Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 26-year-old female with Bartter's syndrome associated with Graves' disease is reported. This patient had a history of Graves' disease from the age of 22 and anti-thyroid drug (Methimazole) had been administered for 2 years. Thyroid function returned to normal but general fatigue and polyuria continued. Hypokalemia was diagnosed at 25 years of age and she was referred to our hospital for evaluation. Blood pressure was normal and laboratory data revealed normal thyroid function, hypokalemic alkalosis, high plasma renin activity and high plasma aldosterone concentration. She showed normal pressor sensitivity to norepinephrine infusion, grossly diminished pressor sensitivity to exogenous angiotensin II infusion compared with the normal. A renal biopsy specimen showed juxtaglomerular cell hyperplasia. Electron microscopy confirmed lacis cell (agranular cell) proliferation.
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PMID:Bartter's syndrome--case report. 15 51

Postpartum thyroid dysfunction (PPTD) refers to the syndromes of transient hyperthyroidism, transient hypothyroidism, or both, occurring sequentially in the first 12 months postpartum. Approximately 5 to 9% of women develop the disorder in this period. PPTD is most often subclinical but some women will experience symptoms such as lack of energy and depression in the hypothyroid phase. The thyroid gland, which normally enlarges during pregnancy, will remain enlarged or enlarge further in the postpartum period in a significant number of affected women, instead of returning to the prepregnancy size as in unaffected women. The gland is painless and histologically demonstrates lymphocytic infiltration. PPTD is strongly associated with the presence of antimicrosomal and/or antithyroglobulin antibodies, which occur in up to 76% of cases. Antibody activity tends to increase in the postpartum period and to peak at the time of onset of the disorder. TSH receptor antibodies are not seen and the gland has low radioiodine uptake, distinguishing PPTD from Graves' disease. The HLA associations are controversial, as is the role of dietary iodine. The etiology of PPTD is almost certainly immunological, reflecting the phenomenon of rebound from the relative immune tolerance of pregnancy. Detection of the disorder is important in order to reassure or treat those who are symptomatic and because PPTD may recur in subsequent pregnancies. In addition, up to one third of affected women will go on to develop permanent hypothyroidism 2 to 4 years later. The role of screening for PPTD remains to be clarified.
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PMID:Postpartum thyroid dysfunction. 152 73

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

We have reported two cases of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with Graves' disease. Case 1: a 45-year-old woman noticed a diffuse goiter, palpitation and emaciation in 1977. Laboratory studies confirmed that she had Graves' disease, and she was treated with antithyroid drug. In 1986, when the hyperthyroidism was subsided, she showed progressive symmetrical weakness and numbness in her limbs, and she was almost in tetraplegia at 1987. Markedly slowed motor and sensory nerve conductions and elevated CSF proteins as well as clinical manifestations confirmed the diagnosis of CIDP. Following corticosteroid-pulse therapy and plasmapheresis resulted in good recovery in both motor and sensory impairment, though two-times of relapses were observed. Case 2: a 33-year-old man first noticed weakness in his legs in 1977, motor and sensory disturbances progressed for 12 years. Slowed nerve conduction, high CSF proteins and two-times of relapses in early phase indicated that the CIDP was the diagnosis. In 1989 he complained general fatigue, hyperhidrosis and body-weight loss. The serum thyroid hormone levels were high, and other laboratory studies confirmed the presence of Graves' disease. The cases with both CIDP and Graves' disease has rarely been reported. The background mechanism of this association is not well understood, but the susceptibility to CIDP and Graves' disease may be related to the HLA antigens and immunoglobulin Gm allotypes of which are the genes linked to the major histocompatibility complex and controlling immune responses. The present two cases commonly shared several HLA-DR antigens, but their significance should be confirmed by examining many cases.
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PMID:[Two cases of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with Graves' disease]. 178 65

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

A 31-year-old female was well until few years ago when she was diagnosed as having Graves' disease. Methimazole (MMI) and Lugol's solution were prescribed. But 7 months later, she stopped taking them arbitrarily. Three months later, thirst and general fatigue appeared. Therefore insulin (60u/day) and MMI (30 mg/day) were administered and continued for 40 days. However no remarkable effect was brought about. She was then transferred to the radioisotope ward of Kumamoto Univ. Hospital and was treated with regular insulin only. Ten days later, she fell into thyroid storm associated with diabetic ketoacidosis and was transferred to our ward. We began to administer large volumes of transfusion, regular insulin, MMI, Lugol's solution, propranolol, hydrocortisone and digitalis. In 24 hours, ketoacidosis disappeared and she became alert. For hyperthyroidism, the dosage of MMI was increased to 60 approximately 45 mg/day and was continued for a month; however, her thyroid function did not normalize and agranulocytosis developed. MMI was discontinued, and she was treated with 131I. About a year later, she became euthyroid. Her diabetes mellitus was difficult to control during the hyperthyroid state but it was under good control with monocomponent lente insulin (36u/day) when the euthyroid state was resumed.
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PMID:[A case of thyroid storm associated with diabetic ketoacidosis (author's transl)]. 677 5

We present two cases of systemic lupus erythematosus (SLE) associated with both Basedow's disease and fatty liver. The first case is a 46-year-old Japanese female who was admitted because of high fever and general fatigue. She had been diagnosed as having Basedow's disease and treated with thiamazole for over 4 years. Since thiamazole-induced lupus was unlikely because of high titer anti-nuclear antibody and anti-DNA antibody and low levels of complements, a diagnosis of SLE was made. The upper abdominal ultrasound study and the specimen obtained by liver biopsy performed before initiating steroid therapy demonstrated marked fatty liver. SLE itself is considered as an etiology of fatty liver in this case. The second case was a 25-year-old Japanese female with SLE. She had been treated with prednisolone for 13 years and was complicated with Basedow's disease 10 years later. Fatty liver was also demonstrated in this patient on ultrasonography, and was thought to be resulted from long-term steroid hormone administration.
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PMID:[Two cases of systemic lupus erythematosus associated with fatty liver and Basedow's disease]. 817 1

Various diseases often occur after delivery but the systemic examinations have not been studied before. Thyroid dysfunction frequently (4.4%) occurs after delivery through an immune rebound mechanism. If postpartum women complain of the symptoms caused by thyrotoxicosis (palpitation, weight loss, increased sweating, finger tremor, fatigue) or hypothyroidism (edema, cold intolerance, hoarseness, sleepiness, fatigue), it is essential to examine thyroid hormones, thyroid stimulating hormone, anti-thyroid microsomal antibody (MCHA) and anti-TSH receptor antibody. To predict who will develop postpartum thyroid dysfunction, the measurement of MCHA during pregnancy is useful because 62% of the subjects with positive MCHA show thyroid dysfunction after delivery. The individuals at high risk of postpartum onset of Graves' thyrotoxicosis can be found early in their pregnancy by the detection of thyroid stimulating antibody (TSAb). Other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, autoimmune hypophysitis and so on, also could develop after delivery. These findings indicate that laboratory tests in the postpartum period are essential to diagnose postpartum onset of autoimmune diseases and the measurement of autoantibodies in early pregnancy is useful for prediction of their onset in the postpartum period.
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PMID:[Postgravid health care and laboratory tests]. 855 72

A fifty-year-old woman was admitted to our hospital because of palpitation and general fatigue. She had received hemithyroidectomy for thyroid papillary adenocarcinoma at 28 years of age. She had experienced episodes of repeated painless thyroiditis five times over the last 12 years. At her sixth episode of thyrotoxicosis, she was suspected to have Graves' disease and admitted to our hospital. Laboratory findings revealed thyrotoxicosis with positive thyroid stimulating antibody and high radioactive iodine uptake, i.e. Graves' disease. Painless thyroiditis often relapses but rarely develops into Graves' disease. This is a rare case in which repeated painless thyroiditis was followed by Graves' disease. The relation between painless thyroiditis and Graves' disease is discussed.
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PMID:A case of repeated painless thyroiditis followed by Graves' disease. 882 26


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