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)

1. In hypertension, the beta-adrenoreceptor-blocker-withdrawal syndrome comprises tachycardia, sweating, tremor and general malaise, symptoms resembling thyrotoxicosis. 2. The effect of abrupt cessation of propranolol on serum concentrations of thyroxine (T4) and triiodothyronine (T3) was therefore investigated in five patients with uncomplicated essential hypertension, treated with propranolol in doses from 160 to 480 mg/day. 3. Four of the five patients developed one or more of the above-mentioned symptoms within 2-6 days after withdrawal of propranolol. 4. A mean relative increase in serum free T3 of 51% (range 22-74%) was found in these four patients on the day of onset of symptoms. 5. The increase in free T3 in the five patients correlated positively with total serum propranolol on the last day the drug was given (r = 0.91, 2P = 0.03). 6. As an increase in T3 was found only in patients suffering the withdrawal syndrome, and was maximal the day the symptoms appeared, despite a variation in time of onset from 2 to 6 days, it is suggested that the beta-adrenoreceptor-blocker-withdrawal syndrome, at least partially, is caused by rebound increased production of T3, induced by the well-known inhibition of the monodeiodination of T4 to T3 during beta-adrenoreceptor blockade. 7. This assumption may explain the clinical symptoms and the reported transient increased beta-adrenoreceptor sensitivity with unchanged serum concentrations of catecholamines.
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PMID:The pathogenesis of propranolol-withdrawal syndrome in essential hypertension. 54 Apr 62

The effect of abrupt withdrawal of propranolol on serum concentrations of triiodothyronine (T3) and thyroxine (T4) was investigated in 5 patients with uncomplicated essential hypertension. The patients had been treated from 2 to 18 mo before the study was begun. Doses varied from 160 to 480 mg propranolol daily. Four of the patients studied developed tachycardia, sweating, or tremor within 2 to 6 days after withdrawal of propranolol. In 1 patient reversible ischemic ECG changes were recorded. The serum concentrations of free T3 increased in the 4 patients suffering from withdrawal symptoms. The mean increase on the day the symptoms started was 51% (range, 22 to 74, 2 p = 0.01). This increase in serum-free T3 correlated positively with the serum propranolol concentration on the last day propranolol was given (r = 0.91, 2 p = 0.03). In the one patient, who did not develop withdrawal symptoms, the serum concentration of propranolol was very low, and the free T3 level remained unchanged. No significant changes in serum concentrations of free T4 or total thyroid hormones were found in any of the patients. We suggest that the propranolol withdrawal symptoms are, at least partially, caused by an increase in the thyroid hormone, T3.
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PMID:Propranolol withdrawal and thyroid hormones in patients with essential hypertension. 64 76

The authors tested in an open, uncontrolled trial in a group of 23 patients with essential hypertension grade I-II (WHO classification) the effect of Metoprolol OROS. The OROS system is a new form of Metoprolol administration which makes it possible to maintain by a single dose per day a steady plasma concentration, while preserving the cardioselectivity and total 24-hour effectiveness during treatment of hypertension and angina pectoris. After eight weeks of Metoprolol OROS administration, in doses gradually adjusted to the therapeutic action, gradually a significant decrease of the heart rate (HR) occurred, of the systolic blood pressure (BPs) and diastolic blood pressure (BPd) (p less than 0.01 for all values) in a recumbent as well as upright position. A reduction of the BPd in an upright position by greater than or equal to 10 mm Hg was achieved in 85% of the patients, in 73.9% of the patients the BPd in an upright position dropped below 95 mm Hg. Four patients developed side-effects which were mild to medium severe (vertigo, palpitations, fatigue, sensation of tremor, tension in the lower extremities). Two patients discontinued treatment early, the main reason in both being palpitations which were under better conversely, in two patients palpitations which were not adequately controlled by previous metoprolol treatment, disappeared completely during Metoprolol OROS treatment. During the trial no significant changes in the investigated laboratory values incl. total cholesterol were recorded, Metoprolol OROS administered once per day is an effective, safe and well tolerated preparation in treatment of mild to medium severe essential hypertension.
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PMID:[The effect of OROS metoprolol in mild and moderately severe essential hypertension]. 239 74

Alpha methyltyrosine (alpha-MPT) was administered to 52 patients from 4 days to 10 months; 22 patients were cases of pheochromocytoma and 20 had essential hypertension. Inhibition of catecholamine synthesis in the range of 50-80% was achieved with divided daily drug dosage of from 1.0 to 4.0 g. Striking clinical benefit was noted in patients with pheochromocytoma in whom the drug was used in preparation for surgery and during chronic medical management. The drug appeared to have limited usefulness when used in essential hypertension, unless added to existing therapy with conventional agents. No beneficial effects were noted in thyrotoxicosis, glaucoma, and Raynaud's phenomenon. Untoward effects in order of decreasing incidence were: sedation (with insomnia on withdrawal), anxiety, tremor, diarrhea, and galactorrhea. Drug crystalluria, which has been observed in animals and is currently restrictive of clinical trials, was not observed in these studies. Evidence is presented that the minor conversion of alpha-MPT to methyldopa probably does not contribute significantly to the central and peripheral effects of the drug.
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PMID:Biochemical and pharmacologic effects of alpha-methyltyrosine in man. 563 45

A limitation of clonidine therapy is the syndrome of rebound hypertension and sympathetic overactivity after withdrawal. Ten patients, four male, six female, aged 28--64 years, with essential hypertension, were treated for one year with an imidazoline derivative, tiamenidine. Blood pressure fell from an average of 178/108 mm Hg pretreatment to 152/86 mm Hg after 1 year. Tiamenidine was then withdrawn in hospital, replaced by identical placebo under single blind conditions and observations made over 96 h. The study was interrupted in five patients (4 patients within 36 h) because blood pressure rose to greater than 30 mm Hg (systolic) or greater than 20 mm Hg (diastolic) above pretreatment values. For the group, blood pressure was maximal at 194/112 mm Hg, 18 h post withdrawal, significantly higher than pretreatment (p less than 0.005). Headache, tremor, flushing and insomnia were noted. Saliva production rose 100% at 24 h. Plasma noradrenaline rose within 24 h with an accompanying rise in urinary metanephrine and catecholamine excretion. Tiamenidine appears to share with other imidazolines rebound cardiovascular and autonomic effects following abrupt withdrawal.
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PMID:Changes in blood pressure, heart rate, and sympathetic activity on abrupt withdrawal of tiamenidine (HOE 440) in essential hypertension. 746 Oct 12

We studied 30 patients whose primary complaint was head tremor in an attempt to characterize neurophysiological aspects of their abnormal movement. Based on family medical history and physical examination, 23 patients had definite or probable essential tremor (essential head tremor, EHT). The remaining seven had mild dystonic signs accompanying their head tremor (head tremor plus dystonic signs, HT + DS). We recorded head movement and the electromyographic (EMG) activity of the sternomastoid and splenius capitis muscles, determined the spontaneous blinking rate, and measured the excitability recovery curve of the blink reflex and of the masseteric inhibitory reflex. All patients had tremor bursts at a frequency ranging between 3 and 9 Hz in at least one of the muscles examined. The predominant pattern seen when patients were sitting relaxed and facing forward was that of synchronized EMG bursts in both splenius capitis muscles. Maintenance of extreme head postures demonstrated two types of additional abnormalities: type 1 (enhancement of tremor), which was observed in 11 patients (47.8%) with EHT and in two (28.5%) with HT + DS; and type 2 (activation of neck muscles not required for maintenance of the posture), which was observed in two patients (8.7%) with EHT and in five (71.5%) with HT + DS (chi 2 = 26.4; p < 0.001). Mean blinking rate per minute was 24.9 +/- 14.6 in patients with EHT and 42.3 +/- 10.5 in patients with HT + DS (paired t test, p = 0.001). The blink reflex and masseteric inhibitory reflex excitability recovery curves showed an abnormal interneuronal excitability enhancement in seven (30.4%) of the 23 patients with EHT and in two (28.5%) of the seven with HT + DS (chi 2 = 3.1; p > 0.05). Abnormal patterns of EMG activity of the neck muscles correlated well with the presence of mild dystonic signs. However, the analysis of brainstem interneuronal excitability did not enable recognition of those patients with head tremor who could potentially develop cervical dystonia. The enhancement of brainstem interneuronal excitability found in approximately 30% of patients with head tremor could be related to plastic changes triggered by increased activity of the cranial muscles.
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PMID:Neurophysiological investigations in patients with head tremor. 925 Oct 77

Lithium carbonate is considered to be a first-line treatment for bipolar disorder; however, this drug has a narrow therapeutic window, and lithium intoxication is commonly induced by various drugs interaction and situations. We herein report a case of lithium intoxication induced by the administration of an antihypertensive agent targeting the angiotensin 1 (AT1) subtype of the angiotensin II receptor in a 65-year-old woman with a 40-year history of bipolar disorder type 1, and 1-year history of essential hypertension. Her bipolar disorder had been well-controlled with 600 mg/day of lithium carbonate for more than 10 years. She was later diagnosed with hypertension and the AT1 receptor blocker, azilsartan was thereafter administrated on a daily basis. After 3 weeks of azilsartan administration, she presented with progressive action tremor and showed a gradual deterioration of her physical state. Four months after the start of azilsartan administration, she presented with alternating episodes of diarrhea and constipation. Two weeks before admission to our hospital, she presented with mild consciousness disturbances, myoclonus, truncal ataxia, and appetite loss. She was diagnosed to have lithium intoxication based on an elevated serum lithium concentration of 3.28 mEq/l.It is therefore important to evaluate the serum lithium concentration after the administration of antihypertensive agents, and consider lithium-antihypertensive agent interactions when selecting antihypertensive agents in elderly patients receiving long-term lithium carbonate treatment.
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PMID:A case of lithium intoxication induced by an antihypertensive angiotensin 1 subtype-specific angiotensin II receptor blocker in an elderly patient with bipolar disorder and hypertension. 2753 87