Input: Hydrocortisone - induced hypertension in humans: pressor responsiveness and sympathetic function. Oral hydrocortisone increases blood pressure and enhances pressor responsiveness in normal human subjects. We studied the effects of 1 week of oral hydrocortisone (200 mg / day) on blood pressure, cardiac output, total peripheral resistance, forearm vascular resistance, and norepinephrine spillover to plasma in eight healthy male volunteers. Although diastolic blood pressure remained unchanged, systolic blood pressure increased from 119 to 135 mm Hg (SED + / - 3. 4, p less than 0. 01), associated with an increased cardiac output (5. 85 - 7. 73 l / min, SED + / - 0. 46, p less than 0. 01). Total peripheral vascular resistance fell from 15. 1 to 12. 2 mm Hg / l / min (SED + / - 1. 03, p less than 0. 05). Resting forearm vascular resistance remained unchanged, but the reflex response to the cold pressor test was accentuated, the rise in resistance increasing from 10. 5 mm Hg / ml / 100 ml / min (R units) before treatment to 32. 6 R units after treatment (SED + / - 6. 4, p less than 0. 025). The rise in forearm vascular resistance accompanying intra - arterial norepinephrine (25, 50, and 100 ng / min) was also significantly greater after hydrocortisone, increasing from an average of 14. 9 + / - 2. 4 R units before treatment to 35. 1 + / - 5. 5 R units after hydrocortisone (SED + / - 6. 0, p less than 0. 05). A shift to the left in the dose - response relation and fall in threshold suggested increased sensitivity to norepinephrine after treatment. Measurement of resting norepinephrine spillover rate to plasma and norepinephrine uptake indicated that overall resting sympathetic nervous system activity was not increased. The rise in resting blood pressure with hydrocortisone is associated with an increased cardiac output (presumably due to increased blood volume). (ABSTRACT TRUNCATED AT 250 WORDS)

Hydrocortisone

hydrocortisone

hydrocortisone

norepinephrine

norepinephrine

hydrocortisone

hydrocortisone

norepinephrine

norepinephrine

norepinephrine

hydrocortisone

hypertension

increased cardiac output

rise in resting blood pressure

increased cardiac output

Hydrocortisone

hypertension

Hydrocortisone

rise in resting blood pressure

hydrocortisone

hypertension

hydrocortisone

rise in resting blood pressure

hydrocortisone

hypertension

hydrocortisone

rise in resting blood pressure

hydrocortisone

hypertension

hydrocortisone

rise in resting blood pressure

hydrocortisone

hypertension

hydrocortisone

rise in resting blood pressure

hydrocortisone

hypertension

hydrocortisone

rise in resting blood pressure


Input: Effects of suprofen on the isolated perfused rat kidney. Although suprofen has been associated with the development of acute renal failure in greater than 100 subjects, the mechanism of damage remains unclear. The direct nephrotoxic effects of a single dose of 15 mg of suprofen were compared in the recirculating isolated rat kidney perfused with cell - free buffer with or without the addition of 5 mg / dL of uric acid. There were no significant differences in renal sodium excretion, oxygen consumption, or urinary flow rates in kidneys perfused with suprofen compared with the drug - free control groups. In contrast, a significant decline in glomerular filtration rate was found after the introduction of suprofen to the kidney perfused with uric acid; no changes were found with suprofen in the absence of uric acid. A significant decrease in the baseline excretion rate of uric acid was found in rats given suprofen, compared with drug - free controls. However, the fractional excretion of uric acid was unchanged between the groups over the experimental period. In summary, suprofen causes acute declines in renal function, most likely by directly altering the intrarenal distribution of uric acid.

suprofen

suprofen

suprofen

uric acid

sodium

oxygen

suprofen

suprofen

uric acid

suprofen

uric acid

uric acid

suprofen

uric acid

suprofen

uric acid

acute renal failure

nephrotoxic

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function

suprofen

acute renal failure

suprofen

acute declines in renal function


Input: Cocaine - induced brainstem seizures and behavior. A variety of abnormal sensory / motor behaviors associated with electrical discharges recorded from the bilateral brainstem were induced in adult WKY rats by mechanical (electrode implants) and DC electrical current stimulations and by acute and chronic administration of cocaine. The electrode implant implicated one side or the other of the reticular system of the brainstem but subjects were not incapacitated by the stimulations. Cocaine (40 mg / kg) was injected subcutaneously for an acute experiment and subsequent 20 mg / kg doses twice daily for 3 days in a chronic study. Cocaine generated more abnormal behaviors in the brainstem perturbation group, especially the electrically perturbated subjects. The abnormal behaviors were yawning, retrocollis, hyperactivity, hypersensitivity, " beating drum " behavior, squealing, head bobbing, circling, sniffing, abnormal posturing, and facial twitching. Shifts in the power frequency spectra of the discharge patterns were noted between quiet and pacing behavioral states. Hypersensitivity to various auditory, tactile, and visual stimulation was present and shifts in the brainstem ambient power spectral frequency occurred in response to tactile stimulation. These findings suggest that the brainstem generates and propagates pathological discharges that can be elicited by mechanical and DC electrical perturbation. Cocaine was found to activate the discharge system and thus induce abnormal behaviors that are generated at the discharge site and at distant sites to which the discharge propagates. Cognitive functions may also be involved since dopaminergic and serotonergic cellular elements at the brainstem level are also implicated.

Cocaine

cocaine

Cocaine

Cocaine

Cocaine

seizures

hyperactivity

hypersensitivity

Hypersensitivity

Cocaine

seizures

cocaine

seizures

Cocaine

seizures

Cocaine

seizures

Cocaine

seizures


Input: Increased sulfation and decreased 7alpha - hydroxylation of deoxycholic acid in ethinyl estradiol - induced cholestasis in rats. Deoxycholic acid conjugation, transport capacity, and metabolism were compared in control and ethinyl estradiol - treated rats. Control rats were found to have a lower capacity to transport deoxycholic acid than taurodeoxycholic acid, and both were decreased by ethinyl estradiol treatment. During [24 - 14C] sodium deoxycholate infusion, [14C] biliary bile acid secretion increased, but bile flow did not change significantly in either control or ethinyl estradiol - treated rats. Ethinyl estradiol - treated animals excreted significantly less 14C as taurocholic acid than did control animals, consistent with an impairment of 7alpha - hydroxylation of taurodeoxycholic acid. Ethinyl estradiol treatment did not impair conjugation of deoxycholic acid, but did result in an increase in sulfation of taurodeoxycholic acid from 1. 5% in controls to nearly 4. 0% (P less than 0. 01). These results are consistent with the hypothesis that the rat has a poorer tolerance for deoxycholic acid than do certain other species. Furthermore, the rat converts deoxycholic acid, a poor choleretic, to taurocholic acid, a good choleretic. When this conversion is impaired with ethinyl estradiol treatment, sulfation may be an important alternate pathway for excretion of this potentially harmful bile acid.

deoxycholic acid

ethinyl estradiol

Deoxycholic acid

ethinyl estradiol

deoxycholic acid

taurodeoxycholic acid

ethinyl estradiol

sodium deoxycholate

bile acid

ethinyl estradiol

Ethinyl estradiol

taurocholic acid

taurodeoxycholic acid

Ethinyl estradiol

deoxycholic acid

taurodeoxycholic acid

deoxycholic acid

deoxycholic acid

taurocholic acid

ethinyl estradiol

bile acid

cholestasis

ethinyl estradiol

cholestasis

ethinyl estradiol

cholestasis

ethinyl estradiol

cholestasis

ethinyl estradiol

cholestasis

Ethinyl estradiol

cholestasis

Ethinyl estradiol

cholestasis

ethinyl estradiol

cholestasis


Input: Effects of ouabain on myocardial oxygen supply and demand in patients with chronic coronary artery disease. A hemodynamic, volumetric, and metabolic study in patients without heart failure. The effects of digitalis glycosides on myocardial oxygen supply and demand are of particular interest in the presence of obstructive coronary artery disease, but have not been measured previously in man. We assessed the effects of ouabain (0. 015 mg / kg body weight) on hemodynamic, volumetric, and metabolic parameters in 11 patients with severe chronic coronary artery disease without clinical congestive heart failure. Because the protocol was long and involved interventions which might affect the determinations, we also studied in nine patients using an identical protocol except that ouabain administration was omitted. Left ventricular end - diastolic pressure and left ventricular end - diastolic volume fell in each patient given ouabain, even though they were initially elevated in only two patients. Left ventricular end - diastolic pressure fell from 11. 5 + / - 1. 4 (mean + / - SE) to 5. 6 + / - 0. 9 mm Hg (P less than 0. 001) and left ventricular end - diastolic volume fell from 100 + / - 17 to 82 + / - 12 ml / m2 (P less than 0. 01) 1 h after ouabain infusion was completed. The maximum velocity of contractile element shortening increased from 1. 68 + / - 0. 11 ml / s to 2. 18 + / - 0. 21 muscle - lengths / s (P less than 0. 05) and is consistent with an increase in contractility. No significant change in these parameters occurred in the control patients. No significant change in myocardial oxygen consumption occurred after ouabain administration but this may be related to a greater decrease in mean arterial pressure in the ouabain patients than in the control patients. We conclude that in patients with chronic coronary artery disease who are not in clinical congestive heart failure left ventricular end - diastolic volume falls after ouabain administration even when it is initially normal. Though this fall would be associated with a decrease in wall tension, and, therefore, of myocardial oxygen consumption, it may not be of sufficient magnitude to prevent a net increase in myocardial oxygen consumption. Nevertheless, compensatory mechanisms prevent a deterioration of resting myocardial metabolism.

ouabain

oxygen

digitalis glycosides

oxygen

ouabain

ouabain

ouabain

ouabain

oxygen

ouabain

ouabain

ouabain

oxygen

oxygen

coronary artery disease

heart failure

coronary artery disease

coronary artery disease

congestive heart failure

coronary artery disease

congestive heart failure

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls

ouabain

left ventricular end - diastolic volume falls


Input: Prolongation of the QT interval related to cisapride - diltiazem interaction. Cisapride, a cytochrome P450 3A4 (CYP3A4) substrate, is widely prescribed for the treatment of gastrointestinal motility disorders. Prolongation of QT interval, torsades de pointes, and sudden cardiac death have been reported after concomitant administration with erythromycin or azole antifungal agents, but not with other CYP3A4 inhibitors. A possible drug interaction occurred in a 45 - year - old woman who was taking cisapride for gastroesophageal reflux disorder and diltiazem, an agent that has inhibitory effect on CYP3A4, for hypertension. The patient was in near syncope and had QT - interval prolongation. After discontinuing cisapride, the QT interval returned to normal and symptoms did not recur. We suggest that caution be taken when cisapride is prescribed with any potent inhibitor of CYP3A4, including diltiazem.

Prolongation of the QT interval

gastrointestinal motility disorders

Prolongation of QT interval

torsades de pointes

sudden cardiac death

gastroesophageal reflux disorder

hypertension

syncope

QT - interval prolongation

cisapride

diltiazem

Cisapride

erythromycin

azole

cisapride

diltiazem

cisapride

cisapride

diltiazem

azole

sudden cardiac death

azole

Prolongation of the QT interval

azole

Prolongation of QT interval

azole

QT - interval prolongation

diltiazem

Prolongation of the QT interval

diltiazem

Prolongation of QT interval

diltiazem

QT - interval prolongation

diltiazem

Prolongation of the QT interval

diltiazem

Prolongation of QT interval

diltiazem

QT - interval prolongation

diltiazem

Prolongation of the QT interval

diltiazem

Prolongation of QT interval

diltiazem

QT - interval prolongation

azole

torsades de pointes

cisapride

sudden cardiac death

Cisapride

sudden cardiac death

cisapride

sudden cardiac death

cisapride

sudden cardiac death

cisapride

sudden cardiac death

erythromycin

torsades de pointes

erythromycin

Prolongation of the QT interval

erythromycin

Prolongation of QT interval

erythromycin

QT - interval prolongation

cisapride

Prolongation of the QT interval

cisapride

Prolongation of QT interval

cisapride

QT - interval prolongation

Cisapride

Prolongation of the QT interval

Cisapride

Prolongation of QT interval

Cisapride

QT - interval prolongation

cisapride

Prolongation of the QT interval

cisapride

Prolongation of QT interval

cisapride

QT - interval prolongation

cisapride

Prolongation of the QT interval

cisapride

Prolongation of QT interval

cisapride

QT - interval prolongation

cisapride

Prolongation of the QT interval

cisapride

Prolongation of QT interval

cisapride

QT - interval prolongation

cisapride

torsades de pointes

Cisapride

torsades de pointes

cisapride

torsades de pointes

cisapride

torsades de pointes

cisapride

torsades de pointes

erythromycin

sudden cardiac death


Input: Paclitaxel combined with carboplatin in the first - line treatment of advanced ovarian cancer. In a phase I study to determine the maximum tolerated dose of paclitaxel (Taxol; Bristol - Myers Squibb Company, Princeton, NJ) given as a 3 - hour infusion in combination with carboplatin administered every 21 days to women with advanced ovarian cancer, paclitaxel doses were escalated as follows: level 1, 135 mg / m2; level 2, 160 mg / m2; level 3, 185 mg / m2; and level 4, 210 mg / m2. The fixed dose of carboplatin at levels 1 through 4 was given to achieve an area under the concentration - time curve (AUC) of 5 using the Calvert formula. In levels 5 and 6 the carboplatin dose was targeted at AUCs of 6 and 7. 5, respectively, combined with a fixed paclitaxel dose of 185 mg / m2. To date, 30 previously untreated patients, all with a good performance status (Eastern Cooperative Oncology Group 0 to 2) have been entered into this ongoing study. The dose - limiting toxicity of the combination was myelosuppression (leukopenia, granulocytopenia, and thrombocytopenia). Neurotoxicity was largely moderate. So far, 14 patients are evaluable for response; of these, eight (57%) showed objective (complete or partial) response and disease stabilized in six patients. No patient had disease progression. We conclude that the combination of paclitaxel 185 mg / m2 administered as a 3 - hour infusion followed immediately by a 1 - hour infusion of carboplatin at an AUC of 6 can be administered safely in a 21 - day schedule in the outpatient setting. The recommended dose for phase III studies is paclitaxel 185 mg / m2 and carboplatin AUC 6.

Paclitaxel

carboplatin

paclitaxel

Taxol

carboplatin

paclitaxel

carboplatin

carboplatin

paclitaxel

paclitaxel

carboplatin

paclitaxel

carboplatin

ovarian cancer

ovarian cancer

toxicity

myelosuppression

leukopenia

granulocytopenia

thrombocytopenia

Neurotoxicity

Paclitaxel

thrombocytopenia

paclitaxel

thrombocytopenia

Taxol

thrombocytopenia

paclitaxel

thrombocytopenia

paclitaxel

thrombocytopenia

paclitaxel

thrombocytopenia

paclitaxel

thrombocytopenia

Paclitaxel

granulocytopenia

paclitaxel

granulocytopenia

Taxol

granulocytopenia

paclitaxel

granulocytopenia

paclitaxel

granulocytopenia

paclitaxel

granulocytopenia

paclitaxel

granulocytopenia

carboplatin

granulocytopenia

carboplatin

granulocytopenia

carboplatin

granulocytopenia

carboplatin

granulocytopenia

carboplatin

granulocytopenia

carboplatin

granulocytopenia

Paclitaxel

leukopenia

paclitaxel

leukopenia

Taxol

leukopenia

paclitaxel

leukopenia

paclitaxel

leukopenia

paclitaxel

leukopenia

paclitaxel

leukopenia

carboplatin

leukopenia

carboplatin

leukopenia

carboplatin

leukopenia

carboplatin

leukopenia

carboplatin

leukopenia

carboplatin

leukopenia

carboplatin

thrombocytopenia

carboplatin

thrombocytopenia

carboplatin

thrombocytopenia

carboplatin

thrombocytopenia

carboplatin

thrombocytopenia

carboplatin

thrombocytopenia

carboplatin

Neurotoxicity

carboplatin

Neurotoxicity

carboplatin

Neurotoxicity

carboplatin

Neurotoxicity

carboplatin

Neurotoxicity

carboplatin

Neurotoxicity

Paclitaxel

Neurotoxicity

paclitaxel

Neurotoxicity

Taxol

Neurotoxicity

paclitaxel

Neurotoxicity

paclitaxel

Neurotoxicity

paclitaxel

Neurotoxicity

paclitaxel

Neurotoxicity


Input: Treatment of tacrolimus - related adverse effects by conversion to cyclosporine in liver transplant recipients. When tacrolimus side effects persist despite dose reduction, conversion to cyclosporine - based immunosuppression (CyA) is necessary. We characterized tacrolimus side effects that warranted discontinuation of the drug, and outcomes after conversion. Of 388 liver recipients who received tacrolimus as primary immunosuppression, 70 required conversion to CyA. We recorded indication for conversion, whether conversion was early or late after transplantation, tacrolimus dose and trough blood level at conversion, and incidence of rejection after conversion. Conversion was early in 29 patients (41. 4%) and late in 41 (58. 6%). Indications for early conversion were neurotoxicity (20), (insulin - dependent) diabetes mellitus (IDDM) (5), nephrotoxicity (3), gastrointestinal (GI) toxicity (6), and cardiomyopathy (1), and for late conversion were neurotoxicity (15), IDDM (12), nephrotoxicity (3), GI toxicity (5), hepatotoxicity (6), post - transplant lmphoproliferate disease (PTLD) (2), cardiomyopathy (1), hemolytic anemia (1), and pruritus (1). All early - conversion patients showed improvement / resolution of symptoms. Among late - conversion patients, 37 (90. 2%) had improvement / resolution; in 4 (9. 8%), adverse effects persisted. The overall rejection rate was 30%. Sixty - two patients (88. 6%) are alive with functioning grafts 686 + / - 362 days (range, 154 - 1433 days) after conversion. When tacrolimus side effects are unresponsive to dose reduction, conversion to CyA can be accomplished safely, with no increased risk of rejection and excellent long - term outcome.

tacrolimus

cyclosporine

tacrolimus

cyclosporine

tacrolimus

tacrolimus

tacrolimus

tacrolimus

neurotoxicity

(insulin - dependent) diabetes mellitus

IDDM

nephrotoxicity

gastrointestinal (GI) toxicity

cardiomyopathy

neurotoxicity

IDDM

nephrotoxicity

GI toxicity

hepatotoxicity

post - transplant lmphoproliferate disease

PTLD

cardiomyopathy

hemolytic anemia

pruritus

tacrolimus

hemolytic anemia

tacrolimus

hemolytic anemia

tacrolimus

hemolytic anemia

tacrolimus

hemolytic anemia

tacrolimus

hemolytic anemia

tacrolimus

hemolytic anemia

tacrolimus

(insulin - dependent) diabetes mellitus

tacrolimus

IDDM

tacrolimus

IDDM

tacrolimus

(insulin - dependent) diabetes mellitus

tacrolimus

IDDM

tacrolimus

IDDM

tacrolimus

(insulin - dependent) diabetes mellitus

tacrolimus

IDDM

tacrolimus

IDDM

tacrolimus

(insulin - dependent) diabetes mellitus

tacrolimus

IDDM

tacrolimus

IDDM

tacrolimus

(insulin - dependent) diabetes mellitus

tacrolimus

IDDM

tacrolimus

IDDM

tacrolimus

(insulin - dependent) diabetes mellitus

tacrolimus

IDDM

tacrolimus

IDDM

tacrolimus

pruritus

tacrolimus

pruritus

tacrolimus

pruritus

tacrolimus

pruritus

tacrolimus

pruritus

tacrolimus

pruritus

tacrolimus

post - transplant lmphoproliferate disease

tacrolimus

PTLD

tacrolimus

post - transplant lmphoproliferate disease

tacrolimus

PTLD

tacrolimus

post - transplant lmphoproliferate disease

tacrolimus

PTLD

tacrolimus

post - transplant lmphoproliferate disease

tacrolimus

PTLD

tacrolimus

post - transplant lmphoproliferate disease

tacrolimus

PTLD

tacrolimus

post - transplant lmphoproliferate disease

tacrolimus

PTLD

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

cardiomyopathy

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

neurotoxicity

tacrolimus

gastrointestinal (GI) toxicity

tacrolimus

GI toxicity

tacrolimus

gastrointestinal (GI) toxicity

tacrolimus

GI toxicity

tacrolimus

gastrointestinal (GI) toxicity

tacrolimus

GI toxicity

tacrolimus

gastrointestinal (GI) toxicity

tacrolimus

GI toxicity

tacrolimus

gastrointestinal (GI) toxicity

tacrolimus

GI toxicity

tacrolimus

gastrointestinal (GI) toxicity

tacrolimus

GI toxicity

tacrolimus

hepatotoxicity

tacrolimus

hepatotoxicity

tacrolimus

hepatotoxicity

tacrolimus

hepatotoxicity

tacrolimus

hepatotoxicity

tacrolimus

hepatotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity


Input: Relative efficacy and toxicity of netilmicin and tobramycin in oncology patients. We prospectively compared the efficacy and safety of netilmicin sulfate or tobramycin sulfate in conjunction with piperacillin sodium in 118 immunocompromised patients with presumed severe infections. The two treatment regimens were equally efficacious. Nephrotoxicity occurred in a similar proportion in patients treated with netilmicin and tobramycin (17% vs 11%). Ototoxicity occurred in four (9. 5%) of 42 netilmicin and piperacillin and in 12 (22%) of 54 tobramycin and piperacillin - treated patients. Of those evaluated with posttherapy audiograms, three of four netilmicin and piperacillin - treated patients had auditory thresholds return to baseline compared with one of nine tobramycin and piperacillin - treated patients. The number of greater than or equal to 15 - dB increases in auditory threshold as a proportion of total greater than or equal to 15 - dB changes (increases and decreases) was significantly lower in netilmicin and piperacillin - vs tobramycin and piperacillin - treated patients (18 of 78 vs 67 of 115). We conclude that aminoglycoside - associated ototoxicity was less severe and more often reversible with netilmicin than with tobramycin.

toxicity

infections

Nephrotoxicity

Ototoxicity

ototoxicity

netilmicin

tobramycin

netilmicin sulfate

tobramycin sulfate

piperacillin sodium

netilmicin

tobramycin

netilmicin

piperacillin

tobramycin

piperacillin

netilmicin

piperacillin

tobramycin

piperacillin

netilmicin

piperacillin

tobramycin

piperacillin

aminoglycoside

netilmicin

tobramycin

tobramycin

Ototoxicity

tobramycin

ototoxicity

tobramycin sulfate

Ototoxicity

tobramycin sulfate

ototoxicity

tobramycin

Ototoxicity

tobramycin

ototoxicity

tobramycin

Ototoxicity

tobramycin

ototoxicity

tobramycin

Ototoxicity

tobramycin

ototoxicity

tobramycin

Ototoxicity

tobramycin

ototoxicity

tobramycin

Ototoxicity

tobramycin

ototoxicity

netilmicin

Ototoxicity

netilmicin

ototoxicity

netilmicin sulfate

Ototoxicity

netilmicin sulfate

ototoxicity

netilmicin

Ototoxicity

netilmicin

ototoxicity

netilmicin

Ototoxicity

netilmicin

ototoxicity

netilmicin

Ototoxicity

netilmicin

ototoxicity

netilmicin

Ototoxicity

netilmicin

ototoxicity

netilmicin

Ototoxicity

netilmicin

ototoxicity

netilmicin

Nephrotoxicity

netilmicin sulfate

Nephrotoxicity

netilmicin

Nephrotoxicity

netilmicin

Nephrotoxicity

netilmicin

Nephrotoxicity

netilmicin

Nephrotoxicity

netilmicin

Nephrotoxicity

piperacillin sodium

Ototoxicity

piperacillin sodium

ototoxicity

piperacillin

Ototoxicity

piperacillin

ototoxicity

piperacillin

Ototoxicity

piperacillin

ototoxicity

piperacillin

Ototoxicity

piperacillin

ototoxicity

piperacillin

Ototoxicity

piperacillin

ototoxicity

piperacillin

Ototoxicity

piperacillin

ototoxicity

piperacillin

Ototoxicity

piperacillin

ototoxicity

piperacillin sodium

Nephrotoxicity

piperacillin

Nephrotoxicity

piperacillin

Nephrotoxicity

piperacillin

Nephrotoxicity

piperacillin

Nephrotoxicity

piperacillin

Nephrotoxicity

piperacillin

Nephrotoxicity

tobramycin

Nephrotoxicity

tobramycin sulfate

Nephrotoxicity

tobramycin

Nephrotoxicity

tobramycin

Nephrotoxicity

tobramycin

Nephrotoxicity

tobramycin

Nephrotoxicity

tobramycin

Nephrotoxicity


Input: Effect of prostaglandin synthetase inhibitors on experimentally induced convulsions in rats. To investigate the relationship of prostaglandins (PGs) to seizure induction, the effects of six PG synthetase inhibitors on convulsions induced by flurothyl, picrotoxin, pentetrazol (PTZ), electroshock or bicuculline were evaluated. Ibuprofen, sulindac, mefenamic acid, and low dose meclofenamic acid increased the latency - to - onset in the flurothyl and / or PTZ models; the electroshock, picrotoxin and bicuculline models were not significantly affected by any of the pretreatment agents. These results suggest that PGs are involved in the mechanism (s) underlying fluorthyl - and PTZ - induced convulsions, but not picrotoxin -, electroshock -, or bicuculline - induced convulsions.

prostaglandin

prostaglandins

PGs

flurothyl

picrotoxin

pentetrazol

PTZ

bicuculline

Ibuprofen

sulindac

mefenamic acid

meclofenamic acid

flurothyl

PTZ

picrotoxin

bicuculline

PGs

fluorthyl

PTZ

picrotoxin

bicuculline

convulsions

seizure

convulsions

convulsions

convulsions

flurothyl

convulsions

flurothyl

seizure

flurothyl

convulsions

flurothyl

convulsions

flurothyl

convulsions

flurothyl

convulsions

flurothyl

seizure

flurothyl

convulsions

flurothyl

convulsions

flurothyl

convulsions

fluorthyl

convulsions

fluorthyl

seizure

fluorthyl

convulsions

fluorthyl

convulsions

fluorthyl

convulsions

bicuculline

convulsions

bicuculline

seizure

bicuculline

convulsions

bicuculline

convulsions

bicuculline

convulsions

bicuculline

convulsions

bicuculline

seizure

bicuculline

convulsions

bicuculline

convulsions

bicuculline

convulsions

bicuculline

convulsions

bicuculline

seizure

bicuculline

convulsions

bicuculline

convulsions

bicuculline

convulsions

pentetrazol

convulsions

pentetrazol

seizure

pentetrazol

convulsions

pentetrazol

convulsions

pentetrazol

convulsions

PTZ

convulsions

PTZ

seizure

PTZ

convulsions

PTZ

convulsions

PTZ

convulsions

PTZ

convulsions

PTZ

seizure

PTZ

convulsions

PTZ

convulsions

PTZ

convulsions

PTZ

convulsions

PTZ

seizure

PTZ

convulsions

PTZ

convulsions

PTZ

convulsions

picrotoxin

convulsions

picrotoxin

seizure

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

seizure

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

seizure

picrotoxin

convulsions

picrotoxin

convulsions

picrotoxin

convulsions


Input: Angiotensin - converting enzyme (ACE) inhibitor - associated angioedema of the stomach and small intestine: a case report. This is a case report on a 45 - year old African - American female with newly diagnosed hypertension, who was started on a combination pill of amlodipine / benazapril 10 / 5 mg. The very next day, she presented at the emergency room (ER) with abdominal pain, nausea and vomiting. Physical exam, complete metabolic panel, and hemogram were in the normal range. She was discharged from the ER after a few hours of treatment with fluid and analgesics. However, she returned to the ER the next day with the same complaints. This time the physical exam was significant for a distended abdomen with dullness to percussion. CT scan of the abdomen revealed markedly thickened antrum of the stomach, duodenum and jejunum, along with fluid in the abdominal and pelvic cavity. Angiotensin - converting enzyme inhibitor (ACEI) - induced angioedema was suspected, and anti - hypertensive medications were discontinued. Her symptoms improved within the next 24 hours, and repeat CT after 72 hours revealed marked improvement in stomach and small bowel thickening and resolution of ascites. The recognition of angiotensin - converting enzyme (ACE) and angiotensin receptor blocker (ARB) intestinal angioedema constitutes a challenge to primary care physicians, internists, emergency room personal and surgeons.

angioedema

hypertension

abdominal pain

nausea

vomiting

angioedema

hypertensive

ascites

intestinal angioedema

intestinal

angioedema

amlodipine

benazapril

angiotensin

angiotensin

benazapril

angioedema

benazapril

angioedema

benazapril

intestinal angioedema

benazapril

angioedema

amlodipine

angioedema

amlodipine

angioedema

amlodipine

intestinal angioedema

amlodipine

angioedema

benazapril

intestinal

amlodipine

intestinal


Input: Valproic acid I: time course of lipid peroxidation biomarkers, liver toxicity, and valproic acid metabolite levels in rats. A single dose of valproic acid (VPA), which is a widely used antiepileptic drug, is associated with oxidative stress in rats, as recently demonstrated by elevated levels of 15 - F (2t) - isoprostane (15 - F (2t) - IsoP). To determine whether there was a temporal relationship between VPA - associated oxidative stress and hepatotoxicity, adult male Sprague - Dawley rats were treated ip with VPA (500 mg / kg) or 0. 9% saline (vehicle) once daily for 2, 4, 7, 10, or 14 days. Oxidative stress was assessed by determining plasma and liver levels of 15 - F (2t) - IsoP, lipid hydroperoxides (LPO), and thiobarbituric acid reactive substances (TBARs). Plasma and liver 15 - F (2t) - IsoP were elevated and reached a plateau after day 2 of VPA treatment compared to control. Liver LPO levels were not elevated until day 7 of treatment (1. 8 - fold versus control, p < 0. 05). Liver and plasma TBARs were not increased until 14 days (2 - fold vs. control, p < 0. 05). Liver toxicity was evaluated based on serum levels of alpha - glutathione S - transferase (alpha - GST) and by histology. Serum alpha - GST levels were significantly elevated by day 4, which corresponded to hepatotoxicity as shown by the increasing incidence of inflammation of the liver capsule, necrosis, and steatosis throughout the study. The liver levels of beta - oxidation metabolites of VPA were decreased by day 14, while the levels of 4 - ene - VPA and (E) - 2, 4 - diene - VPA were not elevated throughout the study. Overall, these findings indicate that VPA treatment results in oxidative stress, as measured by levels of 15 - F (2t) - IsoP, which precedes the onset of necrosis, steatosis, and elevated levels of serum alpha - GST.

Valproic acid

valproic acid

valproic acid

VPA

15 - F (2t) - isoprostane

15 - F (2t) - IsoP

VPA

VPA

15 - F (2t) - IsoP

lipid hydroperoxides

LPO

thiobarbituric acid reactive substances

TBARs

15 - F (2t) - IsoP

VPA

LPO

TBARs

glutathione

VPA

4 - ene - VPA

2, 4 - diene - VPA

VPA

15 - F (2t) - IsoP

liver toxicity

hepatotoxicity

Liver toxicity

hepatotoxicity

inflammation

necrosis

steatosis

necrosis

steatosis

thiobarbituric acid reactive substances

liver toxicity

thiobarbituric acid reactive substances

hepatotoxicity

thiobarbituric acid reactive substances

Liver toxicity

thiobarbituric acid reactive substances

hepatotoxicity

TBARs

liver toxicity

TBARs

hepatotoxicity

TBARs

Liver toxicity

TBARs

hepatotoxicity

TBARs

liver toxicity

TBARs

hepatotoxicity

TBARs

Liver toxicity

TBARs

hepatotoxicity

Valproic acid

steatosis

Valproic acid

steatosis

valproic acid

steatosis

valproic acid

steatosis

valproic acid

steatosis

valproic acid

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

VPA

steatosis

Valproic acid

necrosis

Valproic acid

necrosis

valproic acid

necrosis

valproic acid

necrosis

valproic acid

necrosis

valproic acid

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

VPA

necrosis

15 - F (2t) - isoprostane

liver toxicity

15 - F (2t) - isoprostane

hepatotoxicity

15 - F (2t) - isoprostane

Liver toxicity

15 - F (2t) - isoprostane

hepatotoxicity

15 - F (2t) - IsoP

liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

Liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

Liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

Liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

15 - F (2t) - IsoP

Liver toxicity

15 - F (2t) - IsoP

hepatotoxicity

Valproic acid

liver toxicity

Valproic acid

hepatotoxicity

Valproic acid

Liver toxicity

Valproic acid

hepatotoxicity

valproic acid

liver toxicity

valproic acid

hepatotoxicity

valproic acid

Liver toxicity

valproic acid

hepatotoxicity

valproic acid

liver toxicity

valproic acid

hepatotoxicity

valproic acid

Liver toxicity

valproic acid

hepatotoxicity

VPA

liver toxicity

VPA

hepatotoxicity

VPA

Liver toxicity

VPA

hepatotoxicity

VPA

liver toxicity

VPA

hepatotoxicity

VPA

Liver toxicity

VPA

hepatotoxicity

VPA

liver toxicity

VPA

hepatotoxicity

VPA

Liver toxicity

VPA

hepatotoxicity

VPA

liver toxicity

VPA

hepatotoxicity

VPA

Liver toxicity

VPA

hepatotoxicity

VPA

liver toxicity

VPA

hepatotoxicity

VPA

Liver toxicity

VPA

hepatotoxicity

VPA

liver toxicity

VPA

hepatotoxicity

VPA

Liver toxicity

VPA

hepatotoxicity

lipid hydroperoxides

liver toxicity

lipid hydroperoxides

hepatotoxicity

lipid hydroperoxides

Liver toxicity

lipid hydroperoxides

hepatotoxicity

LPO

liver toxicity

LPO

hepatotoxicity

LPO

Liver toxicity

LPO

hepatotoxicity

LPO

liver toxicity

LPO

hepatotoxicity

LPO

Liver toxicity

LPO

hepatotoxicity


Input: Pheochromocytoma unmasked by amisulpride and tiapride. OBJECTIVE: To describe the unmasking of pheochromocytoma in a patient treated with amisulpride and tiapride. CASE SUMMARY: A 42 - year - old white man developed acute hypertension with severe headache and vomiting 2 hours after the first doses of amisulpride 100 mg and tiapride 100 mg. Both drugs were immediately discontinued, and the patient recovered after subsequent nicardipine and verapamil treatment. Abdominal ultrasound showed an adrenal mass, and postoperative histologic examination confirmed the diagnosis of pheochromocytoma. DISCUSSION: Drug - induced symptoms of pheochromocytoma are often associated with the use of substituted benzamide drugs, but the underlying mechanism is unknown. In our case, use of the Naranjo probability scale indicated a possible relationship between the hypertensive crisis and amisulpride and tiapride therapy. CONCLUSIONS: As of March 24, 2005, this is the first reported case of amisulpride - and tiapride - induced hypertensive crisis in a patient with pheochromocytoma. Physicians and other healthcare professionals should be aware of this potential adverse effect of tiapride and amisulpride.

Pheochromocytoma

pheochromocytoma

hypertension

headache

vomiting

pheochromocytoma

pheochromocytoma

hypertensive

hypertensive

pheochromocytoma

amisulpride

tiapride

amisulpride

tiapride

amisulpride

tiapride

nicardipine

verapamil

benzamide

amisulpride

tiapride

amisulpride

tiapride

tiapride

amisulpride

amisulpride

hypertension

amisulpride

hypertensive

amisulpride

hypertensive

amisulpride

hypertension

amisulpride

hypertensive

amisulpride

hypertensive

amisulpride

hypertension

amisulpride

hypertensive

amisulpride

hypertensive

amisulpride

hypertension

amisulpride

hypertensive

amisulpride

hypertensive

amisulpride

hypertension

amisulpride

hypertensive

amisulpride

hypertensive

amisulpride

hypertension

amisulpride

hypertensive

amisulpride

hypertensive

amisulpride

vomiting

amisulpride

vomiting

amisulpride

vomiting

amisulpride

vomiting

amisulpride

vomiting

amisulpride

vomiting

amisulpride

headache

amisulpride

headache

amisulpride

headache

amisulpride

headache

amisulpride

headache

amisulpride

headache

tiapride

vomiting

tiapride

vomiting

tiapride

vomiting

tiapride

vomiting

tiapride

vomiting

tiapride

vomiting

tiapride

headache

tiapride

headache

tiapride

headache

tiapride

headache

tiapride

headache

tiapride

headache

tiapride

hypertension

tiapride

hypertensive

tiapride

hypertensive

tiapride

hypertension

tiapride

hypertensive

tiapride

hypertensive

tiapride

hypertension

tiapride

hypertensive

tiapride

hypertensive

tiapride

hypertension

tiapride

hypertensive

tiapride

hypertensive

tiapride

hypertension

tiapride

hypertensive

tiapride

hypertensive

tiapride

hypertension

tiapride

hypertensive

tiapride

hypertensive


Input: Quantitative drug levels in stimulant psychosis: relationship to symptom severity, catecholamines and hyperkinesia. To examine the relationship between quantitative stimulant drug levels, catecholamines, and psychotic symptoms, nineteen patients in a psychiatric emergency service with a diagnosis of amphetamine - or cocaine - induced psychosis were interviewed, and plasma and urine were collected for quantitative assays of stimulant drug and catecholamine metabolite levels. Methamphetamine or amphetamine levels were related to several psychopathology scores and the global hyperkinesia rating. HVA levels were related to global hyperkinesia but not to psychopathology ratings. Although many other factors such as sensitization may play a role, intensity of stimulant - induced psychotic symptoms and stereotypies appears to be at least in part dose - related.

psychosis

hyperkinesia

psychotic symptoms

psychiatric

psychosis

hyperkinesia

hyperkinesia

psychotic symptoms

stereotypies

catecholamines

catecholamines

amphetamine

cocaine

catecholamine

Methamphetamine

amphetamine

amphetamine

hyperkinesia

amphetamine

hyperkinesia

amphetamine

hyperkinesia

amphetamine

hyperkinesia

amphetamine

hyperkinesia

amphetamine

hyperkinesia

cocaine

hyperkinesia

cocaine

hyperkinesia

cocaine

hyperkinesia

Methamphetamine

psychosis

Methamphetamine

psychotic symptoms

Methamphetamine

psychosis

Methamphetamine

psychotic symptoms

cocaine

psychosis

cocaine

psychotic symptoms

cocaine

psychosis

cocaine

psychotic symptoms

Methamphetamine

hyperkinesia

Methamphetamine

hyperkinesia

Methamphetamine

hyperkinesia

amphetamine

psychosis

amphetamine

psychotic symptoms

amphetamine

psychosis

amphetamine

psychotic symptoms

amphetamine

psychosis

amphetamine

psychotic symptoms

amphetamine

psychosis

amphetamine

psychotic symptoms


Input: Delayed asystolic cardiac arrest after diltiazem overdose; resuscitation with high dose intravenous calcium. A 51 year old man took a mixed overdose including 1. 8 - 3. 6 g of diltiazem, paracetamol, aspirin, isosorbide nitrate, and alcohol. He initially presented to hospital after six hours with mild hypotension and was treated with activated charcoal and intravenous fluids. Eighteen hours after the overdose he had two generalised tonic - clonic seizures. The patient remained unresponsive with junctional bradycardia, unrecordable blood pressure, and then became asystolic. He was resuscitated with high dose (13. 5 g) intravenous calcium and adrenaline (epinephrine). He required inotropic support and temporary pacing over the next 48 hours. This case suggests there is a role for aggressive high dose intravenous calcium therapy in severe diltiazem overdose, particularly with the onset of asystole. It should be considered early in cases of cardiac arrest after diltiazem overdose. The case also highlights the problems with delayed toxicity when whole bowel irrigation is not administered.

asystolic

cardiac arrest

overdose

overdose

hypotension

overdose

tonic - clonic seizures

bradycardia

asystolic

overdose

asystole

cardiac arrest

overdose

toxicity

diltiazem

calcium

diltiazem

paracetamol

aspirin

isosorbide

nitrate

alcohol

calcium

adrenaline

epinephrine

calcium

diltiazem

diltiazem

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

overdose

diltiazem

hypotension

diltiazem

hypotension

diltiazem

hypotension

diltiazem

hypotension

diltiazem

asystolic

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

asystole

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

asystole

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

asystole

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

cardiac arrest

diltiazem

asystolic

diltiazem

asystole

diltiazem

cardiac arrest

diltiazem

bradycardia

diltiazem

bradycardia

diltiazem

bradycardia

diltiazem

bradycardia


Input: Renal papillary necrosis due to naproxen. A 31 - year - old man with rheumatoid arthritis, who had previously been treated with sulindac, fenoprofen calcium, high dose salicylates and gold salts, developed renal papillary necrosis (RPN) 4 months after institution of naproxen therapy. No other factor predisposing to RPN could be discovered. Sulindac was substituted for naproxen and no further adverse renal effects occurred over the next 12 months. We review previous reports linking RPN to antiinflammatory drug use and discuss possible advantages of sulindac in patients who have experienced renal toxicity from other antiinflammatory agents.

Renal papillary necrosis

rheumatoid arthritis

renal papillary necrosis

RPN

RPN

RPN

renal toxicity

naproxen

sulindac

fenoprofen calcium

salicylates

gold

naproxen

Sulindac

naproxen

sulindac

naproxen

Renal papillary necrosis

naproxen

renal papillary necrosis

naproxen

RPN

naproxen

RPN

naproxen

RPN

naproxen

Renal papillary necrosis

naproxen

renal papillary necrosis

naproxen

RPN

naproxen

RPN

naproxen

RPN

naproxen

Renal papillary necrosis

naproxen

renal papillary necrosis

naproxen

RPN

naproxen

RPN

naproxen

RPN


Input: Adverse interaction between beta - adrenergic blocking drugs and verapamil - - report of three cases. Three patients with ischaemic heart disease developed profound cardiac failure, hypotension and bradycardia during combined therapy with verapamil and beta - adrenergic blocking drugs. This clinical picture resolved completely with cessation of the combined therapy. Baseline left ventricular function, assessed by cardiac catheterisation or nuclear angiography, was normal in two patients and only mildly reduced in the other. Simultaneously administration of beta - adrenergic blocking drugs and verapamil may result in profound adverse interactions and should only be administered with great caution.

beta - adrenergic blocking drugs

verapamil

verapamil

beta - adrenergic blocking drugs

beta - adrenergic blocking drugs

verapamil

ischaemic heart disease

cardiac failure

hypotension

bradycardia

verapamil

hypotension

verapamil

hypotension

verapamil

hypotension

beta - adrenergic blocking drugs

cardiac failure

beta - adrenergic blocking drugs

cardiac failure

beta - adrenergic blocking drugs

cardiac failure

verapamil

bradycardia

verapamil

bradycardia

verapamil

bradycardia

verapamil

cardiac failure

verapamil

cardiac failure

verapamil

cardiac failure

beta - adrenergic blocking drugs

hypotension

beta - adrenergic blocking drugs

hypotension

beta - adrenergic blocking drugs

hypotension

beta - adrenergic blocking drugs

bradycardia

beta - adrenergic blocking drugs

bradycardia

beta - adrenergic blocking drugs

bradycardia


Input: Adverse reactions to bendrofluazide and propranolol for the treatment of mild hypertension. Report of Medical Research Council Working Party on Mild to Moderate Hypertension. Participants in the Medical Research Council treatment trial for mild hypertension are randomly allocated to one of four treatment groups: bendrofluazide, propranolol, or a placebo for either of these drugs. The trial is single - blind. 23 582 patient - years of observation have been completed so far, 10 684 on active drugs and 12 898 on placebos. The results show an association between bendrofluazide treatment and impotence, and impotence also occurred more frequently in patients taking propranolol than in those taking placebos. Other adverse reactions significantly linked with active drugs include impaired glucose tolerance in men and women and gout in men, associated with bendrofluazide treatment, and Raynaud' s phenomenon and dyspnoea in men and women taking propranolol. No corneal disease is known to have occurred in the propranolol group. Mean serum potassium level fell, and urea and uric acid levels rose, in men and women taking bendrofluazide. In the propranolol group, serum potassium and uric acid levels rose in both sexes, but the urea level rose significantly in women only.

bendrofluazide

propranolol

bendrofluazide

propranolol

bendrofluazide

propranolol

bendrofluazide

propranolol

propranolol

potassium

urea

uric acid

bendrofluazide

propranolol

potassium

uric acid

urea

hypertension

Hypertension

hypertension

impotence

impotence

impaired glucose tolerance

gout

Raynaud' s phenomenon

dyspnoea

corneal disease

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

bendrofluazide

impotence

propranolol

Raynaud' s phenomenon

propranolol

Raynaud' s phenomenon

propranolol

Raynaud' s phenomenon

propranolol

Raynaud' s phenomenon

propranolol

Raynaud' s phenomenon

propranolol

Raynaud' s phenomenon

bendrofluazide

impaired glucose tolerance

bendrofluazide

impaired glucose tolerance

bendrofluazide

impaired glucose tolerance

bendrofluazide

impaired glucose tolerance

bendrofluazide

impaired glucose tolerance

bendrofluazide

gout

bendrofluazide

gout

bendrofluazide

gout

bendrofluazide

gout

bendrofluazide

gout

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

impotence

propranolol

dyspnoea

propranolol

dyspnoea

propranolol

dyspnoea

propranolol

dyspnoea

propranolol

dyspnoea

propranolol

dyspnoea


Input: Dexmedetomidine and cardiac protection for non - cardiac surgery: a meta - analysis of randomised controlled trials. We conducted a systematic review of the effects of dexmedetomidine on cardiac outcomes following non - cardiac surgery. We included prospective, randomised peri - operative studies of dexmedetomidine that reported mortality, cardiac morbidity or adverse drug events. A PubMed Central and EMBASE search was conducted up to July 2007. The reference lists of identified papers were examined for further trials. Of 425 studies identified, 20 were included in the meta - analysis (840 patients). Dexmedetomidine was associated with a trend towards improved cardiac outcomes; all - cause mortality (OR 0. 27, 95% CI 0. 01 - 7. 13, p = 0. 44), non - fatal myocardial infarction (OR 0. 26, 95% CI 0. 04 - 1. 60, p = 0. 14), and myocardial ischaemia (OR 0. 65, 95% CI 0. 26 - 1. 63, p = 0. 36). Peri - operative hypotension (26%, OR 3. 80, 95% CI 1. 91 - 7. 54, p = 0. 0001) and bradycardia (17%, OR 5. 45, 95% CI 2. 98 - 9. 95, p < 0. 00001) were significantly increased. An anticholinergic did not reduce the incidence of bradycardia (p = 0. 43). A randomised placebo - controlled trial of dexmedetomidine is warranted.

Dexmedetomidine

dexmedetomidine

dexmedetomidine

Dexmedetomidine

dexmedetomidine

myocardial infarction

myocardial ischaemia

hypotension

bradycardia

bradycardia

Dexmedetomidine

bradycardia

Dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

Dexmedetomidine

bradycardia

Dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

dexmedetomidine

bradycardia

Dexmedetomidine

hypotension

dexmedetomidine

hypotension

dexmedetomidine

hypotension

Dexmedetomidine

hypotension

dexmedetomidine

hypotension


Input: Differential diagnosis of high serum creatine kinase levels in systemic lupus erythematosus. We report the clinical and bioptic findings for a 57 - year - old woman with severe chloroquine - induced myopathy. Since 1989, she had been suffering from systemic lupus erythematosus (SLE) with renal involvement and undergone periods of treatment with azathioprine and cyclophosphamide. Additional therapy with chloroquine (CQ) was started because of arthralgia. At the same time, slightly increased creatine kinase (CK) levels were noted. Myositis was suspected, and the patient was treated with steroids. The CK increase persisted, however, and she developed progressive muscular weakness and muscular atrophy. Routine controls revealed markedly elevated CK levels of 1, 700 U / l. The neurological and electrophysiological findings were not typical of myositis. Thus, muscle biopsy of the deltoid muscle was performed in order to exclude polymyositis or toxic myopathy. As it revealed chloroquine - induced myopathy, medication was stopped. Discriminating between primary SLE - induced affection of the musculoskeletal system and drug - induced side effects is important for appropriate treatment of SLE patients.

creatine

chloroquine

azathioprine

cyclophosphamide

chloroquine

CQ

creatine

steroids

chloroquine

systemic lupus erythematosus

myopathy

systemic lupus erythematosus

SLE

renal involvement

arthralgia

Myositis

muscular weakness

muscular atrophy

myositis

polymyositis

myopathy

myopathy

SLE

affection of the musculoskeletal system

SLE

chloroquine

muscular weakness

chloroquine

muscular weakness

CQ

muscular weakness

chloroquine

muscular weakness

chloroquine

muscular atrophy

chloroquine

muscular atrophy

CQ

muscular atrophy

chloroquine

muscular atrophy


Input: Intravenous ribavirin treatment for severe adenovirus disease in immunocompromised children. BACKGROUND: Adenovirus is an important cause of morbidity and mortality in the immunocompromised host. The incidence of severe adenovirus disease in pediatrics is increasing in association with growing numbers of immunocompromised children, where case fatality rates as high as 50% to 80% have been reported. There are no approved antiviral agents with proven efficacy for the treatment of severe adenovirus disease, nor are there any prospective randomized, controlled trials of potentially useful anti - adenovirus therapies. Apparent clinical success in the treatment of severe adenovirus disease is limited to a few case reports and small series. Experience is greatest with intravenous ribavirin and cidofovir. Ribavirin, a guanosine analogue, has broad antiviral activity against both RNA and DNA viruses, including documented activity against adenovirus in vitro. Ribavirin is licensed in aerosol form for the treatment of respiratory syncytial virus infection, and orally in combination with interferon to treat hepatitis C. Intravenous ribavirin is the treatment of choice for infection with hemorrhagic fever viruses. The most common adverse effect of intravenous ribavirin is reversible mild anemia. The use of cidofovir in severe adenovirus infection has been limited by adverse effects, the most significant of which is nephrotoxicity. OBJECTIVE: We report our experience with intravenous ribavirin therapy for severe adenovirus disease in a series of immunocompromised children and review the literature. DESIGN / METHODS: We retrospectively reviewed the medical records of 5 children treated with intravenous ribavirin for documented severe adenovirus disease. Two patients developed adenovirus hemorrhagic cystitis after cardiac and bone marrow transplants, respectively. The bone marrow transplant patient also received intravenous cidofovir for progressive disseminated disease. An additional 3 children developed adenovirus pneumonia; 2 were neonates, 1 of whom had partial DiGeorge syndrome. The remaining infant had recently undergone a cardiac transplant. Intravenous ribavirin was administered on a compassionate - use protocol. RESULTS: Complete clinical recovery followed later by viral clearance was observed in 2 children: the cardiac transplant recipient with adenovirus hemorrhagic cystitis and the immunocompetent neonate with adenovirus pneumonia. The remaining 3 children died of adenovirus disease. Intravenous ribavirin therapy was well tolerated. Use of cidofovir in 1 child was associated with progressive renal failure and neutropenia. DISCUSSION: Our series of patients is representative of the spectrum of immunocompromised children at greatest risk for severe adenovirus disease, namely solid - organ and bone marrow transplant recipients, neonates, and children with immunodeficiency. Although intravenous ribavirin was not effective for all children with severe adenovirus disease in this series or in the literature, therapy is unlikely to be of benefit if begun late in the course of the infection. Early identification, eg by polymerase chain reaction of those patients at risk of disseminated adenovirus disease may permit earlier antiviral treatment and better evaluation of therapeutic response. CONCLUSIONS: Two of 5 children with severe adenovirus disease treated with intravenous ribavirin recovered. The availability of newer rapid diagnostic techniques, such as polymerase chain reaction, may make earlier, more effective treatment of adenovirus infection possible. Given the seriousness and increasing prevalence of adenovirus disease in certain hosts, especially children, a large, multicenter clinical trial of potentially useful anti - adenoviral therapies, such as intravenous ribavirin, is clearly required to demonstrate the most effective and least toxic therapy.

ribavirin

ribavirin

cidofovir

Ribavirin

guanosine

Ribavirin

ribavirin

ribavirin

cidofovir

ribavirin

ribavirin

cidofovir

ribavirin

ribavirin

cidofovir

ribavirin

ribavirin

ribavirin

adenovirus disease

adenovirus disease

adenovirus disease

adenovirus disease

respiratory syncytial virus infection

hepatitis C

infection with hemorrhagic fever viruses

anemia

adenovirus infection

nephrotoxicity

adenovirus disease

adenovirus disease

hemorrhagic cystitis

hemorrhagic

cystitis

adenovirus pneumonia

adenovirus

pneumonia

DiGeorge syndrome

hemorrhagic cystitis

hemorrhagic

cystitis

adenovirus pneumonia

adenovirus

pneumonia

adenovirus disease

progressive renal failure

neutropenia

adenovirus disease

immunodeficiency

adenovirus disease

infection

adenovirus disease

adenovirus disease

adenovirus infection

adenovirus disease

cidofovir

progressive renal failure

cidofovir

progressive renal failure

cidofovir

progressive renal failure

cidofovir

progressive renal failure

cidofovir

neutropenia

cidofovir

neutropenia

cidofovir

neutropenia

cidofovir

neutropenia


Input: Hepatotoxicity of amiodarone. Amiodarone has proved very effective in the treatment of otherwise resistant cardiac tachyarrhythmias. The use of amiodarone has, however, been limited due to its serious side - effects. A patient with cholestatic hepatitis due to amiodarone treatment is presented below and a review of the hepatotoxicity of amiodarone is given. It is concluded that solid evidence exists of hepatic injury due to amiodarone treatment, including steatosis, alterations resembling alcoholic hepatitis, cholestatic hepatitis and micronodular cirrhosis of the liver. Patients receiving amiodarone should be regularly screened with respect to hepatic enzyme levels. Therapy should be discontinued on the suspicion of cholestatic injury or hepatomegaly.

Hepatotoxicity

tachyarrhythmias

cholestatic hepatitis

cholestatic

hepatitis

hepatotoxicity

hepatic injury

steatosis

alcoholic hepatitis

cholestatic hepatitis

cholestatic

hepatitis

cirrhosis of the liver

cholestatic injury

hepatomegaly

amiodarone

Amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic injury

Amiodarone

cholestatic hepatitis

Amiodarone

cholestatic

Amiodarone

cholestatic hepatitis

Amiodarone

cholestatic

Amiodarone

cholestatic injury

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic injury

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic injury

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic injury

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic injury

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic hepatitis

amiodarone

cholestatic

amiodarone

cholestatic injury

amiodarone

Hepatotoxicity

amiodarone

hepatitis

amiodarone

hepatotoxicity

amiodarone

hepatic injury

amiodarone

hepatitis

Amiodarone

Hepatotoxicity

Amiodarone

hepatitis

Amiodarone

hepatotoxicity

Amiodarone

hepatic injury

Amiodarone

hepatitis

amiodarone

Hepatotoxicity

amiodarone

hepatitis

amiodarone

hepatotoxicity

amiodarone

hepatic injury

amiodarone

hepatitis

amiodarone

Hepatotoxicity

amiodarone

hepatitis

amiodarone

hepatotoxicity

amiodarone

hepatic injury

amiodarone

hepatitis

amiodarone

Hepatotoxicity

amiodarone

hepatitis

amiodarone

hepatotoxicity

amiodarone

hepatic injury

amiodarone

hepatitis

amiodarone

Hepatotoxicity

amiodarone

hepatitis

amiodarone

hepatotoxicity

amiodarone

hepatic injury

amiodarone

hepatitis

amiodarone

Hepatotoxicity

amiodarone

hepatitis

amiodarone

hepatotoxicity

amiodarone

hepatic injury

amiodarone

hepatitis

amiodarone

cirrhosis of the liver

Amiodarone

cirrhosis of the liver

amiodarone

cirrhosis of the liver

amiodarone

cirrhosis of the liver

amiodarone

cirrhosis of the liver

amiodarone

cirrhosis of the liver

amiodarone

cirrhosis of the liver

amiodarone

steatosis

Amiodarone

steatosis

amiodarone

steatosis

amiodarone

steatosis

amiodarone

steatosis

amiodarone

steatosis

amiodarone

steatosis


Input: Catalepsy induced by combinations of ketamine and morphine: potentiation, antagonism, tolerance and cross - tolerance in the rat. Previous studies demonstrated that both ketamine and morphine induced analgesia and catalepsy in the rat. Pre - treatment with ketamine produced cross - tolerance to morphine, whereas pretreatment with morphine did not induce cross - tolerance to ketamine but rather augmented the cataleptic response; this augmentation was attributed to residual morphine in the brain. The present studies explored the duration of the loss of righting reflex induced by sub - effective doses of ketamine and morphine, administered simultaneously. There was mutual potentiation between sub - effective doses of ketamine and morphine, but sub - effective doses of ketamine partly antagonized fully - effective doses of morphine. Latency to the loss of righting reflex, rigidity and behavior on recovery, reflected the relative predominance of ketamine or morphine in each combination. Naloxone inhibited the induced cataleptic effects. The degree and time course of development of tolerance to daily administration of sub - effective dose combinations of ketamine and morphine were similar. Rats, tolerant to ketamine - dominant combinations, were cross - tolerant to both drugs, while those tolerant to morphine - dominant combinations were cross - tolerant to morphine but showed either no cross - tolerance or an augmented response to ketamine. While the mutual potentiation, antagonism and tolerance suggest common mechanisms for the induced catalepsy, differences in latency, rigidity and behavior, asymmetry of cross - tolerance and a widely - different ID50 for naloxone would argue against an action at a single opioid site.

Catalepsy

analgesia

catalepsy

cataleptic

rigidity

cataleptic

catalepsy

rigidity

ketamine

morphine

ketamine

morphine

ketamine

morphine

morphine

ketamine

morphine

ketamine

morphine

ketamine

morphine

ketamine

morphine

ketamine

morphine

Naloxone

ketamine

morphine

ketamine

morphine

morphine

ketamine

naloxone

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

morphine

Catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

cataleptic

morphine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy

ketamine

Catalepsy

ketamine

catalepsy

ketamine

cataleptic

ketamine

cataleptic

ketamine

catalepsy


Input: Acute renal failure in patients with AIDS on tenofovir while receiving prolonged vancomycin course for osteomyelitis. Renal failure developed after a prolonged course of vancomycin therapy in 2 patients who were receiving tenofovir disoproxil fumarate as part of an antiretroviral regimen. Tenofovir has been implicated in the development of Fanconi syndrome and renal insufficiency because of its effects on the proximal renal tubule. Vancomycin nephrotoxicity is infrequent but may result from coadministration with a nephrotoxic agent. Clinicians should be aware that tenofovir may raise the risk of renal failure during prolonged administration of vancomycin.

Acute renal failure

AIDS

osteomyelitis

Renal failure

Fanconi syndrome

renal insufficiency

nephrotoxicity

nephrotoxic

renal failure

tenofovir

vancomycin

vancomycin

tenofovir disoproxil fumarate

Tenofovir

Vancomycin

tenofovir

vancomycin

vancomycin

Acute renal failure

vancomycin

Acute renal failure

Vancomycin

Acute renal failure

vancomycin

Acute renal failure

tenofovir disoproxil fumarate

Acute renal failure


Input: Delayed leukoencephalopathy with stroke - like presentation in chemotherapy recipients. BACKGROUND: A transient leukoencephalopathy mimicking cerebrovascular accident has been described as a complication of chemotherapy, most commonly in recipients of intrathecal methotrexate for childhood leukaemia. Recently published neuroimaging data suggest a common pathophysiology associated with a variety of chemotherapy agents and modes of administration. METHODS: We reviewed the medical literature for single reports and case series of patients presenting with stroke - like episodes while receiving systemic or intrathecal chemotherapy. We only included studies providing detailed neuroimaging data. Patients with cerebrovascular accidents were excluded. RESULTS: We identified 27 reports of toxic leukoencephalopathy in patients treated with methotrexate (intrathecal, systemic), 5 - fluorouracil and its derivative carmofur, and capecitabine. Diffusion weighted imaging (DWI) of all patients revealed well demarcated hyperintense lesions within the subcortical white matter of the cerebral hemispheres and the corpus callosum, corresponding to areas of decreased proton diffusion on apparent diffusion coefficient (ADC) maps (available in 21 / 27 patients). Lesions exceeded the confines of adjacent vascular territories. Complete resolution of symptoms within 1 - 4 days was accompanied by normalisation of ADC abnormalities. However, fluid attenuated inversion recovery (FLAIR) sequences frequently revealed persistent white matter abnormalities. CONCLUSIONS: Several pathophysiological models of delayed leukoencephalopathy after exposure to intrathecal or systemic chemotherapy have been proposed. DWI findings in this cohort are indicative of cytotoxic oedema within cerebral white matter and lend support to an at least partially reversible metabolic derangement as the basis for this syndrome.

leukoencephalopathy

stroke

leukoencephalopathy

cerebrovascular accident

leukaemia

stroke

cerebrovascular accidents

leukoencephalopathy

lesions within the subcortical white matter

white matter abnormalities

leukoencephalopathy

cytotoxic oedema within cerebral white matter

methotrexate

methotrexate

5 - fluorouracil

carmofur

capecitabine

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

lesions within the subcortical white matter

methotrexate

white matter abnormalities

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

lesions within the subcortical white matter

methotrexate

white matter abnormalities

methotrexate

leukoencephalopathy

carmofur

leukoencephalopathy

carmofur

leukoencephalopathy

carmofur

leukoencephalopathy

carmofur

lesions within the subcortical white matter

carmofur

white matter abnormalities

carmofur

leukoencephalopathy

5 - fluorouracil

leukoencephalopathy

5 - fluorouracil

leukoencephalopathy

5 - fluorouracil

leukoencephalopathy

5 - fluorouracil

lesions within the subcortical white matter

5 - fluorouracil

white matter abnormalities

5 - fluorouracil

leukoencephalopathy

capecitabine

leukoencephalopathy

capecitabine

leukoencephalopathy

capecitabine

leukoencephalopathy

capecitabine

lesions within the subcortical white matter

capecitabine

white matter abnormalities

capecitabine

leukoencephalopathy


Input: Down - regulation of norepinephrine transporter function induced by chronic administration of desipramine linking to the alteration of sensitivity of local - anesthetics - induced convulsions and the counteraction by co - administration with local anesthetics. Alterations of norepinephrine transporter (NET) function by chronic inhibition of NET in relation to sensitization to seizures induce by cocaine and local anesthetics were studied in mice. Daily administration of desipramine, an inhibitor of the NET, for 5 days decreased [(3) H] norepinephrine uptake in the P2 fractions of hippocampus but not cortex, striatum or amygdalae. Co - administration of lidocaine, bupivacaine or tricaine with desipramine reversed this effect. Daily treatment of cocaine increased [(3) H] norepinephrine uptake into the hippocampus. Daily administration of desipramine increased the incidence of appearance of lidocaine - induced convulsions and decreased that of cocaine - induced convulsions. Co - administration of lidocaine with desipramine reversed the changes of convulsive activity of lidocaine and cocaine induced by repeated administration of desipramine. These results suggest that down - regulation of hippocampal NET induced by chronic administration of desipramine may be relevant to desipramine - induced sensitization of lidocaine convulsions. Inhibition of Na (+) channels by local anesthetics may regulate desipramine - induced down - regulation of NET function. Repeated administration of cocaine induces up - regulation of hippocampal NET function. Desipramine - induced sensitization of lidocaine seizures may have a mechanism distinct from kindling resulting from repeated administration of cocaine.

norepinephrine

desipramine

norepinephrine

cocaine

desipramine

norepinephrine

lidocaine

bupivacaine

tricaine

desipramine

cocaine

norepinephrine

desipramine

lidocaine

cocaine

lidocaine

desipramine

lidocaine

cocaine

desipramine

desipramine

desipramine

lidocaine

desipramine

cocaine

Desipramine

lidocaine

cocaine

convulsions

seizures

convulsions

convulsions

convulsive

convulsions

seizures

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

convulsions

cocaine

convulsive

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

convulsions

cocaine

convulsive

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

convulsions

cocaine

convulsive

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

convulsions

cocaine

convulsive

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

convulsions

cocaine

convulsive

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

seizures

cocaine

convulsions

cocaine

convulsions

cocaine

convulsive

cocaine

convulsions

cocaine

seizures

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsive

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsive

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsive

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsive

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsive

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

seizures

lidocaine

convulsions

lidocaine

convulsions

lidocaine

convulsive

lidocaine

convulsions

lidocaine

seizures


Input: Definition and management of anemia in patients infected with hepatitis C virus. Chronic infection with hepatitis C virus (HCV) can progress to cirrhosis, hepatocellular carcinoma, and end - stage liver disease. The current best treatment for HCV infection is combination therapy with pegylated interferon and ribavirin. Although this regimen produces sustained virologic responses (SVRs) in approximately 50% of patients, it can be associated with a potentially dose - limiting hemolytic anemia. Hemoglobin concentrations decrease mainly as a result of ribavirin - induced hemolysis, and this anemia can be problematic in patients with HCV infection, especially those who have comorbid renal or cardiovascular disorders. In general, anemia can increase the risk of morbidity and mortality, and may have negative effects on cerebral function and quality of life. Although ribavirin - associated anemia can be reversed by dose reduction or discontinuation, this approach compromises outcomes by significantly decreasing SVR rates. Recombinant human erythropoietin has been used to manage ribavirin - associated anemia but has other potential disadvantages. Viramidine, a liver - targeting prodrug of ribavirin, has the potential to maintain the virologic efficacy of ribavirin while decreasing the risk of hemolytic anemia in patients with chronic hepatitis C.

anemia

infected with hepatitis C virus

Chronic infection with hepatitis C virus

cirrhosis

hepatocellular carcinoma

end - stage liver disease

HCV infection

hemolytic anemia

hemolysis

anemia

HCV infection

renal or cardiovascular disorders

renal or cardiovascular disorders

cardiovascular disorders

anemia

anemia

anemia

hemolytic anemia

chronic hepatitis C

interferon

ribavirin

ribavirin

ribavirin

ribavirin

Viramidine

ribavirin

ribavirin

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

interferon

hemolytic anemia

interferon

hemolytic anemia


Input: Calcium carbonate toxicity: the updated milk - alkali syndrome; report of 3 cases and review of the literature. OBJECTIVE: To describe 3 patients with calcium carbonate - induced hypercalcemia and gain insights into the cause and management of the milk - alkali syndrome. METHODS: We report the clinical and laboratory data in 3 patients who presented with severe hypercalcemia (corrected serum calcium > or = 14 mg / dL) and review the pertinent literature on milk - alkali syndrome. RESULTS: The 3 patients had acute renal insufficiency, relative metabolic alkalosis, and low parathyroid hormone (PTH), PTH - related peptide, and 1, 25 - dihydroxyvitamin D concentrations. No malignant lesion was found. Treatment included aggressive hydration and varied amounts of furosemide. The 2 patients with the higher serum calcium concentrations received pamidronate intravenously (60 and 30 mg, respectively), which caused severe hypocalcemia. Of the 3 patients, 2 were ingesting acceptable doses of elemental calcium (1 g and 2 g daily, respectively) in the form of calcium carbonate. In addition to our highlighted cases, we review the history, classification, pathophysiologic features, and treatment of milk - alkali syndrome and summarize the cases reported from early 1995 to November 2003. CONCLUSION: Milk - alkali syndrome may be a common cause of unexplained hypercalcemia and can be precipitated by small amounts of orally ingested calcium carbonate in susceptible persons. Treatment with hydration, furosemide, and discontinuation of the calcium and vitamin D source is adequate. Pamidronate treatment is associated with considerable risk for hypocalcemia, even in cases of initially severe hypercalcemia.

Calcium carbonate

calcium carbonate

calcium

1, 25 - dihydroxyvitamin D

furosemide

calcium

pamidronate

calcium

calcium carbonate

calcium carbonate

furosemide

calcium

vitamin D

Pamidronate

toxicity

milk - alkali syndrome

hypercalcemia

milk - alkali syndrome

hypercalcemia

milk - alkali syndrome

acute renal insufficiency

metabolic alkalosis

hypocalcemia

milk - alkali syndrome

Milk - alkali syndrome

hypercalcemia

hypocalcemia

hypercalcemia

pamidronate

hypocalcemia

pamidronate

hypocalcemia

Pamidronate

hypocalcemia

Pamidronate

hypocalcemia

Calcium carbonate

milk - alkali syndrome

Calcium carbonate

hypercalcemia

Calcium carbonate

milk - alkali syndrome

Calcium carbonate

hypercalcemia

Calcium carbonate

milk - alkali syndrome

Calcium carbonate

milk - alkali syndrome

Calcium carbonate

Milk - alkali syndrome

Calcium carbonate

hypercalcemia

Calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

milk - alkali syndrome

calcium carbonate

Milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

milk - alkali syndrome

calcium carbonate

Milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

milk - alkali syndrome

calcium carbonate

milk - alkali syndrome

calcium carbonate

Milk - alkali syndrome

calcium carbonate

hypercalcemia

calcium carbonate

hypercalcemia


Input: Management strategies for ribavirin - induced hemolytic anemia in the treatment of hepatitis C: clinical and economic implications. OBJECTIVES: Recently published studies have demonstrated increased efficacy and cost - effectiveness of combination therapy with interferon and alpha - 2b / ribavirin compared with interferon - alpha monotherapy in the treatment of chronic hepatitis C (CHC). Combination therapy is associated with a clinically important adverse effect: ribavirin - induced hemolytic anemia (RIHA). The objective of this study was to evaluate the direct health - care costs and management of RIHA during treatment of CHC in a clinical trial setting. METHODS: A systematic literature review was conducted to synthesize information on the incidence and management of RIHA. Decision - analytic techniques were used to estimate the cost of treating RIHA. Uncertainty was evaluated using sensitivity analyses. RESULTS: RIHA, defined as a reduction in hemoglobin to less than 100 g / L, occurs in approximately 7% to 9% of patients treated with combination therapy. The standard of care for management of RIHA is reduction or discontinuation of the ribavirin dosage. We estimated the direct cost of treating clinically significant RIHA to be 170 per patient receiving combination therapy per 48 - week treatment course (range 68 - 692). The results of the one - way sensitivity analyses ranged from 57 to 317. In comparison, the cost of 48 weeks of combination therapy is 16, 459. CONCLUSIONS: The direct cost of treating clinically significant RIHA is 1% (170 / 16, 459) of drug treatment costs. Questions remain about the optimal dose of ribavirin and the incidence of RIHA in a real - world population. Despite these uncertainties, this initial evaluation of the direct cost of treating RIHA provides an estimate of the cost and management implications of this clinically important adverse effect.

ribavirin

ribavirin

interferon - alpha

ribavirin

ribavirin

ribavirin

hemolytic anemia

hepatitis C

chronic hepatitis C

CHC

hemolytic anemia

RIHA

RIHA

CHC

RIHA

RIHA

RIHA

RIHA

RIHA

RIHA

RIHA

RIHA

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

hemolytic anemia

ribavirin

hemolytic anemia

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

ribavirin

RIHA

interferon - alpha

hemolytic anemia

interferon - alpha

hemolytic anemia

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA

interferon - alpha

RIHA


Input: Effects of amine pretreatment on ketamine catatonia in pinealectomized or hypophysectomized animals. The present studies were designed to clarify the role of catecholamines and pineal idolamines on ketamine - induced catatonia in the intact, pinealectomized or hypophysectomized chick and rat. In the pinealectomized chick, pretreatment with dopamine increased the duration of catatonia (DOC) after ketamine, but pretreatment with norepinephrine did not. The pineal indolamines exhibited mixed actions. Serotonin and N - acetyl serotonin which augmented ketamine DOC, did not do so in the absence of the pineal gland, whereas melatonin potentiated the ketamine DOC in both the intact and pinealectomized chick. Ketamine was more potent in the hypophysectomized chick and the circadian rhythm noted in the intact chick was absent; furthermore, melatonin did not augment the ketamine DOC whereas dopamine continued to do so. This study did not demonstrate a species difference regarding the role of the amines on the pineal in spite of the immature blood - brain barrier in the young chick and the intact barrier in the rat. In addition, these data indicate a direct role of the pituitary in the augmentation of ketamine DOC induced by melatonin. Furthermore, dopamine appeared to act on systems more closely involved with the induction of ketamine catatonia rather than directly on the pituitary.

amine

ketamine

catecholamines

ketamine

dopamine

ketamine

norepinephrine

Serotonin

N - acetyl serotonin

ketamine

melatonin

ketamine

Ketamine

melatonin

ketamine

dopamine

amines

ketamine

melatonin

dopamine

ketamine

catatonia

catatonia

catatonia

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

melatonin

catatonia

Serotonin

catatonia

Serotonin

catatonia

Serotonin

catatonia

Serotonin

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

dopamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

Ketamine

catatonia

Ketamine

catatonia

Ketamine

catatonia

Ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia

ketamine

catatonia


Input: Multicenter, double - blind, multiple - dose, parallel - groups efficacy and safety trial of azelastine, chlorpheniramine, and placebo in the treatment of spring allergic rhinitis. Azelastine, a novel antiallergic medication, was compared with chlorpheniramine maleate and placebo for efficacy and safety in the treatment of spring allergic rhinitis in a multicenter, double - blind, multiple - dose, parallel - groups study. One hundred fifty - five subjects participated. Subjects ranged in age from 18 to 60 years of age and had at least a 2 - year history of spring allergic rhinitis, confirmed by positive skin test to spring aeroallergens. Medications were given four times daily; the azelastine groups received 0. 5, 1. 0, or 2. 0 mg in the morning and evening with placebo in the early and late afternoon; the chlorpheniramine group received 4. 0 mg four times daily. Daily subject symptom cards were completed during a screening period to assess pretreatment symptoms and during a 4 - week treatment period while subjects received study medications. Individual symptoms, total symptoms, and major symptoms were compared to determine efficacy of medication. Elicited, volunteered, and observed adverse experiences were recorded for each subject and compared among groups. Vital signs, body weights, serum chemistry values, complete blood cell counts, urine studies, and electrocardiograms were obtained for each subject and compared among groups. Symptoms relief in the group receiving the highest concentration of azelastine (2. 0 mg twice daily) was statistically greater than in the placebo group during all weeks of the study. Lower doses of azelastine were statistically more effective than placebo only during portions of the first 3 weeks of the study. In contrast, although the chlorpheniramine group did have fewer symptoms than the placebo group during the study, the difference never reached statistical significance during any week of the study. There were no serious side effects in any of the treatment groups. Drowsiness and altered taste perception were increased significantly over placebo only in the high - dose azelastine group. Azelastine appears to be a safe, efficacious medication for seasonal allergic rhinitis.

azelastine

chlorpheniramine

Azelastine

chlorpheniramine maleate

azelastine

chlorpheniramine

azelastine

azelastine

chlorpheniramine

azelastine

Azelastine

spring allergic rhinitis

spring allergic rhinitis

spring allergic rhinitis

Drowsiness

altered taste perception

seasonal allergic rhinitis

azelastine

Drowsiness

Azelastine

Drowsiness

azelastine

Drowsiness

azelastine

Drowsiness

azelastine

Drowsiness

azelastine

Drowsiness

Azelastine

Drowsiness

azelastine

altered taste perception

Azelastine

altered taste perception

azelastine

altered taste perception

azelastine

altered taste perception

azelastine

altered taste perception

azelastine

altered taste perception

Azelastine

altered taste perception


Input: Obsolete but dangerous antacid preparations. One case of acute hypercalcaemia and two of recurrent nephrolithiasis are reported in patients who had regularly consumed large amounts of calcium carbon - ate - sodium bicarbonate powders for more than 20 years. The powders had been obtained from pharmacists unknown to the patients' medical practitioners. It is suggested that these preparations were responsible for the patient' s problems, and that such powders should no longer be freely obtainable.

hypercalcaemia

nephrolithiasis

calcium carbon - ate

sodium bicarbonate

calcium carbon - ate

hypercalcaemia

sodium bicarbonate

nephrolithiasis

sodium bicarbonate

hypercalcaemia

calcium carbon - ate

nephrolithiasis


Input: Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids. The long - term use of nondepolarizing neuromuscular blocking agents (ND - NMBA) has recently been implicated as a cause of prolonged muscle weakness, although the site of the lesion and the predisposing factors have been unclear. We report 3 patients (age 37 - 52 years) with acute respiratory insufficiency who developed prolonged weakness following the discontinuation of ND - NMBAs. Two patients also received intravenous corticosteroids. Renal function was normal but hepatic function was impaired in all patients, and all had acidosis. Electrophysiologic studies revealed low amplitude compound motor action potentials, normal sensory studies, and fibrillations. Repetitive stimulation at 2 Hz showed a decremental response in 2 patients. The serum vecuronium level measured in 1 patient 14 days after the drug had been discontinued was 172 ng / mL. A muscle biopsy in this patient showed loss of thick, myosin filaments. The weakness in these patients is due to pathology at both the neuromuscular junction (most likely due to ND - NMBA) and muscle (most likely due to corticosteroids). Hepatic dysfunction and acidosis are contributing risk factors.

paralysis

muscle weakness

respiratory insufficiency

weakness

acidosis

loss of thick, myosin filaments

weakness

pathology at both the neuromuscular junction

Hepatic dysfunction

acidosis

nondepolarizing neuromuscular blocking agents

corticosteroids

nondepolarizing neuromuscular blocking agents

ND - NMBA

ND - NMBAs

corticosteroids

vecuronium

ND - NMBA

corticosteroids

nondepolarizing neuromuscular blocking agents

muscle weakness

nondepolarizing neuromuscular blocking agents

weakness

nondepolarizing neuromuscular blocking agents

weakness

nondepolarizing neuromuscular blocking agents

muscle weakness

nondepolarizing neuromuscular blocking agents

weakness

nondepolarizing neuromuscular blocking agents

weakness

ND - NMBA

muscle weakness

ND - NMBA

weakness

ND - NMBA

weakness

ND - NMBAs

muscle weakness

ND - NMBAs

weakness

ND - NMBAs

weakness

ND - NMBA

muscle weakness

ND - NMBA

weakness

ND - NMBA

weakness

corticosteroids

loss of thick, myosin filaments

corticosteroids

loss of thick, myosin filaments

corticosteroids

loss of thick, myosin filaments

nondepolarizing neuromuscular blocking agents

pathology at both the neuromuscular junction

nondepolarizing neuromuscular blocking agents

pathology at both the neuromuscular junction

ND - NMBA

pathology at both the neuromuscular junction

ND - NMBAs

pathology at both the neuromuscular junction

ND - NMBA

pathology at both the neuromuscular junction


Input: Prostaglandin E2 - induced bladder hyperactivity in normal, conscious rats: involvement of tachykinins? In normal conscious rats investigated by continuous cystometry, intravesically instilled prostaglandin (PG) E2 facilitated micturition and increased basal intravesical pressure. The effect was attenuated by both the NK1 receptor selective antagonist RP 67, 580 and the NK2 receptor selective antagonist SR 48, 968, given intra - arterially, suggesting that it was mediated by stimulation of both NK1 and NK2 receptors. Intra - arterially given PGE2 produced a distinct increase in bladder pressure before initiating a micturition reflex, indicating that the PG had a direct contractant effect on the detrusor smooth muscle. The effect of intra - arterial PGE2 could not be blocked by intra - arterial RP 67, 580 or SR 48, 968, which opens the possibility that the micturition reflex elicited by intra - arterial PGE2 was mediated by pathways other than the reflex initiated when the PG was given intravesically. The present results thus suggest that intra - arterial PGE2, given near the bladder, may initiate micturition in the normal rat chiefly by directly contracting the smooth muscle of the detrusor. However, when given intravesically, PGE2 may stimulate micturition by releasing tachykinins from nerves in and / or immediately below the urothelium. These tachykinins, in turn, initiate a micturition reflex by stimulating NK1 and NK2 receptors. Prostanoids may, via release of tachykinins, contribute to both urge and bladder hyperactivity seen in inflammatory conditions of the lower urinary tract.

Prostaglandin E2

tachykinins

prostaglandin (PG) E2

RP 67, 580

SR 48, 968

PG

RP 67, 580

SR 48, 968

PG

tachykinins

tachykinins

Prostanoids

tachykinins

bladder hyperactivity

bladder hyperactivity

Prostaglandin E2

bladder hyperactivity

Prostaglandin E2

bladder hyperactivity

prostaglandin (PG) E2

bladder hyperactivity

prostaglandin (PG) E2

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity

bladder hyperactivity


Input: Thiazide diuretics, hypokalemia and cardiac arrhythmias. Thiazide diuretics are widely accepted as the cornerstone of antihypertensive treatment programs. Hypokalemia is a commonly encountered metabolic consequence of chronic thiazide therapy. We treated 38 patients (22 low renin, 16 normal renin) with moderate diastolic hypertension with hydrochlorothiazide (HCTC) administered on a twice daily schedule. Initial dose was 50 mg and the dose was increased at monthly intervals to 100 mg, 150 mg and 200 mg daily until blood pressure normalized. The serum K during the control period was 4. 5 + / - 0. 2 mEq / l an on 50, 100, 150 and 200 mg HCTZ daily 3. 9 + / - 0. 3, 3. 4 + / - 0. 2, 2. 9 + / - 0. 2, and 2. 4 + / - 0. 3 mEq / l, respectively. Corresponding figures for whole body K were 4107 + / - 208, 3722 + / - 319, 3628 + / - 257, 3551 + / - 336, and 3269 + / - 380 mEq, respectively. In 13 patients we observed the effects of HCTZ therapy (100 mg daily) on the occurrence of PVC' s during rest as well as during static and dynamic exercise. During rest we observed 0. 6 + / - 0. 08 PVC beats / min + / - SEM and during static and dynamic exercise 0. 6 + / - 0. 06 and 0. 8 + / - 0. 15, respectively. Corresponding figures during HCTZ therapy 100 mg daily were 1. 4 + / - 0. 1, 3. 6 + / - 0. 7 and 5. 7 4 / - 0. 8, respectively. The occurrence of PVC' s correlated significantly with the fall in serum K + observed r = 0. 72, p less than 0. 001. In conclusion we found that thiazide diuretics cause hypokalemia and depletion of body potassium. The more profound hypokalemia, the greater the propensity for the occurrence of PVC' s.

Thiazide

Thiazide

thiazide

hydrochlorothiazide

HCTC

K

HCTZ

K

HCTZ

HCTZ

K

thiazide

potassium

hypokalemia

cardiac arrhythmias

Hypokalemia

diastolic hypertension

hypokalemia

hypokalemia

hydrochlorothiazide

hypokalemia

hydrochlorothiazide

Hypokalemia

hydrochlorothiazide

hypokalemia

hydrochlorothiazide

hypokalemia

HCTC

hypokalemia

HCTC

Hypokalemia

HCTC

hypokalemia

HCTC

hypokalemia

HCTZ

hypokalemia

HCTZ

Hypokalemia

HCTZ

hypokalemia

HCTZ

hypokalemia

HCTZ

hypokalemia

HCTZ

Hypokalemia

HCTZ

hypokalemia

HCTZ

hypokalemia

HCTZ

hypokalemia

HCTZ

Hypokalemia

HCTZ

hypokalemia

HCTZ

hypokalemia

hydrochlorothiazide

cardiac arrhythmias

HCTC

cardiac arrhythmias

HCTZ

cardiac arrhythmias

HCTZ

cardiac arrhythmias

HCTZ

cardiac arrhythmias