Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnostic and therapeutic potential of intravenous adenosine was studied in 64 patients during 92 episodes of regular sustained tachycardia. In 40 patients who had narrow complex tachycardias (QRS less than 0.12 s) adenosine (2.5-25 mg) restored sinus rhythm in 25 with junctional tachycardias (46 of 48 episodes) and produced atrioventricular block to reveal atrial or sinus tachycardia in 15. In 24 patients with broad complex tachycardias (QRS greater than or equal to 0.12 s) adenosine terminated the tachycardias in six patients and revealed atrial or sinus arrhythmias in four. The tachycardias persisted in 14 patients despite doses up to 20 mg, but adenosine allowed the diagnosis of ventricular tachycardia with retrograde atrial activation in two patients by producing transient ventriculoatrial dissociation. Diagnosis based on adenosine induced atrioventricular nodal block was correct in all patients with narrow complex tachycardias and in 92% of those with broad complex tachycardias, compared with correct electrocardiographic diagnoses in 90% and 75% respectively. Adenosine gave diagnostic information additional to the electrocardiogram in 25%. The response to adenosine in broad complex tachycardias identified those of supraventricular origin with 90% sensitivity, 93% specificity, and 92% predictive accuracy. Adenosine restored sinus rhythm in all patients with junctional reentrant tachycardias, but in 10 (35%) the arrhythmias recurred within two minutes. Symptomatic side effects (dyspnoea, chest pain, flushing, headache) were reported by 40 (63%) patients and, although transient, were severe in 23 (36%). There were ventricular pauses of over 2 s in 16% of patients, the longest pause being 6.1 s. Adenosine is of value in the diagnosis and treatment of narrow and broad complex tachycardias, but its use is limited by symptomatic side effects, a tenfold range in minimal effective dosage, occasional action at sites other than the atrioventricular node, and early recurrence or arrhythmia.
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PMID:Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. 278 11

A large hypertensive population of patients in general practice was used to assess the tolerability of nifedipine in previously untreated patients and was compared with other antihypertensive drugs in previously treated patients. A total of 3972 patients with a sitting diastolic blood pressure between 95 and 115 mmHg were treated with 20 mg nifedipine twice daily for 1 month. In non-responders the dose was increased to 40 mg twice daily for a second month; responders continued to take 20 mg twice daily. A total of 2772 patients had been previously untreated for hypertension, whereas 857 had previously been treated with beta-blockers alone or in combination and 346 had received diuretics alone or in combination. Adverse events were recorded for 28 days prior to treatment being initiated with or changed to nifedipine and for two 28-day nifedipine treatment periods. Flushing and headache, which diminished with time, occurred during nifedipine treatment. Ankle oedema did not diminish with time. Reductions were seen in occurrences of dyspnoea, impotence, lethargy and cold extremities.
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PMID:General practice data derived tolerability assessment of antihypertensive drugs. 280 16

A randomised double blind parallel group study was performed to compare the efficacy and acceptability of slow release nifedipine (maximum dose 40 mg twice a day) with those of atenolol (maximum dose 100 mg once a day) as single agents for the treatment of essential hypertension. Of 410 patients recruited almost exclusively from general practices in 22 centres in the United Kingdom 210 received nifedipine and 200 atenolol. Both drugs significantly reduced blood pressure, and control--a reduction of the diastolic pressure to less than 95 mm Hg--was obtained in about 65% of patients. Those who received nifedipine had more pronounced reductions in systolic pressure than those who received atenolol. One hundred and forty nine patients who failed to respond adequately to either atenolol or nifedipine in low doses were given both drugs once daily for eight weeks in a fixed combination capsule that contained atenolol 50 mg and nifedipine 20 mg. All patients showed further reductions in blood pressure, although those who were taking beta atenolol before the combination capsule had more pronounced reductions in systolic pressures. Twenty six patients (12%) were withdrawn because of adverse effects while taking nifedipine compared with 19 (10%) taking atenolol. Flushing and oedema were more common after the calcium antagonist, whereas diarrhoea and dyspepsia were more common after atenolol. The frequencies of headaches, dizziness, fatigue, and dyspnoea were equally distributed between the two groups. When the fixed combination capsule was taken side effects such as flushing and oedema continued. Nifedipine was more effective than atenolol in lowering systolic blood pressure, although neither drug used alone controlled the pressure of more than two thirds of the patients studied. When used in a fixed combination slightly better control of blood pressure was achieved with a lower dose of each drug.
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PMID:Nifedipine and atenolol singly and combined for treatment of essential hypertension: comparative multicentre study in general practice in the United Kingdom. Nifedipine-Atenolol Study Review Committee. 289 83

A patient with a 12 hour history of headache, breathlessness and hypotension developed acute renal failure necessitating haemodialysis for 12 days. During recovery she developed hypertension, tachycardia and facial flushing. Investigations revealed a right adrenal phaeochromocytoma. Whilst postural hypotension is common in phaeochromocytoma, profound shock with acute renal failure is rare. This may have been precipitated by concomitant drug therapy, myocardial necrosis or by necrosis within the tumour.
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PMID:Phaeochromocytoma presenting with cardiogenic shock and acute renal failure. 333 32

The combination of nifedipine and atenolol must be evaluated in terms of risks and benefits to the hypertensive patient. Disadvantages with single-agent therapy justify trials of combination regimens. beta-Blockers may be unacceptable to some patients because of gastrointestinal upset, musculoskeletal symptoms, tiredness, malaise, insomnia, depression or confusion, sweating, breathlessness or cold extremities. The side effect profile varies from patient to patient and between different beta-blockers. Calcium antagonists also have characteristic side effects, including severe headaches, flushing and oedema, tachycardia and possibly worrying palpitations, and polyuria. Combining a calcium antagonist and a beta-blocker can reduce some side effects; for example, tachycardia is offset by addition of beta-blocker to calcium antagonist therapy, and beta-blocker-induced cold extremities may be reversed with a drug such as nifedipine. Moreover, the antihypertensive efficacy is increased, which is useful in previously resistant patients. However, an excessive fall in blood pressure is a possible adverse effect of the combination. There is also the possibility of precipitating heart failure in patients with cardiomegaly and severely compromised left ventricular function. The combination of nifedipine and atenolol was evaluated in 25 patients in a randomised, crossover trial following a month's treatment with atenolol 50mg twice daily. Patients received either atenolol 50mg twice daily alone, or atenolol 50mg twice daily with sustained release nifedipine 20mg or 40mg twice daily, or placebo twice daily during three 4-week treatment periods. Additional antihypertensive benefit was obtained by addition of the low dose of nifedipine compared with atenolol alone, but no further advantage was obtained with the higher nifedipine dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aims of combination therapy--improved quality of life or better blood pressure control? 337 14

Surgical treatment was applied to 18 patients for intrathoracic struma. Dyspnoea, dysphagia, recurrent palsy, and dilatated cervical veins with facial flushing were indications for surgery. Surgical access routes depended on localisation of the intrathoracic struma and its connection to the thyroid gland. Goitre located in the anterior mediastinum (substernal) can be extirpated, using the cervical approach (Kocher). Sternotomy was found to be necessary only in cases with tracheal resection. Goitres located in the posterior mediastinum were removed by means of right or left thoracotomy. Postoperative "collapse" of the posterior tracheal wall in patients with extreme dislocation of the trachea was successfully avoided by means of intratracheal intubation for 24 hours.
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PMID:[Surgical treatment of intrathoracic struma]. 363 Apr 55

We questioned 113 patients with subsequently diagnosed sustained ventricular tachycardia (VT) regarding the symptoms that prompted their seeking hospital treatment, eliciting the following: 15% of patients had lost consciousness, 15% had near syncope, 35% had mild lightheadedness and 35% had no cerebral symptoms. Patients with preexisting congestive heart failure or a VT rate of 200 beats per minute or greater more often lost consciousness. Other symptoms included palpitations in 57% of patients, chest pain in 27%, dyspnea in 25%, weakness in 6%, nausea or diaphoresis in 3% each and flushing in 2%. In approximately 50% of patients who had mild lightheadedness or no cerebral symptoms, their condition was incorrectly diagnosed as supraventricular tachycardia based on the absence of severe symptoms during the tachycardia. In some patients, VT may be associated with mild or atypical symptoms. The differentiation of supraventricular from ventricular tachycardia should be based on electrocardiographic criteria and should not be influenced by the nature or severity of a patient's symptoms. The severity of cerebral symptoms is at least partially related to the VT rate and a patient's underlying heart disease.
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PMID:Clinical symptoms in patients with sustained ventricular tachycardia. 399 9

According to the United States Food and Drug Administration, untoward reactions to capillary hemodialyzers occur at a rate of 3.5 of every 100,000 dialyzers sold. Allergic symptoms immediately after initiation of dialysis consist of burning retrosternal pain, sensation of diffuse heat, cold perspiration, periorbital and facial edema, flushing, laryngeal stridor, bronchial hypersecretion, hypotension, bradycardia, and loss of consciousness. In 1982 Popli et al. reported four patients suffering from such allergic manifestations; three were successfully managed after being taken off dialysis. These investigators thought that inadequate rinsing of cuprammonium cellulose capillary dialyzers was responsible for the reactions, and recommended rinsing the blood compartment with 2 liters of normal saline, and the dialysate compartment with 10 liters of dialysate, both in a single-pass fashion over 20 minutes. Nichols and Platts (1982) (3) reported 15 patients with urticaria, severe bronchospasm, and shock occurring immediately after the blood had been returned from the dialyzer. These authors suggested that the sterilizing agent, ethylene oxide (ETO), was responsible. Poothullil et al. (1975) (4) described a patient with pruritus, severe dyspnea, and hypotension during dialysis. On the basis of a positive skin prick test (dermal reaction to ETO-exposed human albumin) and of antigen-induced histamine release from peripheral leucocytes, these workers suggested that ETO was responsible for the allergic reactions. Marshall et al. (1984) (5) reported that 8.9% of hemodialysis patients had positive skin tests to ETO and that 12.1% were ETO-radioallergosorbent test (RAST) positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Three cases of hemodialysis-associated hypersensitivity reactions. 405 93

Therapy to decrease the load in congestive heart failure is now classified as acute and chronic vasodilator therapy. In this symposium, we presented prostacyclin (PG I2) as an acute and prazosin as a chronic vasodilator. Their hemodynamic and clinical effectiveness were evaluated and their effect on the sympathetic nervous system was also studied. We studied the effect of intravenous prostacyclin infusion in doses of 22 +/- 11 ng/kg/min in nine patients with severe congestive heart failure refractory to digitalis and diuretic drugs. After prostacyclin infusion, mean pulmonary capillary wedge pressure decreased from 21.0 +/- 7.9 to 15.0 +/- 6.6 mmHg (p less than 0.001), mean arterial pressure from 98.9 +/- 12.8 to 76.2 +/- 7.0 mmHg (p less than 0.001), systemic vascular resistance from 2,574 +/- 384 to 1,368 +/- 283 dynes X sec X cm-5 (p less than 0.001), pulmonary vascular resistance from 1,008 +/- 451 to 443 +/- 135 dynes X sec X cm-5 (p less than 0.001) and pulmonary arteriolar resistance from 330 +/- 111 to 189 +/- 73 dynes X sec X cm-5 (p less than 0.001). The cardiac index increased from 2.0 +/- 0.37 to 3.2 +/- 0.59 l/min/m2 (p less than 0.001), and the stroke index from 27.6 +/- 8.69 to 42.0 +/- 0.62 ml/m2 (p less than 0.001). Moreover, prostacyclin therapy counteracted the sensation of coldness of the limbs and face, and patients felt warmth and mild flushing of the face. The effect of prazosin on the exercise duration time until dyspnea was evaluated by the treadmill test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostacyclin and prazosin in the treatment of congestive heart failure; with special reference to the sympathetic nervous system. 637 Dec 82

Contrast media reactions may be classified as anaphylactoid, vasomotor, severe or life threatening, and fatal. Anaphylactoid reactions mimic immunoglobulin E-mediated hypersensitivity in that signs may consist of urticaria, angioedema, wheezing, dyspnea, hypotension, or shock. These reactions occur in 2% to 8% of all contrast media infusions. Vasomotor reactions occur in 5% to 8% of patients and consist of nausea, vomiting, flushing, and warmth. Severe reactions during which there is a concern for life occur about once per 1000 procedures. Fatalities have occurred in from 1:3000 procedures for intravenous cholangiography to between 1:10,000 to 1:100,000 procedures for intravenous urography. The pathogenesis of contrast media reactions is unknown, and various mechanisms may be associated with different clinical features. Radiocontrast media infusions can cause rises in plasma histamine and complement activation by either classic or alternate pathways or nonsequentially, yet adverse reactions may or may not occur. Abnormalities in the complement system or an increased conversion of prekallikrein to kallikrein has been demonstrated in some patients who have had anaphylactoid reactions. It is unknown if these mechanisms can explain the pathogenesis of anaphylactoid contrast media reactions. When patients who have had definite anaphylactoid reactions require a repeat procedure, the incidence of reactions ranges from 35% to 60% for intravascular infusion. Pretreatment with prednisone and diphenhydramine has been demonstrated to reduce this reaction rate to 9% in 465 procedures. Prednisone-diphenhydramine and ephedrine have further reduced the reaction rate to 3.1% in 192 procedures. These results are statistically significant (X2 = 5.4996, p = 0.019). Emergency equipment should be available should a severe reaction occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contrast media reactions. 649 Nov 7


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