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

Hypertensive emergencies in hemodialysis require immediate therapy, usually by parenteral drug administration; however, sublingual medications may have potential in this special condition. Sublingual captopril (25 mg), nifedipine (10 mg) and prazosin (2 mg) were prescribed to determine the effectiveness and safety of each medication in the treatment of hypertensive emergencies during hemodialysis. Blood pressure and heart rate were measured continuously up to 120 min postdose. The response rates were 83% for captopril, 90% for nifedipine and 11% for prazosin. The significant hypotensive effects of both sublingual captopril and nifedipine occurred at 10 min and continued up to 120 min. The reduction of systolic blood pressure occurred earlier in nifedipine than captopril (10 vs. 15 min). No significant difference in heart rate between them was noted. There were no side effects in the captopril group but flushing, tachycardia and headache were observed in 4 patients of the nifedipine group. We concluded that sublingual captopril and nifedipine were effective but captopril seemed to have less side effects than nifedipine and may be an excellent alternative to sublingual nifedipine in the urgent treatment of hypertensive emergencies in hemodialysis. Prazosin was not recommended because of its low response rate.
Nephron 1993
PMID:Comparison of sublingual captopril, nifedipine and prazosin in hypertensive emergencies during hemodialysis. 824 94

We report a case of renovascular hypertension associated with neurofibromatosis complicated by moderate proteinuria. A 16-year-old female was admitted to Kensei General Hospital with a complaint of headache and a blood pressure of 230/120 mm Hg. She was referred to us for further evaluation of the hypertension. On examination, cafe-au-lait spots were seen over her extremities and flank, and a bruit was heard in the right upper abdomen. The urinary protein excretion was 2.1 g/day. The plasma renin activity (PRA) and plasma aldosterone concentration were high, but the levels of catecholamines were normal. The renogram was asymmetric and on venous sampling, the PRA in the right renal vein was 58.3 ng/ml/h and that in the left was 22.1 ng/ml/h. CT scan detected an approximately 10-mm mass in the proximal right renal artery. Arteriography disclosed severe stenosis in the right renal artery and the superior mesenteric artery. Therefore, we concluded that her hypertension resulted from stenosis of the right renal artery due to neurofibromatosis. Accordingly, she underwent an operation to reconstruct that artery. After the operation, her blood pressure and PRA normalized without administration of any anti-hypertensive drug and urinary protein disappeared.
Nephron 1996
PMID:A case of renovascular hypertension associated with neurofibromatosis. 873 Apr 48

Adverse effects of amlodipine besylate, a widely used antihypertensive medication, include peripheral edema, flushing, headache, pruritus, and rash. An adverse renal effect attributable to the medication has hitherto not been reported in the literature. We herein report a case of amlodipine besylate induced acute interstitial nephritis.
Nephron 2000 Aug
PMID:Amlodipine besylate induced acute interstitial nephritis. 1094 Jul 49

Sumatriptan and butorphanol nasal sprays are commonly used agents for the management of migraine headaches. Under certain circumstances, these two agents may be administered closely in time. However, the possibility of a pharmacokinetic interaction and the safety of this regime have not been examined. In this crossover design study, 24 healthy subjects received the following four treatments, each separated by at least 7 days: 1 mg butorphanol (Stadol NS7); 20 mg sumatriptan (Imitrex Nasal Spray); or both formulations together with butorphanol administered either 1 or 30 min after sumatriptan. Serial plasma samples were collected for 24 h post-dose and analysed for butorphanol and/or sumatriptan by HPLC-MS/MS. Butorphanol plasma concentrations were reduced when it was administered 1 min (mean 28.6% decrease in AUC(0-infinity)), but not 30 min, after sumatriptan. The pharmacokinetics of sumatriptan were not substantially altered by butorphanol. The combination of nasally administered sumatriptan and butorphanol appeared safe. However, if butorphanol nasal spray is administered <30 min after sumatriptan nasal spray, the analgesic effect of butorphanol may be diminished due to reduced nasal absorption resulting from probable transient vasoconstriction of nasal blood vessels by sumatriptan.
Cephalalgia 2002 May
PMID:A pharmacokinetic interaction study between butorphanol and sumatriptan nasal sprays in healthy subjects: importance of the timing of butorphanol administration. 1210 90

In earlier studies, a reduction in intradialytic procedures was observed in patients with severe intradialytic hypotension symptomatology by the use of blood volume controlled biofeedback systems. However, few data are present on the use of biofeedback-controlled treatments in patients experiencing minor intradialytic symptoms. In the present study, 157 standard and 158 biofeedback-controlled treatments were compared during a 2-month period in 16 hemodialysis patients. Both the percentage of hypotensive episodes (6.3 +/- 11.3 vs. 15.8 +/- 18.3%; p < 0.05) as well as other intradialytic symptoms (cramps, nausea, headache, abdominal pain) (11.0 +/- 12.8 vs. 18.1 +/- 16.9%; p < 0.05) were significantly less during biofeedback-controlled treatments compared to standard dialysis treatments, despite a similar decline in relative blood volume (8.8 +/- 3.5 vs. 8.3 +/- 3.1%; p = n.s.). Interdialytic weight gain and intradialytic rise in plasma sodium levels were comparable. Concluding, in this short-term preliminary study, blood volume controlled biofeedback improved dialysis tolerance also in patients with minor intradialytic symptomatology.
Nephron 2002
PMID:Blood volume control by biofeedback and dialysis-induced symptomatology. A short-term clinical study. 1237 44

We describe a 74-year-old man with rheumatoid arthritis (RA) who developed syndrome of inappropriate secretion of antidiuretic hormone (SIADH) 1.5 months after commencement of mizoribin prescription when his arthritis was improved. He noticed nausea and headache and serum Na fell as low as 118 mEq/l. Normal urinary Na excretion without hypotension or hemoconcentration negated the possibility of dehydration resulting from urinary Na loss. Serum antidiuretic hormone (ADH) remained elevated at 0.59 pg/ml in spite of a significant reduction in serum osmolality to 254 mosm/kg. He had no organic disease likely to cause SIADH. Despite infusion of hypertonic saline, his serum Na was not restored to normal. Shortly after mizoribin withdrawal, his serum Na increased significantly from 128 to 139 mEq/l and plasma osmolality from 265 to 287 mosm/kg. ADH hypersecretion in relation to plasma osmolality was reversed by mizoribin withdrawal, suggesting that bredinin might adversely induce SIADH. Additional predisposing factors were the patient's age and difficulty in urination due to benign prostatic hypertrophy. In summary, we report herein the first case of SIADH believed to be an adverse effect of mizoribin, which may therefore needed to be added to the list of drugs which can induce SIADH.
Nephron 2002 Dec
PMID:A case of SIADH induced by mizoribin administration. 1239 45

Although not without controversy, an influence of the autonomic nervous system in headache is a matter for current debate. A possible contact site of autonomic and sensory nerves is the dura mater, where they form a dense network accompanying blood vessels. We investigated interactions between autonomic and nociceptive fibres by measuring release of calcitonin gene-related peptide (CGRP) and prostaglandin E2 (PGE2) from the dura mater, in vitro. The parasympathomimetic agent carbachol did not change basal release of CGRP or PGE2, whereas it diminished release induced by a mixture of inflammatory mediators. Norepinephrine did not change induced release of CGRP or PGE2, nor basal release of CGRP. However, basal release of PGE2 was enhanced by norepinephrine, and this enhancement was reduced by serotonin through 5-HT(1D) receptors. We conclude that sympathetic transmitters may control nociceptor sensitivity via increased basal PGE2 levels, a possible mechanism to facilitate headache generation. Parasympathetic transmitters may reduce enhanced nociceptor activity.
Cephalalgia 2006 Mar
PMID:Effect of sympathetic and parasympathetic mediators on the release of calcitonin gene-related peptide and prostaglandin E from rat dura mater, in vitro. 1647 34

We have previously shown decreased lipolysis in both phases of cluster headache (CH), as an indication of a sympathetic dysregulation. Reduced lipolysis could be a result of diminished beta-receptor sensitivity in adipose tissue. The aim of this study was to measure the lipolytic response to noradrenaline in 10 CH patients in remission and in 10 healthy subjects, to estimate beta-receptor function. Microdialysis technique was used to measure the increase of glycerol, the end-product of lipolysis, during infusion of noradrenaline into the adipose tissue. Noradrenaline infusion resulted in a distinct elevation of glycerol. The average glycerol increase was significantly higher in CH patients (121% +/- 48) than in healthy subjects (77% +/- 41) (P < 0.05), which indicates increased beta-receptor response to noradrenaline in CH patients in remission. This may be due to up-regulated beta-receptor sensitivity, secondary to reduced sympathetic outflow and a primary autonomic disturbance in CH.
Cephalalgia 2006 Jul
PMID:beta-Receptor response to noradrenaline in cluster headache. A study of adipose tissue lipolysis. 1677 98

Reninoma (juxtaglomerular cell tumor) is a rare cause of renin-mediated hypertension. Reninomas are usually diagnosed in adolescents and young adults with occasional reports in younger children. Patients typically present with a long history of headaches leading to a diagnosis of severe hypertension that responds well to antihypertensive treatment targeting the renin-angiotensin-aldosterone system. The clue to clinical diagnosis is the presence of hypokalemia and metabolic alkalosis on the first blood sample drawn before any treatment is instituted. Elevated blood levels of renin and aldosterone confirm the clinical suspicion of renin-mediated hypertension. Diagnostic imaging is employed to identify the source of excessive renin production. While renal ultrasound can miss reninoma, contrast CT or magnetic resonance imaging of the kidneys are diagnostic modalities of choice leading to the correct diagnosis. Renal vein renin sampling with lateralization might help to identify the site of excessive renin production. Nephron-sparing surgery is curative with maintenance of normal blood pressure after discontinuation of antihypertensive medications in the majority of patients. In this paper, we present the case of reninoma in an adolescent girl emphasizing clinical presentation, diagnostic evaluation, and medical and surgical treatment of this rare tumor. We also discuss important points in the management of children presenting with renin-mediated hypertension.
...
PMID:Reninoma: an uncommon cause of Renin-mediated hypertension. 2517 79


<< Previous 1 2