Input: Caffeine challenge test in panic disorder and depression with panic attacks. Our aim was to observe if patients with panic disorder (PD) and patients with major depression with panic attacks (MDP) (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria) respond in a similar way to the induction of panic attacks by an oral caffeine challenge test. We randomly selected 29 patients with PD, 27 with MDP, 25 with major depression without panic attacks (MD), and 28 healthy volunteers. The patients had no psychotropic drug for at least a 4 - week period. In a randomized double - blind experiment performed in 2 occasions 7 days apart, 480 mg caffeine and a caffeine - free (placebo) solution were administered in a coffee form and anxiety scales were applied before and after each test. A total of 58. 6% (n = 17) of patients with PD, 44. 4% (n = 12) of patients with MDP, 12. 0% (n = 3) of patients with MD, and 7. 1% (n = 2) of control subjects had a panic attack after the 480 - mg caffeine challenge test (chi (2) (3) = 16. 22, P =. 001). The patients with PD and MDP were more sensitive to caffeine than were patients with MD and healthy volunteers. No panic attack was observed after the caffeine - free solution intake. The patients with MD had a lower heart rate response to the test than all the other groups (2 - way analysis of variance, group by time interaction with Greenhouse - Geisser correction: F (3, 762) = 2. 85, P =. 026). Our data suggest that there is an association between panic attacks, no matter if associated with PD or MDP, and hyperreactivity to an oral caffeine challenge test.

Caffeine

caffeine

caffeine

caffeine

caffeine

caffeine

caffeine

caffeine

panic disorder

depression

panic attacks

panic disorder

PD

major depression

panic attacks

MDP

Mental Disorders

panic attacks

PD

MDP

major depression

panic attacks

MD

anxiety

PD

MDP

MD

panic attack

PD

MDP

MD

panic attack

MD

panic attacks

PD

MDP

Caffeine

panic disorder

Caffeine

panic attacks

Caffeine

panic disorder

Caffeine

PD

Caffeine

panic attacks

Caffeine

MDP

Caffeine

panic attacks

Caffeine

PD

Caffeine

MDP

Caffeine

panic attacks

Caffeine

PD

Caffeine

MDP

Caffeine

panic attack

Caffeine

PD

Caffeine

MDP

Caffeine

panic attack

Caffeine

panic attacks

Caffeine

PD

Caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic disorder

caffeine

panic attacks

caffeine

panic disorder

caffeine

PD

caffeine

panic attacks

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attacks

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

PD

caffeine

MDP

caffeine

panic attack

caffeine

panic attacks

caffeine

PD

caffeine

MDP


Input: Mitral annuloplasty as a ventricular restoration method for the failing left ventricle: a pilot study. BACKGROUND AND AIM OF THE STUDY: Undersized mitral annuloplasty (MAP) is effective in patients with dilated cardiomyopathy and functional mitral regurgitation (MR) since, as well as addressing the MR, the MAP may also reshape the dilated left ventricular (LV) base. However, the direct benefits of this possible reshaping on LV function in the absence of underlying MR remain incompletely understood. The study aim was to identify these benefits in a canine model of acute heart failure. METHODS: Six dogs underwent MAP with a prosthetic band on the posterior mitral annulus, using four mattress sutures. The sutures were passed individually through four tourniquets and exteriorized untied via the left atriotomy. Sonomicrometry crystals were implanted around the mitral annulus and left ventricle to measure geometry and regional function. Acute heart failure was induced by propranolol and volume loading after weaning from cardiopulmonary bypass; an absence of MR was confirmed by echocardiography. MAP was accomplished by cinching the tourniquets. Data were acquired at baseline, after induction of acute heart failure, and after MAP. RESULTS: MAP decreased mitral annular dimensions in both commissure - commissure and septal - lateral directions. Concomitantly, the diastolic diameter of the LV base and LV sphericity decreased (i. e., improved) from 37. 4 + / - 9. 3 to 35. 9 + / - 10 mm (p = 0. 063), and from 67. 9 + / - 18. 6% to 65. 3 + / - 18. 9% (p = 0. 016), respectively. Decreases were evident in both LV end - diastolic pressure (from 17 + / - 7 to 15 + / - 6 mmHg, p = 0. 0480 and Tau (from 48 + / - 8 to 45 + / - 8 ms, p < 0. 01), while fractional shortening at the LV base increased from 7. 7 + / - 4. 5% to 9. 4 + / - 4. 5% (p = 0. 045). After MAP, increases were identified in both cardiac output (from 1. 54 + / - 0. 57 to 1. 65 + / - 0. 57 1 / min) and Emax (from 1. 86 + / - 0. 9 to 2. 41 + / - 1. 31 mmHg / ml). CONCLUSION: The data acquired suggest that isolated MAP may have certain benefits on LV dimension / function in acute heart failure, even in the absence of MR. However, further investigations are warranted in a model of chronic heart failure.

failing left ventricle

dilated cardiomyopathy

mitral regurgitation

MR

MR

MR

heart failure

heart failure

MR

heart failure

heart failure

MR

heart failure

propranolol

propranolol

failing left ventricle

propranolol

heart failure

propranolol

heart failure

propranolol

heart failure

propranolol

heart failure

propranolol

heart failure


Input: Piperacillin / tazobactam - induced seizure rapidly reversed by high flux hemodialysis in a patient on peritoneal dialysis. Despite popular use of piperacillin, the dire neurotoxicity associated with piperacillin still goes unrecognized, leading to a delay in appropriate management. We report a 57 - year - old woman with end - stage renal disease receiving continuous ambulatory peritoneal dialysis (CAPD), who developed slurred speech, tremor, bizarre behavior, progressive mental confusion, and 2 episodes of generalized tonic - clonic seizure (GTCS) after 5 doses of piperacillin / tazobactam (2 g / 250 mg) were given for bronchiectasis with secondary infection. The laboratory data revealed normal plasma electrolyte and ammonia levels but leukocytosis. Neurologic examinations showed dysarthria and bilateral Babinski sign. Computed tomography of brain and electroencephalogram were unremarkable. Despite the use of antiepileptic agents, another GTCS episode recurred after the sixth dose of piperacillin / tazobactam. Brain magnetic resonance imaging did not demonstrate acute infarction and organic brain lesions. Initiation of high - flux hemodialysis rapidly reversed the neurologic symptoms within 4 hours. Piperacillin - induced encephalopathy should be considered in any uremic patients with unexplained neurological manifestations. CAPD is inefficient in removing piperacillin, whereas hemodialysis can rapidly terminate the piperacillin - induced encephalopathy.

Piperacillin / tazobactam

piperacillin

piperacillin

piperacillin / tazobactam

ammonia

piperacillin / tazobactam

Piperacillin

piperacillin

piperacillin

seizure

neurotoxicity

end - stage renal disease

tremor

confusion

tonic - clonic seizure

GTCS

bronchiectasis

secondary infection

leukocytosis

dysarthria

GTCS

infarction

organic brain lesions

encephalopathy

uremic

encephalopathy

Piperacillin / tazobactam

confusion

piperacillin / tazobactam

confusion

piperacillin / tazobactam

confusion

Piperacillin / tazobactam

tonic - clonic seizure

Piperacillin / tazobactam

GTCS

Piperacillin / tazobactam

GTCS

piperacillin / tazobactam

tonic - clonic seizure

piperacillin / tazobactam

GTCS

piperacillin / tazobactam

GTCS

piperacillin / tazobactam

tonic - clonic seizure

piperacillin / tazobactam

GTCS

piperacillin / tazobactam

GTCS

Piperacillin / tazobactam

tremor

piperacillin / tazobactam

tremor

piperacillin / tazobactam

tremor


Input: Frequency of transient ipsilateral vocal cord paralysis in patients undergoing carotid endarterectomy under local anesthesia. BACKGROUND: Especially because of improvements in clinical neurologic monitoring, carotid endarterectomy done under local anesthesia has become the technique of choice in several centers. Temporary ipsilateral vocal nerve palsies due to local anesthetics have been described, however. Such complications are most important in situations where there is a pre - existing contralateral paralysis. We therefore examined the effect of local anesthesia on vocal cord function to better understand its possible consequences. METHODS: This prospective study included 28 patients undergoing carotid endarterectomy under local anesthesia. Vocal cord function was evaluated before, during, and after surgery (postoperative day 1) using flexible laryngoscopy. Anesthesia was performed by injecting 20 to 40 mL of a mixture of long - acting (ropivacaine) and short - acting (prilocaine) anesthetic. RESULTS: All patients had normal vocal cord function preoperatively. Twelve patients (43%) were found to have intraoperative ipsilateral vocal cord paralysis. It resolved in all cases < or = 24 hours. There were no significant differences in operating time or volume or frequency of anesthetic administration in patients with temporary vocal cord paralysis compared with those without. CONCLUSION: Local anesthesia led to temporary ipsilateral vocal cord paralysis in almost half of these patients. Because pre - existing paralysis is of a relevant frequency (up to 3%), a preoperative evaluation of vocal cord function before carotid endarterectomy under local anesthesia is recommended to avoid intraoperative bilateral paralysis. In patients with preoperative contralateral vocal cord paralysis, surgery under general anesthesia should be considered.

vocal cord paralysis

vocal nerve palsies

paralysis

vocal cord paralysis

vocal cord paralysis

vocal cord paralysis

paralysis

paralysis

vocal cord paralysis

ropivacaine

prilocaine

prilocaine

vocal cord paralysis

prilocaine

vocal nerve palsies

prilocaine

vocal cord paralysis

prilocaine

vocal cord paralysis

prilocaine

vocal cord paralysis

prilocaine

vocal cord paralysis


Input: Neuroprotective effects of melatonin upon the offspring cerebellar cortex in the rat model of BCNU - induced cortical dysplasia. Cortical dysplasia is a malformation characterized by defects in proliferation, migration and maturation. This study was designed to evaluate the alterations in offspring rat cerebellum induced by maternal exposure to carmustine - [1, 3 - bis (2 - chloroethyl) - 1 - nitrosoure] (BCNU) and to investigate the effects of exogenous melatonin upon cerebellar BCNU - induced cortical dysplasia, using histological and biochemical analyses. Pregnant Wistar rats were assigned to five groups: intact - control, saline - control, melatonin - treated, BCNU - exposed and BCNU - exposed plus melatonin. Rats were exposed to BCNU on embryonic day 15 and melatonin was given until delivery. Immuno / histochemistry and electron microscopy were carried out on the offspring cerebellum, and levels of malondialdehyde and superoxide dismutase were determined. Histopathologically, typical findings were observed in the cerebella from the control groups, but the findings consistent with early embryonic development were noted in BCNU - exposed cortical dysplasia group. There was a marked increase in the number of TUNEL positive cells and nestin positive cells in BCNU - exposed group, but a decreased immunoreactivity to glial fibrillary acidic protein, synaptophysin and transforming growth factor beta1 was observed, indicating a delayed maturation, and melatonin significantly reversed these changes. Malondialdehyde level in BCNU - exposed group was higher than those in control groups and melatonin decreased malondialdehyde levels in BCNU group (P < 0. 01), while there were no significant differences in the superoxide dismutase levels between these groups. These data suggest that exposure of animals to BCNU during pregnancy leads to delayed maturation of offspring cerebellum and melatonin protects the cerebellum against the effects of BCNU.

melatonin

BCNU

carmustine

1, 3 - bis (2 - chloroethyl) - 1 - nitrosoure

BCNU

melatonin

BCNU

melatonin

BCNU

BCNU

melatonin

BCNU

melatonin

malondialdehyde

superoxide

BCNU

BCNU

melatonin

Malondialdehyde

BCNU

melatonin

malondialdehyde

BCNU

superoxide

BCNU

melatonin

BCNU

cortical dysplasia

Cortical dysplasia

cortical dysplasia

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

carmustine

cortical dysplasia

carmustine

Cortical dysplasia

carmustine

cortical dysplasia

carmustine

cortical dysplasia

1, 3 - bis (2 - chloroethyl) - 1 - nitrosoure

cortical dysplasia

1, 3 - bis (2 - chloroethyl) - 1 - nitrosoure

Cortical dysplasia

1, 3 - bis (2 - chloroethyl) - 1 - nitrosoure

cortical dysplasia

1, 3 - bis (2 - chloroethyl) - 1 - nitrosoure

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia

BCNU

Cortical dysplasia

BCNU

cortical dysplasia

BCNU

cortical dysplasia


Input: Myo - inositol - 1 - phosphate (MIP) synthase inhibition: in - vivo study in rats. Lithium and valproate are the prototypic mood stabilizers and have diverse structures and targets. Both drugs influence inositol metabolism. Lithium inhibits IMPase and valproate inhibits MIP synthase. This study shows that MIP synthase inhibition does not replicate or augment the effects of lithium in the inositol sensitive pilocarpine - induced seizures model. This lack of effects may stem from the low contribution of de - novo synthesis to cellular inositol supply or to the inhibition of the de - novo synthesis by lithium itself.

Myo - inositol - 1 - phosphate

MIP

Lithium

valproate

inositol

Lithium

valproate

MIP

MIP

lithium

inositol

pilocarpine

inositol

lithium

seizures

pilocarpine

seizures


Input: Non - steroidal anti - inflammatory drugs - associated acute interstitial nephritis with granular tubular basement membrane deposits. Acute tubulo - interstitial nephritis (ATIN) is an important cause of acute renal failure resulting from a variety of insults, including immune complex - mediated tubulo - interstitial injury, but drugs such as non - steroidal anti - inflammatory drugs (NSAIDs) are a far more frequent cause. Overall, as an entity, ATIN remains under - diagnosed, as symptoms resolve spontaneously if the medication is stopped. We report on a 14 - year - old boy who developed acute renal failure 2 weeks after aortic valve surgery. He was put on aspirin following surgery and took ibuprofen for fever for nearly a week prior to presentation. He then presented to the emergency department feeling quite ill and was found to have a blood urea nitrogen (BUN) concentration of of 147 mg / dl, creatinine of 15. 3 mg / dl and serum potassium of 8. 7 mEq / l. Dialysis was immediately initiated. A kidney biopsy showed inflammatory infiltrate consistent with ATIN. However, in the tubular basement membrane (TBM), very intense granular deposits of polyclonal IgG and C3 were noted. He needed dialysis for 2 weeks and was treated successfully with steroids for 6 months. His renal recovery and disappearance of proteinuria took a year. In conclusion, this is a first report of NSAIDs - associated ATIN, showing deposits of granular immune complex present only in the TBM and not in the glomeruli.

interstitial nephritis

Acute tubulo - interstitial nephritis

ATIN

acute renal failure

tubulo - interstitial injury

ATIN

acute renal failure

fever

ATIN

proteinuria

ATIN

aspirin

ibuprofen

blood urea nitrogen

BUN

creatinine

potassium

steroids

ibuprofen

acute renal failure

ibuprofen

acute renal failure

ibuprofen

interstitial nephritis

ibuprofen

tubulo - interstitial injury


Input: Rifampicin - associated segmental necrotizing glomerulonephritis in staphylococcal endocarditis. Segmental necrotising glomerulonephritis has been reported as complication of rifampicin therapy in patients receiving treatment for tuberculosis. Changing epidemiology of infections such as infective endocarditis (IE) has led to an increase in the use of rifampicin for Staphylococcal infections. We describe a case of a patient with Staphylococcal IE who developed acute renal failure secondary to a segmental necrotising glomerulonephritis while being treated with rifampicin, and review the literature regarding this complication of rifampicin therapy.

Rifampicin

rifampicin

rifampicin

rifampicin

rifampicin

glomerulonephritis

staphylococcal endocarditis

staphylococcal

endocarditis

glomerulonephritis

tuberculosis

infections

infective endocarditis

IE

Staphylococcal infections

Staphylococcal IE

Staphylococcal

IE

acute renal failure

glomerulonephritis

Rifampicin

acute renal failure

rifampicin

acute renal failure

rifampicin

acute renal failure

rifampicin

acute renal failure

rifampicin

acute renal failure

Rifampicin

glomerulonephritis

Rifampicin

glomerulonephritis

Rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis

rifampicin

glomerulonephritis


Input: Rate of YMDD motif mutants in lamivudine - untreated Iranian patients with chronic hepatitis B virus infection. BACKGROUND: Lamivudine is used for the treatment of chronic hepatitis B patients. Recent studies show that the YMDD motif mutants (resistant hepatitis B virus) occur as natural genome variability in lamivudine - untreated chronic hepatitis B patients. In this study we aimed to determine the rate of YMDD motif mutants in lamivudine - untreated chronic hepatitis B patients in Iran. PATIENTS AND METHODS: A total of 77 chronic hepatitis B patients who had not been treated with lamivudine were included in the study. Serum samples from patients were tested by polymerase chain reaction - restriction fragment length polymorphism (PCR - RFLP) for detection of YMDD motif mutants. All patients were also tested for liver enzymes, anti - HCV, HBeAg, and anti - HBe. RESULTS: Of the 77 patients enrolled in the study, 73% were male and 27% were female. Mean ALT and AST levels were 124. 4 + / - 73. 4 and 103. 1 + / - 81 IU / l, respectively. HBeAg was positive in 40% and anti - HBe in 60% of the patients. Anti - HCV was negative in all of them. YMDD motif mutants were not detected in any of the patients despite the liver enzyme levels and the presence of HBeAg or anti - HBe. CONCLUSION: Although the natural occurrence of YMDD motif mutants in lamivudine - untreated patients with chronic hepatitis B has been reported, these mutants were not detected in Iranian lamivudine - untreated chronic hepatitis B patients.

lamivudine

Lamivudine

lamivudine

lamivudine

lamivudine

HBeAg

HBeAg

HBeAg

lamivudine

lamivudine

chronic hepatitis B virus infection

chronic hepatitis B

hepatitis B

chronic hepatitis B

chronic hepatitis B

chronic hepatitis B

chronic hepatitis B

chronic hepatitis B

HBeAg

chronic hepatitis B virus infection

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B virus infection

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B virus infection

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B

HBeAg

chronic hepatitis B


Input: Branch retinal vein occlusion and fluoxetine. A case of branch retinal vein occlusion associated with fluoxetine - induced secondary hypertension is described. Although an infrequent complication of selective serotonin reuptake inhibitor therapy, it is important that ophthalmologists are aware that these agents can cause hypertension because this class of drugs is widely prescribed.

retinal vein occlusion

retinal vein occlusion

hypertension

hypertension

fluoxetine

fluoxetine

serotonin

fluoxetine

retinal vein occlusion

fluoxetine

retinal vein occlusion

fluoxetine

retinal vein occlusion

fluoxetine

retinal vein occlusion

fluoxetine

hypertension

fluoxetine

hypertension

fluoxetine

hypertension

fluoxetine

hypertension


Input: The differential effects of bupivacaine and lidocaine on prostaglandin E2 release, cyclooxygenase gene expression and pain in a clinical pain model. BACKGROUND: In addition to blocking nociceptive input from surgical sites, long - acting local anesthetics might directly modulate inflammation. In the present study, we describe the proinflammatory effects of bupivacaine on local prostaglandin E2 (PGE2) production and cyclooxygenase (COX) gene expression that increases postoperative pain in human subjects. METHODS: Subjects (n = 114) undergoing extraction of impacted third molars received either 2% lidocaine or 0. 5% bupivacaine before surgery and either rofecoxib 50 mg or placebo orally 90 min before surgery and for the following 48 h. Oral mucosal biopsies were taken before surgery and 48 h after surgery. After extraction, a microdialysis probe was placed at the surgical site for PGE2 and thromboxane B2 (TXB2) measurements. RESULTS: The bupivacaine / rofecoxib group reported significantly less pain, as assessed by a visual analog scale, compared with the other three treatment groups over the first 4 h. However, the bupivacaine / placebo group reported significantly more pain at 24 h and PGE2 levels during the first 4 h were significantly higher than the other three treatment groups. Moreover, bupivacaine significantly increased COX - 2 gene expression at 48 h as compared with the lidocaine / placebo group. Thromboxane levels were not significantly affected by any of the treatments, indicating that the effects seen were attributable to inhibition of COX - 2, but not COX - 1. CONCLUSIONS: These results suggest that bupivacaine stimulates COX - 2 gene expression after tissue injury, which is associated with higher PGE2 production and pain after the local anesthetic effect dissipates.

bupivacaine

lidocaine

prostaglandin E2

bupivacaine

prostaglandin E2

lidocaine

bupivacaine

rofecoxib

thromboxane B2

bupivacaine

rofecoxib

bupivacaine

bupivacaine

lidocaine

Thromboxane

bupivacaine

pain

pain

inflammation

postoperative pain

pain

pain

tissue injury

pain

bupivacaine

inflammation

bupivacaine

inflammation

bupivacaine

inflammation

bupivacaine

inflammation

bupivacaine

inflammation

bupivacaine

inflammation

bupivacaine

inflammation

bupivacaine

postoperative pain

bupivacaine

postoperative pain

bupivacaine

postoperative pain

bupivacaine

postoperative pain

bupivacaine

postoperative pain

bupivacaine

postoperative pain

bupivacaine

postoperative pain


Input: p75NTR expression in rat urinary bladder sensory neurons and spinal cord with cyclophosphamide - induced cystitis. A role for nerve growth factor (NGF) in contributing to increased voiding frequency and altered sensation from the urinary bladder has been suggested. Previous studies have examined the expression and regulation of tyrosine kinase receptors (Trks) in micturition reflexes with urinary bladder inflammation. The present studies examine the expression and regulation of another receptor known to bind NGF, p75 (NTR), after various durations of bladder inflammation induced by cyclophosphamide (CYP). CYP - induced cystitis increased (P < or = 0. 001) p75 (NTR) expression in the superficial lateral and medial dorsal horn in L1 - L2 and L6 - S1 spinal segments. The number of p75 (NTR) - immunoreactive (- IR) cells in the lumbosacral dorsal root ganglia (DRG) also increased (P < or = 0. 05) with CYP - induced cystitis (acute, intermediate, and chronic). Quantitative, real - time polymerase chain reaction also demonstrated significant increases (P < or = 0. 01) in p75 (NTR) mRNA in DRG with intermediate and chronic CYP - induced cystitis. Retrograde dye - tracing techniques with Fastblue were used to identify presumptive bladder afferent cells in the lumbosacral DRG. In bladder afferent cells in DRG, p75 (NTR) - IR was also increased (P < or = 0. 01) with cystitis. In addition to increases in p75 (NTR) - IR in DRG cell bodies, increases (P < or = 0. 001) in pericellular (encircling DRG cells) p75 (NTR) - IR in DRG also increased. Confocal analyses demonstrated that pericellular p75 (NTR) - IR was not colocalized with the glial marker, glial fibrillary acidic protein (GFAP). These studies demonstrate that p75 (NTR) expression in micturition reflexes is present constitutively and modified by bladder inflammation. The functional significance of p75 (NTR) expression in micturition reflexes remains to be determined.

cyclophosphamide

tyrosine

cyclophosphamide

CYP

CYP

CYP

CYP

cystitis

urinary bladder inflammation

bladder inflammation

cystitis

cystitis

cystitis

cystitis

bladder inflammation

cyclophosphamide

cystitis

cyclophosphamide

urinary bladder inflammation

cyclophosphamide

bladder inflammation

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

bladder inflammation

cyclophosphamide

cystitis

cyclophosphamide

urinary bladder inflammation

cyclophosphamide

bladder inflammation

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

bladder inflammation

CYP

cystitis

CYP

urinary bladder inflammation

CYP

bladder inflammation

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

bladder inflammation

CYP

cystitis

CYP

urinary bladder inflammation

CYP

bladder inflammation

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

bladder inflammation

CYP

cystitis

CYP

urinary bladder inflammation

CYP

bladder inflammation

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

bladder inflammation

CYP

cystitis

CYP

urinary bladder inflammation

CYP

bladder inflammation

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

bladder inflammation


Input: Azathioprine - induced suicidal erythrocyte death. BACKGROUND: Azathioprine is widely used as an immunosuppressive drug. The side effects of azathioprine include anemia, which has been attributed to bone marrow suppression. Alternatively, anemia could result from accelerated suicidal erythrocyte death or eryptosis, which is characterized by exposure of phosphatidylserine (PS) at the erythrocyte surface and by cell shrinkage. METHODS: The present experiments explored whether azathioprine influences eryptosis. According to annexin V binding, erythrocytes from patients indeed showed a significant increase of PS exposure within 1 week of treatment with azathioprine. In a second series, cytosolic Ca2 + activity (Fluo3 fluorescence), cell volume (forward scatter), and PS - exposure (annexin V binding) were determined by FACS analysis in erythrocytes from healthy volunteers. RESULTS: Exposure to azathioprine (> or = 2 microg / mL) for 48 hours increased cytosolic Ca2 + activity and annexin V binding and decreased forward scatter. The effect of azathioprine on both annexin V binding and forward scatter was significantly blunted in the nominal absence of extracellular Ca2 +. CONCLUSIONS: Azathioprine triggers suicidal erythrocyte death, an effect presumably contributing to azathioprine - induced anemia.

Azathioprine

Azathioprine

azathioprine

phosphatidylserine

PS

azathioprine

PS

azathioprine

PS

azathioprine

azathioprine

Azathioprine

azathioprine

anemia

anemia

anemia

Azathioprine

anemia

Azathioprine

anemia

Azathioprine

anemia

Azathioprine

anemia

Azathioprine

anemia

Azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

Azathioprine

anemia

Azathioprine

anemia

Azathioprine

anemia

azathioprine

anemia

azathioprine

anemia

azathioprine

anemia


Input: Clinical comparison of cardiorespiratory effects during unilateral and conventional spinal anaesthesia. BACKGROUND: Spinal anaesthesia is widely employed in clinical practice but has the main drawback of post - spinal block hypotension. Efforts must therefore continue to be made to obviate this setback OBJECTIVE: To evaluate the cardiovascular and respiratory changes during unilateral and conventional spinal anaesthesia. METHODS: With ethical approval, we studied 74 American Society of Anesthesiologists (ASA), physical status class 1 and 2 patients scheduled for elective unilateral lower limb surgery. Patients were randomly allocated into one of two groups: lateral and conventional spinal anaesthesia groups. In the lateral position with operative side down, patients recived 10 mg (2mls) of 0. 5% hyperbaric bupivacaine through a 25 - gauge spinal needle. Patients in the unilateral group were maintained in the lateral position for 15 minutes following spinal injection while those in the conventional group were turned supine immediately after injection. Blood pressure, heart rate, respiratory rate and oxygen saturation were monitored over 1 hour. RESULTS: Three patients (8. 1%) in the unilateral group and 5 (13. 5%) in the conventional group developed hypotension, P = 0. 71. Four (10. 8%) patients in the conventional group and 1 (2. 7%) in the unilateral group, P = 0. 17 required epinephrine infusion to treat hypotension. Patients in the conventional group had statistically significant greater fall in the systolic blood pressures at 15, 30 and 45 minutes when compared to the baseline (P = 0. 003, 0. 001 and 0. 004). The mean respiratory rate and oxygen saturations in the two groups were similar. CONCLUSION: Compared to conventional spinal anaesthesia, unilateral spinal anaesthesia was associated with fewer cardiovascular perturbations. Also, the type of spinal block instituted affected neither the respiratory rate nor the arterial oxygen saturation.

hypotension

hypotension

hypotension

bupivacaine

oxygen

epinephrine

oxygen

oxygen

bupivacaine

hypotension

bupivacaine

hypotension

bupivacaine

hypotension


Input: Spectrum of adverse events after generic HAART in southern Indian HIV - infected patients. To determine the incidence of clinically significant adverse events after long - term, fixed - dose, generic highly active antiretroviral therapy (HAART) use among HIV - infected individuals in South India, we examined the experiences of 3154 HIV - infected individuals who received a minimum of 3 months of generic HAART between February 1996 and December 2006 at a tertiary HIV care referral center in South India. The most common regimens were 3TC + d4T + nevirapine (NVP) (54. 8%), zidovudine (AZT) + 3TC + NVP (14. 5%), 3TC + d4T + efavirenz (EFV) (20. 1%), and AZT + 3TC + EFV (5. 4%). The most common adverse events and median CD4 at time of event were rash (15. 2%; CD4, 285 cells / microL) and peripheral neuropathy (9. 0% and 348 cells / microL). Clinically significant anemia (hemoglobin < 7 g / dL) was observed in 5. 4% of patients (CD4, 165 cells / microL) and hepatitis (clinical jaundice with alanine aminotransferase > 5 times upper limits of normal) in 3. 5% of patients (CD4, 260 cells / microL). Women were significantly more likely to experience lactic acidosis, while men were significantly more likely to experience immune reconstitution syndrome (p < 0. 05). Among the patients with 1 year of follow - up, NVP therapy was significantly associated with developing rash and d4T therapy with developing peripheral neuropathy (p < 0. 05). Anemia and hepatitis often occur within 12 weeks of initiating generic HAART. Frequent and early monitoring for these toxicities is warranted in developing countries where generic HAART is increasingly available.

HIV - infected

HIV - infected

HIV - infected

rash

peripheral neuropathy

anemia

hepatitis

jaundice

lactic acidosis

immune reconstitution syndrome

rash

peripheral neuropathy

Anemia

hepatitis

toxicities

nevirapine

NVP

zidovudine

AZT

NVP

efavirenz

EFV

AZT

EFV

alanine

NVP

peripheral neuropathy

peripheral neuropathy

peripheral neuropathy

peripheral neuropathy

peripheral neuropathy

peripheral neuropathy

nevirapine

rash

nevirapine

rash

NVP

rash

NVP

rash

NVP

rash

NVP

rash

NVP

rash

NVP

rash


Input: Thalidomide and sensory neurotoxicity: a neurophysiological study. BACKGROUND: Recent studies confirmed a high incidence of sensory axonal neuropathy in patients treated with different doses of thalidomide. The study' s aims were to measure variations in sural nerve sensory action potential (SAP) amplitude in patients with refractory cutaneous lupus erythematosus (CLE) treated with thalidomide and use these findings to identify the neurotoxic potential of thalidomide and the recovery capacity of sensory fibres after discontinuation of treatment. PATIENTS AND METHODS: Clinical and electrophysiological data in 12 female patients with CLE during treatment with thalidomide and up to 47 months after discontinuation of treatment were analysed. Sural nerve SAP amplitude reduction > or = 40% was the criteria for discontinuing therapy. RESULTS: During treatment, 11 patients showed a reduction in sural nerve SAP amplitude compared to baseline values (9 with a reduction > or = 50% and 2 < 50%). One patient showed no changes in SAP amplitude. Five patients complained of paresthesias and leg cramps. After thalidomide treatment, sural SAP amplitude recovered in 3 patients. At detection of reduction in sural nerve SAP amplitude, the median thalidomide cumulative dose was 21. 4 g. The threshold neurotoxic dosage is lower than previously reported. CONCLUSIONS: Sural nerve SAP amplitude reduction is a reliable and sensitive marker of degeneration and recovery of sensory fibres. This electrophysiological parameter provides information about subclinical neurotoxic potential of thalidomide but is not helpful in predicting the appearance of sensory symptoms.

Thalidomide

thalidomide

thalidomide

thalidomide

thalidomide

thalidomide

thalidomide

thalidomide

sensory neurotoxicity

sensory axonal neuropathy

cutaneous lupus erythematosus

CLE

neurotoxic

CLE

paresthesias

cramps

neurotoxic

neurotoxic

Thalidomide

cramps

thalidomide

cramps

thalidomide

cramps

thalidomide

cramps

thalidomide

cramps

thalidomide

cramps

thalidomide

cramps

thalidomide

cramps

Thalidomide

sensory neurotoxicity

Thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

thalidomide

sensory neurotoxicity

thalidomide

sensory axonal neuropathy

Thalidomide

paresthesias

thalidomide

paresthesias

thalidomide

paresthesias

thalidomide

paresthesias

thalidomide

paresthesias

thalidomide

paresthesias

thalidomide

paresthesias

thalidomide

paresthesias


Input: Amiodarone - related pulmonary mass and unique membranous glomerulonephritis in a patient with valvular heart disease: Diagnostic pitfall and new findings. Amiodarone is an anti - arrhythmic drug for life - threatening tachycardia, but various adverse effects have been reported. Reported herein is an autopsy case of valvular heart disease, in a patient who developed a lung mass (1. 5 cm in diameter) and proteinuria (2. 76 g / day) after treatment with amiodarone for a long time. The lung mass was highly suspected to be lung cancer on CT and positron emission tomography, but histologically the lesion was composed of lymphoplasmacytic infiltrates in alveolar walls and intra - alveolar accumulation of foamy macrophages containing characteristic myelinoid bodies, indicating that it was an amiodarone - related lesion. In addition, the lung tissue had unevenly distributed hemosiderin deposition, and abnormally tortuous capillaries were seen in the mass and in heavily hemosiderotic lung portions outside the mass. In the kidneys, glomeruli had membrane spikes, prominent swelling of podocytes and subepithelial deposits, which were sometimes large and hump - like. Autoimmune diseases, viral hepatitis, malignant neoplasms or other diseases with a known relationship to membranous glomerulonephritis were not found. The present case highlights the possibility that differential diagnosis between an amiodarone - related pulmonary lesion and a neoplasm can be very difficult radiologically, and suggests that membranous glomerulonephritis might be another possible complication of amiodarone treatment.

Amiodarone

Amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

pulmonary mass

membranous glomerulonephritis

valvular heart disease

arrhythmic

tachycardia

valvular heart disease

lung mass

proteinuria

lung mass

lung cancer

hemosiderin

hemosiderotic

Autoimmune diseases

viral hepatitis

neoplasms

membranous glomerulonephritis

pulmonary lesion

neoplasm

membranous glomerulonephritis

Amiodarone

pulmonary mass

Amiodarone

lung mass

Amiodarone

lung mass

Amiodarone

pulmonary lesion

Amiodarone

pulmonary mass

Amiodarone

lung mass

Amiodarone

lung mass

Amiodarone

pulmonary lesion

amiodarone

pulmonary mass

amiodarone

lung mass

amiodarone

lung mass

amiodarone

pulmonary lesion

amiodarone

pulmonary mass

amiodarone

lung mass

amiodarone

lung mass

amiodarone

pulmonary lesion

amiodarone

pulmonary mass

amiodarone

lung mass

amiodarone

lung mass

amiodarone

pulmonary lesion

amiodarone

pulmonary mass

amiodarone

lung mass

amiodarone

lung mass

amiodarone

pulmonary lesion

Amiodarone

membranous glomerulonephritis

Amiodarone

membranous glomerulonephritis

Amiodarone

membranous glomerulonephritis

Amiodarone

membranous glomerulonephritis

Amiodarone

membranous glomerulonephritis

Amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

amiodarone

membranous glomerulonephritis

Amiodarone

hemosiderin

Amiodarone

hemosiderotic

Amiodarone

hemosiderin

Amiodarone

hemosiderotic

amiodarone

hemosiderin

amiodarone

hemosiderotic

amiodarone

hemosiderin

amiodarone

hemosiderotic

amiodarone

hemosiderin

amiodarone

hemosiderotic

amiodarone

hemosiderin

amiodarone

hemosiderotic


Input: Risk of coronary artery disease associated with initial sulphonylurea treatment of patients with type 2 diabetes: a matched case - control study. AIMS: This study sought to assess the risk of developing coronary artery disease (CAD) associated with initial treatment of type 2 diabetes with different sulphonylureas. METHODS: In type 2 diabetic patients, cases who developed CAD were compared retrospectively with controls that did not. The 20 - year risk of CAD at diagnosis of diabetes, using the UKPDS risk engine, was used to match cases with controls. RESULTS: The 76 cases of CAD were compared with 152 controls. The hazard of developing CAD (95% CI) associated with initial treatment increased by 2. 4 - fold (1. 3 - 4. 3, P = 0. 004) with glibenclamide; 2 - fold (0. 9 - 4. 6, P = 0. 099) with glipizide; 2. 9 - fold (1. 6 - 5. 1, P = 0. 000) with either, and was unchanged with metformin. The hazard decreased 0. 3 - fold (0. 7 - 1. 7, P = 0. 385) with glimepiride, 0. 4 - fold (0. 7 - 1. 3, P = 0. 192) with gliclazide, and 0. 4 - fold (0. 7 - 1. 1, P = 0. 09) with either. CONCLUSIONS: Initiating treatment of type 2 diabetes with glibenclamide or glipizide is associated with increased risk of CAD in comparison to gliclazide or glimepiride. If confirmed, this may be important because most Indian patients receive the cheaper older sulphonylureas, and present guidelines do not distinguish between individual agents.

coronary artery disease

type 2 diabetes

coronary artery disease

CAD

type 2 diabetes

type 2 diabetic

CAD

CAD

diabetes

CAD

CAD

type 2 diabetes

CAD

sulphonylurea

sulphonylureas

glibenclamide

glipizide

metformin

glimepiride

gliclazide

glibenclamide

glipizide

gliclazide

glimepiride

sulphonylureas

glibenclamide

coronary artery disease

glibenclamide

coronary artery disease

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

coronary artery disease

glibenclamide

coronary artery disease

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD

glibenclamide

CAD


Input: Reduced progression of adriamycin nephropathy in spontaneously hypertensive rats treated by losartan. BACKGROUND: The aim of the study was to investigate the antihypertensive effects of angiotensin II type - 1 receptor blocker, losartan, and its potential in slowing down renal disease progression in spontaneously hypertensive rats (SHR) with adriamycin (ADR) nephropathy. METHODS: Six - month - old female SHR were randomly selected in six groups. Two control groups (SH (6), SH (12)) received vehicle. Groups ADR (6), ADR + LOS (6) and ADR (12), and ADR + LOS (12) received ADR (2 mg / kg / b. w. i. v.) twice in a 3 - week interval. Group ADR + LOS (6) received losartan (10 mg / kg / b. w. / day by gavages) for 6 weeks and group ADR + LOS (12) for 12 weeks after second injection of ADR. Animals were killed after 6 or 12 weeks, respectively. Haemodynamic measurements were performed on anaesthetized animals, blood and urine samples were taken for biochemical analysis and the left kidney was processed for morphological studies. RESULTS: Short - term losartan treatment, besides antihypertensive effect, improved glomerular filtration rate and ameliorated glomerulosclerosis resulting in decreased proteinuria. Prolonged treatment with losartan showed further reduction of glomerulosclerosis associated with reduced progression of tubular atrophy and interstitial fibrosis, thus preventing heavy proteinuria and chronic renal failure. Losartan reduced uraemia and increased urea clearance in advanced ADR nephropathy in SHR. Histological examination showed that losartan could prevent tubular atrophy, interstitial infiltration and fibrosis in ADR nephropathy. CONCLUSION: Losartan reduces the rate of progression of ADR - induced focal segmental glomerulosclerosis to end - stage renal disease in SHR.

adriamycin

losartan

angiotensin II

losartan

adriamycin

ADR

ADR

ADR

LOS

ADR

ADR

LOS

ADR

ADR

LOS

losartan

ADR

LOS

ADR

losartan

losartan

Losartan

urea

ADR

losartan

ADR

Losartan

ADR

nephropathy

hypertensive

renal disease

hypertensive

nephropathy

glomerulosclerosis

proteinuria

glomerulosclerosis

atrophy

interstitial fibrosis

proteinuria

chronic renal failure

uraemia

nephropathy

atrophy

fibrosis

nephropathy

focal segmental glomerulosclerosis

end - stage renal disease

adriamycin

uraemia

adriamycin

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

ADR

uraemia

adriamycin

focal segmental glomerulosclerosis

adriamycin

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

ADR

focal segmental glomerulosclerosis

adriamycin

proteinuria

adriamycin

proteinuria

adriamycin

proteinuria

adriamycin

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria

ADR

proteinuria


Input: The risks of aprotinin and tranexamic acid in cardiac surgery: a one - year follow - up of 1188 consecutive patients. BACKGROUND: Our aim was to investigate postoperative complications and mortality after administration of aprotinin compared to tranexamic acid in an unselected, consecutive cohort. METHODS: Perioperative data from consecutive cardiac surgery patients were prospectively collected between September 2005 and June 2006 in a university - affiliated clinic (n = 1188). During the first 5 mo, 596 patients received aprotinin (Group A); in the next 5 mo, 592 patients were treated with tranexamic acid (Group T). Except for antifibrinolytic therapy, the anesthetic and surgical protocols remained unchanged. RESULTS: The pre - and intraoperative variables were comparable between the treatment groups. Postoperatively, a significantly higher incidence of seizures was found in Group T (4. 6% vs 1. 2%, P < 0. 001). This difference was also significant in the primary valve surgery and the high risk surgery subgroups (7. 9% vs 1. 2%, P = 0. 003; 7. 3% vs 2. 4%, P = 0. 035, respectively). Persistent atrial fibrillation (7. 9% vs 2. 3%, P = 0. 020) and renal failure (9. 7% vs 1. 7%, P = 0. 002) were also more common in Group T, in the primary valve surgery subgroup. On the contrary, among primary coronary artery bypass surgery patients, there were more acute myocardial infarctions and renal dysfunction in Group A (5. 8% vs 2. 0%, P = 0. 027; 22. 5% vs 15. 2%, P = 0. 036, respectively). The 1 - yr mortality was significantly higher after aprotinin treatment in the high risk surgery group (17. 7% vs 9. 8%, P = 0. 034). CONCLUSION: Both antifibrinolytic drugs bear the risk of adverse outcome depending on the type of cardiac surgery. Administration of aprotinin should be avoided in coronary artery bypass graft and high risk patients, whereas administration of tranexamic acid is not recommended in valve surgery.

tranexamic acid

tranexamic acid

tranexamic acid

tranexamic acid

seizures

renal failure

myocardial infarctions

renal dysfunction

tranexamic acid

renal failure

tranexamic acid

renal failure

tranexamic acid

renal failure

tranexamic acid

renal failure

tranexamic acid

seizures

tranexamic acid

seizures

tranexamic acid

seizures

tranexamic acid

seizures


Input: The biological properties of the optical isomers of propranolol and their effects on cardiac arrhythmias. 1. The optical isomers of propranolol have been compared for their beta - blocking and antiarrhythmic activities. 2. In blocking the positive inotropic and chronotropic responses to isoprenaline, (+) - propranolol had less than one hundredth the potency of (-) - propranolol. At dose levels of (+) - propranolol which attenuated the responses to isoprenaline, there was a significant prolongation of the PR interval of the electrocardiogram. 3. The metabolic responses to isoprenaline in dogs (an increase in circulating glucose, lactate and free fatty acids) were all blocked by (-) - propranolol. (+) - Propranolol had no effect on fatty acid mobilization but significantly reduced the increments in both lactate and glucose. 4. Both isomers of propranolol possessed similar depressant potency on isolated atrial muscle taken from guinea - pigs. 5. The isomers of propranolol exhibited similar local anaesthetic potencies on an isolated frog nerve preparation at a level approximately three times that of procaine. The racemic compound was significantly less potent than either isomer. 6. Both isomers of propranolol were capable of preventing adrenaline - induced cardiac arrhythmias in cats anaesthetized with halothane, but the mean dose of (-) - propranolol was 0. 09 + / - 0. 02 mg / kg whereas that of (+) - propranolol was 4. 2 + / - 1. 2 mg / kg. At the effective dose level of (+) - propranolol there was a significant prolongation of the PR interval of the electrocardiogram. Blockade of arrhythmias with both isomers was surmountable by increasing the dose of adrenaline. 7. Both isomers of propranolol were also capable of reversing ventricular tachycardia caused by ouabain in anaesthetized cats and dogs. The dose of (-) - propranolol was significantly smaller than that of (+) - propranolol in both species but much higher than that required to produce evidence of beta - blockade. 8. The implications of these results are discussed.

propranolol

propranolol

isoprenaline

propranolol

propranolol

propranolol

isoprenaline

isoprenaline

glucose

lactate

fatty acids

propranolol

Propranolol

fatty acid

lactate

glucose

propranolol

propranolol

procaine

propranolol

adrenaline

halothane

propranolol

propranolol

propranolol

adrenaline

propranolol

ouabain

propranolol

propranolol

cardiac arrhythmias

cardiac arrhythmias

arrhythmias

ventricular tachycardia

halothane

cardiac arrhythmias

halothane

cardiac arrhythmias

halothane

arrhythmias

ouabain

ventricular tachycardia

adrenaline

cardiac arrhythmias

adrenaline

cardiac arrhythmias

adrenaline

arrhythmias

adrenaline

cardiac arrhythmias

adrenaline

cardiac arrhythmias

adrenaline

arrhythmias


Input: Topotecan in combination with radiotherapy in unresectable glioblastoma: a phase 2 study. Improving glioblastoma multiforme (GBM) treatment with radio - chemotherapy remains a challenge. Topotecan is an attractive option as it exhibits growth inhibition of human glioma as well as brain penetration. The present study assessed the combination of radiotherapy (60 Gy / 30 fractions / 40 days) and topotecan (0. 9 mg / m (2) / day on days 1 - 5 on weeks 1, 3 and 5) in 50 adults with histologically proven and untreated GBM. The incidence of non - hematological toxicities was low and grade 3 - 4 hematological toxicities were reported in 20 patients (mainly lymphopenia and neutropenia). Partial response and stabilization rates were 2% and 32%, respectively, with an overall time to progression of 12 weeks. One - year overall survival (OS) rate was 42%, with a median OS of 40 weeks. Topotecan in combination with radiotherapy was well tolerated. However, while response and stabilization concerned one - third of the patients, the study did not show increased benefits in terms of survival in patients with unresectable GBM.

Topotecan

Topotecan

topotecan

Topotecan

glioblastoma

glioblastoma multiforme

GBM

glioma

GBM

toxicities

toxicities

lymphopenia

neutropenia

GBM

Topotecan

neutropenia

Topotecan

neutropenia

topotecan

neutropenia

Topotecan

neutropenia

Topotecan

lymphopenia

Topotecan

lymphopenia

topotecan

lymphopenia

Topotecan

lymphopenia


Input: Long - term lithium therapy leading to hyperparathyroidism: a case report. PURPOSE: This paper reviews the effect of chronic lithium therapy on serum calcium level and parathyroid glands, its pathogenesis, and treatment options. We examined the case of a lithium - treated patient who had recurrent hypercalcemia to better understand the disease process. CONCLUSION: Primary hyperparathyroidism is a rare but potentially life - threatening side effect of long - term lithium therapy. Careful patient selection and long - term follow - up can reduce morbidity. PRACTICAL IMPLICATIONS: As much as 15% of lithium - treated patients become hypercalcemic. By routinely monitoring serum calcium levels, healthcare providers can improve the quality of life of this patient group.

lithium

lithium

calcium

lithium

lithium

lithium

calcium

hyperparathyroidism

hypercalcemia

Primary hyperparathyroidism

hypercalcemic

lithium

hyperparathyroidism

lithium

hyperparathyroidism

lithium

hyperparathyroidism

lithium

hyperparathyroidism

lithium

hyperparathyroidism

lithium

hypercalcemia

lithium

hypercalcemic

lithium

hypercalcemia

lithium

hypercalcemic

lithium

hypercalcemia

lithium

hypercalcemic

lithium

hypercalcemia

lithium

hypercalcemic

lithium

hypercalcemia

lithium

hypercalcemic


Input: Comparison of laryngeal mask with endotracheal tube for anesthesia in endoscopic sinus surgery. BACKGROUND: The purpose of this study was to compare surgical conditions, including the amount of intraoperative bleeding as well as intraoperative blood pressure, during functional endoscopic sinus surgery (FESS) using flexible reinforced laryngeal mask airway (FRLMA) versus endotracheal tube (ETT) in maintaining controlled hypotension anesthesia induced by propofol - remifentanil total i. v. anesthesia (TIVA). METHODS: Sixty normotensive American Society of Anesthesiologists I - II adult patients undergoing FESS under controlled hypotension anesthesia caused by propofol - remifentanil - TIVA were randomly assigned into two groups: group I, FRLMA; group II, ETT. Hemorrhage was measured and the visibility of the operative field was evaluated according to a six - point scale. RESULTS: Controlled hypotension was achieved within a shorter period using laryngeal mask using lower rates of remifentanil infusion and lower total dose of remifentanil. CONCLUSION: In summary, our results indicate that airway management using FRLMA during controlled hypotension anesthesia provided better surgical conditions in terms of quality of operative field and blood loss and allowed for convenient induced hypotension with low doses of remifentanil during TIVA in patients undergoing FESS.

bleeding

hypotension

hypotension

Hemorrhage

hypotension

hypotension

hypotension

propofol

remifentanil

propofol

remifentanil

remifentanil

remifentanil

remifentanil

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

propofol

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension

remifentanil

hypotension


Input: Nonalcoholic fatty liver disease during valproate therapy. Valproic acid (VPA) is effective for the treatment of many types of epilepsy, but its use can be associated with an increase in body weight. We report a case of nonalcoholic fatty liver disease (NAFLD) arising in a child who developed obesity during VPA treatment. Laboratory data revealed hyperinsulinemia with insulin resistance. After the withdrawal of VPA therapy, our patient showed a significant weight loss, a decrease of body mass index, and normalization of metabolic and endocrine parameters; moreover, ultrasound measurements showed a complete normalization. The present case suggests that obesity, hyperinsulinemia, insulin resistance, and long - term treatment with VPA may be all associated with the development of NAFLD; this side effect is reversible after VPA withdrawal.

Nonalcoholic fatty liver disease

epilepsy

nonalcoholic fatty liver disease

NAFLD

obesity

hyperinsulinemia

insulin resistance

weight loss

obesity

hyperinsulinemia

insulin resistance

NAFLD

valproate

Valproic acid

VPA

VPA

VPA

VPA

VPA

valproate

obesity

valproate

obesity

Valproic acid

obesity

Valproic acid

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

VPA

obesity

valproate

hyperinsulinemia

valproate

hyperinsulinemia

Valproic acid

hyperinsulinemia

Valproic acid

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

VPA

hyperinsulinemia

valproate

Nonalcoholic fatty liver disease

valproate

nonalcoholic fatty liver disease

valproate

NAFLD

valproate

NAFLD

Valproic acid

Nonalcoholic fatty liver disease

Valproic acid

nonalcoholic fatty liver disease

Valproic acid

NAFLD

Valproic acid

NAFLD

VPA

Nonalcoholic fatty liver disease

VPA

nonalcoholic fatty liver disease

VPA

NAFLD

VPA

NAFLD

VPA

Nonalcoholic fatty liver disease

VPA

nonalcoholic fatty liver disease

VPA

NAFLD

VPA

NAFLD

VPA

Nonalcoholic fatty liver disease

VPA

nonalcoholic fatty liver disease

VPA

NAFLD

VPA

NAFLD

VPA

Nonalcoholic fatty liver disease

VPA

nonalcoholic fatty liver disease

VPA

NAFLD

VPA

NAFLD

VPA

Nonalcoholic fatty liver disease

VPA

nonalcoholic fatty liver disease

VPA

NAFLD

VPA

NAFLD

valproate

insulin resistance

valproate

insulin resistance

Valproic acid

insulin resistance

Valproic acid

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance

VPA

insulin resistance


Input: Carbimazole induced ANCA positive vasculitis. Anti - thyroid drugs, like carbimazole and propylthiouracil (PTU) are commonly prescribed for the treatment of hyperthyroidism. One should be aware of the side effects of antithyroid medications. Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis is a potentially life - threatening adverse effect of antithyroidmedications. We report a patient with Graves' disease who developed ANCA positive carbimazole induced vasculitis. The episode was characterized by a vasculitic skin rash associated with large joint arthritis, pyrexia and parotiditis but no renal or pulmonary involvement. He was referred to us for neurological evaluation because he had difficulty in getting up from squatting position and was suspected to have myositis. Carbimazole and methimazole have a lower incidence of reported ANCA positive side effects than PUT. To the best of our knowledge this is the first ANCA positive carbimazole induced vasculitis case reported from India.

Carbimazole

Anti - thyroid drugs

carbimazole

propylthiouracil

PTU

antithyroid medications

antithyroidmedications

carbimazole

Carbimazole

methimazole

carbimazole

ANCA positive vasculitis

hyperthyroidism

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

Graves' disease

vasculitis

vasculitic

skin rash

arthritis

pyrexia

parotiditis

myositis

vasculitis

Anti - thyroid drugs

parotiditis

antithyroid medications

parotiditis

antithyroidmedications

parotiditis

Anti - thyroid drugs

ANCA positive vasculitis

Anti - thyroid drugs

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

antithyroid medications

ANCA positive vasculitis

antithyroid medications

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

antithyroidmedications

ANCA positive vasculitis

antithyroidmedications

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

Anti - thyroid drugs

arthritis

antithyroid medications

arthritis

antithyroidmedications

arthritis

Carbimazole

parotiditis

carbimazole

parotiditis

carbimazole

parotiditis

Carbimazole

parotiditis

carbimazole

parotiditis

Carbimazole

pyrexia

carbimazole

pyrexia

carbimazole

pyrexia

Carbimazole

pyrexia

carbimazole

pyrexia

Anti - thyroid drugs

pyrexia

antithyroid medications

pyrexia

antithyroidmedications

pyrexia

Carbimazole

arthritis

carbimazole

arthritis

carbimazole

arthritis

Carbimazole

arthritis

carbimazole

arthritis

Carbimazole

ANCA positive vasculitis

Carbimazole

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

carbimazole

ANCA positive vasculitis

carbimazole

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

carbimazole

ANCA positive vasculitis

carbimazole

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

Carbimazole

ANCA positive vasculitis

Carbimazole

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis

carbimazole

ANCA positive vasculitis

carbimazole

Antineutrophil cytoplasmic antibody (ANCA) - - associated vasculitis


Input: Aspirin for the primary prevention of cardiovascular events: an update of the evidence for the U. S. Preventive Services Task Force. BACKGROUND: Coronary heart disease and cerebrovascular disease are leading causes of death in the United States. In 2002, the U. S. Preventive Services Task Force (USPSTF) strongly recommended that clinicians discuss aspirin with adults who are at increased risk for coronary heart disease. PURPOSE: To determine the benefits and harms of taking aspirin for the primary prevention of myocardial infarctions, strokes, and death. DATA SOURCES: MEDLINE and Cochrane Library (search dates, 1 January 2001 to 28 August 2008), recent systematic reviews, reference lists of retrieved articles, and suggestions from experts. STUDY SELECTION: English - language randomized, controlled trials (RCTs); case - control studies; meta - analyses; and systematic reviews of aspirin versus control for the primary prevention of cardiovascular disease (CVD) were selected to answer the following questions: Does aspirin decrease coronary heart events, strokes, death from coronary heart events or stroke, or all - cause mortality in adults without known CVD? Does aspirin increase gastrointestinal bleeding or hemorrhagic strokes? DATA EXTRACTION: All studies were reviewed, abstracted, and rated for quality by using predefined USPSTF criteria. DATA SYNTHESIS: New evidence from 1 good - quality RCT, 1 good - quality meta - analysis, and 2 fair - quality subanalyses of RCTs demonstrates that aspirin use reduces the number of CVD events in patients without known CVD. Men in these studies experienced fewer myocardial infarctions and women experienced fewer ischemic strokes. Aspirin does not seem to affect CVD mortality or all - cause mortality in either men or women. The use of aspirin for primary prevention increases the risk for major bleeding events, primarily gastrointestinal bleeding events, in both men and women. Men have an increased risk for hemorrhagic strokes with aspirin use. A new RCT and meta - analysis suggest that the risk for hemorrhagic strokes in women is not statistically significantly increased. LIMITATIONS: New evidence on aspirin for the primary prevention of CVD is limited. The dose of aspirin used in the RCTs varied, which prevented the estimation of the most appropriate dose for primary prevention. Several of the RCTs were conducted within populations of health professionals, which potentially limits generalizability. CONCLUSION: Aspirin reduces the risk for myocardial infarction in men and strokes in women. Aspirin use increases the risk for serious bleeding events.

Aspirin

aspirin

aspirin

aspirin

aspirin

aspirin

aspirin

Aspirin

aspirin

aspirin

aspirin

aspirin

Aspirin

Aspirin

Coronary heart disease

cerebrovascular disease

coronary heart disease

myocardial infarctions

strokes

cardiovascular disease

CVD

strokes

stroke

CVD

gastrointestinal bleeding

hemorrhagic strokes

hemorrhagic

strokes

CVD

CVD

myocardial infarctions

strokes

CVD

bleeding

gastrointestinal bleeding

hemorrhagic strokes

hemorrhagic

strokes

hemorrhagic strokes

hemorrhagic

strokes

CVD

myocardial infarction

strokes

bleeding

Aspirin

strokes

Aspirin

strokes

Aspirin

stroke

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

stroke

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

strokes

aspirin

stroke

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

hemorrhagic strokes

aspirin

strokes

aspirin

strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

stroke

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

stroke

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

hemorrhagic strokes

Aspirin

strokes

Aspirin

strokes

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

hemorrhagic

Aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding

Aspirin

gastrointestinal bleeding


Input: Reducing harm associated with anticoagulation: practical considerations of argatroban therapy in heparin - induced thrombocytopenia. Argatroban is a hepatically metabolized, direct thrombin inhibitor used for prophylaxis or treatment of thrombosis in heparin - induced thrombocytopenia (HIT) and for patients with or at risk of HIT undergoing percutaneous coronary intervention (PCI). The objective of this review is to summarize practical considerations of argatroban therapy in HIT. The US FDA - recommended argatroban dose in HIT is 2 microg / kg / min (reduced in patients with hepatic impairment and in paediatric patients), adjusted to achieve activated partial thromboplastin times (aPTTs) 1. 5 - 3 times baseline (not > 100 seconds). Contemporary experiences indicate that reduced doses are also needed in patients with conditions associated with hepatic hypoperfusion, e. g. heart failure, yet are unnecessary for renal dysfunction, adult age, sex, race / ethnicity or obesity. Argatroban 0. 5 - 1. 2 microg / kg / min typically supports therapeutic aPTTs. The FDA - recommended dose during PCI is 25 microg / kg / min (350 microg / kg initial bolus), adjusted to achieve activated clotting times (ACTs) of 300 - 450 sec. For PCI, argatroban has not been investigated in hepatically impaired patients; dose adjustment is unnecessary for adult age, sex, race / ethnicity or obesity, and lesser doses may be adequate with concurrent glycoprotein IIb / IIIa inhibition. Argatroban prolongs the International Normalized Ratio, and published approaches for monitoring the argatroban - to - warfarin transition should be followed. Major bleeding with argatroban is 0 - 10% in the non - interventional setting and 0 - 5. 8% periprocedurally. Argatroban has no specific antidote, and if excessive anticoagulation occurs, argatroban infusion should be stopped or reduced. Improved familiarity of healthcare professionals with argatroban therapy in HIT, including in special populations and during PCI, may facilitate reduction of harm associated with HIT (e. g. fewer thromboses) or its treatment (e. g. fewer argatroban medication errors).

argatroban

heparin

Argatroban

heparin

argatroban

argatroban

Argatroban

argatroban

Argatroban

argatroban

warfarin

argatroban

Argatroban

argatroban

argatroban

argatroban

thrombocytopenia

thrombosis

thrombocytopenia

HIT

HIT

HIT

HIT

hepatic impairment

heart failure

renal dysfunction

obesity

obesity

bleeding

HIT

HIT

argatroban

bleeding

Argatroban

bleeding

argatroban

bleeding

argatroban

bleeding

Argatroban

bleeding

argatroban

bleeding

Argatroban

bleeding

argatroban

bleeding

argatroban

bleeding

Argatroban

bleeding

argatroban

bleeding

argatroban

bleeding

argatroban

bleeding


Input: Rhabdomyolysis and brain ischemic stroke in a heroin - dependent male under methadone maintenance therapy. OBJECTIVE: There are several complications associated with heroin abuse, some of which are life - threatening. Methadone may aggravate this problem. METHOD: A clinical case description. RESULTS: A 33 - year - old man presented with rhabdomyolysis and cerebral ischemic stroke after intravenous heroin. He had used heroin since age 20, and had used 150 mg methadone daily for 6 months. He was found unconsciousness at home and was sent to our hospital. In the ER, his opiate level was 4497 ng / ml. In the ICU, we found rhabdomyolysis, acute renal failure and acute respiratory failure. After transfer to an internal ward, we noted aphasia and weakness of his left limbs. After MRI, we found cerebral ischemic infarction. CONCLUSION: Those using methadone and heroin simultaneously may increase risk of rhabdomyolysis and ischemic stroke. Patients under methadone maintenance therapy should be warned regarding these serious adverse events. Hypotheses of heroin - related rhabdomyolysis and stroke in heroin abusers are discussed.

Rhabdomyolysis

ischemic stroke

heroin abuse

rhabdomyolysis

ischemic stroke

unconsciousness

rhabdomyolysis

acute renal failure

respiratory failure

aphasia

weakness

cerebral ischemic infarction

rhabdomyolysis

ischemic stroke

rhabdomyolysis

stroke

heroin

methadone

Methadone

heroin

heroin

methadone

methadone

heroin

methadone

heroin

heroin

heroin

Rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

Rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

Rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

Rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

Rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

Rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

heroin

rhabdomyolysis

methadone

Rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

Methadone

Rhabdomyolysis

Methadone

rhabdomyolysis

Methadone

rhabdomyolysis

Methadone

rhabdomyolysis

Methadone

rhabdomyolysis

methadone

Rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

Rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

Rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

methadone

rhabdomyolysis

heroin

stroke

heroin

stroke

heroin

stroke

heroin

stroke

heroin

stroke

heroin

stroke

methadone

stroke

Methadone

stroke

methadone

stroke

methadone

stroke

methadone

stroke


Input: Increased vulnerability to 6 - hydroxydopamine lesion and reduced development of dyskinesias in mice lacking CB1 cannabinoid receptors. Motor impairment, dopamine (DA) neuronal activity and proenkephalin (PENK) gene expression in the caudate - putamen (CPu) were measured in 6 - OHDA - lesioned and treated (L - DOPA + benserazide) CB1 KO and WT mice. A lesion induced by 6 - OHDA produced more severe motor deterioration in CB1 KO mice accompanied by more loss of DA neurons and increased PENK gene expression in the CPu. Oxidative / nitrosative and neuroinflammatory parameters were estimated in the CPu and cingulate cortex (Cg). CB1 KO mice exhibited higher MDA levels and iNOS protein expression in the CPu and Cg compared to WT mice. Treatment with L - DOPA + benserazide (12 weeks) resulted in less severe dyskinesias in CB1 KO than in WT mice. The results revealed that the lack of cannabinoid CB1 receptors increased the severity of motor impairment and DA lesion, and reduced L - DOPA - induced dyskinesias. These results suggest that activation of CB1 receptors offers neuroprotection against dopaminergic lesion and the development of L - DOPA - induced dyskinesias.

6 - hydroxydopamine

dopamine

DA

proenkephalin

PENK

6 - OHDA

L - DOPA + benserazide

6 - OHDA

DA

PENK

MDA

L - DOPA + benserazide

DA

L - DOPA

L - DOPA

dyskinesias

dyskinesias

dyskinesias

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias

L - DOPA

dyskinesias


Input: Animal model of mania induced by ouabain: Evidence of oxidative stress in submitochondrial particles of the rat brain. The intracerebroventricular (ICV) administration of ouabain (a Na (+) / K (+) - ATPase inhibitor) in rats has been suggested to mimic some symptoms of human bipolar mania. Clinical studies have shown that bipolar disorder may be related to mitochondrial dysfunction. Herein, we investigated the behavioral and biochemical effects induced by the ICV administration of ouabain in rats. To achieve this aim, the effects of ouabain injection immediately after and 7 days following a single ICV administration (at concentrations of 10 (- 2) and 10 (- 3) M) on locomotion was measured using the open - field test. Additionally, thiobarbituric acid reactive substances (TBARSs) and superoxide production were measured in submitochondrial particles of the prefrontal cortex, hippocampus, striatum and amygdala. Our findings demonstrated that ouabain at 10 (- 2) and 10 (- 3) M induced hyperlocomotion in rats, and this response remained up to 7 days following a single ICV injection. In addition, we observed that the persistent increase in the rat spontaneous locomotion is associated with increased TBARS levels and superoxide generation in submitochondrial particles in the prefrontal cortex, striatum and amygdala. In conclusion, ouabain - induced mania - like behavior may provide a useful animal model to test the hypothesis of the involvement of oxidative stress in bipolar disorder.

mania

bipolar mania

bipolar disorder

mitochondrial dysfunction

hyperlocomotion

mania

bipolar disorder

ouabain

ouabain

K

ouabain

ouabain

thiobarbituric acid

superoxide

ouabain

superoxide

ouabain

ouabain

mania

ouabain

bipolar mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar mania

ouabain

bipolar disorder

ouabain

mania

ouabain

bipolar disorder


Input: Intraoperative dialysis during liver transplantation with citrate dialysate. Liver transplantation for acutely ill patients with fulminant liver failure carries high intraoperative and immediate postoperative risks. These are increased with the presence of concomitant acute kidney injury (AKI) and intraoperative dialysis is sometimes required to allow the transplant to proceed. The derangements in the procoagulant and anticoagulant pathways during fulminant liver failure can lead to difficulties with anticoagulation during dialysis, especially when continued in the operating room. Systemic anticoagulation is unsafe and regional citrate anticoagulation in the absence of a functional liver carries the risk of citrate toxicity. Citrate dialysate, a new dialysate with citric acid can be used for anticoagulation in patients who cannot tolerate heparin or regional citrate. We report a case of a 40 - year - old female with acetaminophen - induced fulminant liver failure with associated AKI who underwent intraoperative dialytic support during liver transplantation anticoagulated with citrate dialysate during the entire procedure. The patient tolerated the procedure well without any signs of citrate toxicity and maintained adequate anticoagulation for patency of the dialysis circuit. Citrate dialysate is a safe alternative for intradialytic support of liver transplantation in fulminant liver failure.

citrate

citrate

citrate

Citrate

citric acid

heparin

citrate

acetaminophen

citrate

citrate

Citrate

fulminant liver failure

acute kidney injury

AKI

fulminant liver failure

toxicity

fulminant liver failure

AKI

toxicity

fulminant liver failure

acetaminophen

fulminant liver failure

acetaminophen

fulminant liver failure

acetaminophen

fulminant liver failure

acetaminophen

fulminant liver failure

acetaminophen

acute kidney injury

acetaminophen

AKI

acetaminophen

AKI


Input: Delirium in a patient with toxic flecainide plasma concentrations: the role of a pharmacokinetic drug interaction with paroxetine. OBJECTIVE: To describe a case of flecainide - induced delirium associated with a pharmacokinetic drug interaction with paroxetine. CASE SUMMARY: A 69 - year - old white female presented to the emergency department with a history of confusion and paranoia over the past several days. On admission the patient was taking carvedilol 12 mg twice daily, warfarin 2 mg / day, folic acid 1 mg / day, levothyroxine 100 microg / day, pantoprazole 40 mg / day, paroxetine 40 mg / day, and flecainide 100 mg twice daily. Flecainide had been started 2 weeks prior for atrial fibrillation. Laboratory test findings on admission were notable only for a flecainide plasma concentration of 1360 microg / L (reference range 200 - 1000). A metabolic drug interaction between flecainide and paroxetine, which the patient had been taking for more than 5 years, was considered. Paroxetine was discontinued and the dose of flecainide was reduced to 50 mg twice daily. Her delirium resolved 3 days later. DISCUSSION: Flecainide and pharmacologically similar agents that interact with sodium channels may cause delirium in susceptible patients. A MEDLINE search (1966 - January 2009) revealed one in vivo pharmacokinetic study on the interaction between flecainide, a CYP2D6 substrate, and paroxetine, a CYP2D6 inhibitor, as well as 3 case reports of flecainide - induced delirium. According to the Naranjo probability scale, flecainide was the probable cause of the patient' s delirium; the Horn Drug Interaction Probability Scale indicates a possible pharmacokinetic drug interaction between flecainide and paroxetine. CONCLUSIONS: Supratherapeutic flecainide plasma concentrations may cause delirium. Because toxicity may occur when flecainide is prescribed with paroxetine and other potent CYP2D6 inhibitors, flecainide plasma concentrations should be monitored closely with commencement of CYP2D6 inhibitors.

Delirium

delirium

confusion

paranoia

atrial fibrillation

delirium

delirium

delirium

delirium

delirium

toxicity

flecainide

paroxetine

flecainide

paroxetine

carvedilol

warfarin

folic acid

levothyroxine

pantoprazole

paroxetine

flecainide

Flecainide

flecainide

flecainide

paroxetine

Paroxetine

flecainide

Flecainide

sodium

flecainide

paroxetine

flecainide

flecainide

flecainide

paroxetine

flecainide

flecainide

paroxetine

flecainide

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

Flecainide

Delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

Flecainide

Delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

Flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

Delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

flecainide

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

Paroxetine

Delirium

Paroxetine

delirium

Paroxetine

delirium

Paroxetine

delirium

Paroxetine

delirium

Paroxetine

delirium

Paroxetine

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

Delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium

paroxetine

delirium


Input: Efficacy of everolimus (RAD001) in patients with advanced NSCLC previously treated with chemotherapy alone or with chemotherapy and EGFR inhibitors. BACKGROUND: Treatment options are scarce in pretreated advanced non - small - cell lung cancer (NSCLC) patients. RAD001, an oral inhibitor of the mammalian target of rapamycin (mTOR), has shown phase I efficacy in NSCLC. METHODS: Stage IIIb or IV NSCLC patients, with two or fewer prior chemotherapy regimens, one platinum based (stratum 1) or both chemotherapy and epidermal growth factor receptor tyrosine kinase inhibitors (stratum 2), received RAD001 10 mg / day until progression or unacceptable toxicity. Primary objective was overall response rate (ORR). Analyses of markers associated with the mTOR pathway were carried out on archival tumor from a subgroup using immunohistochemistry (IHC) and direct mutation sequencing. RESULTS: Eighty - five patients were enrolled, 42 in stratum 1 and 43 in stratum. ORR was 4. 7% (7. 1% stratum 1; 2. 3% stratum 2). Overall disease control rate was 47. 1%. Median progression - free survivals (PFSs) were 2. 6 (stratum 1) and 2. 7 months (stratum 2). Common > or = grade 3 events were fatigue, dyspnea, stomatitis, anemia, and thrombocytopenia. Pneumonitis, probably or possibly related, mainly grade 1 / 2, occurred in 25%. Cox regression analysis of IHC scores found that only phospho AKT (pAKT) was a significant independent predictor of worse PFS. CONCLUSIONS: RAD001 10 mg / day was well tolerated, showing modest clinical activity in pretreated NSCLC. Evaluation of RAD001 plus standard therapy for metastatic NSCLC continues.

everolimus

rapamycin

platinum

tyrosine

NSCLC

non - small - cell lung cancer

NSCLC

NSCLC

NSCLC

toxicity

tumor

fatigue

dyspnea

stomatitis

anemia

thrombocytopenia

Pneumonitis

NSCLC

NSCLC

everolimus

thrombocytopenia

thrombocytopenia

thrombocytopenia

thrombocytopenia

thrombocytopenia

thrombocytopenia

everolimus

stomatitis

stomatitis

stomatitis

stomatitis

stomatitis

stomatitis

everolimus

anemia

anemia

anemia

anemia

anemia

anemia

everolimus

fatigue

fatigue

fatigue

fatigue

fatigue

fatigue

everolimus

dyspnea

dyspnea

dyspnea

dyspnea

dyspnea

dyspnea


Input: Posttransplant anemia: the role of sirolimus. Posttransplant anemia is a common problem that may hinder patients' quality of life. It occurs in 12 to 76% of patients, and is most common in the immediate posttransplant period. A variety of factors have been identified that increase the risk of posttransplant anemia, of which the level of renal function is most important. Sirolimus, a mammalian target of rapamycin inhibitor, has been implicated as playing a special role in posttransplant anemia. This review considers anemia associated with sirolimus, including its presentation, mechanisms, and management.

anemia

anemia

anemia

anemia

anemia

sirolimus

Sirolimus

rapamycin

sirolimus

sirolimus

anemia

sirolimus

anemia

sirolimus

anemia

sirolimus

anemia

sirolimus

anemia

Sirolimus

anemia

Sirolimus

anemia

Sirolimus

anemia

Sirolimus

anemia

Sirolimus

anemia

rapamycin

anemia

rapamycin

anemia

rapamycin

anemia

rapamycin

anemia

rapamycin

anemia

sirolimus

anemia

sirolimus

anemia

sirolimus

anemia

sirolimus

anemia

sirolimus

anemia


Input: Coronary computerized tomography angiography for rapid discharge of low - risk patients with cocaine - associated chest pain. BACKGROUND: Most patients presenting to emergency departments (EDs) with cocaine - associated chest pain are admitted for at least 12 hours and receive a " rule out acute coronary syndrome " protocol, often with noninvasive testing prior to discharge. In patients without cocaine use, coronary computerized tomography angiography (CTA) has been shown to be useful for identifying a group of patients at low risk for cardiac events who can be safely discharged. It is unclear whether a coronary CTA strategy would be efficacious in cocaine - associated chest pain, as coronary vasospasm may account for some of the ischemia. We studied whether a negative coronary CTA in patients with cocaine - associated chest pain could identify a subset safe for discharge. METHODS: We prospectively evaluated the safety of coronary CTA for low - risk patients who presented to the ED with cocaineassociated chest pain (self - reported or positive urine test). Consecutive patients received either immediate coronary CTA in the ED (without serial markers) or underwent coronary CTA after a brief observation period with serial cardiac marker measurements. Patients with negative coronary CTA (maximal stenosis less than 50%) were discharged. The main outcome was 30 - day cardiovascular death or myocardial infarction. RESULTS: A total of 59 patients with cocaine - associated chest pain were evaluated. Patients had a mean age of 45. 6 + / - 6. 6 yrs and were 86% black, 66% male. Seventy - nine percent had a normal or nonspecific ECG and 85% had a TIMI score < 2. Twenty patients received coronary CTA immediately in the ED, 18 of whom were discharged following CTA (90%). Thirty - nine received coronary CTA after a brief observation period, with 37 discharged home following CTA (95%). Six patients had coronary stenosis > or = 50%. During the 30 - day follow - up period, no patients died of a cardiovascular event (0%; 95% CI, 0 - 6. 1%) and no patient sustained a nonfatal myocardial infarction (0%; 95% CI, 0 - 6. 1%). CONCLUSIONS: Although cocaine - associated myocardial ischemia can result from coronary vasoconstriction, patients with cocaine associated chest pain, a non - ischemic ECG, and a TIMI risk score < 2 may be safely discharged from the ED after a negative coronary CTA with a low risk of 30 - day adverse events.

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

chest pain

chest pain

acute coronary syndrome

chest pain

coronary vasospasm

ischemia

chest pain

chest pain

stenosis

myocardial infarction

chest pain

coronary stenosis

myocardial infarction

myocardial ischemia

chest pain

ischemic

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

chest pain

cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia

cocaine

myocardial ischemia