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)

The concentration of 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), kallikrein-like enzymes and beta-glucuronidase were quantified in the cerebrospinal fluid (CSF) during spontaneous migraine attacks. Plasma levels of kallikrein-like enzymes and beta-glucuronidase, as well as urinary levels of 5-HIAA as free acid and glucuronides were also measured. Correlation of these biochemical findings with various clinical variables showed that 5-HIAA in the CSF did not correlate with either the time sequences of migraine attacks or with clinical division of migraine into classical and common migraine. CSF 5-HIAA correlated positively with HVA, EEG photostimulation, the triggering of food and the therapeutic effect of the so-called antiserotonin treatment, and negatively with esterase activity. Urinary 5-HIAA showed a significant increase during the early headache stage.
 ...
PMID:Changes in serotonin metabolism during migraine attacks. 97 98

Forty-six sclerotherapy sessions were performed on liver cirrhotics with high-risk esophageal varices using GT XIII, a sclerosant composed of gelatin, thrombin and coagulation factor XIII. GT XIII was effective for the prevention of temporary symptoms and transient hypotension observed in 55 sclerotherapy sessions using thrombin. In 42 (91%) sessions, patients underwent sclerotherapy with no symptoms, and in the other four (9%) sessions, only slight symptoms of general fatigue and headache were observed. Changes in the mean arterial pressure were significantly smaller in sessions using GT XIII than in those using thrombin (-12.3 +/- 13.6 vs. -26.8 +/- 20.7 mmHg, P less than 0.01). Changes in coagulation tests, similar to those of disseminated intravascular coagulation (DIC), were also reduced in sessions using GT XIII. Urinary kallikrein and kinin excretion significantly increased after the procedure (P less than 0.01), indicating activation of the renal kallikrein-kinin system. Increases in urinary kallikrein and kinin excretion showed a significant relationship with the consumed plasma fibrinogen levels (r = -0.51, P less than 0.01 and r = -0.58, P less than 0.01, respectively), and it was suggested that activation of the glandular kallikrein-kinin system caused by abrupt DIC-like changes in the hemostatic system might play a role in manifestations of temporary complications occurring with the use of hemostatic agents containing thrombin.
 ...
PMID:Effects of endoscopic variceal sclerotherapy using GT XIII on blood coagulation tests and the renal kallikrein-kinin system. 222 47

We performed an epidemiological study on the atrial natriuretic factor pattern in a young population. Subjects were recruited in the Ospedale Militare Principale of Rome among young men liable to conscription, whose hospitalization was due either to essential hypertension or to other pathologies (not influencing our study, such as headache etc.). The recruitment lead to the formation of three different groups: normotensives, normotensives with family history of hypertension (mother and/or father) and hypertensives. On the morning of the study (after 7 days of pharmacological wash-out, under a diet containing 120 mEq of Na+/die), blood samples were taken. Plasma atrial natriuretic factor, renin activity and aldosterone were assayed by RIA. Digoxin-like immunoreactive substance was assayed by a solid-phase radioimmunoassay, following the extraction of plasma. Serum creatinine, sodium, potassium and urinary sodium and potassium (24 h before the study) were assayed by standard methods. Urinary kallikrein was assayed by chromogenic substrate S-2266. So far, we have studied 60 subjects (26 hypertensives, 21 normotensives and 13 normotensives with family history) and we wish to discuss in this article the preliminary results concerning the atrial natriuretic factor and its relationship with renin activity, aldosterone and blood pressure. Our results show that the mean plasma levels of atrial natriuretic factor in the hypertensive group were higher, although not significantly, than those of the other two groups and that the normotensives with family history had slightly higher levels as compared to normotensives (Delta % = + 7.4).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Atrial natriuretic factor: an epidemiological study. Preliminary results]. 252 19

Enalapril maleate is a new angiotensin converting enzyme inhibitor marketed in the U.S. by Merck Sharp and Dohme. It has been demonstrated to actively interfere with the renin-angiotensin-aldosterone system. This is reflected by both hemodynamic (decreased blood pressure) and humoral (increased plasma renin, angiotensin I, and decreased angiotensin II) responses to enalapril therapy. Activity in the kallikrein-bradykinin system is still controversial. Enalapril maleate is a prodrug which is quickly absorbed, hydrolyzed by the liver to the active metabolite enalaprilic acid, and excreted 33 percent in the bile and 61 percent in the urine. The therapeutic dosage range is 10-40 mg/d, maximum of 40 mg, given once or twice daily. The onset and duration of action are dose related. Vertigo and headache have been the most commonly reported side effects. Clinical comparison of enalapril to hydrochlorothiazide, beta-adrenergic blockers, and captopril find it efficacious in the treatment of essential hypertension. Efficacy in treating congestive heart failure and hypertension secondary to renal artery stenosis has also been demonstrated for both angiotensin converting enzyme inhibitors. The overall efficacy and safety of enalapril and captopril appear equivalent when used at low doses in patients with uncomplicated hypertension.
 ...
PMID:Enalapril: a new angiotensin converting enzyme inhibitor. 300 62

Recombinant gamma interferon (rHuIFN-gamma) has been recognized to increase mRNA and protein levels of C1 inhibitor (C1 INH) in various human cells. Further, when administered to patients with colon cancer, it increased plasma C1 INH levels. A prospective trial was initiated to determine whether rHuIFN-gamma could elevate plasma C1 INH levels in six normal volunteers and two patients with type I angioedema. After 1 month of observation of plasma C1 INH levels, rHuIFN-gamma was administered subcutaneously at 25 micrograms/M2 daily for 4 consecutive days. All healthy volunteers and patients experienced local erythema, headache, myalgias, and chills during the administration of rHuIFN-gamma. C1 INH, prekallikrein, high-molecular-weight kininogen, and factor XII levels in plasma were not influenced by the rHuIFN-gamma administration. One patient with hereditary angioedema (HAE) had an attack of angioedema 3 days after completion of rHuIFN-gamma therapy. During the attack, circulating cleaved high-molecular-weight kininogen, kallikrein-alpha 2-macroglobulin complexes, and an altered 50 kd form of kallikrein were detected in the patient's plasma. Additional studies showed that rHuIFN-gamma treatment resulted in decreased total fibrinolytic activity. It was found that immediately after rHuIFN-gamma treatment, tissue plasminogen activator activity and antigen levels were not significantly decreased in volunteers. Plasminogen activator inhibitor levels rose significantly, but this activity was not due to plasminogen activator inhibitor-1 antigen, whose value significantly fell. These data suggest that rHuIFN-gamma may stimulate the expression of another plasminogen activator inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Administration of gamma interferon in human subjects decreases plasminogen activation and fibrinolysis without influencing C1 inhibitor. 830 Nov 99