Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 17-year-old women received 12,000 rads of alpha-particle radiation for the treatment of Cushing's disease. One day after the completion of therapy, the patient developed nausea, vomiting, headache, and postural hypotension. Laboratory evaluation demonstrated a marked fall of the previously elevated urinary 17-hydroxycorticosteroids (17-OHCS) and undetectable plasma cortisols. The urinary 17-OHCS transiently returned to supranormal levels but over a 2 1/2-week period decreased and then remained low. The patient also demonstrated a subnormal urinary aldosterone excretion in relation to plasma renin activity (PRA) during 10 mEq/24 h sodium restriction. The remainder of the endocrine evaluation was normal, suggesting that pituitary function otherwise remained intact. One and one-half years after alpha-particle therapy, the patients's urinary 17-OHCS were normal and responded normally to metyrapone. The relationship between urinary aldosterone excretion and PRA also was normal. It is postulated that there was an infarction of an ACTH secreting pituitary tumor leaving the remainder of the pituitary intact. Achronically elevated circulating level of ACTH with sudden loss of ACTH secretion appeared to have been responsible for the initial low urinary aldosterone as well as the low urinary 17-OHCS. This is the first reported case of a presumed pituitary tumor infarction in association with alpha-particle pituitary radiation.
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PMID:Rapid appearance of transient secondary adrenocortical insufficiency after alpha-particle radiation therapy for Cushing's disease. 18 95

Intramuscularly administered methylprednisolone sodium phosphate (Medrol Stabisol) in single doses of 40, 80, or 160 mg (methylprednisolone equivalents) had a similar effect as the same doses of methylprednisolone sodium succinate (Solu-Medrol) with regard to eosinophil suppression, elevation of glucose, white blood count differential shifts (lympholytic effect), urinary excretion of sodium and potassium, and localized (pain) and systemic side effects. The average plasma methylprednisolone concentration was approximately 20% higher after the intramuscular administration of methylprednisolone sodium phosphate than after methylprednisolone sodium succinate. The differences in plasma methylprednisolone levels produced by the two esters suggest that either hydrolysis of the succinate ester occurs more slowly or the succinate ester distributes more extensively. This difference in plasma level, however, is not reflected in any other pharmacologic evaluation of the two esters, e.g., both eosinophil depression and hyperglycemic response were identical. No clinically significant changes in the vital signs, standard hematology, and clinical chemistry parameters evaluated were noted after 21 successive doses (q.i.d. for five days with one dose in the morning of day 6) of 80 mg methylprednisolone sodium phosphate. An increase was noted in the systolic blood pressure from a pretreatment mean of 113 mm Hg to a posttreatment mean of 123 mm Hg and an increase in the body weight from a pretreatment mean of 177 pounds to a posttreatment mean of 183 pounds. No signs of adrenal suppression were found as judged by plasma cortisol and ACTH levels. Six (6/12) subjects of the methylprednisolone sodium phosphate group, one (1/12) subject of the vehicle group, and one (1/12) subject of the placebo (sterile saline) group reported the following systemic side effects: gas in stomach, headaches, anorectal itching, and dryness of itching of the skin. No trend was observed for any side effect reported. In these double-blind, randomized studies, single (40, 80, and 160 mg) and multiple (80 mg) intramuscular doses of methylprednisolone sodium phosphate were tolerated in healthy volunteers as well as the same doses of methylprednisolone sodium succinate and similar volumes of vehicle or placebo.
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PMID:The clinical pharmacology of methylprednisolone sodium phosphate. I. Intramuscular route of administration. 32 97

One hundred and two patients with either rheumatoid arthritis or osteo-arthrosis were treated for prolonged periods with diclophenac sodium (Voltaren; Geigy) to evaluate the efficacy and tolerability of the drug. Fifty-seven patients completed a trial of 12 months. A total of 70% showed an improvement in functional class, and 40% of the total had complete functional capacity by the end of the trial. The drug was well tolerated. The side-effects (heartburn, abdominal cramps, headache and dizziness) were mild and in most cases did not require cessation of treatment. In 9 patients the Coombs test became positive during the trial, but this did not require cessation of therapy.
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PMID:A long-term study of diclophenac sodium in the treatment of rheumatoid arthritis and osteo-arthrosis. 35 28

In a double-blind crossover trial conducted on a multicentre basis, 109 patients with "classic" or "definite" rheumatoid arthritis were treated for two weeks with diclofenac sodium (Voltaren, 25 mg t.i.d.) and indomethacin (25 mg t.i.d). Both drugs led to a clear-cut decrease in morning stiffness, as well as to a significant improvement in pain at rest and on movement. In these respects no significant difference between the two-drugs was observed. As regards their effect on status of rheumatoid condition, however, a trend towards a significant improvement was discernible, in the investigator's opinion, only in response to diclofenac sodium. "Unwanted effects" were mentioned by 25 patients before the trial, by 31 during treatment with diclofenac sodium, and by 33 during treatment with indomethacin. While the patients were receiving indomethacin, five of them discontinued treatment on account of side effects (headache in three cases, headache and tiredness in one case, and an allergic skin reaction in one case) and one of them, who complained of headache, lowered the dosage; treatment with diclofenac sodium was discontinued because of side effects by only one patient, who had developed an allergic skin reaction.
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PMID:Diclofenac sodium (Voltaren) and indomethacin in the ambulatory treatment of rheumatoid arthritis: a double-blind multicentre study. 35 46

Hemodynamic monitoring after a single dose (10 mg) of nifedipine in 27 primary hypertensive subjects (diastolic pressure greater than 110 mm Hg) documented that this calcium antagonistic agent exerts a potent arteriolar vasodilating action, which results in prompt (-21% of control at 30 minutes) and persistent (-16% of control at 120 minutes) fall in mean arterial pressure associated with a rise in cardiac output and pulse rate. The same patients received oral treatment for 3 weeks. Hourly pressure readings showed that 1) the antihypertensive response to each dose lasts 8--12 hours; and 2) nifedipine every 6 hours significantly reduced blood pressure throughout the 24 hours, without postural hypotension. Side effect were short-lasting (headache in five patients, palpitation without arrhythmias in eight patients, burning sensation in the face and legs in five patients and sporadic extrasystoles in five patients) and tended to disappear with continued treatment. Development of drug resistance, sodium retention, plasma volume expansion, renin release or angina pectoris were not observed during the study. Although these findings seem to differentiate nifedipine from other vasodilators currently used in the treatment of hypertension, broader experience and more prolonged trials with nifedipine as an antihypertensive agent will be needed before conclusions can be drawn on these particular aspects.
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PMID:Treatment of hypertension with nifedipine, a calcium antagonistic agent. 37 56

1 The cardiovascular effects of a new substance (PR--G 138) with vasodilating action were analysed in 12 patients with moderately severe essential hypertension on a 60 mEq sodium diet in a metabolic ward. To prevent tachycardia, propranolol 40 mg four times daily was given during the control period until blood pressure (BP) was stabilized, and continued throughout the study. 2 The compound was effective in every patient except one, who also was resistant to hydrallazine and diazoxide. Mean arterial pressure was lowered from a mean control value of 121 +/- 11 supine and 118 +/- 13 standing to 98 +/- 18 and 95+/- 15 mm Hg (P less than 0.001) respectively after a single oral dosage of 5 to 15 mg PR--G 138. The effect was maximal after 1--2 h and lasted up to 6 h. 3 With adequate dosage, there was no orthostatic reaction. Pulse rate and plasma renin activity did not rise during PR--G 138 treatment, and cardiac output increased only slightly, doubtlessly as a result of the propranolol therapy. In most patients 5 mg of the drug was sufficient to cause a drop of BP to normal levels. Exercise tolerance (bicycle ergometry) was constant or improved during drug action. One patient complained of headache, but no other side effects were seen provided that propranolol was taken when the drug was given. During 3 months treatments on an out-patient basis the effect was sustained in four of eight patients. No toxic effects have been noticed.
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PMID:Clinical evaluation of a new antihypertensive vasodilating agent PR--G 138 Cl. 38 24

This investigation was undertaken to define the "adequate" sodium concentration in the dialytic fluid allowing to maintain a stable plasma effective osmolality during dialysis. Isonatric dialysate is shown to miss this aim by inducing a predictable postdialytic hypernatremia. To avoid this effect a new approach was made. 17 clinically stabilized patients, previously dialyzed over a period of at least 2 years with a dialysate sodium concentration of 133 mEq/l, underwent dialysis with the "adequate" sodium concentration in the dialysate for over 3 years. During dialysis cramps, headache, hypotension, hypertensive crises and postdialytic weakness were reduced in frequency and nearly disappeared. No deterioration in blood pressure control occurred and improvement in some general parameters (hematocrit, glucose and insulin metabolism, well-being) was reported after prolonged treatment.
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PMID:Hemodialysis with "adequate" sodium concentration in dialysate. 46 5

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

Design and evaluation of the controlled clinical trial are thoroughly discussed by giving an example for testing a sodium pentosan polysulphate/nicotinic acid combination (Compuron). 60 patients with cerebral vascular disorders were randomly allocated to the two treatments and received medication over a period of eight weeks. A detailed biostatistical analysis of the data led to the following conclusions: 1. Regarding the target symptoms headache, nausea, sleep disturbance, reduced alertness, reduced ability for contacts and moods significant differences in favor of the active medication beginning with the sixth treatment week. 2. Regarding the psychological tests substantial and statistically highly significant (P less than 0.001) therapeutic effects. 3. Statistically significant decrease of the cholesterol and triglycerides level, absolutely as well as relative to placeo medication. 4. No treatment related side effects during the entire trial period of eight weeks.
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PMID:[Design and evaluation of the controlled clinical trial/demonstrated by an efficacy test of the combination pentosan polysulphate/nicotinic acid in disturbed cerebral circulation (author's transl)]. 78 68

Out of 19 patients with extrinsic bronchial asthma challenged with 123 mug histamine acid phosphate by intravenous infusion only 13 responded with a fall in FEV1 of over 10% (mean 16%). Seventeen of these patients were given histamine 2 mg/ml by aerosol, and all responded with a mean decrease in FEV1 of 37.8%. When challenged with allergen extract by aerosol the mean decrease in FEV1 was 37.5%. After 40 mg sodium cromoglycate 15 of the 17 patients showed significant protection against allergen challenge with a mean decrease in FEV1 of only 23.6%. Inhalation of 40 mg sodium cromoglycate, however, failed to protect against histamine given by either the intravenous or aerosol route. Histamine given intravenously to asthmatic patients produces less of a bronchial response than when given by aerosol, even though the intravenous route produces many more systemic symptoms, such as flushing and throbbing headache. The protection of sodium cromoglycate against an allergen inhalation challenge is not due to histamine antagonsim.
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PMID:Bronchial reactivity to histamine before and after sodium cromoglycate in bronchial asthma. 81 11


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