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)

A case of hyperthyroidism occurring in a 68 year old man receiving lithium carbonate (1 g/day) for 5 years is reported. The clinical history of the patient, treated for bipolar affective disorder, was remarkable for transient hypothyroidism followed several months later by tremor, increased free thyroxine and triiodothyronine, and decreased TSH levels which led to lithium withdrawal. Two months later, clinical and biological signs were unchanged, Tc99m-scan displayed a homogeneous and increased isotope uptake. In this setting, high levels of autoantibodies against TSH-receptor, and grade I exophthalmos and slightly ocular muscle enlargement at CT-scan favored the diagnosis of Graves' disease (perhaps facilitated by lithium therapy). Carbimazole treatment was effective in controlling hyperthyroidism. Review of the literature disclosed 44 cases of hyperthyroidism occurring in lithium-treated patients. Most of these cases concerned specific thyroid diseases, particularly with an autoimmune mechanism. There is also evidence for an actual role of lithium in increasing intrathyroid iodide pool and for an impact of lithium on the immune system. Thus, the hypothesis that lithium may trigger the development of an autoimmune thyroid disease in predisposed patients deserves further investigation.
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PMID:[Lithium therapy and hyperthyroidism: disease caused or facilitated by lithium? Review of the literature apropos of a case of hyperthyroidism preceded by transient hypothyroidism]. 808 84

A case of 43-year-old woman with Hashimoto's encephalopathy who experienced three relapses closely associated with the menstrual cycle is reported. In April 1992, she began to experience occasional tremors in her arms. Three months later, she experienced a generalized seizure and was transferred to our hospital. Hashimoto's thyroiditis was diagnosed on the basis of high thyroid microsomal titer and mild hypothyroidism. Neurological findings in admission included action tremor in both hands, myoclonus in all extremities, cerebellar ataxia, confusion, and hyperreflexia. Cerebrospinal fluid showed elevated protein level without pleocytosis. Electroencephalogram showed diffuse slowing and magnetic resonance imaging of brain was normal. Hashimoto's encephalopathy was diagnosed from these findings. These episodes of remission and exacerbation were observed during the admission. Her symptoms started at ovulation, worsened during the luteal phase, and improved when menstruation started. After the third relapse, she was treated with oral thyroxine for hypothyroidism and with an estrogen and progesterone combination to regulate the menstrual cycle. Her thyroid function gradually became euthyroid and she did not experience any subsequent relapses. The relation between the relapsing course and menstrual cycle suggests that the periodic alteration of gonadotrophic and/or gonadal hormones or the menstrual regulating center itself in the brain may be an important factor of pathogenetic mechanism of the disorder.
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PMID:[A case of Hashimoto's encephalopathy with a relapsing course related to menstrual cycle]. 829 82

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

Hypothyroidism, which is treatable by hormone substitution, is one of the most frequent causes of symptomatic dementia. The effectiveness of hormone therapy for improving mental status is well established, but full reversibility of symptoms is unusual. We report the case of a woman whose disease began with progressive cognitive deterioration and tremor; laboratory tests revealed subclinical hypothyroidism, which was watched carefully over the next three years. When thyroid hormone therapy was begun, there was marked clinical improvement, which reversed only when the patient voluntarily withdrew treatment for a few weeks.
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PMID:[Subclinical hypothyroidism as a cause of reversible cognitive deterioration]. 900 50

We report a 47-year-old Japanese man who presented with visual disturbance due to a pituitary tumor with suprasellar extension. The patient had mild secondary hypothyroidism preoperatively, and was started on administration of levothyroxine sodium immediately before transsphenoidal surgery. After the operation, levothyroxine sodium was continued for several months. Pathological examination of the surgical specimen, together with endocrinological investigation revealed that the suprasellar tumor was a FSH-producing pituitary adenoma. Since 3 months after the operation, he has developed muscle weakness and finger tremor. He was found to be thyrotoxicosis, and levothyroxine sodium was discontinued. Seven weeks after levothyroxine sodium was discontinued, thyrotoxicosis continued, with a positive thyrotropin binding inhibitory immunoglobulin (TBII) and a high diffuse 123I-uptake by the thyroid. He was started on thiamazole 30 mg/day. Although his thyroid dysfunction improved within 2 months, hyperthyroidism worsened repeatedly on attempts to discontinue thiamazole, and he required continuous treatment at 2.5 mg/day. Patients with occult autoimmune thyroiditis rarely progress to thyrotoxicosis after operations on other endocrine organs such as the adrenal or parathyroid gland. In patients with pituitary adenoma, thyroid function and thyroid-associated autoantibodies should be investigated pre- and post-operatively.
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PMID:Manifestation of primary hyperthyroidism after pituitary adenomectomy: a case report. 962 7

Successful lithium treatment of manic disorders was reported in 1949 by John Cade. This marked the beginning of the pharmacological era in psychiatry. In spite of the emergence of alternative drugs with antimanic and moodstabilising properties, lithium remains the primary long-term treatment for preventing relapse of bipolar disorders. Among the adverse effects of lithium treatment are unintentional lithium intoxication, nephropathy, hypothyroidism, hypercalcemia, hyperparathyroidism, diarrhoea, tremor, weight gain, and effects on the fetus and the newborn child. Early detection or prevention of adverse effects, particularly lithium intoxication, is vital for safety. Therefore, P-lithium and P-creatinine are assessed every 4 months (and pre-lithium) while thyroid and parathyroid function, weight, 24 h consumption of liquids (or 24 h urinary output), B-glucose, and blood pressure are assessed annually (and pre-lithium). Urinary concentrating capacity and glomerular filtration rate are always measured after 5 years of lithium treatment, and always when clinically indicated. Patient education and annual reinforcement of his/her knowledge of pertinent aspects of the treatment and of risk factors for lithium intoxication are important aspects for ensuring safety.
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PMID:[Adverse effects of lithium treatment and safety routines]. 1519 Jul 55

In response to the increase of resistant depressive disorders and in spite of improved treatments, numerous studies were conducted in the last thirty Years aiming at assessing the pre-morbid thyroid state of depressed patients resistant to well conducted tricyclic treatments. "Minimal" thyroid abnormalities were evidenced as well as central thyroid disorders which may not be detected by peripheral-i.e plasmatic- dosages. Regarding the premorbid thyroid status, the hypothesis of subclinical hypothyroidism was considered by many Authors. It is marked by four grades including T3 and T4 decreased levels, basal TSH concentration abnormalities as well as increased TSH response to TRH stimulation, and the presence of antimicrosomal and antithyroglobulin antibodies. Although, there are different views on the existence or not of these abnormalities, we'll focus our attention on a metaanalysis including six studies. It shows in a population with a resistant depression, 52% of patients with subclinical hypothyroidism, against 8 to 17% in patients with simple depression and 5% in the overall population.Similarly, antithyroid antibody levels (group IV hypothyroidism) were significantly higher in depressed patients (9% to 20% against 7,5% in the overall population). For many Years, a central hypothyroidism was hypothesized on the basis of an exhausted T3-T4 transference mechanism and a lowered TRH hypothalamic biodisponibility.In the last Years, new data emerged on the role of transthyretin, a cerebral carrier T4 protein, whose concentration in the CSF was found significantly lower in depressed patients than in a control group, the lowest levels being observed in the most severely depressed. This decreased level of transthyretin would result in a lower central T4 biodisponibility-hence, in view of a T4-T3 desiodation insufficiency, a T3 deficit is observed. A low transthyretin level associated or not to subclinical hypothyroidism could be a factor of depressive vulnerability on one hand, of resistance to tricyclic treatment on the other one. Conversely, subclinical hypothyroidism could be a predictive factor of a good response to a potentializing strategy. The pharmacological mechanisms involved in this potentializing phenomenon are now well known: they consist in an interaction between depression, adrenergic receptors and thyroid hormones biodisponibility. The decreased norepinephrine level observed in depressive patients is associated, in case of increased thyroid hormones biodisponibility, with a higher sensitivity of adre-nergic receptors, mostly betaadrenergic. This seems to underly the recovery process. According to some Authors, the serotoninergic system might be involved in the potentialization of tricyclics by thyroid hormones. We know that in animals with hypothyroidism, the serotonin synthesis is decreased and that the administration of T3 increases the brain levels of serotonin and its 5HIA catabolite. In addition, T3 could correct the down-regulation induced by serotoninergics on beta-adrenergic receptors. On the basis of numerous studies carried out on the potentializing of tricyclics, we suggest practical modalities of treatment - which until today did not materialize in every day practice in the absence of a clear consensus based on statistically reliable data: after four to six weeks of inefficient tricyclic or serotoninergic treatment on a correct dosage testified by plasmatic dosages, it is recommended to initiate a T3 treatment on a effective posology (25 to 50 micrograms per day), which must be reached in 2 or 3 days, except in case of rare and transitory side effects (sweating, shaking, tachycardia, nervousness, anxiety). If the treatment is not rapidly efficient, it must be discontinued in case there is no improvement after 3 weeks. Until today, there is no consensus about the duration of a T3 treatment. It is important to take into account the predictive criteria of good or bad response to a T3 potentialization, since they have direct consequences on the management of depressed patients. For example, a high degree of chronic evolution with resistance to numerous treatments, associated disorders according to the DSM IV axis I and a comorbidity of addiction, point to a bad prognosis of a potentialization treatment. In addition, we'll examine the few recent studies on the potentializing of serotoninergic antidepressant drugs by thyroid hormones.
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PMID:[Potentializing of tricyclics and serotoninergics by thyroid hormones in resistant depressive disorders]. 1523 25

The aim of this observational prospective study was to assess the incidence rate and the characteristics of adverse drug reactions (ADRs) induced by amiodarone during the long-term follow-up of 98 French patients. Inclusions were performed between March 1994 and April 1997. Eligible patients were consecutive outpatients for whom amiodarone was initiated for the first time. The treatment had to be taken for at least 6 months if no ADR required its withdrawal. A cohort of 57 men and 41 women, mean age 72.6 years (SD: 8.6), was followed for a mean period of 38 months. The incidence rate of ADRs during the overall follow-up period was 13.91 cases for 100 person-years. Recorded ADRs were 13 hypothyroidism (incidence rate for 100 person-years: 4.61 [95% confidence interval: 4.58-4.63], 5 hyperthyroidism (1.62 [1.60-1.63]), 10 bradycardia and/or conduction ADRs (3.48 [3.46-3.50]), 7 photosensitivity (2.27 [2.25-2.28]), 1 storage disease (0.33 [0.32-0.33]), 3 interstitial pneumonitis (0.97 [0.96-0.98]), 2 peripheral neuropathies (0.65 [0.64-0.66]), 1 tremor (0.32 [0.32-0.33]) and 1 gastrointestinal disturbances (0.32 [0.32-0.33])). Thyroid and cardiac ADRs occurred mainly during the first 6 months. According to the French system of pharmacovigilance, 27 ADRs were "probable/likely" and 14 were "possible." Hypothyroidism, cardiac ADRs, and photosensitivity were the most frequent ADRs. None of the ADRs had a fatal outcome in this study.
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PMID:Incidence rate of adverse drug reactions during long-term follow-up of patients newly treated with amiodarone. 1685 66

We determined the prevalence of self-reported late-effects in survivors of autologous hematopoietic cell transplantation (HCT) for Hodgkin lymphoma (HL, n = 92) and non-Hodgkin lymphoma (NHL, n = 184) using a 255-item questionnaire and compared them to 319 sibling controls in the Bone Marrow Transplant Survivor Study. Median age at HCT was 39 years (range: 13-69) and median posttransplant follow-up was 6 years (range: 2-17). Median age at survey was 46 years (range: 21-73) for survivors and 44 years (range: 19-79) for siblings. Compared to siblings, HCT survivors reported a significantly higher frequency of cataracts, dry mouth, hypothyroidism, bone impairments (osteoporosis and avascular necrosis), congestive heart failure, exercise-induced shortness of breath, neurosensory impairments, inability to attend work or school, and poor overall health. Compared to those receiving no total-body irradiation (TBI), patients treated with TBI-based conditioning had higher risks of cataracts (odds-ratio [OR] 4.9, 95% confidence interval [CI] 1.5-15.5) and dry mouth (OR 3.4, 95% CI 1.1-10.4). Females had a greater likelihood of reporting osteoporosis (OR 8.7, 95% CI: 1.8-41.7), congestive heart failure (OR 4.3, 95% CI 1.1-17.2), and abnormal balance, tremor, or weakness (OR 2.4, 95% CI 1.0-5.5). HL and NHL survivors of autologous HCT have a high prevalence of long-term health-related complications and require continued monitoring for late effects of transplantation.
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PMID:Late effects in survivors of Hodgkin and non-Hodgkin lymphoma treated with autologous hematopoietic cell transplantation: a report from the bone marrow transplant survivor study. 1788 51

Neurological manifestations of thyroid autoimmunity are heterogeneous and nonspecific. The most frequently adopted name for this entity is Hashimoto's encephalopathy although this eponym has been recently contested. In the absence of specific clinical features, diagnosis is suggested by the presence of elevated levels of anti-thyroid antibodies in the appropriate clinical context. We describe a patient with recurrent focal seizures, palatal tremor and elevated anti-thyroid antibodies but no encephalopathy. Her past medical history was marked by recurrent miscarriages. The markedly elevated thyroid antibodies, the temporal relationship between neurological symptoms and hypothyroidism, and the absence of another explanation to her symptoms suggest a causal role of thyroid autoimmunity. In the clinical setting of recurrent spontaneous miscarriages, elevated levels of anti-thyroid antibodies and neurological deficits not attributed to another disease entity, Hashimoto's encephalopathy should be suspected.
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PMID:Palatal tremor, focal seizures, repeated miscarriages and elevated anti-thyroid antibodies. 1824 87


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