Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Japan, mass screening tests on newborns for Cretinism have been performed since 1984, Cretinism is a very rare condition. We report the clinical course and complications of longitudinal thyroid hormone replacement therapy (liothyronine sodium: T3) of two women with Cretinism and ectopic thyroid gland for the past 33 years until 2001. They were born in April 1951 (Case 1) and in January 1952 (Case 2). On admission in June 1968, they were 17 and 16 years old. They had short stature, mental retardation, macroglossia, saddle nose, retardation of bone maturation, edematous face, coexistence of permanent teeth and deciduous teeth, abdominal distention, hypotonia, anemia, hypophosphatemia and hypercholesterolemia. After admission, Case 2 had an appendectomy for appendicitis. She was found to have a right ovarian cyst, but was not operated upon. Later, the right ovarian cyst disappeared during thyroid hormone replacement therapy. The complication in this case was NIDDM. Over secretion of thyroid hormone in for example, hyperthyroidism sometimes induces NIDDM. On their admission, a levothyroxine sodium (T4: Thyradin S) was unavailable in Japan, so we had no choice but to treat them with liothyronine sodium for thyroid hormone replacement therapy. We suspect that liothyronine sodium replacement therapy probably induced NIDDM. They experienced improved bone maturation, anemia, hypophsphatemia and hypercholesterolemia, but their intellectual and mental disabilities were not improved.
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PMID:The longitudinal course of two cases with cretinism diagnosed after adolescence. 1280 80

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.
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PMID:Iron deficiency anaemia in childhood and thyroid function. 1281 Apr 11

Often patients in whom there is little to suggest myxedema or cretinism have subclinical hypothyroidism. Once the condition is suspected, it can be diagnosed by determination of protein-bound iodine and, if the PBI is low, by response to therapy with thyroid hormone. Patients in the following categories should have protein-bound iodine determination: Those having (1) a history of previous treatment for hypothyroidism; (2) suboptimal development in children; (3) ovarian dysfunction, infertility, habitual abortion or unusual menopausal disorders; (4) symptoms of malaise and debility, such as undue fatigue, somnolence, mental asthenia and anxiety; (5) unexplained anemia; (6) colloid goiter, adenomatous goiter and cancer of the thyroid gland. If hypothyroidism is diagnosed, administration of thyroid hormone in increasing amounts, as determined by serial serum PBI tests, should be carried out indefinitely. Instruction of the patient is essential.
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PMID:Subclinical hypothyroidism. Recognition and treatment. 1398 2

Data on the effect of maternal malnutrition and/or anemia on thyroid hormone regulation in human fetuses are scarce, and would be of great importance in examining the relevance of Barker's hypothesis, which proposes adaptation of fetuses to undernutrition leading to permanent metabolic and endocrine changes that form the basis of adult diseases. To examine the quantitative variations in thyroid hormone profile of neonates born to malnourished and/or anemic mothers, we quantitated the T3, T4, rT3 and TSH levels in cord blood of neonates and maternal blood of their corresponding mothers that are malnourished and/or anemic. Further, we classified neonates born to each of these groups of mothers into Small for Gestational Age (SGA) or Appropriate for Gestational Age (AGA) based on the intrauterine growth curve for our population, and examined the thyroid hormone profile in these neonates. Our results show that firstly, the effects of malnutrition or anemia on thyroid hormone profile are distinct, secondly, significantly higher levels of cord blood T4 and correspondingly lower levels of T3 and rT3 are observed in the neonates born to anemic and malnourished mothers and thirdly, decreases in cord blood T3 levels were observed in Small for Gestational Age neonates born to anemic mothers. These observations lead us to speculate that alterations in the pituitary-thyroid function result in beneficial adaptations to the hostile intrauterine environment in malnutrition related growth retardation and anemia.
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PMID:Thyroid hormone dysregulation in intrauterine growth retardation associated with maternal malnutrition and/or anemia. 1627 87

The purpose of this retrospective study was to report clinical and clinicopathologic findings, response to treatment, and outcome of hypothyroid dogs treated with levothyroxine intravenously (IV). Seven levothyroxine IV treated hypothyroid dogs and 799 other hypothyroid dogs examined during the same period were included. Rottweiler dogs were overrepresented in the group of levothyroxine IV-treated hypothyroid dogs compared with other hypothyroid dogs (P < .0001). Common physical examination abnormalities were obese or overweight body condition (5 dogs), mental dullness (5 dogs), and nonpitting edema (4 dogs). Anemia (4 dogs) and hypercholesterolemia (5) were common, although 1 dog had neither. Concurrent disease (most commonly infection) was observed in 5 dogs. Glucocorticoids and nonsteroidal antiinflammatory drugs had been administered to 2 dogs before examination. Surgery was performed in 2 dogs before treatment with levothyroxine IV. Four of the 7 dogs received 4-5 microg/kg of levothyroxine IV. Subjective improvement in mentation or ambulation (6 of 7 dogs) and systolic hypotension (2 of 2 dogs) occurred within 30 hours of levothyroxine IV administration. Six of the 7 dogs responded well to therapy and were discharged from the hospital. It was concluded that physical examination and clinicopathologic findings of dogs with a hypothyroid crisis are nonspecific, although Rottweiler dogs may be at increased risk. Concurrent disorder, such as infection, concurrent administration of thyroid hormone-altering medication, and surgery, may be associated with development of a hypothyroid crisis. Resolution of abnormal mentation, ambulation, and systolic hypotension should be expected within 30 hours. Prognosis is good in most treated dogs.
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PMID:Hypothyroid dogs treated with intravenous levothyroxine. 1649 20

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.
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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

Glycated albumin (GA) is used alongside glycated hemoglobin (HbA(1C)) as an indicator of glycemic control. Although serum GA levels are affected mainly by plasma glucose, they are also influenced by serum albumin metabolism. Thyroid hormone is known to promote albumin catabolism, and it is thus thought to affect serum GA levels. In the present study, the effects of thyroid hormone on serum GA measurements were investigated in patients with thyroid dysfunction. Six patients with untreated hypothyroidism and 17 patients with untreated thyrotoxicosis were investigated. Patients who had anemia or diabetes were excluded. A total of 25 non-diabetic, euthyroid individuals were enrolled as controls. HbA(1C), serum GA, thyroid-stimulating hormone (TSH), free triiodothyronine (T(3)), and free thyroxine (T(4)) levels were measured in all these subjects, and their relationships were examined. Although no intergroup differences were observed for HbA(1C), serum GA was significantly higher among patients with hypothyroidism than controls, and significantly lower among patients with thyrotoxicosis. Serum GA had a significant positive correlation with serum TSH and significant inverse correlations with free T(3) and free T(4). Thyroid hormone levels are inversely associated with serum GA levels. Cautions are necessary when evaluating serum GA levels in patients with thyroid dysfunction.
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PMID:Effects of thyroid hormone on serum glycated albumin levels: study on non-diabetic subjects. 1924 49

Thyroid hormones play a crucial role in the metabolic activities of adults, affecting almost every organ system. All types of thyroid diseases are encountered in the elderly. As symptoms and signs of thyroid diseases may overlap with what is considered to be "normal aging," the presence of a thyroid disorder may go undiagnosed in the elderly. This potential problem is further compounded in elderly patients with chronic kidney disease (CKD), where the presence of an underlying hormonal problem such as hypothyroidism may be erroneously attributed to multiple comorbidities, the aging process, or the kidney disease. Frailty is being recognized as a contributing factor to the poor outcomes (hospitalization and high mortality) in elderly patients with CKD. Predisposing factors leading to frailty in elderly with CKD such as increased inflammatory markers, anemia, low testosterone, sarcopenia, and depression are associated with thyroid hormonal abnormalities. These associations are remarkable and raise the question of whether routine monitoring and screening for thyroid hormone changes in elderly CKD patients might be helpful in identifying reversible causes of frailty. In this review, we will focus on the associations between thyroid hormone abnormalities and the predisposing factors of frailty in elderly patients with CKD. If a cause-effect relationship of thyroid hormone abnormalities and factors predisposing to frailty in CKD patients is established, identification and treatment of thyroid abnormalities in this population would assume increased importance.
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PMID:Thyroid hormone abnormalities and frailty in elderly patients with chronic kidney disease: a hypothesis. 2063 25

Polychlorinated biphenyls (PCBs), persistent chemicals widely used for industrial purposes, have been banned in most parts of the world for decades. Owing to their bioaccumulative nature, PCBs are still found in high concentrations in marine mammals, particularly those that occupy upper trophic positions. While PCB-related health effects have been well-documented in some mammals, studies among dolphins and whales are limited. We conducted health evaluations of bottlenose dolphins (Tursiops truncatus) near a site on the Georgia, United States coast heavily contaminated by Aroclor 1268, an uncommon PCB mixture primarily comprised of octa- through deca-chlorobiphenyl congeners. A high proportion (26%) of sampled dolphins suffered anaemia, a finding previously reported from primate laboratory studies using high doses of a more common PCB mixture, Aroclor 1254. In addition, the dolphins showed reduced thyroid hormone levels and total thyroxine, free thyroxine and triiodothyronine negatively correlated with PCB concentration measured in blubber (p = 0.039, < 0.001, 0.009, respectively). Similarly, T-lymphocyte proliferation and indices of innate immunity decreased with blubber PCB concentration, suggesting an increased susceptibility to infectious disease. Other persistent contaminants such as DDT which could potentially confound results were similar in the Georgia dolphins when compared with previously sampled reference sites, and therefore probably did not contribute to the observed correlations. Our results clearly demonstrate that dolphins are vulnerable to PCB-related toxic effects, at least partially mediated through the endocrine system. The severity of the effects suggests that the PCB mixture to which the Georgia dolphins were exposed has substantial toxic potential and further studies are warranted to elucidate mechanisms and potential impacts on other top-level predators, including humans, who regularly consume fish from the same marine waters.
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PMID:Anaemia, hypothyroidism and immune suppression associated with polychlorinated biphenyl exposure in bottlenose dolphins (Tursiops truncatus). 2161 98

Hypothyroidism is a systemic disease resulting from either thyroid gland's anatomical and functional absence or lack of hypophyseal stimulation, both of which can lead to deficiency in thyroid hormone (TH) production. TH is essential for human and animal development, growth, and function of multiple organs. Children with deficient TH can develop alterations in central nervous system (CNS), striated muscle, bone tissue, liver, bone marrow, and cardiorespiratory system. Among the clinical outlook are signs like breathing difficulty, cardiac insufficiency, dysphagia, and repeated bronchial aspiration, constipation, muscle weakness, cognitive alterations, cochlear dysfunction, reduced height, defects in temperature regulation, anaemia, jaundice, susceptibility to infection, and others. Experimental and clinical studies have shown that TH is very essential for normal brain development. Other research work based on mice pointed out that a reduced level of TH in pregnant mother leads to congenital hypothyroidism in animal models and it is associated with mental retardation, deep neurologic deficiency that impacts on cognitive, learning, and memory functions. The principal experimental model studies that have focused on hypothyroidism are reviewed in this study. This is important on considering the fact that almost all animal species require thyroid hormones for their metabolism.
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PMID:Experimental models of developmental hypothyroidism. 2220 41


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