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

Acute thyrotoxicosis following the ingestion of massive doses of thyroid hormone may pose diagnostic problems when the intoxication is clandestine, and may endanger life. The authors report here the case of a previously euthyroid young woman. The outcome was favourable, though assisted ventilation was required for a number of days. The particular features of this case (relatively low blood thyroxinelevels, anaemia and thrombocytopaenia following regression of the thyrotoxicosis, presence of parotid swelling) are discussed in the context of data from the literature.
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PMID:[Drug-induced thyrotosic crisis or the dangers of an allegedly homeopathic preparation (author's transl)]. 60 26

A comparison of concentrations of 2,3-diphosphoglycerate (2,3-DPG) and adenosine-triphosphate (ATP) in the red cells of cretins and normal controls living at 3,700 m in the Nepal Himalayas has shown that 2,3-DPG and ATP levels were higher in the cretins. A negative correlation between hemoglobin and 2.3-DPG level was found. Chronic hypoxia appears to have provided the additional stress required to differentiate the significance of thyroid hormone deficiency in producing anemia from its effect on 2,3-DPG levels. If thyroid hormone is in fact one regulator of 2,3-DPG, the anemia of hypothyroidism appears to be more significant. This also suggest that the anemia of hypothyroidism, is at least in part, "pathologic" as opposed to "adaptive".
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PMID:Erythrocyte 2,3-diphosphoglycerate and adenosine-triphosphate in cretins living at high altitude. 82 72

In this report we describe 26 pregnancies complicated by hypothyroidism cared for over 6.5 years at AIIMS, New Delhi. In 2 women hypothyroidism was diagnosed during pregnancy; others were diagnosed before pregnancy and continued to receive thyroxine replacement therapy throughout pregnancy. The thyroxine treatment needed readjustment in 7 (26.9%) pregnancies to maintain euthyroidism. Maternal complications included anaemia (23.0%), pregnancy induced hypertension (26.9%), postpartum haemorrhage (7.7%), intrauterine growth retardation (15.4%), postdatism (30.8%), and deficient lactation (19.2%). Perinatal mortality was 3.9%. No case of stillbirth occurred probably because of intensive fetal monitoring and timely termination of pregnancies on evidence of intrauterine fetal compromise. One neonatal death occurred due to fetal thyrotoxicosis. In these cases close surveillance during pregnancy is needed to maintain optimum thyroid hormone concentration, and intensive fetal monitoring is required to achieve a good perinatal outcome.
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PMID:Hypothyroidism complicating pregnancy. 144 36

Mutant cats were developed with non-goitrous primary hypothyroidism. They were clinically characterized by severely retarded growth, mild anaemia and high mortality in the young. They responded markedly to thyroid hormone replacement. Thyroid glands in the mutants were normal in position but slightly reduced in size. Laboratory studies revealed low serum concentrations of thyroxine (T4) and tri-iodothyronine (T3), and increased serum concentrations of TSH. Administration of TRH induced no further increase in TSH. Administration of exogenous TSH after suppression of endogenous TSH by T3 did not increase the serum concentration of T4 in the mutants, in sharp contrast with the threefold increase in serum T4 observed in the normal litter-mates. These findings suggest that the underlying pathogenesis of this disorder is unresponsive to TSH. Moreover, we found that the mutants were transmitted in an autosomal recessive manner.
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PMID:Inherited primary hypothyroidism with thyrotrophin resistance in Japanese cats. 190 88

Congenital hypothyroid dwarfism was diagnosed in a family of Giant Schnauzers. Three female and two male puppies from different litters were evaluated for dwarfism, lethargy, somnolence, gait abnormalities, and constipation. On physical examination, disproportionate dwarfism (n = 5), macroglossia (n = 3), hypothermia (n = 3), delayed dental eruption (n = 3), ataxia (n = 2), and abdominal distension (n = 1) were identified. Results of initial laboratory tests showed anemia (n = 4), hypercholesterolemia (n = 4), hypercalcemia (n = 2), and transudative abdominal effusion (n = 1). Radiographic skeletal surveys disclosed epiphyseal dysgenesis and delayed skeletal maturation (n = 5). A diagnosis of hypothyroidism was established on the basis of low basal serum thyroxine concentrations that failed to increase following the administration of TSH (n = 5) and markedly reduced to absent thyroid image when evaluated with gamma camera imaging of the thyroid gland (n = 4). In the two dogs that were most thoroughly evaluated, the results of thyroid histology, prolonged TSH testing, and repeat thyroid imaging, after three daily injections of TSH, were all consistent with secondary or tertiary, rather than primary, hypothyroidism. When TSH was administered over a period of 3 consecutive days (5 IU/day, subcutaneously), serum thyroid hormone response became normal and resulted in a normal thyroid image in the two dogs re-evaluated with gamma camera imaging. Daily treatment with oral levothyroxine (20 micrograms/kg) resulted in complete remission in puppies (n = 4) treated prior to 4 months of age. The other puppy failed to attain normal breed standards for height.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congenital hypothyroid dwarfism in a family of giant schnauzers. 174 85

Ten women with iron-deficiency anemia, 8 with depleted iron stores (nonanemic), and 12 control women, all of similar body fatness, were exposed to a 28 degrees C water bath to test the hypothesis that iron-deficiency anemia impairs thermoregulatory performance. The anemic women had lower rectal temperatures than did control women (36.0 +/- 0.2 vs 36.2 +/- 0.1 degree C, respectively, P = 0.001) and a lower rate of oxygen consumption (5.28 +/- 0.26 vs 5.99 +/- 0.29 mL.min-1.kg body wt-1, respectively, P = 0.04) at 100 min of cold exposure. Plasma thyroxine and triiodothyronine concentrations were significantly (P less than 0.002) lower in anemic than in control women at baseline and during cold exposure. Responses of iron-depleted subjects were similar to those of control subjects. Iron supplementation corrected the anemia, significantly (P = 0.03) improved rectal temperature at 100 min, and partially normalized plasma thyroid hormone concentrations. Plasma catecholamines were unaffected by iron status. This experiment demonstrates a functional consequence of iron-deficiency anemia in the balance of heat production and loss and suggests that thyroid-hormone metabolism may be responsible.
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PMID:Impaired thermoregulation and thyroid function in iron-deficiency anemia. 223 56

Iron-deficient anemic rats have previously been shown to have low plasma levels of thyroid hormone and a poor plasma thyroid hormone response to acute cold exposure. As an initial exploration, we examined thyroid hormone metabolism during iron deficiency in age-matched rats from three aspects: 1) plasma TSH (thyrotropin, thyroid stimulating hormone), T4 (thyroxine) and T3 (triiodothyronine) responses to graded doses of exogenous TRH (thyrotropin releasing hormone), 2) plasma T3 kinetics, and 3) rates of hepatic T3 production. Iron-deficient anemic rats had lower basal TSH values and blunted TSH responses to intravenous TRH injection at three different doses (10, 25 and 50 ng TRH/100 g body wt). Iron-deficient anemic rats also had a significant decrease in plasma T3 turnover (42 vs. 88 ng/h in controls), and significantly lower hepatic T4-5'-deiodinase activities than controls [26 vs. 44.0 ng T3/(mg protein.20 min)]. Thus, decreased rates of T3 production in iron-deficient anemic rats, as documented by turnover studies, may be related to decreased deiodinase activity and reduced peripheral formation of T3. The dampened TSH responses to TRH further facilitate or perpetuate this T3 deficiency. We propose that this abnormal thyroid state is partially responsible for impaired thermogenesis in iron-deficiency anemia.
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PMID:Evidence for thyroid hormone deficiency in iron-deficient anemic rats. 249 73

A patient with Graves' disease associated with severe muscle weakness who was finally diagnosed as polymyositis by pathological examination of the muscle is reported. A 28-year-old women was incidentally found to have hyperthyroidism when she consulted a hospital for the evaluation and treatment of anemia in 1979. She was treated with methimazole for approximately a month when she stopped the medication by herself. Approximately two yr later (Nov. 4, 1981) she consulted another hospital with complaints of palpitation and muscle weakness. Diagnosis of hyperthyroidism due to Graves' disease and thyrotoxic myopathy were made, followed by the treatment with radioiodine (4 mCi of 131I). She was further treated with propylthiouracil (PTU). Four yr after the treatment, serum thyroid hormone concentration declined to the lower level than normal and serum TSH concentration increased. She was subsequently treated with synthetic I-T4. Despite the fact she became euthyroid with the treatment, muscle weakness as well as elevated concentrations of muscle enzymes were not improved. Muscle biopsy was made in July 1983, and she was diagnosed as immune polymyositis and treatment with prednisolone and cyclophosphamide in addition to PTU or I-T4, was started. With the treatment, serum LDH decreased to the normal range. However she still has muscle weakness and serum concentrations of CPK and aldolase are still in higher levels than normal range.
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PMID:A case of Graves' disease associated with polymyositis. 209 Jun 76

Dysfunctional uterine bleeding (DUB), menstrual bleeding not explained by organic pathology in the pelvis or systemic deseases that exacerbate bleeding, is suspected when a reproductive-aged woman has excessive menstrual flow. Ovulatory DUB is most common in parous women aged 30-45 years. Cycles are regular and predictable and menstrual flows are preceded by breas soreness, mood or energy changes, or pelvic discomfort. Hypochronic microcytic anemia may result from the amount, rapidity, and duration of bleeding. Current evidence supports the hypothesis that DUB is associated with an increased total amount of prostaglandin in the uterus. Prostacyclin appears to be a likely cause of menorrhagia because it is locally produced within the intima of vessels and is a powerful vasodilator and effective inhibitor of platelet aggregation. DUB diagnosis requires careful exclusion of organic pathology through a detailed history, complete physical examination, and a complete blood count. A beta-human chorionic gonadotrophin measurement to rule out obstetric accident, curettage, hysteroscopy, biopsy, or laparoscopic visualization may be appropriate under different conditions. Curettage, thyroid hormone administration, ergot alkaloids, vitamin and mineral preparations, and iron therapy do little to correct the basic problem. Aspirin should be avoided in the week before and on the days of flow since in analgesic doses it inhibits the platelet thromboxanes that promote platelet agggregation and local vasoconstriction. Bed rest or reduced physical activity on days of flow is also advisable. Nonsteroidal antiinflammatory drugs are effective in reducing blood loss in women with DUB. The durgs are prostaglandin synthetase inhibitors, but the biochemical modifications causing an improved bleeding pattern are not well understood. All such drugs are effective, but some women experience greater relief with 1 formulation than another. Medroxyprogesterone acetate, 10 mg dialy for 7 days before the onset of flow, reduces bleeding in some women although the mechanism of action is unclear. Oral contraceptives (OCs) containing progestins derived from 19-nortestosterone inhibit endometrial proliferation, so ther is little tissue to be shed and little local prostaglandin to stimulate bleeding. Nonsmoking women under 40 years old with DUB who desire reversible contraception are excellent candidates for OCs. Aminocaproic acid is very expensive and has annoying gastrointestinal side effects. but is cost-effective for women with chronic anemia or life threatening uterine hemorrhage who wish to avoid hysterectomy. Danazol is of little usefulness because of its expense and side effects. Hysterectomy is an acceptable therapeutic option for many women.
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PMID:Dysfunctional uterine bleeding in ovulatory women. 388 Aug 90

Nineteen patients with overt hypothyroidism were examined for the prevalence of myocardial disfunction, respiratory disturbances, peripheral neuropathy, and visual failure due to pituitary enlargement. Prevalences of pericardial effusion and myocardial disfunction (decrease PEP/LVET) were 50% and 75%, respectively. The degree of decreased myocardial function did not parallel with the grade of pericardial effusion. Arterial blood analysis indicated a frequent incidence of hypoxia in hypothyroidism. The incidence of hypoxia was 69%. The hypoxia was improved by thyroxine replacement therapy. In 6 patients examined for the ventilatory control, all had the index for hypercapnic ventilatory drive lower than normal control. It was suggested that the hypoxia in hypothyroidism was caused by a depression of the respiratory center in the brain and by anemia. Sensory nerve conduction was diminished in 6 of 11 hypothyroid patients and motor conduction in 6 of 15 was studied. In distal segments of sensory nerves, the abnormality frequently appeared before clinical symptoms of polyneuropathy. Visual field defect was detected in 71% of patients suffering of primary hypothyroidism. The most common characteristic change was the defect in the central visual field. All cases of visual field defect were cured by thyroid hormone replacement therapy. Two cases with deteriorated visual failure who did not improve during physiological replacement, were successively treated with over dosage of thyroid hormone.
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PMID:Unusual manifestations in primary hypothyroidism. 622 84


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