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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects on blood of abnormal thyroid hormone secretion were investigated in a prospective study involving 80 patients. Anaemia, when present, could usually be ascribed to association with another pathology. In non-anaemic patients an excess or a deficiency of thyroid hormones had opposite effects on erythrocytes. Leucocytes as a whole were not influenced by hypothyroidism, but untreated hyperthyroidism seemed to be responsible for a relative decrease in the number of neutrophils and a relative increase in the number of eosinophils and mononucleate cells. Platelet counts were unaffected by variations in thyroid hormone levels. Excluding the effects on blood of synthetic antithyroid drugs, the changes observed were generally reversible after correction of the abnormal hormone secretion.
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PMID:[Hematologic repercussions of disorders of thyroid secretion]. 623 Jun 10

When exposed to an ambient temperature of 4 degrees C, iron-deficient anemic rats become hypothermic. This lesion is related more to anemia than to tissue iron deficiency, since exchange transfusion to hematocrits over 25 restored normal thermoregulatory performance. Likewise poor cold responses were induced in control rats by transfusion to low hematocrits. Cold sensitivity in all anemic animals was paralleled by poor thyroid responses: there was a significant positive correlation between hematocrit and percent rise in triiodothyronine (r = 0.63) and thyroxine (r = 0.53) during 6 h at 4 degrees C. Basal levels of thyroid-stimulating hormone (TSH) were similar in control and iron-deficient animals: after cold exposure, TSH rose to higher levels in those animals with hematocrits over 25 than in those with lower hematocrits. Diminished O2 delivery to tissues responsible for heat production is probably a major component of the cold sensitivity of anemic rats. The novel finding that thyroid hormone responses are compromised by anemia implies effects on hormonal regulation that may also contribute to this functional lesion.
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PMID:Effect of iron-deficiency anemia on hormone levels and thermoregulation during cold exposure. 674 20

Data from the National Thyrotoxicosis Therapy Follow-Up Study (NTTFS) are presented here to document the existence of anemia in hyperthyroidism, a mild and reversible anemia that is simultaneously ameliorated with reversal of the hyperthyroid state. Among 20,600 women entered into the NTTF study with no previous history of hematological disorders, the prevalence of anemia was found to range from 10-15%, appearing to be higher in those selected for treatment with 131I when compared to those selected for surgery. An attempt is made to verify the recent hypothesis that thyroid hormone levels in the supraphysiologic range may suppress erythrogenesis. Two statistically significant regression models are consistent with a hypothesis of thyrotoxic bone marrow suppression. However, both associations are weak enough to suggest that some other physiologic improvement underlies the amelioration of anemia when hyperthyroidism is reversed. The degree of improvement in hematological status is similar for women in both treatment groups. Among 4464 women for whom serial hematological tests are obtained, over 3/4 of anemic patients are no longer anemic after an average 6.2 yr of follow-up. Clinicians are reassured that radioactive iodine exposure causes no further insult to the bone marrow, no matter what the cumulative dosage. The highly fractionated low dose bone marrow exposures to radiation account for the minimal hematological risks of 131I treatment.
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PMID:Effect of 131I on the anemia of hyperthyroidism. 685 67

Although the liver is the major site of erythropoietin (Ep) production in the fetus, this function is assumed by kidneys in the adult. The mechanisms underlying the liver to kidney switch of Ep formation are not understood. We studied the natural progression of this transition in sheep by measuring Ep production in response to anemia in normal and bilaterally nephrectomized fetal and newborn sheep beginning at about 80 d gestation (normal gestation: 140 d). Removal of both kidneys before induction of anemia did not affect Ep formation up to about 120 d of gestation. A significant reduction (29%, P < 0.02) in Ep synthesis was first noted at about 130 d of gestation (initiation of switch). This level of nephrectomy-induced reduction of Ep formation persisted until about 15 d after birth. Thereafter, bilateral nephrectomy caused further significant decreases (P < 0.05) in Ep production, gradually resulting in near total absence of Ep production at about day 40 postpartum (completion of switch). Chronic administration of testosterone (12 mg/wk) or estradiole benzoate (1.5 mg/d, 5 d/wk) to the fetus/newborn beginning at 85-90 d of gestation enhanced or suppressed erythropoiesis, respectively, but failed to affect the time at which the liver to kidney switch was initiated and/or completed. By contrast, a significant delay (P < 0.001) in the onset, but not completion of the switch occurred in animals that were either thyroidectomized or rendered chronically anemic beginning in the second third of the gestation period. Administration of thyroxin (1.2 mg/d, 5 d/wk) to thyroidectomized fetus/newborns not only prevented the delay in the initiation of the switch, but also accelerated the rate at which the switch was completed. These results demonstrate that in sheep (a) the liver to kidney switch of Ep production is initiated in utero during the last third of the gestation period, but is completed after birth, (b) this transition occurs gradually; the assumption of Ep producing capacity by the kidney is not preceded by an abrupt loss of hepatic Ep formation; and (c) the switch is not affected by changes in sex hormone levels during the prenatal-postnatal growth periods, but is profoundly influenced by alterations in thyroid hormone and oxygen supply-demand levels.
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PMID:Studies on the liver to kidney switch of erythropoietin production. 720 72

A new autosomal recessive mutation that causes hypothyroidism has been identified in mice. The gene, herein named hypothyroid (hyt), has been mapped on chromosome 12 approximately 30 units from the centromere. The mutants are characterized by retarded growth, infertility, mild anemia, elevated serum cholesterol, very low to undetectable serum thyroxine, and elevated serum thyroid-stimulating hormone. Thyroid glands are in the normal location but are reduced in size and hypoplastic. Mutant mice respond to thyroid hormone therapy by improved growth and fertility. These findings suggest that the hyt mutant gene results in primary hypothyroidism unresponsive to thyroid-stimulating hormone.
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PMID:Inherited primary hypothyroidism in mice. 720 19

Hypothyroidism in dogs should be diagnosed by integrating the history, clinical symptoms and thyroid hormone assay. Affected dogs have a slow onset of decreased activity, cold intolerance, and skin changes of thickening and mild hyperpigmentation. The hair coat becomes dry and coarse, and alopecia develops in friction areas. The non-specific clinico-pathological changes of a mild anaemia and hypercholesterolaemia do not occur consistently. The easiest and best documented thyroid hormone assay is serum thyroxine (T4). The most accurate diagnosis is made using either the thyrotropin (TSH) stimulation test or thyroid gland biopsy. The condition is controlled by thyroxine replacement therapy at a dose rate of 30--50 mcg/kg/day in 2 divided doses, for the life of the dog.
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PMID:The diagnosis and treatment of canine hypothyroidism. 745 58

The importance of selenium as an essential trace element for man has been increasingly recognized during the last several years. Selenium deficiency has been associated with cases of congestive cardiomyopathy, skeletal myopathy, anemia, enhanced cancer risk, elevated incidence of cardiovascular disease, immune system alterations, hair and nail changes, and abnormalities in thyroid hormone metabolism. These symptoms are frequently present in chronic uremic patients. Nevertheless, the prevalence and significance of selenium deficiency in the uremic syndrome is still not clearly defined. This article reviews the selenium status in chronic uremic patients, the supposed pathogenetic mechanisms of selenium disturbance in uremia, and the possible role of selenium deficiency on some uremic abnormalities.
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PMID:Selenium in uremia. 762 25

For several decades, very-low-energy diets (VLEDs) have been used by obese individuals to achieve weight loss. During the weight loss, patients often have dramatic drops in circulating thyroid hormone concentrations and experience cold intolerance. Because poor iron status is known to alter thermogenesis, we investigated the possibility that iron intake interacts with energy intake during weight loss in obese individuals. The effects on indicators of iron and thyroid status of increasing the iron content of a VLED from 18 to 27 mg/d during 12 wk of a VLED were compared with the effects on the same indicators of increasing energy intake from 1752 kJ(420 kcal) to 3347 kJ(800 kcal)/d. Although all VLED groups initially had 30% declines in plasma transferrin saturation, increases in plasma ferritin concentrations, and decreases in plasma thyroid hormone concentrations, patients who received iron supplementation had significantly higher circulating concentrations of triiodothyronine and thyroxine at the end of the VLED than did patients who received only the recommended dietary allowance of iron. The patients who received iron supplementation also had a more rapid return of iron indicators to normal values over the course of the VLED. The transitory fall in iron delivery to bone marrow was not associated with anemia. These data suggest that higher thyroid hormone concentrations can be maintained during VLEDs that provide higher iron intakes.
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PMID:Changes in iron status during weight loss with very-low-energy diets. 920 76

Hydrops fetalis (HF) consists of an abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin edema. Almost all observed cases of HF are of the nonimmune type, the causes of which remain undetermined in 15% of patients. We report a newborn infant with nonimmune hydrops fetalis (NIHF) and congenital hypothyroidism. The infant's mother was healthy and there were no malformations of the placenta or umbilical cord. The infant did not show any structural abnormalities of his central nervous, cardiovascular, gastrointestinal, or urinary tract systems, and there was no evidence of anemia, infectious disease, or inborn error of metabolism. An immune-based process was unlikely, because the blood group of the mother and infant was A-positive and results of an indirect Coombs test in the mother and a direct Coombs test in the infant were negative. The patient's condition gradually improved with mechanical ventilation, repeated thoracocentesis, and total parenteral nutrition. By day 5 of age the skin edema, pericardial effusion, and ascites disappeared, but accumulation of significant amounts of chylous pleural fluid persisted. Because of lethargy, FT4 and thyroid-stimulating hormone levels were obtained and showed hypothyroidism. Thyroid hormone supplementation was then started, and within 4 days the infant became more vigorous and was weaned from mechanical ventilation. After 7 days, the chylothorax resolved completely as the serum thyroxine level normalized. No reaccumulation of pleural effusion was noticed. The infant started to gain weight and was discharged from the hospital at 35 days of age. A possible pathophysiologic association between congenital hypothyroidism and NIHF is discussed. NIHF may be caused by lymphatic congestion attributable to an impairment of lymphatic flow and a delayed return of lymph to the vascular compartment. There could be a possibility that because of thyroid hormone deficiency in this patient, there was reduced adrenergic stimulation of the lymphatic system. This could result in a sluggish flow of the lymph with engorgement of the lymphatic system, leakage of lymph into the pleura and the interstitial spaces, and the production of chylothorax with NIHF. Animal studies demonstrate a direct relationship between lymph flow rate or lung liquid clearance and adrenergic receptor activity in the lymphatic system. These observations support our hypothesis that deficient adrenergic activity in congenital hypothyroidism might lead to chylothorax with NIHF in the fetus. We speculate that thyroid hormone may play a role in the regulation of adrenergic receptors in the lymphatic system and lungs, thus modulating both the lymphatic flow rate and lung liquid clearance, and facilitating the resolution of chylothorax. Examination of thyroid functions should be included in the investigation of fetuses and neonates with NIHF of an obscure origin.
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PMID:Congenital hypothyroidism and nonimmune hydrops fetalis: associated? 1061 Apr 98

The toxicity of 3,3',4,4'-tetrachloroazobenzene (TCAB) was evaluated in 13-week gavage studies in male and female F344/N rats and B6C3F1 mice. In addition to histopathology, evaluations included clinical chemistry, hematology, thyroid hormone analyses, and reproductive parameters. Groups of 10 rats and 10 mice of each sex were exposed to TCAB at dose levels of 0, 0.1, 1, 3, 10, or 30 mg/kg for 5 days a week for 13 weeks. In the rat studies, the major effects for both males and females included a 10% decrease in terminal body weight at 30 mg/kg/day, an increase in hematopoietic cell proliferation in the spleen at 10 and 30 mg/kg/day, and a responsive anemia at 10 and 30 mg/kg/day. A 15 to 30% decrease in platelet counts and a 20 to 40% decrease in thymus weights was observed at 10 and 30 mg/kg/day. An increase in liver weight up to 15% was found at 3 mg/kg/day and higher doses in males and at 10 and 30 mg/kg/day in females, respectively. An increase in spleen weights up to 15% was observed at 10 and 30 mg/kg/day in males and at 30 mg/kg/day in females. A marked decrease in circulating total thyroxine (TT4) was found in both males and females at all dose levels tested. TT4 could hardly be detected at 10 and 30 mg TCAB/kg/day. In addition, hyperplasia of the forestomach was increased at 3 mg/kg/day and higher doses in males and at 30 mg/kg/day in females. In the mouse studies, an increase in liver and spleen weight was observed up to approximately 25% in both males and females at 10 and 30 mg/kg/day. Hyperplasia of the forestomach was observed at 1 mg/kg/day and higher doses in both males and females. In males, a 30% decrease in thymus weights at 30 mg/kg/day and a 60% decrease in epididymal sperm density at 3 and 30 mg/kg/day was observed. Also in males, centrilobular hypertrophy of hepatocytes and an increase in hematopoietic cell proliferation in the spleen was observed at 3 mg/kg/day and higher doses. Based on the current study and information in the literature, TCAB has dioxin-like properties. Comparison of the effects of TCAB in the present study and in the literature to those with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) indicates that TCAB is from two to six orders of magnitude less potent than TCDD depending on the end point.
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PMID:Toxicity of 3,3',4,4'-tetrachloroazobenzene in rats and mice. 1019 80


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