 1998;23(1):27-31
Influence of aluminium on erythropoiesis, iron metabolism and some
functional characteristics of erythrocytes in rats.
Ganchev T, Dyankov E, Zacharieva R, Pachalieva I, Velikova M, Kavaldjieva B
Medical Univesity of Varna, Department of Physiology, Bulgaria.
The increased aluminium (Al) levels in serum of patients with chronic renal
failure on hemodialysis are associated with impaired erythropoiesis and iron
metabolism. The long term Al loading of rats (20 to 90 days) has similar
effect. Data are still lacking about the effects after short-term aluminium
treatment. The 7 day's treatment with Al2(SO4)3 in a dose 67.5 mg/kg b. w.,
i. m. m. significantly decreased hemoglobin, hematocrit, incorporation of
59Fe in newly formed erythrocytes and increased reticulocytes in absolute
and relative counts. We observed a mild degree hypochromic, ferropenic,
microcytic anemia and polychromazia in the available macrocytes. The
immature erythroblasts were predominant forms in the erythroblastogram while
the number of mature erythroblasts was decreased. Index of maturation of
erythroblasts was lower, indicating inhibited erythroblast maturation.
Plasma iron, TIBC, transferrin saturation and 59Fe absorption in the
experimental group were significantly decreased. Spontaneous and mechanical
hemolysis of erythrocytes were lower while erythrocyte deformability was
increased. Obviously, Al treatment inhibits erythropoiesis and iron
metabolism, probably hinders hemoglobin synthesis and erythroid cell
maturation but does not affect the studied functional characteristics of
mature erythrocytes negatively.
PMID: 10347617, UI: 99276965
- What about mercury from dental amalgam fillings? Can mercury
cause anemia? The following study indicates that it does.
|: Sci Total Environ 1990 Dec 1;99(1-2):23-35
The relationship between mercury from dental amalgam and the
Department of Physiology, College of Veterinary Medicine and Biological
Sciences, Colorado State University, Fort Collins 80523.
The findings presented here suggest that mercury poisoning from dental
amalgam may play a role in the etiology of cardiovascular disorders.
Comparisons between subjects with and without amalgam showed amalgam-bearing
subjects had significantly higher blood pressure, lower heart rate, lower
hemoglobin, and lower hematocrit. Hemoglobin, hematocrit, and red blood
cells were significantly lower when correlated to increased levels of urine
mercury. The amalgam subjects had a greater incidence of chest pains,
tachycardia, anemia, fatigue, tiring easily, and being tired in the morning.
The data suggest that inorganic mercury poisoning from dental amalgam does
affect the cardiovascular system.
PMID: 2270468, UI: 91102526
- Here's another study indicating that mercury intoxication causes anemia
where the patient used Mercurochrome as a topical antiseptic. No one
uses Mercurochrome anymore, do they? Anyone know if this product is
still sold? If you have this or any other mercury compound in your
medicine chest, get rid of it now.
|Acta Med Scand 1979;205(6):463-6
A case of merbromin (Mercurochrome) intoxication possibly resulting in
Slee PH, den Ottolander GJ, de Wolff FA
A patient is described who appeared to be suffering from mercury
intoxication caused by local application of merbromin to an operation wound
and who developed aplastic anemia, which we ascribed to merbromin.
PMID: 88168, UI: 79206133
As the following study states, a great many factors can affect the blood
and lead to anemia.
|Folia Med Cracov 1993;34(1-4):29-47
Immunotoxic and hematotoxic effects of occupational exposures.
Department of Hematology, Collegium Medicum, Jagiellonian University,
The toxic effects of environmental factors at work places on the
hematopoietic and immune systems are of basic importance due to the time of
exposure, lasting on average 8 hours daily during one week. Porphyrinurias
and porphyrias have been observed after exposure to hexachlorobenzene,
chlorinated dibenzodioxins, polychlorinated biphenyls, polybrominated
biphenyls, vinyl chloride and lead. Aplastic anemia may occur after exposure
to benzene, pesticides, arsenic, cadmium and copper compounds. Megaloblastic
anemia has been noted in subjects exposed to arsenic, chlordane, benzene and
nitrous oxide. Methemoglobinemia is induced by aromatic nitro and amino
compounds. Hemolytic reactions caused by arsenic, methyl chloride,
naphthalene, lead, cadmium and mercury compounds represent a separate
problem. Immunodeficiencies resulting in decreased antitumor and
antiinfectious immunity have been reported in subjects exposed to asbestos,
ozone, dimethylsulphoxide, vinilidene chloride, and benzene homologues.
Lymphocytopenia may be induced by manganese, lead, toluene and industrial
noise. Neutropenia was marked after exposure to carbon disulphide, arsenic
compounds, benzene and electromagnetic fields. Only a few reports concern
the lymphocyte T3, T4 and T8 subpopulations. Electromagnetic fields
(microwaves) cause an imbalance of that subpopulation, consisting of a
decrease in the T8 cell count. The neutrophil enzymes, such as
myeloperoxidase and alkaline phosphatase, decrease in their activity after
exposure to polychlorinated biphenyls, carbon disulphide, chlorobenzene and
DDT. A majority of agents cited include genotoxic effects reflected in
chromosome aberrations and increased sister chromatid exchange and abnormal
unscheduled DNA synthesis. Leukemia or lymphoma risk is increased after
exposure to pesticides, electromagnetic fields, benzene and irradiation.
ANEMIA AND HYPERTHYROIDISM
What studies show that anemia is associated with hyperthyroidism? In
the following study, 38 out of 100 hyperthyroid patients were found to be have
hypochromic anemia (low hemoglobin). Also the 38 anemic patients had
significantly higher levels of thyroid hormones than the 62 without
anemia. Additionally, the authors state that iron deficiency, B-12
deficiency, and folic acid deficiency could all be excluded as possible causes
of the anemia. This makes sense to me. The conclusion, as I see it:
copper-deficiency anemia. Since copper gets used up in de-activating
thyroid hormones, treating the hyperthyroidism normalized the anemia because the
excessive drain on copper reserves produced by high thyroid hormones was ended.
|Z Gesamte Inn Med 1981 Mar 15;36(6):203-8
[Hyperthyroidism and anemia].
[Article in German]
Hambsch K, Fischer H, Langpeter D, Muller P
In a random test of 100 patients with hyperthyroidism with clinical and
paraclinical ascertainment of the diagnosis in 38 cases normo-hypochromic,
normocytary anaemias of different expression were found. In the patients
with anaemia the serum hormone values were statistically significantly
higher than in the 62 patients without anaemia. Also cardiotoxic and
hepatotoxic findings were more frequently to be proved in patients with
anaemia. A causal iron deficiency, deficit of vitamin B12 or folic acid
as well as a haemolytic component of the induction of anaemia could vastly
be excluded. By means of the treatment of the basic disease and
metabolic balance a normalisation of hemoglobin was achieved without
additional medication. From the results of the examinations is concluded
that above all a thyreotoxic damage is responsible for the development of
the anaemia. In cases of oligo-symptomatic hyperthyroidism part from
hepatotoxicity and cardiotoxicity also anaemias may become a leading
ANEMIA AND HYPOTHYROIDISM
The following study states that 20-60% of patients with hypothyroidism are
anemic. It also states that "Anemia is often the first
sign of hypothyroidism." Very important is the observation that
anemia in hypothyroidism is often not diagnosed because hypothyroids have a
lower volume of plasma which causes a false high estimation of the amount of
hemoglobin in the blood.
|Med Pregl 1999 Mar-May;52(3-5):136-40
[Anemia in hypothyroidism].
[Article in Serbo-Croatian (Roman)]
Antonijevic N, Nesovic M, Trbojevic B, Milosevic R
Poliklinika Vizim, Beograd.
INTRODUCTION: Anemias are diagnosed in 20-60% patients with
hypothyroidism. Real values of the degree of anemia are estimated by
radioisotopic analysis due to the lower volume of plasma in
hypothyroidism causing false high levels of hemoglobin in blood. Anemia
is often the first sign of hypothyroidism. Diagnosis of hypothyroidism
should be considered in every case of anemia with uncertain etiology because
sometimes signs of overt hypothyroidism needn't necessarily be evident.
Microcytic, macrocytic and normocytic are regularly described anemias.
CLASSIFICATION: Microcytic anemia is usually ascribed to malabsorption of
iron and loss of iron by menorrhagia. Macrocytic anemia is caused by
malabsorption of vitamin B12, folic acid, pernicious anemia and inadequate
nutrition. Pernicious anemia occurs 20 times more frequently in patients
with hypothyroidism than generally. Macrocytosis is found in up to 55%
patients with hypothyroidism and may result from the insufficiency of the
thyroid hormones themselves without nutritive deficit. Normocytic anemia,
so-called uncomplicated anemia, arises due to thyroid hormones deficit
itself not followed by nutritive deficit. This type of anemia is considered
to be an adaptation to a decreased basal metabolism. Thyroid hormones
directly or indirectly, through erythropoietin, stimulate growth of
erythroid colonies (BFU-E, CFU-E). Normocytic anemia is characterized by
reticulopenia, hypoplasia of erythroid lineage, decreased level of
erythropoietin, mainly regular erythrocyte survival. Acanthocytosis findings
in cytologic blood smear suggest hypothyroidism in about 90% of cases.
The following study shows that anemia is also present in congenital
hypothyroidism (in infants born with hypothyroidism) just as it is found in
adult hypothyroids. Note that the authors of this study, as most
researchers in the field, try to attribute the anemia to the effect of low
thyroid hormones, despite the fact that the anemia persists even after thyroid
hormone supplementation. It seems that no one is seeing that the same
mineral deficiencies which cause anemia (iron and zinc), cause
|J Endocrinol Invest 1996 Oct;19(9):613-9
Anemia in infants with congenital hypothyroidism diagnosed by neonatal
Franzese A, Salerno M, Argenziano A, Buongiovanni C, Limauro R, Tenore A
Dipartimento di Pediatria, Universita di Napoli, Italy.
Although anemia is a common finding in adult hypothyroid patients, there
are no studies on anemia in hypothyroid infants. The aim of this study,
therefore, was to review the hematologic status during the first year of
life in 50 infants with congenital hypothyroidism detected through the
regional neonatal screening program. The mean age at diagnosis was 23.7 +/-
6.5 days and treatment was initially begun with a mean L-thyroxine dose of
6.8 +/- 1.3 micrograms/kg/day. Clinical and haematological assessments were
performed at diagnosis, 3, 6 and 12 months of age. The patients were divided
in 2 groups based on whether T4 serum concentration at diagnosis was < 3
micrograms/dl (Group A) or > or = 3 micrograms/dl (Group B). Data for
hemoglobin (Hb), hematocrit (Ht), red cells count (RCC), mean corpuscular
volume (MCV), mean corpuscular hemoglobin (MCH), serum iron and ferritin
were expressed as Standard Deviation Score (SDS). Although at diagnosis the
mean value of Hb-SDS, Ht-SDS and RCC-SDS were in the low-normal range in
both groups, at 3 months of age the values in Group A (Hb -1.9 +/- 0.79; Ht
-2.34 +/- 1.02; RCC -1.56 +/- 1.25) were significantly lower than in Group B
(Hb -1.14 +/- 0.78, p < 0.005; Ht -1.59 +/- 0.94, p < 0.05; RCC -0.55
+/- 1.32, p < 0.02). A rise of the Hb, Ht and RCC values was observed in
both groups from 6 to 12 months. The mean values of MCV-SDS and MCH-SDS were
in the normal range at diagnosis in both groups, decrease progressively at 3
and 6 months and returned to normal at 12 months of age; no differences were
found between the 2 groups at any time. Mean Hb levels at 3 months of age
were correlated with mean serum T4 at diagnosis (r = 0.30, p < 0.05). The
present results indicate that anemia is a frequent finding in infants with
congenital hypothyroidism and is depended on the degree of neonatal
hypothyroidism and imply that hypothyroidism during development may produce
persisting changes even after thyroid replacement has begun.
- Iron deficiency may be a factor in anemia,
hypothyroidism, and myxedema (pretibial myxedema is a swelling of the front
of the shin from fibroblast proliferation, a condition associated with
thyroid disease and thyroid eye disease). There are not many
studies which have looked at iron levels in myxedema, but the following
study is suggestive.
|Lik Sprava 1999 Jun;(4):148-50
[Iron-deficiency anemia as a hematological mask of myxedema].
[Article in Ukrainian]
An atypical course of myxedema manifested by iron-deficiency anemia is
described that proved to be a diagnostic challenge. Pathogenetic mechanisms
of origination are analyzed.
There are numerous studies to suggest that both hypothyroidism and
hyperthyroidism are diseases which stem from the same deficiencies which cause
Other studies indicate that the same metals which we have seen contribute
to thyroid disease also contribute to anemia. It appears that toxicities from
metals like cadmium, mercury, lead, and aluminum are involved in the etiologies
of both diseases.
An understanding of anemia can be very important for the person suffering
from thyroid disease. The symptoms of anemia listed above should be
watched for so that you can more closely monitor the effects of your supplement
and eating programs on your thyroid disease. By eating to correct anemia,
you should be able to correct your thyroid disease.
Thalassemia is an inherited form of anemia and there are two main types:
alpha-thalassemia in which there is a decreased rate of synthesis of the alpha
chains of hemoglobin; and beta-thalassemia in which there is a decreased
rate of synthesis of the beta chains of hemoglobin.
- Cardiac arryhthmia (irregular heart rate) is a symptom of thalassemia
induced anemia as it is of anemia caused by nutrient deficiencies.
Amiodarone is a potassium channel blocking drug which is used to control the
cardiac arryhthmia caused by thalassemia.
- Amiodarone is known to induce hypothyroidism and hyperthyroidism.
Following is a study about thyroid dysfunction induced by Amiodarone
|J Endocrinol Invest 1999 Jan;22(1):55-63
High prevalence of thyroid dysfunction in adult patients with
beta-thalassemia major submitted to amiodarone treatment.
Mariotti S, Loviselli A, Murenu S, Sau F, Valentino L, Mandas A, Vacquer S,
Martino E, Balestrieri A, Lai ME
Dipartimento di Scienze Mediche M. Aresu, Universita di Cagliari, Italy.
Amiodarone may induce hyper- or hypothyroidism. Patients with
beta-Thalassemia Major (beta-Thal) have an increased prevalence of primary
hypothyroidism and often require amiodarone for hemosyderotic cardiomyopathy.
Aim of this study was to retrospectively evaluate thyroid function in beta-Thal
adult patients on long-term amiodarone. The study group consisted of
twenty-two (21 males, 1 female; age: 23-36 yr) beta-Thal patients submitted
to long-term (3-48 months) amiodarone therapy from January 1991 to July
1996. Controls included 73 beta-Thal patients (23 males and 50 females aged
25-35 yr) not treated with amiodarone. In all cases serum free thyroid
hormones, thyrotropin and thyroid autoantibodies were evaluated. A higher
prevalence of overt hypothyroidism (5/22 [22.7%]) as compared to controls
(3/73 [4.1%], p=0.02) was found in beta-Thal patients < or = 3 months
after starting amiodarone, while the prevalence of subclinical
hypothyroidism was similar in amiodarone-treated (18.2%) and untreated (15%)
beta-Thal patients. Overt hypothyroidism resolved spontaneously after
amiodarone withdrawal in 1 case, while the remaining patients were
maintained euthyroid on amiodarone by L-thyroxine administration. After
21-47 months of amiodarone therapy, 3 patients (13.6%) developed
thyrotoxicosis (2 overt and 1 subclinical), which remitted shortly after
amiodarone withdrawal. No case of hyperthyroidism was observed in beta-Thal
controls (p=0.012 vs amiodarone-treated patients). In conclusion, amiodarone
administration is often associated in adult beta-Thal patients to a rapid
progression of the pre-existing subclinical hypothyroidism, but transient
thyrotoxicosis may also be observed after a longer period of therapy. These
findings should be carefully considered in the management of these patients.
The following study
shows that anemia and iron deficiency cause
tongue pain. Thus tongue abnormalities may be
a useful indicator of anemia.
|Am J Med Sci
The pathophysiology of
glossal pain in patients with iron
deficiency and anemia.
Osaki T, Ueta E, Arisawa K, Kitamura Y,
Department of Oral Surgery, Kochi Medical
School, Nankoku-city, Japan.
BACKGROUND: It is well known that prolonged
anemia causes atrophy of tongue papillae,
glossal pain, and dysphagia, but it is
uncertain whether iron (Fe) deficiency
induces glossal pain without any objective
manifestation. To resolve this matter, the
relationship between Fe deficiency and
glossal pain was examined. METHODS: Eighteen
patients with Fe deficiency and 7 anemic
patients manifesting spontaneous irritation
or pain of the tongue without any objective
abnormalities participated in this study. To
ascertain the cause of glossal pain and the
oral pathophysiology in Fe deficiency and
anemia, peripheral blood was examined and
the glossal pain threshold and salivary flow
rates (SFRs) were estimated along with
Candida albicans cell culture tests.
RESULTS: Compared with patients with Fe
deficiency, those with anemia had a longer
history of tongue pain. In patients with
anemia, painful areas of the tongue were
more numerous than in patients with Fe
deficiency. Pain thresholds were decreased
in the painful portions, and both
nonstimulated and stimulated SFRs were
suppressed. Each patient was treated with
oral Fe; within 2 months, most patients
exhibited increased serum ferritin level
(P< 0.02, paired t-test), pain threshold
(P < 0.05) and salivation (P < 0.05)
and glossal pain subsided. CONCLUSIONS: Fe
deficiency causes glossal pain and the
degree of glossal pain increases as Fe
deficiency advances to anemia, manifesting
hyposalivation and abnormalities of glossal
Discovery Leads Researchers to New Suspect in Iron
- From: http://www.berkeley.edu/news/berkeleyan/1999/0224/protein.html
- By Kathy
Scalise, Public Affairs
Posted February 24, 1999
If you're slugging down iron pills but remain
weak and anemic, the culprit may not be iron at
all, but another metal: copper. A new genetic find
explaining why is described by a Berkeley
scientist and his colleagues in this month's issue
of the journal Nature Genetics.
The researchers discovered a protein,
hephaestin, that appears critical for moving iron
to the bloodstream. This protein contains copper
and cannot be produced in the absence of copper.
Thus in some cases, having too little copper
present even with an ample iron supply might cause
anemia, said the lead author on the paper,
Assistant Professor Christopher Vulpe of the
Division of Nutrition and Toxicology in the
College of Natural Resources.
The new protein may also help explain what
Vulpe describes as the number one inherited
disease in Caucasians, hemochromatosis. It results
from too much iron in the body and can cause
diabetes if it kills insulin-producing cells in
the pancreas, or "iron heart" if too
much of the metal accumulates in that organ and
causes cardiac arrest.
Vulpe's collaborators on the project included
researchers from UC San Francisco, the University
of Utah and the University of Queensland in
Hephaestin was isolated from mice and named
after the Greek god for metal-working, Hephaestus.
The protein is produced by the gene Heph, also
discovered by the researchers and reported in the
Nature paper, and is tethered to the membrane of
intestinal cells. The researchers suspect it is a
"multi-copper ferroxidase" protein that
contains copper and works on iron molecules.
Vulpe led the original study while a
postdoctoral fellow in the laboratory of Professor
Jane Gitschier of UCSF. Gitschier said in a recent
UCSF statement that "more work needs to be
done to determine if and how often genetic defects
in iron transport occur in humans."
In describing the possible role of the new
protein, Vulpe traced the path of iron through the
Iron, he said, usually originates in the food
supply, either as "heme," a cage of iron
that transports oxygen in blood and comes mainly
from meats, or as "free" iron from other
sources. Both kinds of iron are processed by the
gut -- stomach and intestine -- where they are
converted by means not well understood to a form
of iron readily used by the body. Finally, the
iron winds up in the intestinal epithelial cells,
ready for export to red blood cells, muscle tissue
But somehow "it has to get out of the gut
and into the bloodstream," said Vulpe.
This is particularly difficult, he said,
because the so-called "hydrophobic"
intestinal membrane wants to reject the charged
So hephaestin comes into play. Probably acting
as a helper molecule forming a complex with a yet
unknown transport protein, it allows iron to make
its way through the membrane.
In fact, hephaestin may act like an
"on/off" switch to control the flow of
iron into the body, said Vulpe. Perhaps in the
presence of hephaestin, more iron is pumped into
the blood, and when hephaestin stops production,
the pumping also soon halts.
While a certain amount of iron is vital for
survival, about 10 percent of infants and women of
childbearing age in the U.S. -- about 8.5 million
people -- are iron deficient. Many other people
suffer from having too much iron circulating in
the body, a syndrome called hemochromatosis, which
can also have toxic effects.
When the body functions correctly, excess iron
remains trapped in the intestine and is harmlessly
excreted. Disease results only after too much iron
escapes from the intestine and into the blood.
The UC researchers plan to investigate whether
hephaestin plays a role in hemochromatosis.
They suspect improper regulation of the Heph
gene may result