Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two male patients with 'Hashitoxicosis', who revealed histologic pictures of adenomatous goiter in addition to findings of chronic thyroiditis, are described. Case 1. A 55-year-old man was admitted on May 7, 1981, for evaluation of hyperthyroidism. He had exophthalmos with positive Moebius and von Graefe's signs, and a firm, asymmetrically enlarged non tender thyroid gland with multiple cysts. The BMR was +60%, T4 26.4 micrograms/dl, free T4 7.2 ng/dl, T3 5.62 ng/ml and 24 hr radioiodine uptake 49.5%. TSH was undetectable and did not respond to TRH. 123I scan showed multiple defects in the bilateral upper poles of the thyroid gland. Antithyroglobulin and antimicrosomal antibodies were positive. He then underwent a total thyroidectomy with removal of multinodular goiter. The mutinodular goiter was associated with cystic degeneration which contained the thyroid hormone-rich fluid. Histologic examination revealed multiple adenomatous nodules and lymphocytic infiltration and degeneration in the surrounding tissues of the nodules. Case 2. A 43-year-old man was admitted on May 14, 1975, because of an 8 month history of hand tremor, weight loss (5 kg), facial and upper palpebral edema and an enlarged thyroid. He had mild exophthalmos and a firm, asymmetrically enlarged thyroid gland with multiple nodules. The BMR was +35%, T4 20.0 micrograms/dl, T3(Resomat) 0.78 ng/ml and PBI 20.0 micrograms/dl. TSH was 1.0 muU/ml and responded slightly to TRH. 24 hr radioiodine uptake was 84.4% and did not respond to T3 administration. Antithyroglobulin and antimicrosomal antibodies were positive. 123I scan showed diffusely increased uptake and no defects. Histologic examination of the biopsy specimen of the thyroid gland showed multiple adenomatous nodules in addition to typical findings of chronic thyroiditis in the surrounding tissues of the nodules. From the above observations, it is suggested that multiple adenomatous nodules accompanying chronic thyroiditis show clinical features resembling Basedow's disease rather than Plummer's disease.
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PMID:[2 cases of Hashitoxicosis with histological features of adenomatous goiter]. 668 93

Lithium is the recommended treatment for the prophylaxis of bipolar affective disorder. The drug is also effective in the prophylactic treatment of recurrent unipolar depression, although many psychiatrists prefer to use antidepressant drugs for this indication. The efficacy of lithium is well established in the short term treatment of mania, although neuroleptic drugs are required at the start of treatment for more severely disturbed patients. Lithium augmentation of antidepressant drugs is increasingly popular for the treatment of resistant depression. It is now common practice to maintain serum lithium concentrations in the range 0.5 to 0.8 mmol/L, which is generally as effective as higher concentrations while reducing the incidence of adverse effects and intoxication. Some individuals may nevertheless require higher serum concentrations. Most adverse effects such as tremor and gastrointestinal upset are usually minor and often transient. There is no good evidence of nephrotoxicity with long term treatment, but persistent polyuria can occur. Hypothyroidism, with or without goitre, can occur uncommonly during long term lithium therapy. Prescribers should be alert to, and patients should be educated about, the predisposing factors and early symptoms relating to lithium intoxication. Specialist mood disorder clinics can facilitate safer and more effective lithium treatment.
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PMID:Lithium. Current status in psychiatric disorders. 769 9

A 24-year-old women presented with multiple translucent papules on the periorbital and malar areas. Histological examination demonstrated cystic structures lined with a few layers of flattened epithelial cells. These cells were positive for carcinoembryonic antigen, confirming the histological diagnosis of eccrine hidrocystoma. Physical examination revealed a goiter along with finger tremor and hyperhidrosis. The diagnosis of Graves' diseases was established by endocrinological studies. The skin lesion as well as clinical symptoms disappeared as the thyroid function normalized with treatment. Graves' disease should be considered as one of the underlying diseases or conditions related to the development of the multiple eccrine hidrocystomas.
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PMID:Multiple eccrine hidrocystomas associated with Graves' disease. 891 70

Sarcoidosis is a systemic chronic granulomatous disease of unknown etiology most commonly affecting young females. The disease was first described in the thyroid gland in 1938. Our patient, a 27-year-old male with known sarcoidosis, was referred to the National University Hospital for acute symptoms of thyrotoxicosis (weight loss of 6 kg, tremor, thyroid enlargement, and tachycardia). Laboratory findings showed suppressed serum thyrotropin (TSH, <0.03 mU/L [0.5-4.20]), increased total thyroxine (T4) (223 nmol/L, [60-140]), and triiodothyronine (T3) (8.5 nmol/L, [1.5-2.7]). Furthermore, Tc-99m pertechnetate scintigraphy disclosed diffuse accumulation of the isotope confirming the diagnosis of Graves' disease. During the next 18 months of antithyroid treatment (thiamazole, Thycapzol) hyperthyroidism was difficult to control, the thyroid gland gradually enlarged, and surgery was recommended. Initially, the patient declined surgery but after an additional 18 months, he accepted surgery. During the 36-month period of antithyroid drug treatment TSH was suppressed (<0.01 mU/L) and T3 often elevated despite high doses of thiamazole. Total thyroidectomy was performed, and histologic examination of the removed thyroid tissue confirmed the diagnosis of Graves' disease and also the presence of sarcoid granuloma and metastatic papillary adenocarcinoma with spread to neck lymph nodes. Four months later, a modified radical neck dissection was performed with removal of neck lymph nodes followed by external radiation therapy (2 Gy x 32 fractions to the neck). The concomitant presence of sarcoidosis, papillary carcinoma, and Graves' disease in a thyroid gland, to our knowledge, has not previously been described in the literature.
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PMID:A case of sarcoidosis and sarcoid granuloma, papillary carcinoma, and Graves' disease in the thyroid gland. 1077 43

A 49-year-old man, diagnosed as having Cushing disease in 1976 at the age of 26, underwent a Hardy operation 13 years after treatment with reserpine combined with pituitary radiation. In laboratory examinations before and 2 weeks after the successful surgery, the patient's serum thyroid hormones were found to be normal except for suppressed serum thyroid-stimulating hormone (TSH), and his serum anti-TSH receptor (TRAb) and anti-TSH receptor-stimulating antibodies (TSAb) were negative. Glucocorticoid supplemental treatment was withdrawn on the 15th day after surgery and was restarted on the 48th day, during which time there were no signs of an adrenal crisis. Sinus tachycardia, fine finger tremor, and enlarged thyroid gland, approximately the size of a thumb head, were observed on the 140th day after surgery. Thyrotoxicosis with increased serum TSAb and TRAb and high 24-h thyroid uptake of 123I was noted, indicating a diagnosis of Graves disease. No special treatment was prescribed, but his serum thyroid hormone levels started to decrease on the 140th day after the operation and returned to normal on the 520th day. Serum TRAb also spontaneously decreased, but the timing of the peak of serum TRAb was delayed 230 days from that of the thyroid hormones. This is the first reported case of Graves disease after successful surgery for Cushing disease. We presume that a latent autoimmune process in the thyroid, suppressed by hypercortisolism, developed into overt Graves disease after the abrupt reduction of plasma glucocorticoid levels induced by surgery.
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PMID:Transient Graves disease developing after surgery for Cushing disease. 1190 63

Hashimoto's thyroiditis (HT) and Graves' disease (GD) constitute a spectrum of autoimmune thyroid diseases (AITD). They share an autoimmune pathogenesis, with a cellular and a humoral response to the thyroid gland. As a consequence, dysfunction of the gland itself may develop, characterized by hyperfunction in the case of GD and hypofunction in the case of HT, however at the onset of HT the hyperthyroidism might be observed as a result of a rapid destruction of thyrocytes. An abnormal thyroid echographic pattern characterized by a diffuse low echogeneity has been described in both AITD. This hypoechogeneity is due to three components: increase of intrathyroidal flow, functional changes in thyroid follicles with increased cellularity and decrease of the colloid content, resulting in the reduction of the cell/colloid interface, variable degree of lymphocytic infiltration. The first two components may be reversible during medical treatment and seem to be characteristic for GD, whereas lymphocytic infiltration may rather represent mostly HT. Here we present a 17-year-old girl with typical clinical signs of hyperthyroidism [firm goiter (II degrees), tachycardia, palpitations, nervousness, excessive sweating and tremor]. Laboratory tests were the following: fT3 - 6.59 pg/ml(increasing), fT4 - 1.99 ng/dl(increasing), TSH - 0.02 micro IU/ml(decreasing); anti-Tg-Ab - 840 IU/ml(increasing), anti-TPO-Ab - 190 IU/ml(increasing) (4 months later antithyroid antibodies were 2200 and 70, respectively). Ultrasound examination showed hypoechogeneity of the whole gland and enhanced vascular flow based on power Doppler analysis. Thyroid scan visualized the generally increased uptake of technetium. The girl was put on beta-blocker (propranolol) and later an antithyroid drug (thiamazole) was added. A course of disease was unstable, therefore the fine-needle aspiration biopsy was performed and showed the presence of single groups of normal thyrocytes and scanty colloid with no features of HT. Power Doppler analysis showed still enhanced blood flow within a gland inspite of euthyroid state. After a very unsteady period of the disease, the euthyroid state is maintained although the medical treatment was given up. The full recovery of normal blood flow and normal echogeneity of the thyroid was documented. The latter supports the diagnosis of GD. Follow-up of the thyroid echogeneity is of great diagnostic and prognostic value if the assay of TSHR-Ab is not available. On the other side, it has to be remembered that TSHR-Ab do not have to be positive in patients with GD and can be positive in patients with HT.
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PMID:[Thyroid echogeneity as a useful tool for the differential diagnosis of hyperthyroidism in the course of Graves disease and Hashimoto thyroiditis]. 1281 76

We report herein a case of thyroid mucosa-associated lymphoid tissue (MALT) lymphoma in a patient receiving antithyroid drug therapy for Graves' disease. A 75-year-old woman first presented with finger tremor and was diagnosed with Graves' disease on the basis of clinical and laboratory findings. Three years later, she presented with rapid and painless enlargement of the thyroid. Ultrasonography revealed a circumscribed hypoechoic area bilaterally in each lobe of the thyroid, and fine-needle aspiration biopsy showed diffuse monotonous infiltration of small- to medium-sized atypical lymphoid cells. (67)Ga scintigraphy was positive exclusively in the thyroid. After total thyroidectomy, the patient received radiation therapy for treatment of stage IE primary thyroid lymphoma. Results of histological examination, immunohistochemical analysis, and flow cytometric analysis confirmed MALT lymphoma. To our knowledge, there have been few published reports of primary thyroid lymphoma associated with Graves' disease. Our experience with this case, though rare, indicates that an enlarged thyroid in cases of Graves' disease should be examined carefully for primary thyroid lymphoma.
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PMID:Primary thyroid lymphoma associated with Graves' disease. 1536 Dec 65

Thyrotoxic hypokalemic periodic paralysis (THPP) is a medical emergency characterized by acute attacks of weakness, hypokalemia, and thyrotoxicosis that resolve with the treatment of hyperthyroidism. Attacks are transient, self-limited, associated with hypokalemia and resemble those of familial hypokalemic periodic paralysis (FHPP), an autosomal dominant neurological channelopathy. This study reviews the clinical features and genetic findings of THPP in 25 Brazilian patients. Most patients had weight loss, taquicardia, goiter, tremor, and ophthalmopathy. Most often attacks arose during the night and recovered spontaneously but some patients evolved to total quadriplegia, and few experienced cardiac arrhythmias. All patients had suppressed TSH and elevated T4 and most had positive anti-thyroid antibodies, indicating autoimmunity thyrotoxic etiology. Potassium was low in all patients during the crisis. Prophylactic potassium therapy has not been shown to prevent attacks; however it was useful for curbing the paralysis during the crisis. We identified the mutation R83H in the KCNE3 gene in one sporadic case, and M58V in the KCNE4 gene in one case with family history. Furthermore, we identified other genetic polymorphisms in the CACNA1S, SCN4A, KCNE1, KCNE2, KCNE1L, KCNJ2, KCNJ8 e KCNJ11 genes. We conclude that THPP is the most common treatable cause of acquired periodic paralysis; therefore, it must be included in the differential diagnosis of acute muscle weakness.
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PMID:[Thyrotoxic hypokalemic periodic paralysis, an endocrine emergency: clinical and genetic features in 25 patients]. 1561 33

We analyzed the clinical and laboratory data of 106 children (17 boys and 89 girls, 11.7 +/- 3.4 years old) with newly diagnosed Graves' disease at Chang-Gung Children's Hospital in Taiwan from 1995 to 2005. The earliest age of disease onset was 3.36 years old, and incidence progressively increased throughout childhood, with a peak at 15 years old. Forty-six (48%) of 95 children had a positive family history of thyroid disorders. We divided the children into three groups according to pubertal stage: prepubertal (Tanner stage 1), 34 (32%); pubertal (Tanner stage 2-4), 13 (12%); and postpubertal (Tanner stage 5), 59 (56%). The most common presentations were diffuse goiter, heat intolerance, sweating, palpitations, and weight loss despite an increase in appetite, but there were no significant differences among the three groups. Neuropsychiatric symptoms such as nervousness, hyperactivity and poor school performance are common features in these children. Height standard deviation score (0.33 +/- 1.35) revealed tall stature (0.39 +/- 1.66 in the prepubertal group, -0.066 +/- 0.63 in the pubertal group, and 0.40 +/- 1.23 in the postpubertal group). Bone maturation also was accelerated in all three groups (bone age/chronological age 1.09 +/- 0.22, 1.07 +/- 0.20, and 1.08 +/- 0.08), but there were no significant differences between groups. Body mass index (standard deviation score) was low in all three groups (-0.49 +/- 1.10, -0.68 .0.63, and -0.13 +/- 0.98), with no significant differences between groups. Tachycardia (96%), goiter (94%), fine tremor (92%), bruit (66%), hypertension (63%), and exophthalmos (60%) were the most frequent symptoms. Laboratory findings yielded undetectable TSH levels (<0.03 microIU/mL), increased FT4 (5.54 +/- 2.26 ng/dL), TT4 (18.37 +/- 4.79 microg/dL), and TT3 (450.4 +/- 202.2 ng/dL), with no significant differences between groups. The prevalences of positive TBII, AMCA, and TGAB were 96%, 95%, and 71%, respectively. In conclusion, we did not find any differences in the presentation of Graves' disease among prepubertal, pubertal, and postpubertal patients. An awareness of symptoms is necessary for prompt diagnosis and management of Graves' disease because the disease can seriously interfere with children's growth and development.
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PMID:Clinical and laboratory findings at initial diagnosis in pediatric Graves' disease in Taiwan. 1692 32

Lithium use in mental diseases has changed over the years but remains a cornerstone of treatment in bipolar disorders. In two companion papers, we have reviewed existing (and especially recent) data on lithium efficacy and updated basic knowledge regarding the practical fundamentals of lithium therapy. The present paper reviews safety data on lithium available to date. Gastrointestinal pain or discomfort, diarrhoea, tremor, polyuria, nocturnal urination, weight gain, oedema, flattening of affect and exacerbation of psoriasis are typical complaints of patients receiving long-term lithium therapy. Renal involvement results in a reduced urinary concentrating capacity, expressed as obligate polyuria, with secondary thirst. With long-term therapy, this may result in nephrogenic diabetes insipidus. In addition, glomerular filtration rate falls slightly in about 20% of patients. The view that only a few patients receiving long-term lithium are at increased risk of glomerular impairment and progressive renal insufficiency should be regarded with caution. The risk is increased in case of concomitant diseases or medications. Lithium treatment may inhibit thyroid hormone release and induce goitre. Consequently, the prevalence of both overt and subclinical hypothyroidism is increased, with circulating thyroid auto-antibodies frequently being found. Much less commonly, thyrotoxicosis may also develop in association with lithium therapy. Long-term lithium treatment may also be associated with persistent hyperparathyroidism and hypercalcaemia, as well as with hypermagnesaemia. Overweight of up to 4-10 kg is found in approximately 30% of lithium-treated patients. Most neurological manifestations are benign, for example, the fine postural and/or action tremor present in 4-20% of patients. This is increased by high caffeine consumption and concomitant use of other psychotropic agents. A number of rare, potentially serious neurological adverse effects have been reported, including extrapyramidal symptoms, 'pseudotumour cerebri' or occasionally cerebellar symptoms. Severe neurological sequelae are exceptional. Cognitive disturbances are often mentioned as a lithium-related adverse effect. The few controlled studies do show a statistically significant negative effect of lithium on memory, vigilance, reaction time and tracking. There are frequent reports of mild effects of lithium on cognition at therapeutic serum concentrations. A number of deaths associated with lithium treatment have been reported. The most serious issue is that of non-accidental overdose, i.e. either long-term overdosage or acute overdose on long-term treatment. Progressive renal insufficiency, an exceptional complication of long-term lithium therapy, may also have a fatal outcome. In relation to pregnancy, lithium salts are rated as category D (positive evidence of risk). Therefore, prescription of lithium should be avoided during the first trimester of pregnancy unless the benefit to the mother exceeds the risk to the fetus. Although lithium transfer into breast milk is well established, the long-term fate of babies breast-fed by mothers receiving lithium therapy is unknown. Whether lithium therapy is safe in breast-feeding women is controversial. Although there is no absolute contraindication, it is known that the kidney is particularly sensitive to lithium just after birth. Intoxication in patients on long-term treatment with lithium in the absence of history of acute ingestion is not rare. Contributing factors include change in daily dose, long-term high dosage, kidney disease or drug interaction. In suspected cases, serum concentrations should be obtained early and repeatedly. In addition to supportive measures, haemodialysis is the treatment of choice for severe cases. Thorough knowledge of the limitations and drawbacks of lithium therapy is mandatory for its optimal use, especially at a time when its risk/benefit profile needs to be compared accurately with that of antiepileptic drugs and other mood stabilizing medications.
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PMID:Lithium: updated human knowledge using an evidence-based approach: part III: clinical safety. 1945 1


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