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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Focal or diffuse infiltration of lymphoid cells in auto-immune thyroiditis destroys the parenchyma. In the diffuse form (Hashimoto's disease), the clinical picture is characterized by fatigue and thyroid enlargement. The diagnosis is settled by cytology. All patients must be treated with thyroid hormones to avoid myxoedema. Loss of immunological tolerance and cytotoxic immune reactions is discussed.
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PMID:Human auto-immune thyroiditis. 79 Aug 89

The incidence of pregnant women with thyroid dysfunction has been reported to be around 0.1-0.4%. Graves' disease accounts for more than half of these disorders. The main cause of thyroid disease in pregnancy and puerperium is autoimmune dysfunction. Whether there may be goitre or exophthalmus present, clinical signs as inappropriate weight gain, high systolic pressure, palpitation (greater than or equal to 110/min), emotional lability, fatigue, acceleration of suppression of the Achilles' tendon reflex should induce changes in the biochemical thyroid function tests. Parameters for the diagnosis and management for hyperthyroidism are serum levels of free T4 and TSH, while those of T3, reverse T3, and TSH are for hypothyroidism. Serum anti-microsomal antibodies and anti-thyroglobulin antibodies which have no effect on the fetus are also good markers for severity. The transplacental transfer of maternal TSH receptor antibodies consisting of stimulatory and inhibitory immunoglobulins and maternal thyroid-binding inhibiting immunoglobulins play roles in the development of transient neonatal hyper- or hypothyroidism. Fetal control is achieved by optimal maternal management. Untreated hyperthyroidism may be associated with fetal malformations. This risk may be reduced by antithyroid drug treatment of up to 150 mg/day of propylthiouracil which has less chance of placental passage and less secretion into the mother's milk than methyl-mercapto-imidazol. Maternal thyroid function should be kept in the upper limit of normal range, taking into consideration the fetal dysfunction induced by over-administration of the drug which passes through placenta. Children of hypothyroid women taking inadequate replacement therapy manifested lower IQ values compared to the progeny of euthyroid or hypothyroid women taking adequate therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Thyroid disease]. 170 36

Anti-thyroid peroxidase antibodies were prospectively assayed and compared with anti-microsome and anti-thyroglobulin antibodies in 203 patients (188 women, 15 men; mean age 42 +/- 14 years). These patients consulted for hyperthyroidism (n = 42, including 18 with Graves' disease), fumary hypothyroidism (n = 50, including 20 at the diagnosis stage), euthyroid diffuse or nodular goitre (n = 81) or benign euthyroid nodule (n = 14). Sixteen patients examined for fatigue, gynecomastia, menstrual disorders or overweight had normal thyroid function. Anti-thyroid peroxidase, anti-microsome and anti-thyroglobulin antibodies were assayed by radioimmunology or indirect immunofluorescence. Anti-thyroid peroxidase antibodies were most frequently present in patients with autoimmune thyroid diseases, such as Graves' disease (72%) or primary hypothyroidism (70%), and correlated with anti-microsome antibody levels (r = 0.87; p less than 0.001). Anti-thyroid peroxidase antibodies were absent in patients with benign euthyroid nodule; they were present in 22% of patients with euthyroid goitre and in 12% of control patients; their level decreased during replacement therapy for hypothyroidism. It is concluded that radioimmunological assays of anti-thyroid peroxidase antibodies should replace anti-microsome and anti-thyroglobulin antibodies in thyroid evaluation.
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PMID:[Anti-thyroid peroxidase in non-neoplastic thyroid pathology]. 177 11

A 40-year old female was admitted with complaints of general fatigue and dyspnoea brought on by effort. There were edema on the face, a diffuse and slightly hard goiter on the neck and non-pitting edema in the lower legs. Laboratory findings showed low levels of serum T3 (0.37 ng/ml) and T4 (2.0 micrograms/dl), a very high level of serum TSH (549.8 microU/l), positive thyroid test (x 400) and positive microsome test (x 102,400). The chest roentgenogram showed an enlargement (CTR 62%) of the cardiac silhouette in the shape an ice bag, and the electrocardiogram revealed low QRS voltage with T-wave flattening in all leads. Remarkable pericardial effusion was shown on the two-dimensional echocardiogram. Judging from the indications of hypothyroidism, positive antithyroid antibody and pericardial effusion. This patient was diagnosed as having myxedema heart due to chronic thyroiditis. The levels of plasma alpha-hANP did not elevate so much as the levels in normal controls after right atrial (RA) pacing, although mean right atrial pressure was higher than in normal controls after RA pacing. The levels of plasma alpha-hANP after RA pacing in euthyroid state were higher than those in hypothyroid state. The levels of plasma alpha-hANP after RA pacing became higher after the administration of ATP or db-cAMP both in euthyroid and hypothyroid states. These results indicate that the impaired alpha-hANP secretion in myxedema heart is improved by the administration of thyroxine, ATP or db-cAMP.
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PMID:[A case of myxedema heart showing the improvement of impaired alpha-hANP secretion by administration of ATP and dibutyryl cAMP]. 217 40

We describe an epidemic of self-limited (6 weeks) thyrotoxicosis which affected 12 index cases, 5 household contacts, and 6 retrospectively identified cases in July, August, and September, 1987 in the town of Winterswijk (28,011 inhabitants), The Netherlands. A small goiter was present in 9 of the 12 index patients, tender upon palpation in only 2. Signs and symptoms of thyrotoxicosis were accompanied by a low grade fever in combination with fatigue, headache, myalgia, and a fine desquamation of the palms and soles. The apparent incubation time between family members was 6 days. Thyroid technetium uptake was decreased in 10 of 11 tested patients. Laboratory findings included elevated sedimentation rates (up to 68 mm/h), increased liver enzymes, lymphopenia in 2 patients, and absence of thyroid autoantibodies. HLA-B35, associated with classical subacute thyroiditis, was found in 1 patient only. An etiological agent was not identified. No evidence was found for thyrotoxicosis factitia. After 10 months, all patients were euthyroid, without a goiter or thyroid autoantibodies. Thus, a new variant of thyroiditis, atypical subacute thyroiditis, was probably the cause of this unusual outbreak. It is unclear at present if this variant of thyroiditis is common in communities and represents a separate disease entity.
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PMID:An outbreak of thyrotoxicosis due to atypical subacute thyroiditis. 229 55

In this review, the major types of immune mediated thyroiditis are described and the etiology explained in the light of current theories of autoimmunity. Hashimoto's thyroiditis is a common autoimmune disease. The onset is gradual with patients presenting with symptoms of hypothyroidism, nonspecific symptoms of the autoimmune process itself, or symptoms relating to a goitre. The disease is usually relentless and, except in young patients, permanent replacement with thyroxine is eventually required. Silent thyroiditis is another autoimmune disease of more acute onset. The initial, thyrotoxic, phase lasting several weeks is due to release of thyroid hormone from damaged follicles, and radionuclidic scans show absent uptake. There often follows a hypothyroid phase with final recovery in most patients. Post partum thyroiditis is due to silent thyroiditis, or, less commonly, Hashimoto's thyroiditis, occurring three to six months after delivery. Subacute thyroiditis often follows a viral infection and is not thought to be an autoimmune disease. It presents with severe thyroid pain and tenderness with marked non-specific symptoms such as myalgia and fatigue. The initial, thyrotoxic, phase is also due to release of thyroid hormone, and radionuclidic scans show absent uptake. A hypothyroid phase often follows and recovery is complete. Hashimoto's thyroiditis appears to be due to a congenitally present, antigen specific, T suppressor lymphocyte defect. It is proposed that in silent thyroiditis there is a less severe Ts defect and a correspondingly greater decompensating factor. In post partum thyroiditis, this factor appears to be a general decline in T suppressor lymphocyte function after delivery. Subacute thyroiditis is not an autoimmune disease. The thyroid appears to be an "innocent bystander" in an immune mediated antiviral attack.
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PMID:Thyroiditis. 293 21

Fifty-nine patients with both clinical evidence of thyroid dysfunction and patent diabetes mellitus were investigated in our diabetology department. Patients with euthyroid goitre and iatrogenic or pituitary hypothyroidism were excluded from the study. Among the 45 diabetics with hyperthyroidism, 32 had Graves' disease and 13 had toxic adenoma; 71% were insulin-treated. Hyperthyroidism had passed unnoticed in 7 of these 32 patients because fatigue and loss of weight, which initially were the predominant or sole symptoms, are extremely frequent in uncontrolled diabetes. These symptoms, as well as polyuria, polyphagia and even sweating are common to both diseases. Considerable deterioration in the control of glycaemia was observed in 63% of the insulin-treated patients when hyperthyroidism developed, with a 17 to 212% (mean 82%) increase in insulin dosage in 53%. There was no correlation between the degree of hyperthyroidism and the loss of control. Following treatment of the hyperthyroidism, control was improved in 63%, with an 11-83% (mean 44%) decrease in insulin dosage in 59% of them. Insulin therapy could be withdrawn in only one of the 32 insulin-treated patients. Non-iatrogenic primary hypothyroidism was found in 0.2% of the diabetics investigated. This incidence was significantly higher than the calculated probability of the two diseases occurring by chance in the same patient. Eleven out of 14 patients were insulin-treated. When hypothyroidism developed, 73% of them had their insulin dosage reduced, with a high frequency of hypoglycaemic disorders: repeated "malaise" in 55% and coma in 27%. A higher proportion of vitiligo was also noted: 14% in the total patient population reported, and 18% in insulin-treated patients.
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PMID:[Effect of clinical hyperthyroidism and hypothyroidism on patent diabetes. 59 cases]. 315 40

In this study, 65 women and two men were examined because of symptoms suggesting hypothyroidism (eg, tiredness, lack of energy, weight gain, dry skin, cold intolerance, constipation, galactorrhea, menstrual disturbances). Some also demonstrated biochemical abnormalities (eg, hyperlipoproteinemia, elevation of creatine phosphokinase). Serum thyroxine (T4) and triiodothyronine (T3) and T3 uptake were normal in all patients. The thyrotropin-releasing hormone (TRH) test differentiated the patients into two groups: Group 1 (47 patients) had an exaggerated response of thyroid-stimulating hormone (TSH) to TRH; group 2 (20 patients) had a normal TSH response. Compared with group 2, the group 1 patients had a higher incidence of typical hypothyroid symptoms and goiter and responded more readily to levothyroxine therapy. We concluded that these patients had borderline hypothyroidism. Results of basal thyroid function tests may be within normal limits in such a condition. The TRH test, then, appears to increase diagnostic accuracy and should be routinely performed in patients who have symptoms suggesting hypothyroidism but normal results of basal thyroid function tests.
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PMID:How to detect hypothyroidism when screening tests are normal. Use of the TRH stimulation test. 641 Mar 62

A case of hyperthyroidism associated with pancytopenia has been reported. A 51-year-old woman was hospitalized for the investigation of struma, peripheral edema and fatigue. Hormonal studies revealed hyperfunction of the thyroid gland. Hematological examinations showed normocytic normochromic anemia, leukopenia and thrombocytopenia with hyperplastic bone marrow and increased serum iron levels. Elevations of the anti-thyroidal antibody and anti-microsomal antibody, and a decrease in CH50 titer were observed. A Coombs' test and anti-leukocytic antibody and anti-thrombocytic antibody tests were negative. The numbers of erythrocyte and thrombocyte were normalized after the administration of methimazole for three months as were the findings of the bone marrow and the serum iron level. However, leukopenia was maintained due to the effect of methimazole. It should be suggested that the etiology of pancytopenia might be due to hyperthyroidism. Although the mechanism of pancytopenia in a patient with hyperthyroidism is unclear, it might be related to the reduced life-span of whole blood components and/or partially to the autoimmune mechanism.
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PMID:[Case of hyperthyroidism with pancytopenia]. 666 44

The clinical manifestations of biochemically-confirmed acquired hypothyroidism in nineteen children and adolescents were reviewed to evaluate the symptoms and signs in the early stage of the disease. The group consisted of 14 girls and 5 boys ranging in age from 4 to 15 years. In 13 of the 19 patients with profound biochemical hypothyroidism, classical symptoms were often absent and clinical signs limited. In these patients, hypothyroidism was presumed to have been short in duration and consequence of chronic lymphocytic thyroiditis. In the remaining 6 patients, hypothyroidism was long-standing and clinical presentation classical, including disproportionate weight gain, fatigue, cold intolerance, myxedematous feature, growth retardation and constipation. Goiter was the most consistent finding in both groups and was present in all instances of spontaneously acquired primary hypothyroidism. These observations emphasize the importance of routine examination of the thyroid gland, particularly in preadolescent and adolescent girls. The finding of goiter may be the only detectable sign of hypothyroidism in the early stage of the disease. Biochemical evaluation should not be deferred because of a clinically euthyroid presentation. Replacement therapy must be instituted when findings indicate a hypothyroid state. Failure to recognize and treat hypothyroidism in these pubertal patients may compromise the adult height, since skeletal maturation will proceed under the influence of sex hormones despite the presence of hypothyroidism.
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PMID:Clinical recognition of juvenile hypothyroidism in the early stage. 689 85


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