High blood pressure. Causes, symptoms, treatments

Status epilepticus secondary to hypertensive encephalopathy as the presenting manifestation of Guillain-Barré syndrome.


To determine the risk factors of symptomatic NSAID-induced small intestinal injuries, including diaphragm disease.

This study investigated the efficacy of LMP-420 as an anti-inflammatory agent in acute and chronic colitis induced by oral administration of dextran sulfate sodium (DSS) to mice and in chronic colitis following piroxicam administration to IL-10-deficient mice. The severity of colon inflammation was assessed histologically. TNF levels were measured by enzyme immunoassay.

Intraligamentary mode of delivery of Piroxicam was more efficacious.

We have examined the effects of auranofin and some nonsteroidal anti-inflammatory drugs (NSAID) on the release of gelatinase from rat neutrophils. Two preparations of neutrophils were used, one derived from normal blood and the other from the inflamed pleural fluids of carrageenin-elicited pleurisy. Both neutrophil preparations released gelatinase in response to stimulation by serum-treated zymosan (STZ) or concanavalin A (Con A). Control, blood-derived neutrophils exposed to STZ produced more than a four-fold increase in the release of gelatinase, a response significantly inhibited by the presence of auranofin at 10(-5) and 10(-4) M. Inflamed, pleural neutrophils exposed to STZ produced a doubling in gelatinase release and this was also inhibited by auranofin at 10(-5) and 10(-4) M. The release of gelatinase by control neutrophils (no stimulation) or by neutrophils exposed to Con A was enhanced by 10(-6) M auranofin. In contrast, the NSAIDs aspirin, piroxicam, sulindac, indomethacin and naproxen had no inhibitory action on neutrophil gelatinase release. We conclude that auranofin is an effective inhibitor of gelatinase release from neutrophils and this property may represent a contributory factor assigned to the beneficial therapeutic action of gold salts.

This was a 2-center randomized placebo-controlled trial. One hundred forty-eight patients, between 18 and 70 years of age, were randomly assigned to 6 groups (28 in each group) with the use of computer software: A(gabapentin/ketamine/lornoxicam/ropivacaine); B(gabapentin/placebo/placebo/placebo); C (placebo/ketamine/placebo/placebo); D (placebo/placebo/lornoxicam/placebo); E (placebo/placebo/placebo/ropivacaine); and F (placebo/placebo/placebo/placebo). Only the principal investigator was aware of patients' allocation and provided drugs and placebo in covered prefilled syringes. The primary outcome of the study was the 24-hour morphine consumption. Secondary outcomes were frequency of opioid-related side effects (nausea, vomiting, sedation, pruritus, and dysuria).

Fifty adult patients scheduled for general anaesthesia with endotracheal intubation were enrolled in this randomized, double-blind placebo-controlled study. They were divided into two equal groups to receive intravenously either lornoxicam 16 mg or placebo 30 min before surgery. Mean arterial pressure and heart rate were recorded before and after induction of anaesthesia, and every minute after intubation for 10 min. Serum catecholamine levels were measured before induction and 1 min after intubation.

The case-population approach or population-based case-cohort approach is derived from the case-control design and consists of comparing past exposure to a given risk factor in subjects presenting a given disease or symptom (cases) with the exposure rate to this factor in the whole cohort or in the source population of cases. In the same way as the case-control approach, the case-population approach measures the disproportionality of exposure between cases of a given disease and their source population expressed in the form of an odds ratio approximating the ratio of the risks in exposed and not-exposed populations (relative risk).

Two simple, sensitive and accurate spectrophotometric methods have been proposed for the determination of amoxycillin (AMX), ciprofloxacin (CPF) and piroxicam (PIR) in pure and pharmaceutical preparations. The methods are based on the measurement of absorbances of tris(o-phenanthroline) iron(II) [method A] and tris (bipyridyl) iron(II) [method B] complexes at 510 and at 522 nm, respectively. Reaction conditions have been optimized to obtain coloured complexes of higher sensitivity and longer stability. The absorbances were found to increase linearly with increase in concentrations of AMX, CPF and PIR which were corroborated by correlation coefficient values. The complexes obeyed Beer's law over the concentration range of 0.06-5.2, 0.04-7.2 and 0.2-6.5 microg ml(-1) for AMX, CPF and PIR, respectively, in method A, and of 0.05-8.5, 0.05-9.0 and 0.05-6.5 microg ml(-1) for AMX, CPF and PIR, respectively, in method B. The developed methods have been successfully applied for the determination of AMX, CPF and PIR in bulk drugs and pharmaceutical formulations. The common excipients and additives did not interfere in their determinations. The results obtained by the proposed methods have been statistically compared by means of Student t-test and by the variance ratio F-test.