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Query: UMLS:C0018681 (headache)
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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

During metabolism studies of radiolabeled proteins in 126 participants four patients were suspected of being sensitive to potassium iodide (Kl) because they repeatedly developed urticaria and other symptoms after Kl administration. Two of the four patients suspected of Kl sensitivity and 10 control patients were orally challenged with Kl to document and characterize Kl sensitivity and to evaluate the possible association(s) of Kl sensitivity with urticaria, hypocomplementemia, and vasculitis. The Kl challenges in the two sensitive patients precipitated urticaria, angioedema, polymyalgias, conjunctivitis, and coryza. One of these two patients also developed a severe systemic illness characterized by fever, headache, peritonitis, episcleritis, and pneumonitis. The four sensitive patients were strikingly similar in that they exhibited hypocomplementemia and dermal vasculitis associated with chronic urticaria or systemic lupus erythematosus, suggesting that other patients with similar clinical features may be sensitive to Kl and that Kl may precipitate severe systemic illness in them.
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PMID:Potassium iodide sensitivity in four patients with hypocomplementemic vasculitis. 51 84

A crossover comparison of metoprolol and hydrochlorothiazide has been performed in 20 patients with mild hypertension. Both drugs caused almost identical statistically significant reduction in blood pressure of about 20 mm Hg systolic and 15 mm Hg diastolic. The side effects during active therapy were few and mild, but 5 patients experienced subjective symptoms during the first few days following abrupt withdrawal of metoprolol, namely general malaise, palpitations, headache, sweating and tremor. The symptoms were more pronounced in the standing position and disappeared at once on resumption of beta-blocker therapy, or gradually over 5 - 7 days when placebo tablets were given. In 11 of the 20 patients hydrochlorothiazide produced subnormal serum potassium levels and potassium supplements were given. The serum uric acid level was also significantly increased during hydrochlorothiazide treatment.
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PMID:Comparison of metoprolol as hydrochlorothiazide and antihypertensive agents. 79 49

In 1148 cases the serum digoxin concentration (SDC) was correlated with the extracardiac signs of digitalis intoxication. There is a considerably overlap of SDC levels of patients with and without extracardiac signs of toxicity even though the mean SDC's of these two groups differ significantly. An increasing percentage of clinical intoxicated patients with increasing SDC levels was found at digoxin concentrations of 2.0 ng/ml and higher. At lower SDC levels patients with and without extracardiac signs of digitalis intoxication did not differ significantly in their mean SDC but in mean age and in mean creatinine concentration indicating that at least part of the symptoms in these patients might be due to a more severe illness. We could show that many of the extracardiac signs of digitalis intoxication are also seen in patients with impaired kidney function at low SDC levels and may lead to a wrong diagnosis. The most common complaint in patients with SDC's of 2.0 ng/ml and more is nausea (39.4%), followed by tiredness (30.4%), dizzyness (23.7%), vomiting (23.1%), headache (16.0%), visual disturbances (13,5%), colour (yellow) seeing (6;7%), diarrhea (4.2%) and severe neuro-psychiatric disturbances (3.8%). In patients with digitalis-induced arrhythmias the sequence of symptoms is the same only with a somewhat higher percentage rate. Only about one half of the patients with digitalis-induced arrhythmias and SDC values up to 2.5 ng/ml showed also extracardiac signs of intoxication. Therefore these signs are not to be taken as early symptoms of digitalis intoxication. Divided into subgroups (patients with/without digitalis-induced arrhythmias, patients with SDC values of more/less than 2.0 ng/ml) the patients with and without extracardiac signs of digitalis toxicity are compared with each other in regard to: mean body height and weight, concentration of digoxin, potassium and creatinine, digoxin dosage and mean age. The greatest differences were found between patients with combined cardiac and extracardiac signs of intoxication and patients with neither cardiac nor extracardiac signs of intoxication: These intoxicated patients are of significantly higher mean age and lower body weight, their mean concentration of digoxin and creatinine and the digoxin dosage administered are significantly greater, but there is no significant difference in potassium concentration. An important group of patients, namely the elderly with impaired kidney function, are especially prone to develop digitalis intoxication. In this group, however, the extracardial symptoms are of little benefit in the diagnosis of digitalis intoxication. In these patients rhythm disturbances and intoxication-like symptoms are frequently caused by other reasons. In most cases the SDC value can clarify the diagnosis without withdrawal of the drug.
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PMID:[Digitalis intoxication: specifity and significance of cardiac and extracardiac symptoms. part II. Patients with extracardiac symptoms of digitalis intoxications (author's transl)]. 85 53

In a 31-year old woman with a six year history of headache and hypertension a diagnosis of primary aldosteronism was made on the basis of urine samples containing 45 mug/day of aldosterone. The preoperative systemic blood pressure was 240 mm Hg systolic and 120 mm Hg diastolic. The serum potassium level was 2.6 mEq/L and other laboratory findings were within normal limits. The patient was to undergo operation. Pre-medication consisted of oral pentobarbitone, intramuscular pethidine and atropine. For induction of anaesthesia, enflurane 2.0-2.5% maximum was given with O2 (21/min) and N2O (61/min); no intravenous agents were used. Suxamethonium chloride 40 mg was administered to facilitate endotracheal intubation. Anaesthesia was maintained with enflurane 1.5-2.0% with 50% N2O and O2. Tubocurarine 27 mg was given for muscle relaxation. When the tumour was manipulated, systemic arterial blood pressure was elevated again to 190 mm Hg systolic and 120 mm Hg diastolic. After removal of the tumour, the arterial pressure and heart rate were stable and recovery from anaesthesia was without circulatory or respiratory complications. Plasma aldosterone levels reached a maximum when the tumour was manipulated and fell to normal levels on the second post-operative day. Cortisol levels were not altered markedly even when the tumour was handled. These data imply that adrenocortical response to enflurane anaesthesia as jadged by plasma aldosterone levels would be different from that as estimated by plasma cortisol levels.
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PMID:Enflurane anaesthesia for removal of aldosterone producing adenoma. 126 18

Nicorandil belongs to the class of compounds known as potassium channel activators which are characterised by their arterial vasodilator properties. In addition, nicorandil has venodilating properties which are attributable to a nitrate group in its chemical structure. Therefore, by combining these two vasodilator mechanisms, nicorandil represents a novel type of compound for use in the treatment of angina pectoris. Furthermore, increasing experimental evidence suggests that potassium channel activation may also exert a direct cytoprotective effect by augmenting normal physiological processes which protect the heart against ischaemic events. Comparative studies of up to 3 months' duration suggest that nicorandil is equivalent in efficacy to isosorbide dinitrate, propranolol, atenolol, nifedipine or diltiazem in the treatment of stable angina. Preliminary evidence suggests that an improvement of anginal and ischaemic symptoms is maintained for up to 1 year. Whilst the efficacy of nicorandil in other types of angina has not been extensively studied, preliminary results indicate that intravenous nicorandil is as effective as isosorbide dinitrate in the treatment of unstable angina and is also effective in patients with variant angina. In addition, the limited data available indicate that nicorandil may be effective in patients with unstable and variant angina who are refractory to therapy with conventional antianginal agents, a potentially important area for further study. Headache, mostly of mild to moderate intensity was the most commonly reported adverse event, occurring in one-third of patients receiving the recommended therapeutic regimen of nicorandil 10 to 20mg twice daily. In comparative trials involving a total of 84 patients who received nicorandil, the incidence of headache was similar to that produced by isosorbide mononitrate and isosorbide dinitrate. Headache was most frequent on initiating therapy but declined with continued treatment. To date, approximately 5% of patients participating in European trials have withdrawn due to headache, although this rate may be reduced by using a lower starting dose of nicorandil (5 mg twice daily). In summary, clinical experience thus far indicates that nicorandil, with its novel combination of two distinct vasodilator mechanisms, offers an effective alternative to established vasodilator therapy with conventional nitrates and calcium antagonists in the long term treatment of stable angina pectoris. Further studies are warranted to establish whether the unique pharmacodynamic profile of nicorandil is advantageous for the treatment of other types of angina and/or the ischaemic myocardium.
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PMID:Nicorandil. A review of its pharmacology and therapeutic efficacy in angina pectoris. 128 Oct 76

A double-blind, placebo-controlled, cross-over study in 10 healthy male subjects has been carried out to investigate the non-pulmonary effects of single inhaled doses of salmeterol 100 micrograms, 200 micrograms and 400 micrograms and salbutamol 400 micrograms from a metered-dose inhaler. At all doses tested, salmeterol produced statistically significant changes in pulse rate, tremor, blood glucose and plasma potassium concentrations, compared with placebo. All changes were dosed related. A number of dose-related adverse events including tremor, awareness of heart beat and headache were reported after salmeterol administration.
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PMID:Dose-response study with high-dose inhaled salmeterol in healthy subjects. 134 91

This is the first report from Ethiopia of a case of cryptococcal meningitis in a patient with AIDS. A 20-year-old woman was admitted to Tikur Anbessa Hospital in January 1990 with complaints of generalized pruritic skin lesions of six months, and headache, fever, and poor appetite of three months duration. The headache and low-grade intermittent fever were accompanied by nausea, vomiting, anorexia, and progressive weight loss, without diarrhea. She had had multiple sex partners. Upon admission, after being bedridden for two weeks, she appeared acutely ill and restless. Her temperature was 39.5 degrees Celsius, and she had oral thrush. There was no lymphadenopathy. Widespread, irregular erythematous and whitish macular patches (3 x 5 to 8 x 10 sq. cm in size) with peripheral scaling and tiny vesicles were found on the skin, pubic and perineal regions. She had neck stiffness, but was conscious and well-oriented. Hemoglobin (Hb) was 10.5 g%; the white cell count (WBC) was 3400/cu. mm; the erythrocyte sedimentation rate (ESR) was 92 mm/hr; the platelet count was 175,000/mm; and blood films were negative for hemoparasites. Urinalysis showed 3+ albumin and many pus cells and red cells/HPF. Urine culture was negative, and the VDRL test was nonreactive. Lumbar puncture, which was performed upon arrival, showed clear cerebrospinal fluid (CSF), with normal protein and glucose levels and no cells. CSF culture showed yeast cells, and an India ink preparation was positive for Cryptococcus neoformans. Blood taken for bacterial culture grew yeast cells. Renal and liver function tests, and chest x-rays were normal. A potassium hydroxide (KOH) preparation from a skin snip showed rounded yeast cells. ELISA and Western blot tests were both positive. The patient was given supportive treatment and amphotericin B (0.6 mg/kg daily). Although the fever decreased, the patient's general condition did not improve. She complained of headache, photophobia, nausea, and vomiting. Lumbar puncture was repeated eight days after the start of treatment; CSF culture and India ink preparations were negative. Urea nitrogen (BUN) repeated two weeks later was normal. Four weeks after admission, the patient suddenly vomited massive amounts of fresh blood and died before transfusion could be given. A discussion follows regarding the clinical manifestations, diagnosis, and treatment of this disease, particularly in AIDS patients, with a review of the literature.
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PMID:Cryptococcal meningitis in a young Ethiopian woman with AIDS. 139 20

From 1975 to 1989, 52 patients with primary aldosteronism underwent adrenalectomy. There were 16 men and 36 women. The average age was 42.5 years, ranging from 28 years to 70 years. They were all hypertensive, with average pre-operative diastolic pressures varying from 105 to 140 mm Hg (median 117 mm Hg). The subjective symptoms most frequently reported were headache (71%) and asthenia (53%). In all patients except two, serum potassium concentration was 3.3 mEq/L (median 2.7 mEq/L) at the time of diagnosis. Plasma aldosterone concentration was elevated in all patients, 48 +/- 5.3 ng/mL in the recumbent position and 52.6 +/- 6.0 ng/mL in the upright position. The operations carried out were 50 unilateral and 2 bilateral adrenalectomies. In 4 patients a transperitoneal approach was employed and in the remaining 48 patients an extraperitoneal flank incision was used. The histological findings were 47 adenomas (with dimension ranging from 1 to 4.5 cm), unilateral macronodular hyperplasia in 2 patients, an adenoma plus controlateral hyperplasia in 1 patient, bilateral hyperplasia in 1 patient, and unilateral hyperplasia in 1 patient. After long-term follow-up (median 77 months, range 13 to 189 months), 15 patients remained hypertensive (diastolic blood pressure up to 100 mm Hg). In 9 of these patients the hypertensive illness had been present for more than 5 years prior to operation. In the remaining 37 (71%) patients, the arterial pressure returned to normal and in almost half of the patients this result was evident one or two days after operation.
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PMID:Adrenalectomy in primary aldosteronism: a long-term follow-up study in 52 patients. 141 36

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
Headache 1992 Jan
PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28


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