Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have shown that under experimental conditions ferrous sulfate may reduce the gastrointestinal absorption of orally administered levothyroxine sodium in patients with primary hypothyroidism. We describe a patient who became hypothyroid while taking ferrous sulfate. The hypothyroid status was corrected by increasing the dose of levothyroxine. Subsequently, when ferrous sulfate was discontinued, the patient became hyperthyroid while taking the higher dose of thyroid hormone preparation. Since both hypothyroidism and iron deficiency anemia may coexist, additional thyroid function testing is recommended in patients treated concurrently with ferrous sulfate and L-thyroxine.
 ...
PMID:Ferrous sulfate-induced increase in requirement for thyroxine in a patient with primary hypothyroidism. 919 42

Iron deficiency anemia is associated with lower plasma thyroid hormone concentrations in rodents and, in some studies, in humans. The objective of this project was to determine if plasma triiodothyronine (T3) and thyroxine (T4) kinetics were affected by iron deficiency. Studies were done at a near-thermoneutral temperature (30 degrees C), and a cool environmental temperature (15 degrees C), to determine plasma T3 and T4 kinetics as a function of dietary iron intake and environmental need for the hormones. Weanling male Sprague-Dawley rats were fed either a low Fe diet [iron-deficient group (ID), <5 microg/g Fe] or a control diet [control group (CN), 35 microg/g Fe] at each temperature for 7 wk before the tracer kinetic studies. An additional ID group receiving exogenous thyroid hormone replacement was also used at the cooler temperature. For T4, the disposal rate was >60% lower (89 +/- 6 vs. 256 +/- 53 pmol/h, P < 0.001) in ID rats than in controls at 30 degrees C, and approximately 40% lower (192 +/- 27 vs. 372 +/- 26 pmol/h, P < 0.01) in ID rats at 15 degrees C. Exogenous T4 replacement in a cohort of ID rats at 15 degrees C normalized the T4 concentration and the disposal rate. For T3, the disposal rate was significantly lower in ID rats in a cool environment (92 +/- 11 vs. 129 +/- 11 pmol/h, P < 0.01); thyroxine replacement again normalized the T3 disposal rate (126 +/- 12 pmol/h). Neither liver nor brown fat thyroxine 5'-deiodinase activities were sufficiently different to explain the lower T3 disposal rates in iron deficiency. Thus, plasma thyroid hormone kinetics in iron deficiency anemia are corrected by simply providing more thyroxine. This suggests a central regulatory defect as the primary lesion and not peripheral alterations.
 ...
PMID:Plasma thyroid hormone kinetics are altered in iron-deficient rats. 968 62

Usual causes of intolerance to thyroxine sodium include coronary artery disease, advanced age, untreated adrenal insufficiency, and severe hypothyroidism. We describe 4 patients with iron deficiency anemia and primary hypothyroidism. After treatment with thyroxine sodium, these patients developed palpitations and feelings of restlessness, which necessitated discontinuation of the thyroid hormone. After the anemia was treated with ferrous sulfate for 4 to 7 weeks, they were able to tolerate thyroxine sodium therapy. Iron deficiency anemia coexisting with primary hypothyroidism results in a hyperadrenergic state. In such patients, we postulate that thyroid hormone administration causes palpitations, nervousness, and feelings of restlessness. Correction of any existing pronounced anemia in hypothyroid patients who are intolerant to thyroxine sodium therapy may result in tolerance to this agent.
 ...
PMID:Anemia: a cause of intolerance to thyroxine sodium. 1068 60

Iron plays an important role in thyroid hormone metabolism; thus, iron deficiency anemia may lead to alterations in resting metabolic rate (RMR). Based on this premise, two iron-deficient-anemic female athletes, 18 (A1) and 21 (A2) years of age, were supplemented with 23 mg/day of elemental iron to assess its effects on iron and thyroid hormone status and RMR at 0, 8, and 16 weeks. Anemia was clinically corrected in both subjects (hemoglobin: A1 = 11.0 to 13.0 to 12.6 g/dL and A2 = 11.5 to 13.9 to 12.6 g/dL, 0 to 8 to 16 weeks, respectively). Serum ferritin (SF) concentration also improved in both subjects (A1: 5.0 to 11.0 to 15.0 ng/dL and A2: 5.0 to 16.0 to 20.0 ng/dL; 0 to 8 to 16 weeks, respectively); however, 16 weeks of iron supplementation did not fully replete iron stores. A2 increased dietary iron and ascorbic acid intakes from 8 to 16 weeks, possibly accounting for her higher SF concentrations. RMR and total thyroxine changed over time: A1 increased while A2 decreased in these variables. Although clinical correction of iron deficiency anemia occurred after 16 weeks of low-level iron supplementation, RMR and thyroid hormone metabolism were oppositely affected in the two subjects.
 ...
PMID:Effect of iron supplementation on thyroid hormone levels and resting metabolic rate in two college female athletes: a case study. 1109 70

Studies in animals and humans have shown that iron deficiency anemia (IDA) impairs thyroid metabolism. However, the mechanism is not yet clear. The objective of this study was to investigate whether iron (Fe) deficiency lowers thyroid peroxidase (TPO) activity. TPO is a heme-containing enzyme catalyzing the two initial steps in thyroid hormone synthesis. Male weanling Sprague-Dawley rats (n = 84) were randomly assigned to seven groups. Three groups (ID-3, ID-7, ID-11) were fed an Fe-deficient diet containing 3, 7 and 11 microg Fe/g, respectively. Because IDA reduces food intake, three control groups were pair-fed Fe-sufficient diets (35 microg Fe/g) to each of the ID groups and one control group consumed food ad libitum. After 4 wk, hemoglobin, triiodothyronine (T(3)) and thyroxine (T(4)) were lower in the Fe-deficient groups than in the ad libitum control group (P < 0.001). By multiple regression, food restriction had a significant, independent effect on T(4) (P < 0.0001), but not on T(3). TPO activity (by both guaiacol and iodine assays) was markedly reduced by food restriction (P < 0.05). IDA also independently reduced TPO activity (P < 0.05). Compared with the ad libitum controls, TPO activity per thyroid determined by the guaiacol assay in the ID-3, ID-7 and ID-11 groups was decreased by 56, 45 and 33%, respectively (P < 0.05). These data indicate that Fe deficiency sharply reduces TPO activity and suggest that decreased TPO activity contributes to the adverse effects of IDA on thyroid metabolism.
 ...
PMID:Iron deficiency anemia reduces thyroid peroxidase activity in rats. 1209 75

Studies in animals and adults have indicated iron deficiency anaemia to be associated with altered thyroid hormone metabolism. The aim of the present study was to determine the effect of iron deficiency anaemia on the thyroid function of young children. Concentrations of thyroxine (T4) and triiodothyronine (T3), free thyroid hormones (fT4 and fT3), thyroxine binding globulin (TBG), and thyroid stimulating hormone (TSH) were measured in the basal state and in response to an intravenous bolus of thyrotropin releasing hormone (TRH) in nine children one to three years of age with iron deficiency anaemia (IDA) before and after treatment with oral iron. The results of the anaemic children were also compared to basal and stimulated concentrations of thyroid hormones, TBG, and TSH of eight iron sufficient, age-matched children. Seven of the IDA and 6 of the control children were male. The mean haemoglobin (Hb) and serum ferritin (SF) in the IDA children at baseline were 93g/L (range 81-102) and 6g/L (range 1-12) which increased to 121g/L (range 114-129) and 54g/L (range 19-175), respectively, after a mean of 2.3 months (SD 0.5) of iron therapy. In the control group, mean Hb and SF were 125g/L (range 114-130) and 51 g/L (range 24-144), respectively. The basal values of TBG and thyroid hormones of the IDA children before and after iron treatment were not different from the control children. Similarly, there was no statistical difference in the thyroid hormones in the IDA children before compared to after resolution of the anaemia. Compared to the control children, the TSH response over time to TRH, TSH area under the curve (TSHAUC), and the peak TSH value after stimulation were all lower in the IDA children both before and after resolution of anaemia, but the differences were not significant. Iron therapy and resolution of anaemia had no effect among the IDA children. The time to reach the peak TSH concentration was longer in the IDA children (P=0.08) than the control children before iron therapy. While the time to peak TSH decreased upon resolution of the anaemia, the difference was not significant. There was no effect of Hb concentration, age, or anthropometry with TSH, TSHAUC, or time to peak TSH after TRH stimulation in the IDA children before treatment. Normal thyroid function was preserved in these children with iron deficiency anaemia, however three of nine children had minor abnormalities of hypothalamic-pituitary function. These results indicate that hypothyroidism is unlikely to be a major cause of impaired psychomotor development or growth in young children with iron deficiency anaemia.
 ...
PMID:Iron deficiency anaemia in childhood and thyroid function. 1281 Apr 11

The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain. As any other organ, the brain is elaborated from substances present in the diet (sometimes exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can have an influence on brain structure, and thus on its function, including cognitive and intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning. For instance, to produce energy, the use of glucose by nervous tissue implies the presence of vitamin B1; this vitamin modulates cognitive performance, especially in the elderly. Vitamin B9 preserves brain during its development and memory during ageing. Vitamin B6 is likely to benefit in treating premenstrual depression. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin improves cerebral and cognitive functions in the elderly; it frequently improves the functioning of factors related to the frontal lobe, as well as the language function of those with cognitive disorders. Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron deficiency is linked to perturbation of the development of cognitive functions. Iron deficiency anaemia is common, particularly in women, and is associated, for instance, with apathy, depression and rapid fatigue when exercising. Lithium importance, at least in psychiatry, is known for a long time. Magnesium plays important roles in all the major metabolisms: in oxidation-reduction and in ionic regulation, among others. Zinc participates among others in the perception of taste. An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be linked to Alzheimer disease. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. More specifically, the full genetic potential of the child for physical growth ad mental development may be compromised due to deficiency (even subclinical) of micronutrients. Children and adolescents with poor nutritional status are exposed to alterations of mental and behavioural functions that can be corrected by dietary measures, but only to certain extend. Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse. Brain diseases during aging can also be due to failure for protective mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace elements, vitamins, non essential micronutrients such as polyphenols) related with protection against free radicals. Macronutrients are presented in the accompanying paper.
 ...
PMID:Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. 1706 9

Prasad's syndrome is characterized by geophagia, growth retardation, hypogonadism, and zinc deficiency. We report a 15-year-old boy whose medical history and clinical and laboratory findings were fully compatible with Prasad's syndrome. In addition to severe growth retardation and pubertal delay, iron deficiency anemia and zinc deficiency were determined. His gliadin and endomysium antibodies were negative. The thyroid hormone levels were in normal range but basal gonadotropins and testosterone levels were low for his age. Detailed endocrinological evaluation revealed growth hormone deficiency and hypogonadotropic hypogonadism. Pituitary gland magnetic resonance imaging revealed pituitary hypoplasia. In our opinion, before the diagnosis of Prasad's syndrome, endocrine evaluation should be done in these patients and hypopituitarism should be ruled out. Hypogonadotropic hypogonadism and growth hormone deficiency may be masked by Prasad's syndrome.
 ...
PMID:Hypopituitarism masquerading as Prasad's syndrome: a case report. 2309 50

The aim of the research was to estimate peripheric blood in patients with iron deficiency anemia and different forms of hypothyreosis. 192 patients with diagnosis of iron deficiency anemia and different forms of hypothyreosis were investigated. Among investigated patients 34 (22.9%) were men and 158 (87.5%) - women. The patients' age varied from 21 to 77 years old. Patients were divided into 3 groups: group I - patients with subclinical hypothyreosis; group I A - patients with isolated subclinical hypothyreosis; group I B - patients with subclinical hypothyreosis in combination with iron deficiency condition. Group II A - patients with isolated primary hypothyreosis; group II B - patients with primary hypothyreosis in combination with iron deficiency. According to the results the different degree of blood formation disturbances were detected in the study groups: tissue iron deficiency; light, moderate and heavy degrees of anemia, and the etiology of risk factors of anemic syndrome in the study groups were determined. It was found that the insufficiency of thyroid hormones determined the insufficiency of the formed elements of blood. The iron deficient anemia with deficit of iron- containing enzymes in tissue led to decreased secretion of thyroid hormone from the thyroid gland and hypothyreosis.
 ...
PMID:[Evaluation of peripheric blood in patients with different forms of hypothyreosis and iron deficiencient anemia]. 2534 Dec 38