Input: Famotidine - associated delirium. A series of six cases. Famotidine is a histamine H2 - receptor antagonist used in inpatient settings for prevention of stress ulcers and is showing increasing popularity because of its low cost. Although all of the currently available H2 - receptor antagonists have shown the propensity to cause delirium, only two previously reported cases have been associated with famotidine. The authors report on six cases of famotidine - associated delirium in hospitalized patients who cleared completely upon removal of famotidine. The pharmacokinetics of famotidine are reviewed, with no change in its metabolism in the elderly population seen. The implications of using famotidine in elderly persons are discussed.

Famotidine

Famotidine

famotidine

famotidine

famotidine

famotidine

famotidine

delirium

ulcers

delirium

delirium

Famotidine

delirium

Famotidine

delirium

Famotidine

delirium

Famotidine

delirium

Famotidine

delirium

Famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium

famotidine

delirium


Input: Indomethacin induced hypotension in sodium and volume depleted rats. After a single oral dose of 4 mg / kg indomethacin (IDM) to sodium and volume depleted rats plasma renin activity (PRA) and systolic blood pressure fell significantly within four hours. In sodium repleted animals indomethacin did not change systolic blood pressure (BP) although plasma renin activity was decreased. Thus, indomethacin by inhibition of prostaglandin synthesis may diminish the blood pressure maintaining effect of the stimulated renin - angiotensin system in sodium and volume depletion.

Indomethacin

sodium

indomethacin

IDM

sodium

sodium

indomethacin

indomethacin

prostaglandin

angiotensin

sodium

hypotension

Indomethacin

hypotension

indomethacin

hypotension

IDM

hypotension

indomethacin

hypotension

indomethacin

hypotension


Input: Late - onset scleroderma renal crisis induced by tacrolimus and prednisolone: a case report. Scleroderma renal crisis (SRC) is a rare complication of systemic sclerosis (SSc) but can be severe enough to require temporary or permanent renal replacement therapy. Moderate to high dose corticosteroid use is recognized as a major risk factor for SRC. Furthermore, there have been reports of thrombotic microangiopathy precipitated by cyclosporine in patients with SSc. In this article, we report a patient with SRC induced by tacrolimus and corticosteroids. The aim of this work is to call attention to the risk of tacrolimus use in patients with SSc.

scleroderma renal crisis

Scleroderma renal crisis

SRC

systemic sclerosis

SSc

SRC

thrombotic microangiopathy

SSc

SRC

SSc

tacrolimus

prednisolone

corticosteroid

cyclosporine

tacrolimus

corticosteroids

tacrolimus

cyclosporine

thrombotic microangiopathy

corticosteroid

systemic sclerosis

corticosteroid

SSc

corticosteroid

SSc

corticosteroid

SSc

corticosteroids

systemic sclerosis

corticosteroids

SSc

corticosteroids

SSc

corticosteroids

SSc

tacrolimus

systemic sclerosis

tacrolimus

SSc

tacrolimus

SSc

tacrolimus

SSc

tacrolimus

systemic sclerosis

tacrolimus

SSc

tacrolimus

SSc

tacrolimus

SSc

tacrolimus

systemic sclerosis

tacrolimus

SSc

tacrolimus

SSc

tacrolimus

SSc


Input: The risk and associated factors of methamphetamine psychosis in methamphetamine - dependent patients in Malaysia. OBJECTIVE: The objective of this study was to determine the risk of lifetime and current methamphetamine - induced psychosis in patients with methamphetamine dependence. The association between psychiatric co - morbidity and methamphetamine - induced psychosis was also studied. METHODS: This was a cross - sectional study conducted concurrently at a teaching hospital and a drug rehabilitation center in Malaysia. Patients with the diagnosis of methamphetamine based on DSM - IV were interviewed using the Mini International Neuropsychiatric Interview (M. I. N. I.) for methamphetamine - induced psychosis and other Axis I psychiatric disorders. The information on sociodemographic background and drug use history was obtained from interview or medical records. RESULTS: Of 292 subjects, 47. 9% of the subjects had a past history of psychotic symptoms and 13. 0% of the patients were having current psychotic symptoms. Co - morbid major depressive disorder (OR = 7. 18, 95 CI = 2. 612 - 19. 708), bipolar disorder (OR = 13. 807, 95 CI = 5. 194 - 36. 706), antisocial personality disorder (OR = 12. 619, 95 CI = 6. 702 - 23. 759) and heavy methamphetamine uses were significantly associated with lifetime methamphetamine - induced psychosis after adjusted for other factors. Major depressive disorder (OR = 2. 870, CI = 1. 154 - 7. 142) and antisocial personality disorder (OR = 3. 299, 95 CI = 1. 375 - 7. 914) were the only factors associated with current psychosis. CONCLUSION: There was a high risk of psychosis in patients with methamphetamine dependence. It was associated with co - morbid affective disorder, antisocial personality, and heavy methamphetamine use. It is recommended that all cases of methamphetamine dependence should be screened for psychotic symptoms.

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

methamphetamine

psychosis

psychosis

psychosis

psychosis

psychiatric disorders

psychotic symptoms

psychotic symptoms

depressive disorder

bipolar disorder

antisocial personality disorder

psychosis

Major depressive disorder

antisocial personality disorder

psychosis

psychosis

affective disorder

antisocial personality

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

psychotic symptoms

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychosis

methamphetamine

psychotic symptoms

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

bipolar disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality disorder

methamphetamine

antisocial personality


Input: Cerebellar sensory processing alterations impact motor cortical plasticity in Parkinson' s disease: clues from dyskinetic patients. The plasticity of primary motor cortex (M1) in patients with Parkinson' s disease (PD) and levodopa - induced dyskinesias (LIDs) is severely impaired. We recently reported in young healthy subjects that inhibitory cerebellar stimulation enhanced the sensorimotor plasticity of M1 that was induced by paired associative stimulation (PAS). This study demonstrates that the deficient sensorimotor M1 plasticity in 16 patients with LIDs could be reinstated by a single session of real inhibitory cerebellar stimulation but not sham stimulation. This was evident only when a sensory component was involved in the induction of plasticity, indicating that cerebellar sensory processing function is involved in the resurgence of M1 plasticity. The benefit of inhibitory cerebellar stimulation on LIDs is known. To explore whether this benefit is linked to the restoration of sensorimotor plasticity of M1, we conducted an additional study looking at changes in LIDs and PAS - induced plasticity after 10 sessions of either bilateral, real inhibitory cerebellar stimulation or sham stimulation. Only real and not sham stimulation had an antidyskinetic effect and it was paralleled by a resurgence in the sensorimotor plasticity of M1. These results suggest that alterations in cerebellar sensory processing function, occurring secondary to abnormal basal ganglia signals reaching it, may be an important element contributing to the maladaptive sensorimotor plasticity of M1 and the emergence of abnormal involuntary movements.

Parkinson' s disease

dyskinetic

Parkinson' s disease

PD

dyskinesias

LIDs

LIDs

LIDs

LIDs

abnormal involuntary movements

levodopa

levodopa

dyskinetic

levodopa

dyskinesias

levodopa

LIDs

levodopa

LIDs

levodopa

LIDs

levodopa

LIDs

levodopa

abnormal involuntary movements


Input: The function of P2X3 receptor and NK1 receptor antagonists on cyclophosphamide - induced cystitis in rats. PURPOSE: The purpose of the study is to explore the function of P2X3 and NK1 receptors antagonists on cyclophosphamide (CYP) - induced cystitis in rats. METHODS: Sixty female Sprague - Dawley (SD) rats were randomly divided into three groups. The rats in the control group were intraperitoneally (i. p.) injected with 0. 9% saline (4 ml / kg); the rats in the model group were i. p. injected with CYP (150 mg / kg); and the rats in the intervention group were i. p. injected with CYP with subsequently perfusion of bladder with P2X3 and NK1 receptors' antagonists, Suramin and GR 82334. Spontaneous pain behaviors following the administration of CYP were observed. Urodynamic parameters, bladder pressure - volume curve, maximum voiding pressure (MVP), and maximum cystometric capacity (MCC), were recorded. Pathological changes in bladder tissue were observed. Immunofluorescence was used to detect the expression of P2X3 and NK1 receptors in bladder. RESULTS: Cyclophosphamide treatment increased the spontaneous pain behaviors scores. The incidence of bladder instability during urine storage period of model group was significantly higher than intervention group (X (2) = 7. 619, P = 0. 007) and control group (X (2) = 13. 755, P = 0. 000). MCC in the model group was lower than the control and intervention groups (P < 0. 01). Histological changes evident in model and intervention groups rats' bladder included edema, vasodilation, and infiltration of inflammatory cells. In model group, the expression of P2X3 receptor increased in urothelium and suburothelium, and NK1 receptor increased in suburothelium, while the expression of them in intervention group was lower. CONCLUSIONS: In CYP - induced cystitis, the expression of P2X3 and NK1 receptors increased in urothelium and / or suburothelium. Perfusion of bladder with P2X3 and NK1 receptors antagonists ameliorated the bladder function.

cyclophosphamide

cyclophosphamide

CYP

CYP

CYP

Suramin

GR 82334

CYP

Cyclophosphamide

CYP

cystitis

cystitis

pain

pain

edema

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

Cyclophosphamide

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

cyclophosphamide

pain

cyclophosphamide

pain

cyclophosphamide

pain

cyclophosphamide

pain

CYP

pain

CYP

pain

CYP

pain

CYP

pain

CYP

pain

CYP

pain

CYP

pain

CYP

pain

Cyclophosphamide

pain

Cyclophosphamide

pain

CYP

pain

CYP

pain

cyclophosphamide

edema

cyclophosphamide

edema

CYP

edema

CYP

edema

CYP

edema

CYP

edema

Cyclophosphamide

edema

CYP

edema


Input: Acute hepatitis associated with clopidogrel: a case report and review of the literature. Drug - induced hepatotoxicity is a common cause of acute hepatitis, and the recognition of the responsible drug may be difficult. We describe a case of clopidogrel - related acute hepatitis. The diagnosis is strongly suggested by an accurate medical history and liver biopsy. Reports about cases of hepatotoxicity due to clopidogrel are increasing in the last few years, after the increased use of this drug. In conclusion, we believe that physicians should carefully consider the risk of drug - induced hepatic injury when clopidogrel is prescribed.

hepatitis

hepatotoxicity

hepatitis

hepatitis

hepatotoxicity

hepatic injury

clopidogrel

clopidogrel

clopidogrel

clopidogrel

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatitis

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatic injury

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatitis

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatic injury

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatitis

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatic injury

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatitis

clopidogrel

hepatitis

clopidogrel

hepatotoxicity

clopidogrel

hepatic injury


Input: Bortezomib and dexamethasone as salvage therapy in patients with relapsed / refractory multiple myeloma: analysis of long - term clinical outcomes. Bortezomib (bort) - dexamethasone (dex) is an effective therapy for relapsed / refractory (R / R) multiple myeloma (MM). This retrospective study investigated the combination of bort (1. 3 mg / m (2) on days 1, 4, 8, and 11 every 3 weeks) and dex (20 mg on the day of and the day after bort) as salvage treatment in 85 patients with R / R MM after prior autologous stem cell transplantation or conventional chemotherapy. The median number of prior lines of therapy was 2. Eighty - seven percent of the patients had received immunomodulatory drugs included in some line of therapy before bort - dex. The median number of bort - dex cycles was 6, up to a maximum of 12 cycles. On an intention - to - treat basis, 55% of the patients achieved at least partial response, including 19% CR and 35% achieved at least very good partial response. Median durations of response, time to next therapy and treatment - free interval were 8, 11. 2, and 5. 1 months, respectively. The most relevant adverse event was peripheral neuropathy, which occurred in 78% of the patients (grade II, 38%; grade III, 21%) and led to treatment discontinuation in 6%. With a median follow up of 22 months, median time to progression, progression - free survival (PFS) and overall survival (OS) were 8. 9, 8. 7, and 22 months, respectively. Prolonged PFS and OS were observed in patients achieving CR and receiving bort - dex a single line of prior therapy. Bort - dex was an effective salvage treatment for MM patients, particularly for those in first relapse.

Bortezomib

dexamethasone

Bortezomib

bort

dexamethasone

dex

bort

dex

bort

bort

dex

bort

dex

bort

dex

Bort

dex

multiple myeloma

multiple myeloma

MM

MM

peripheral neuropathy

MM

dexamethasone

peripheral neuropathy

dexamethasone

peripheral neuropathy

dex

peripheral neuropathy

dex

peripheral neuropathy

dex

peripheral neuropathy

dex

peripheral neuropathy

dex

peripheral neuropathy

dex

peripheral neuropathy

Bortezomib

peripheral neuropathy

Bortezomib

peripheral neuropathy

bort

peripheral neuropathy

bort

peripheral neuropathy

bort

peripheral neuropathy

bort

peripheral neuropathy

bort

peripheral neuropathy

bort

peripheral neuropathy

Bort

peripheral neuropathy


Input: Pubertal exposure to Bisphenol A increases anxiety - like behavior and decreases acetylcholinesterase activity of hippocampus in adult male mice. The negative effects of Bisphenol A (BPA) on neurodevelopment and behaviors have been well established. Acetylcholinesterase (AChE) is a regulatory enzyme which is involved in anxiety - like behavior. This study investigated behavioral phenotypes and AChE activity in male mice following BPA exposure during puberty. On postnatal day (PND) 35, male mice were exposed to 50mg BPA / kg diet per day for a period of 35 days. On PND71, a behavioral assay was performed using the elevated plus maze (EPM) and the light / dark test. In addition, AChE activity was measured in the prefrontal cortex, hypothalamus, cerebellum and hippocampus. Results from our behavioral phenotyping indicated that anxiety - like behavior was increased in mice exposed to BPA. AChE activity was significantly decreased in the hippocampus of mice with BPA compared to control mice, whereas no difference was found in the prefrontal cortex, hypothalamus and cerebellum. Our findings showed that pubertal BPA exposure increased anxiety - like behavior, which may be associated with decreased AChE activity of the hippocampus in adult male mice. Further studies are necessary to investigate the cholinergic signaling of the hippocampus in PBE induced anxiety - like behaviors.

Bisphenol A

Bisphenol A

BPA

BPA

BPA

BPA

BPA

BPA

anxiety

anxiety

anxiety

anxiety

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

Bisphenol A

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety

BPA

anxiety


Input: Biochemical effects of Solidago virgaurea extract on experimental cardiotoxicity. Cardiovascular diseases (CVDs) are the major health problem of advanced as well as developing countries of the world. The aim of the present study was to investigate the protective effect of the Solidago virgaurea extract on isoproterenol - induced cardiotoxicity in rats. The subcutaneous injection of isoproterenol (30 mg / kg) into rats twice at an interval of 24 h, for two consecutive days, led to a significant increase in serum lactate dehydrogenase, creatine phosphokinase, alanine transaminase, aspartate transaminase, and angiotensin - converting enzyme activities, total cholesterol, triglycerides, free serum fatty acid, cardiac tissue malondialdehyde (MDA), and nitric oxide levels and a significant decrease in levels of glutathione and superoxide dismutase in cardiac tissue as compared to the normal control group (P < 0. 05). Pretreatment with S. virgaurea extract for 5 weeks at a dose of 250 mg / kg followed by isoproterenol injection significantly prevented the observed alterations. Captopril (50 mg / kg / day, given orally), an inhibitor of angiotensin - converting enzyme used as a standard cardioprotective drug, was used as a positive control in this study. The data of the present study suggest that S. virgaurea extract exerts its protective effect by decreasing MDA level and increasing the antioxidant status in isoproterenol - treated rats. The study emphasizes the beneficial action of S. virgaurea extract as a cardioprotective agent.

cardiotoxicity

Cardiovascular diseases

CVDs

cardiotoxicity

isoproterenol

isoproterenol

lactate

creatine

alanine

aspartate

angiotensin

cholesterol

triglycerides

fatty acid

malondialdehyde

MDA

nitric oxide

glutathione

superoxide

isoproterenol

Captopril

angiotensin

MDA

isoproterenol

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity

isoproterenol

cardiotoxicity


Input: " Real - world " data on the efficacy and safety of lenalidomide and dexamethasone in patients with relapsed / refractory multiple myeloma who were treated according to the standard clinical practice: a study of the Greek Myeloma Study Group. Lenalidomide and dexamethasone (RD) is a standard of care for relapsed / refractory multiple myeloma (RRMM), but there is limited published data on its efficacy and safety in the " real world " (RW), according to the International Society of Pharmacoeconomics and Outcomes Research definition. We studied 212 RRMM patients who received RD in RW. Objective response (> PR (partial response)) rate was 77. 4% (complete response (CR), 20. 2%). Median time to first and best response was 2 and 5 months, respectively. Median time to CR when RD was given as 2nd or > 2 (nd) - line treatment at 4 and 11 months, respectively. Quality of response was independent of previous lines of therapies or previous exposure to thalidomide or bortezomib. Median duration of response was 34. 4 months, and it was higher in patients who received RD until progression (not reached versus 19 months, p < 0. 001). Improvement of humoral immunity occurred in 60% of responders (p < 0. 001) and in the majority of patients who achieved stable disease. Adverse events were reported in 68. 9% of patients (myelosuppression in 49. 4%) and 12. 7% of patients needed hospitalization. Peripheral neuropathy was observed only in 2. 5% of patients and deep vein thrombosis in 5. 7%. Dose reductions were needed in 31% of patients and permanent discontinuation in 38. 9%. Median time to treatment discontinuation was 16. 8 months. Performance status (PS) and initial lenalidomide dose predicted for treatment discontinuation. Extra - medullary relapses occurred in 3. 8% of patients. Our study confirms that RD is effective and safe in RRMM in the RW; it produces durable responses especially in patients who continue on treatment till progression and improves humoral immunity even in patients with stable disease.

lenalidomide

dexamethasone

Lenalidomide

dexamethasone

RD

RD

RD

thalidomide

bortezomib

RD

lenalidomide

RD

multiple myeloma

Myeloma

multiple myeloma

RRMM

RRMM

myelosuppression

Peripheral neuropathy

deep vein thrombosis

RRMM

dexamethasone

Peripheral neuropathy

dexamethasone

Peripheral neuropathy

RD

Peripheral neuropathy

RD

Peripheral neuropathy

RD

Peripheral neuropathy

RD

Peripheral neuropathy

RD

Peripheral neuropathy

dexamethasone

myelosuppression

dexamethasone

myelosuppression

RD

myelosuppression

RD

myelosuppression

RD

myelosuppression

RD

myelosuppression

RD

myelosuppression

dexamethasone

deep vein thrombosis

dexamethasone

deep vein thrombosis

RD

deep vein thrombosis

RD

deep vein thrombosis

RD

deep vein thrombosis

RD

deep vein thrombosis

RD

deep vein thrombosis

lenalidomide

myelosuppression

Lenalidomide

myelosuppression

lenalidomide

myelosuppression

lenalidomide

Peripheral neuropathy

Lenalidomide

Peripheral neuropathy

lenalidomide

Peripheral neuropathy

lenalidomide

deep vein thrombosis

Lenalidomide

deep vein thrombosis

lenalidomide

deep vein thrombosis


Input: The cytogenetic action of ifosfamide, mesna, and their combination on peripheral rabbit lymphocytes: an in vivo / in vitro cytogenetic study. Ifosfamide (IFO) is an alkylating nitrogen mustard, administrated as an antineoplasmic agent. It is characterized by its intense urotoxic action, leading to hemorrhagic cystitis. This side effect of IFO raises the requirement for the co - administration with sodium 2 - sulfanylethanesulfonate (Mesna) aiming to avoid or minimize this effect. IFO and Mesna were administrated separately on rabbit' s lymphocytes in vivo, which were later developed in vitro. Cytogenetic markers for sister chromatid exchanges (SCEs), proliferation rate index (PRI) and Mitotic Index were recorded. Mesna' s action, in conjunction with IFO reduces the frequency of SCEs, in comparison with the SCEs recordings obtained when IFO is administered alone. In addition to this, when high concentrations of Mesna were administered alone significant reductions of the PRI were noted, than with IFO acting at the same concentration on the lymphocytes. Mesna significantly reduces IFO' s genotoxicity, while when administered in high concentrations it acts in an inhibitory fashion on the cytostatic action of the drug.

ifosfamide

mesna

Ifosfamide

IFO

nitrogen

IFO

sodium 2 - sulfanylethanesulfonate

Mesna

IFO

Mesna

Mesna

IFO

IFO

Mesna

IFO

Mesna

IFO

hemorrhagic cystitis

hemorrhagic

cystitis

genotoxicity

ifosfamide

hemorrhagic cystitis

ifosfamide

cystitis

Ifosfamide

hemorrhagic cystitis

Ifosfamide

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

IFO

hemorrhagic cystitis

IFO

cystitis

ifosfamide

hemorrhagic

Ifosfamide

hemorrhagic

IFO

hemorrhagic

IFO

hemorrhagic

IFO

hemorrhagic

IFO

hemorrhagic

IFO

hemorrhagic

IFO

hemorrhagic

IFO

hemorrhagic


Input: Risk factors and predictors of levodopa - induced dyskinesia among multiethnic Malaysians with Parkinson' s disease. Chronic pulsatile levodopa therapy for Parkinson' s disease (PD) leads to the development of motor fluctuations and dyskinesia. We studied the prevalence and predictors of levodopa - induced dyskinesia among multiethnic Malaysian patients with PD. METHODS: This is a cross - sectional study involving 95 patients with PD on uninterrupted levodopa therapy for at least 6 months. The instrument used was the UPDRS questionnaires. The predictors of dyskinesia were determined using multivariate logistic regression analysis. RESULTS: The mean age was 65. 6 + 8. 5 years. The mean onset age was 58. 5 + 9. 8 years. The median disease duration was 6 (7) years. Dyskinesia was present in 44% (n = 42) with median levodopa therapy of 3 years. There were 64. 3% Chinese, 31% Malays, and 3. 7% Indians and other ethnic groups. Eighty - one percent of patients with dyskinesia had clinical fluctuations. Patients with dyskinesia had lower onset age (p < 0. 001), longer duration of levodopa therapy (p < 0. 001), longer disease duration (p < 0. 001), higher total daily levodopa dose (p < 0. 001), and higher total UPDRS scores (p = 0. 005) than patients without dyskinesia. The three significant predictors of dyskinesia were duration of levodopa therapy, onset age, and total daily levodopa dose. CONCLUSIONS: The prevalence of levodopa - induced dyskinesia in our patients was 44%. The most significant predictors were duration of levodopa therapy, total daily levodopa dose, and onset age.

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

dyskinesia

Parkinson' s disease

Parkinson' s disease

PD

dyskinesia

dyskinesia

PD

PD

dyskinesia

Dyskinesia

dyskinesia

dyskinesia

dyskinesia

dyskinesia

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

Dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia


Input: An unexpected diagnosis in a renal - transplant patient with proteinuria treated with everolimus: AL amyloidosis. Proteinuria is an expected complication in transplant patients treated with mammalian target of rapamycin inhibitors (mTOR - i). However, clinical suspicion should always be supported by histological evidence in order to investigate potential alternate diagnoses such as acute or chronic rejection, interstitial fibrosis and tubular atrophy, or recurrent or de novo glomerulopathy. In this case we report the unexpected diagnosis of amyloidosis in a renal - transplant patient with pre - transplant monoclonal gammapathy of undetermined significance who developed proteinuria after conversion from tacrolimus to everolimus.

proteinuria

AL

amyloidosis

Proteinuria

fibrosis

atrophy

glomerulopathy

amyloidosis

proteinuria

everolimus

rapamycin

tacrolimus

everolimus

everolimus

AL

everolimus

amyloidosis

everolimus

amyloidosis

everolimus

AL

everolimus

amyloidosis

everolimus

amyloidosis

everolimus

proteinuria

everolimus

Proteinuria

everolimus

proteinuria

everolimus

proteinuria

everolimus

Proteinuria

everolimus

proteinuria


Input: An investigation of the pattern of kidney injury in HIV - positive persons exposed to tenofovir disoproxil fumarate: an examination of a large population database (MHRA database). The potential for tenofovir to cause a range of kidney syndromes has been established from mechanistic and randomised clinical trials. However, the exact pattern of kidney involvement is still uncertain. We undertook a descriptive analysis of Yellow Card records of 407 HIV - positive persons taking tenofovir disoproxil fumarate (TDF) as part of their antiretroviral therapy regimen and submitted to the Medicines and Healthcare Products Regulatory Agency (MHRA) with suspected kidney adverse effects. Reports that satisfy defined criteria were classified as acute kidney injury, kidney tubular dysfunction and Fanconi syndrome. Of the 407 Yellow Card records analysed, 106 satisfied criteria for TDF - related kidney disease, of which 53 (50%) had features of kidney tubular dysfunction, 35 (33%) were found to have features of glomerular dysfunction and 18 (17%) had Fanconi syndrome. The median TDF exposure was 316 days (interquartile range 120 - 740). The incidence of hospitalisation for TDF kidney adverse effects was high, particularly amongst patients with features of Fanconi syndrome. The pattern of kidney syndromes in this population series mirrors that reported in randomised clinical trials. Cessation of TDF was associated with complete restoration of kidney function in up half of the patients in this report.

kidney injury

acute kidney injury

kidney tubular dysfunction

Fanconi syndrome

kidney disease

kidney tubular dysfunction

glomerular dysfunction

Fanconi syndrome

Fanconi syndrome

tenofovir disoproxil fumarate

tenofovir

tenofovir disoproxil fumarate

TDF

TDF

TDF

TDF

TDF

tenofovir disoproxil fumarate

acute kidney injury

tenofovir disoproxil fumarate

acute kidney injury

TDF

acute kidney injury

TDF

acute kidney injury

TDF

acute kidney injury

TDF

acute kidney injury

TDF

acute kidney injury

tenofovir disoproxil fumarate

Fanconi syndrome

tenofovir disoproxil fumarate

Fanconi syndrome

tenofovir disoproxil fumarate

Fanconi syndrome

tenofovir disoproxil fumarate

Fanconi syndrome

tenofovir disoproxil fumarate

Fanconi syndrome

tenofovir disoproxil fumarate

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome

TDF

Fanconi syndrome


Input: Incidence of postoperative delirium is high even in a population without known risk factors. PURPOSE: Postoperative delirium is a recognized complication in populations at risk. The aim of this study is to assess the prevalence of early postoperative delirium in a population without known risk factors admitted to the ICU for postoperative monitoring after elective major surgery. The secondary outcome investigated is to identify eventual independent risk factors among demographic data and anesthetic drugs used. METHODS: An observational, prospective study was conducted on a consecutive cohort of patients admitted to our ICU within and for at least 24 h after major surgical procedures. Exclusion criteria were any preexisting predisposing factor for delirium or other potentially confounding neurological dysfunctions. Patients were assessed daily using the confusion assessment method for the ICU scale for 3 days after the surgical procedure. Early postoperative delirium incidence risk factors were then assessed through three different multiple regression models. RESULTS: According to the confusion assessment method for the ICU scale, 28% of patients were diagnosed with early postoperative delirium. The use of thiopentone was significantly associated with an eight - fold - higher risk for delirium compared to propofol (57. 1% vs. 7. 1%, RR = 8. 0, X2 = 4. 256; df = 1; 0. 05 < p < 0. 02). CONCLUSION: In this study early postoperative delirium was found to be a very common complication after major surgery, even in a population without known risk factors. Thiopentone was independently associated with an increase in its relative risk.

postoperative delirium

Postoperative delirium

postoperative delirium

delirium

neurological dysfunctions

confusion

postoperative delirium

postoperative delirium

delirium

postoperative delirium

thiopentone

propofol

Thiopentone

thiopentone

postoperative delirium

thiopentone

Postoperative delirium

thiopentone

postoperative delirium

thiopentone

postoperative delirium

thiopentone

postoperative delirium

thiopentone

postoperative delirium

Thiopentone

postoperative delirium

Thiopentone

Postoperative delirium

Thiopentone

postoperative delirium

Thiopentone

postoperative delirium

Thiopentone

postoperative delirium

Thiopentone

postoperative delirium

thiopentone

delirium

thiopentone

delirium

Thiopentone

delirium

Thiopentone

delirium


Input: A single neurotoxic dose of methamphetamine induces a long - lasting depressive - like behaviour in mice. Methamphetamine (METH) triggers a disruption of the monoaminergic system and METH abuse leads to negative emotional states including depressive symptoms during drug withdrawal. However, it is currently unknown if the acute toxic dosage of METH also causes a long - lasting depressive phenotype and persistent monoaminergic deficits. Thus, we now assessed the depressive - like behaviour in mice at early and long - term periods following a single high METH dose (30 mg / kg, i. p.). METH did not alter the motor function and procedural memory of mice as assessed by swimming speed and escape latency to find the platform in a cued version of the water maze task. However, METH significantly increased the immobility time in the tail suspension test at 3 and 49 days post - administration. This depressive - like profile induced by METH was accompanied by a marked depletion of frontostriatal dopaminergic and serotonergic neurotransmission, indicated by a reduction in the levels of dopamine, DOPAC and HVA, tyrosine hydroxylase and serotonin, observed at both 3 and 49 days post - administration. In parallel, another neurochemical feature of depression - - astroglial dysfunction - - was unaffected in the cortex and the striatal levels of the astrocytic protein marker, glial fibrillary acidic protein, were only transiently increased at 3 days. These findings demonstrate for the first time that a single high dose of METH induces long - lasting depressive - like behaviour in mice associated with a persistent disruption of frontostriatal dopaminergic and serotonergic homoeostasis.

neurotoxic

depressive

depressive symptoms

depressive

depressive

depressive

depression

depressive

methamphetamine

Methamphetamine

METH

METH

METH

METH

METH

METH

METH

dopamine

DOPAC

HVA

tyrosine

serotonin

METH

methamphetamine

depressive

methamphetamine

depressive symptoms

methamphetamine

depressive

methamphetamine

depressive

methamphetamine

depressive

methamphetamine

depression

methamphetamine

depressive

Methamphetamine

depressive

Methamphetamine

depressive symptoms

Methamphetamine

depressive

Methamphetamine

depressive

Methamphetamine

depressive

Methamphetamine

depression

Methamphetamine

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive

METH

depressive

METH

depressive symptoms

METH

depressive

METH

depressive

METH

depressive

METH

depression

METH

depressive


Input: Linezolid - induced optic neuropathy. Many systemic antimicrobials have been implicated to cause ocular adverse effects. This is especially relevant in multidrug therapy where more than one drug can cause a similar ocular adverse effect. We describe a case of progressive loss of vision associated with linezolid therapy. A 45 - year - old male patient who was on treatment with multiple second - line anti - tuberculous drugs including linezolid and ethambutol for extensively drug - resistant tuberculosis (XDR - TB) presented to us with painless progressive loss of vision in both eyes. Color vision was defective and fundus examination revealed optic disc edema in both eyes. Ethambutol - induced toxic optic neuropathy was suspected and tablet ethambutol was withdrawn. Deterioration of vision occurred despite withdrawal of ethambutol. Discontinuation of linezolid resulted in marked improvement of vision. Our report emphasizes the need for monitoring of visual function in patients on long - term linezolid treatment.

Linezolid

linezolid

linezolid

ethambutol

Ethambutol

ethambutol

ethambutol

linezolid

linezolid

optic neuropathy

loss of vision

extensively drug - resistant tuberculosis

XDR - TB

loss of vision

optic disc edema

toxic optic neuropathy

Deterioration of vision

Linezolid

optic neuropathy

Linezolid

toxic optic neuropathy

linezolid

optic neuropathy

linezolid

toxic optic neuropathy

linezolid

optic neuropathy

linezolid

toxic optic neuropathy

linezolid

optic neuropathy

linezolid

toxic optic neuropathy

linezolid

optic neuropathy

linezolid

toxic optic neuropathy

Linezolid

optic disc edema

linezolid

optic disc edema

linezolid

optic disc edema

linezolid

optic disc edema

linezolid

optic disc edema


Input: Resuscitation with lipid, epinephrine, or both in levobupivacaine - induced cardiac toxicity in newborn piglets. BACKGROUND: The optimal dosing regimens of lipid emulsion, epinephrine, or both are not yet determined in neonates in cases of local anaesthetic systemic toxicity (LAST). METHODS: Newborn piglets received levobupivacaine until cardiovascular collapse occurred. Standard cardiopulmonary resuscitation was started and electrocardiogram (ECG) was monitored for ventricular tachycardia, fibrillation, or QRS prolongation. Piglets were then randomly allocated to four groups: control (saline), Intralipid () alone, epinephrine alone, or a combination of Intralipd plus epinephrine. Resuscitation continued for 30 min or until there was a return of spontaneous circulation (ROSC) accompanied by a mean arterial pressure at or superior to the baseline pressure and normal sinus rhythm for a period of 30 min. RESULTS: ROSC was achieved in only one of the control piglets compared with most of the treated piglets. Mortality was not significantly different between the three treatment groups, but was significantly lower in all the treatment groups compared with control. The number of ECG abnormalities was zero in the Intralipid only group, but 14 and 17, respectively, in the epinephrine and epinephrine plus lipid groups (P < 0. 05). CONCLUSIONS: Lipid emulsion with or without epinephrine, or epinephrine alone were equally effective in achieving a return to spontaneous circulation in this model of LAST. Epinephrine alone or in combination with lipid was associated with an increased number of ECG abnormalities compared with lipid emulsion alone.

epinephrine

levobupivacaine

epinephrine

levobupivacaine

epinephrine

epinephrine

epinephrine

epinephrine

epinephrine

epinephrine

Epinephrine

cardiac toxicity

toxicity

cardiovascular collapse

ventricular tachycardia

fibrillation

levobupivacaine

cardiovascular collapse

levobupivacaine

cardiovascular collapse


Input: Incidence of heparin - induced thrombocytopenia type II and postoperative recovery of platelet count in liver graft recipients: a retrospective cohort analysis. BACKGROUND: Thrombocytopenia in patients with end - stage liver disease is a common disorder caused mainly by portal hypertension, low levels of thrombopoetin, and endotoxemia. The impact of immune - mediated heparin - induced thrombocytopenia type II (HIT type II) as a cause of thrombocytopenia after liver transplantation is not yet understood, with few literature citations reporting contradictory results. The aim of our study was to demonstrate the perioperative course of thrombocytopenia after liver transplantation and determine the occurrence of clinical HIT type II. METHOD: We retrospectively evaluated the medical records of 205 consecutive adult patients who underwent full - size liver transplantation between January 2006 and December 2010 due to end - stage or malignant liver disease. Preoperative platelet count, postoperative course of platelets, and clinical signs of HIT type II were analyzed. RESULTS: A total of 155 (75. 6%) of 205 patients had thrombocytopenia before transplantation, significantly influenced by Model of End - Stage Liver Disease score and liver cirrhosis. The platelet count exceeded 100, 000 / uL in most of the patients (n = 193) at a medium of 7 d. Regarding HIT II, there were four (1. 95%) patients with a background of HIT type II. CONCLUSIONS: The incidence of HIT in patients with end - stage hepatic failure is, with about 1. 95%, rare. For further reduction of HIT type II, the use of intravenous heparin should be avoided and the prophylactic anticoagulation should be performed with low - molecular - weight heparin after normalization of platelet count.

heparin

heparin

heparin

heparin

thrombocytopenia type II

Thrombocytopenia

end - stage liver disease

portal hypertension

endotoxemia

thrombocytopenia type II

HIT type II

thrombocytopenia

thrombocytopenia

HIT type II

end - stage or malignant liver disease

end - stage or malignant liver disease

malignant liver disease

HIT type II

thrombocytopenia

End - Stage Liver Disease

liver cirrhosis

HIT II

HIT type II

HIT

end - stage hepatic failure

HIT type II

heparin

thrombocytopenia type II

heparin

Thrombocytopenia

heparin

thrombocytopenia type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

HIT II

heparin

HIT type II

heparin

HIT

heparin

HIT type II

heparin

thrombocytopenia type II

heparin

Thrombocytopenia

heparin

thrombocytopenia type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

HIT II

heparin

HIT type II

heparin

HIT

heparin

HIT type II

heparin

thrombocytopenia type II

heparin

Thrombocytopenia

heparin

thrombocytopenia type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

HIT II

heparin

HIT type II

heparin

HIT

heparin

HIT type II

heparin

thrombocytopenia type II

heparin

Thrombocytopenia

heparin

thrombocytopenia type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT type II

heparin

HIT type II

heparin

thrombocytopenia

heparin

HIT II

heparin

HIT type II

heparin

HIT

heparin

HIT type II


Input: Takotsubo syndrome (or apical ballooning syndrome) secondary to Zolmitriptan. Takotsubo syndrome (TS), also known as broken heart syndrome, is characterized by left ventricle apical ballooning with elevated cardiac biomarkers and electrocardiographic changes suggestive of an acute coronary syndrome (ie, ST - segment elevation, T wave inversions, and pathologic Q waves). We report a case of 54 - year - old woman with medical history of mitral valve prolapse and migraines, who was admitted to the hospital for substernal chest pain and electrocardiogram demonstrated 1 / 2 mm ST - segment elevation in leads II, III, aVF, V5, and V6 and positive troponin I. Emergent coronary angiogram revealed normal coronary arteries with moderately reduced left ventricular ejection fraction with wall motion abnormalities consistent with TS. Detailed history obtained retrospectively revealed that the patient took zolmitriptan sparingly only when she had migraines. But before this event, she was taking zolmitriptan 2 - 3 times daily for several days because of a persistent migraine headache. She otherwise reported that she is quite active, rides horses, and does show jumping without any limitations in her physical activity. There was no evidence of any recent stress or status migrainosus. Extensive literature search revealed multiple cases of coronary artery vasospasm secondary to zolmitriptan, but none of the cases were associated with TS.

Takotsubo syndrome

apical ballooning syndrome

Takotsubo syndrome

TS

broken heart syndrome

acute coronary syndrome

mitral valve prolapse

migraines

chest pain

TS

migraines

migraine headache

status migrainosus

coronary artery vasospasm

TS

Zolmitriptan

zolmitriptan

zolmitriptan

zolmitriptan

Zolmitriptan

coronary artery vasospasm

zolmitriptan

coronary artery vasospasm

zolmitriptan

coronary artery vasospasm

zolmitriptan

coronary artery vasospasm

Zolmitriptan

Takotsubo syndrome

Zolmitriptan

apical ballooning syndrome

Zolmitriptan

Takotsubo syndrome

Zolmitriptan

TS

Zolmitriptan

broken heart syndrome

Zolmitriptan

TS

Zolmitriptan

TS

zolmitriptan

Takotsubo syndrome

zolmitriptan

apical ballooning syndrome

zolmitriptan

Takotsubo syndrome

zolmitriptan

TS

zolmitriptan

broken heart syndrome

zolmitriptan

TS

zolmitriptan

TS

zolmitriptan

Takotsubo syndrome

zolmitriptan

apical ballooning syndrome

zolmitriptan

Takotsubo syndrome

zolmitriptan

TS

zolmitriptan

broken heart syndrome

zolmitriptan

TS

zolmitriptan

TS

zolmitriptan

Takotsubo syndrome

zolmitriptan

apical ballooning syndrome

zolmitriptan

Takotsubo syndrome

zolmitriptan

TS

zolmitriptan

broken heart syndrome

zolmitriptan

TS

zolmitriptan

TS


Input: Depression, impulsiveness, sleep, and memory in past and present polydrug users of 3, 4 - methylenedioxymethamphetamine (MDMA, ecstasy). RATIONALE: Ecstasy (3, 4 - methylenedioxymethamphetamine, MDMA) is a worldwide recreational drug of abuse. Unfortunately, the results from human research investigating its psychological effects have been inconsistent. OBJECTIVES: The present study aimed to be the largest to date in sample size and 5HT - related behaviors; the first to compare present ecstasy users with past users after an abstinence of 4 or more years, and the first to include robust controls for other recreational substances. METHODS: A sample of 997 participants (52% male) was recruited to four control groups (non - drug (ND), alcohol / nicotine (AN), cannabis / alcohol / nicotine (CAN), non - ecstasy polydrug (PD)), and two ecstasy polydrug groups (present (MDMA) and past users (EX - MDMA). Participants completed a drug history questionnaire, Beck Depression Inventory, Barratt Impulsiveness Scale, Pittsburgh Sleep Quality Index, and Wechsler Memory Scale - Revised which, in total, provided 13 psychometric measures. RESULTS: While the CAN and PD groups tended to record greater deficits than the non - drug controls, the MDMA and EX - MDMA groups recorded greater deficits than all the control groups on ten of the 13 psychometric measures. Strikingly, despite prolonged abstinence (mean, 4. 98; range, 4 - 9 years), past ecstasy users showed few signs of recovery. Compared with present ecstasy users, the past users showed no change for ten measures, increased impairment for two measures, and improvement on just one measure. CONCLUSIONS: Given this record of impaired memory and clinically significant levels of depression, impulsiveness, and sleep disturbance, the prognosis for the current generation of ecstasy users is a major cause for concern.

Depression

impulsiveness

Depression

Impulsiveness

impaired memory

depression

impulsiveness

sleep disturbance

3, 4 - methylenedioxymethamphetamine

MDMA

ecstasy

Ecstasy

3, 4 - methylenedioxymethamphetamine

MDMA

ecstasy

alcohol

nicotine

AN

cannabis

alcohol

nicotine

CAN

ecstasy

ecstasy

MDMA

MDMA

CAN

MDMA

MDMA

ecstasy

ecstasy

ecstasy

3, 4 - methylenedioxymethamphetamine

sleep disturbance

MDMA

sleep disturbance

ecstasy

sleep disturbance

Ecstasy

sleep disturbance

3, 4 - methylenedioxymethamphetamine

sleep disturbance

MDMA

sleep disturbance

ecstasy

sleep disturbance

ecstasy

sleep disturbance

ecstasy

sleep disturbance

MDMA

sleep disturbance

MDMA

sleep disturbance

MDMA

sleep disturbance

MDMA

sleep disturbance

ecstasy

sleep disturbance

ecstasy

sleep disturbance

ecstasy

sleep disturbance

3, 4 - methylenedioxymethamphetamine

impulsiveness

3, 4 - methylenedioxymethamphetamine

Impulsiveness

3, 4 - methylenedioxymethamphetamine

impulsiveness

MDMA

impulsiveness

MDMA

Impulsiveness

MDMA

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

Ecstasy

impulsiveness

Ecstasy

Impulsiveness

Ecstasy

impulsiveness

3, 4 - methylenedioxymethamphetamine

impulsiveness

3, 4 - methylenedioxymethamphetamine

Impulsiveness

3, 4 - methylenedioxymethamphetamine

impulsiveness

MDMA

impulsiveness

MDMA

Impulsiveness

MDMA

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

MDMA

impulsiveness

MDMA

Impulsiveness

MDMA

impulsiveness

MDMA

impulsiveness

MDMA

Impulsiveness

MDMA

impulsiveness

MDMA

impulsiveness

MDMA

Impulsiveness

MDMA

impulsiveness

MDMA

impulsiveness

MDMA

Impulsiveness

MDMA

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

ecstasy

impulsiveness

ecstasy

Impulsiveness

ecstasy

impulsiveness

3, 4 - methylenedioxymethamphetamine

Depression

3, 4 - methylenedioxymethamphetamine

Depression

3, 4 - methylenedioxymethamphetamine

depression

MDMA

Depression

MDMA

Depression

MDMA

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression

Ecstasy

Depression

Ecstasy

Depression

Ecstasy

depression

3, 4 - methylenedioxymethamphetamine

Depression

3, 4 - methylenedioxymethamphetamine

Depression

3, 4 - methylenedioxymethamphetamine

depression

MDMA

Depression

MDMA

Depression

MDMA

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression

MDMA

Depression

MDMA

Depression

MDMA

depression

MDMA

Depression

MDMA

Depression

MDMA

depression

MDMA

Depression

MDMA

Depression

MDMA

depression

MDMA

Depression

MDMA

Depression

MDMA

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression

ecstasy

Depression

ecstasy

Depression

ecstasy

depression


Input: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson' s disease patients. Levodopa is the most effective symptomatic therapy for Parkinson' s disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson' s disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR) = 0. 615, 95% confidence interval (CI) 0. 426 - 0. 887, P = 0. 009) and visual hallucinations (PR = 0. 515, 95% CI 0. 295 - 0. 899, P = 0. 020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.

levodopa

Levodopa

glutamate

levodopa

levodopa

Parkinson' s disease

Parkinson' s disease

dyskinesia

visual hallucinations

idiopathic Parkinson' s disease

dyskinesia

visual hallucinations

levodopa

visual hallucinations

levodopa

visual hallucinations

Levodopa

visual hallucinations

Levodopa

visual hallucinations

levodopa

visual hallucinations

levodopa

visual hallucinations

levodopa

visual hallucinations

levodopa

visual hallucinations

levodopa

dyskinesia

levodopa

dyskinesia

Levodopa

dyskinesia

Levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia


Input: Crocin improves lipid dysregulation in subacute diazinon exposure through ERK1 / 2 pathway in rat liver. INTRODUCTION: Diazinon Yis one of the most broadly used organophosphorus insecticides in agriculture. It has been shown that exposure to diazinon may interfere with lipid metabolism. Moreover, the hypolipidemic effect of crocin has been established. Earlier studies revealed the major role of Extracellular signal - regulated kinase (ERK) pathways in low - density lipoprotein receptor (LDLr) expression. The aim of this study was to evaluate changes in the regulation of lipid metabolism, ERK and LDLr expression in the liver of rats exposed to subacute diazinon. Furthermore ameliorating effect of crocin on diazinon induced disturbed cholesterol homeostasis was studied. METHODS: 24 Rats were divided into 4 groups and received following treatments for 4 weeks; Corn oil (control), diazinon (15mg / kg per day, orally) and crocin (12. 5 and 25mg / kg per day, intraperitoneally) in combination with diazinon (15 mg / kg). The levels of cholesterol, triglyceride and LDL in blood of rats were analyzed. Moreover mRNA levels of LDLr and ERK1 / 2 as well as protein levels of total and activated forms of ERK1 / 2 in rat liver were evaluated by Western blotting and quantitative real time polymerase chain reaction analysis. RESULTS: Our data showed that subacute exposure to diazinon significantly increased concentrations of cholesterol, triglyceride and LDL. Moreover diazinon decreased ERK1 / 2 protein phosphorylation and LDLr transcript. Crocin reduced inhibition of ERK activation and diazinon - induced hyperlipemia and increased levels of LDLr transcript. CONCLUSIONS: Crocin may be considered as a novel protective agent in diazinon - induced hyperlipemia through modulating of ERK pathway and increase of LDLr expression.

Crocin

diazinon

Diazinon

organophosphorus

diazinon

crocin

diazinon

crocin

diazinon

cholesterol

diazinon

crocin

diazinon

cholesterol

triglyceride

diazinon

cholesterol

triglyceride

diazinon

Crocin

diazinon

Crocin

diazinon

hyperlipemia

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

Diazinon

hyperlipemia

Diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia

diazinon

hyperlipemia


Input: GEM - P chemotherapy is active in the treatment of relapsed Hodgkin lymphoma. Hodgkin lymphoma (HL) is a relatively chemosensitive malignancy. However, for those who relapse, high - dose chemotherapy with autologous stem cell transplant is the treatment of choice which relies on adequate disease control with salvage chemotherapy. Regimens commonly used often require inpatient administration and can be difficult to deliver due to toxicity. Gemcitabine and cisplatin have activity in HL, non - overlapping toxicity with first - line chemotherapeutics, and may be delivered in an outpatient setting. In this retrospective single - centre analysis, patients with relapsed or refractory HL treated with gemcitabine 1, 000 mg / m (2) day (D) 1, D8 and D15; methylprednisolone 1, 000 mg D1 - 5; and cisplatin 100 mg / m (2) D15, every 28 days (GEM - P) were included. Demographic, survival, response and toxicity data were recorded. Forty - one eligible patients were identified: median age 27. One hundred and twenty - two cycles of GEM - P were administered in total (median 3 cycles; range 1 - 6). Twenty of 41 (48%) patients received GEM - P as second - line treatment and 11 / 41 (27%) as third - line therapy. Overall response rate (ORR) to GEM - P in the entire cohort was 80% (complete response (CR) 37%, partial response 44%) with 14 / 15 CR confirmed as a metabolic CR on PET and ORR of 85% in the 20 second - line patients. The most common grade 3 / 4 toxicities were haematological: neutropenia 54% and thrombocytopenia 51%. Median follow - up from the start of GEM - P was 4. 5 years. Following GEM - P, 5 - year progression - free survival was 46% (95% confidence interval (CI), 30 - 62%) and 5 - year overall survival was 59% (95% CI, 43 - 74%). Fourteen of 41 patients proceeded directly to autologous transplant. GEM - P is a salvage chemotherapy with relatively high response rates, leading to successful transplantation in appropriate patients, in the treatment of relapsed or refractory HL.

GEM

Gemcitabine

cisplatin

gemcitabine

methylprednisolone

cisplatin

GEM

GEM

GEM

GEM

GEM

GEM

GEM

Hodgkin lymphoma

Hodgkin lymphoma

HL

malignancy

toxicity

HL

toxicity

HL

toxicity

toxicities

neutropenia

thrombocytopenia

HL

methylprednisolone

neutropenia

GEM

thrombocytopenia

Gemcitabine

thrombocytopenia

gemcitabine

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

GEM

thrombocytopenia

methylprednisolone

thrombocytopenia

GEM

neutropenia

Gemcitabine

neutropenia

gemcitabine

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia

GEM

neutropenia


Input: Basal functioning of the hypothalamic - pituitary - adrenal (HPA) axis and psychological distress in recreational ecstasy polydrug users. RATIONALE: Ecstasy (MDMA) is a psychostimulant drug which is increasingly associated with psychobiological dysfunction. While some recent studies suggest acute changes in neuroendocrine function, less is known about long - term changes in HPA functionality in recreational users. OBJECTIVES: The current study is the first to explore the effects of ecstasy - polydrug use on psychological distress and basal functioning of the HPA axis through assessing the secretion of cortisol across the diurnal period. METHOD: Seventy - six participants (21 nonusers, 29 light ecstasy - polydrug users, 26 heavy ecstasy - polydrug users) completed a substance use inventory and measures of psychological distress at baseline, then two consecutive days of cortisol sampling (on awakening, 30 min post awakening, between 1400 and 1600 hours and pre bedtime). On day 2, participants also attended the laboratory to complete a 20 - min multitasking stressor. RESULTS: Both user groups exhibited significantly greater levels of anxiety and depression than nonusers. On day 1, all participants exhibited a typical cortisol profile, though light users had significantly elevated levels pre - bed. On day 2, heavy users demonstrated elevated levels upon awakening and all ecstasy - polydrug users demonstrated elevated pre - bed levels compared to non - users. Significant between group differences were also observed in afternoon cortisol levels and in overall cortisol secretion across the day. CONCLUSIONS: The increases in anxiety and depression are in line with previous observations in recreational ecstasy - polydrug users. Dysregulated diurnal cortisol may be indicative of inappropriate anticipation of forthcoming demands and hypersecretion may lead to the increased psychological and physical morbidity associated with heavy recreational use of ecstasy.

ecstasy

Ecstasy

MDMA

ecstasy

cortisol

ecstasy

ecstasy

cortisol

cortisol

ecstasy

cortisol

cortisol

ecstasy

cortisol

ecstasy

psychobiological dysfunction

anxiety

depression

anxiety

depression

ecstasy

depression

ecstasy

depression

Ecstasy

depression

Ecstasy

depression

MDMA

depression

MDMA

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression

ecstasy

depression


Input: Ifosfamide related encephalopathy: the need for a timely EEG evaluation. BACKGROUND: Ifosfamide is an alkylating agent useful in the treatment of a wide range of cancers including sarcomas, lymphoma, gynecologic and testicular cancers. Encephalopathy has been reported in 10 - 40% of patients receiving high - dose IV ifosfamide. OBJECTIVE: To highlight the role of electroencephalogram (EEG) in the early detection and management of ifosfamide related encephalopathy. METHODS: Retrospective chart review including clinical data and EEG recordings was done on five patients, admitted to MD Anderson Cancer Center between years 2009 and 2012, who developed ifosfamide related acute encephalopathy. RESULTS: All five patients experienced symptoms of encephalopathy soon after (within 12 h - 2 days) receiving ifosfamide. Two patients developed generalized convulsions while one patient developed continuous non - convulsive status epilepticus (NCSE) that required ICU admission and intubation. Initial EEG showed epileptiform discharges in three patients; run of triphasic waves in one patient and moderate degree diffuse generalized slowing. Mixed pattern with the presence of both sharps and triphasic waves were also noted. Repeat EEGs within 24_h of symptom onset showed marked improvement that was correlated with clinical improvement. CONCLUSIONS: Severity of ifosfamide related encephalopathy correlates with EEG changes. We suggest a timely EEG evaluation for patients receiving ifosfamide who develop features of encephalopathy.

Ifosfamide

Ifosfamide

ifosfamide

ifosfamide

ifosfamide

ifosfamide

ifosfamide

ifosfamide

encephalopathy

cancers

sarcomas

lymphoma

gynecologic and testicular cancers

Encephalopathy

encephalopathy

Cancer

encephalopathy

encephalopathy

convulsions

non - convulsive status epilepticus

NCSE

encephalopathy

encephalopathy

Ifosfamide

convulsions

Ifosfamide

convulsions

ifosfamide

convulsions

ifosfamide

convulsions

ifosfamide

convulsions

ifosfamide

convulsions

ifosfamide

convulsions

ifosfamide

convulsions

Ifosfamide

non - convulsive status epilepticus

Ifosfamide

NCSE

Ifosfamide

non - convulsive status epilepticus

Ifosfamide

NCSE

ifosfamide

non - convulsive status epilepticus

ifosfamide

NCSE

ifosfamide

non - convulsive status epilepticus

ifosfamide

NCSE

ifosfamide

non - convulsive status epilepticus

ifosfamide

NCSE

ifosfamide

non - convulsive status epilepticus

ifosfamide

NCSE

ifosfamide

non - convulsive status epilepticus

ifosfamide

NCSE

ifosfamide

non - convulsive status epilepticus

ifosfamide

NCSE


Input: Incidence of contrast - induced nephropathy in hospitalised patients with cancer. OBJECTIVES: To determine the frequency of and possible factors related to contrast - induced nephropathy (CIN) in hospitalised patients with cancer. METHODS: Ninety adult patients were enrolled. Patients with risk factors for acute renal failure were excluded. Blood samples were examined the day before contrast - enhanced computed tomography (CT) and serially for 3 days thereafter. CIN was defined as an increase in serum creatinine (Cr) of 0. 5 mg / dl or more, or elevation of Cr to 25% over baseline. Relationships between CIN and possible risk factors were investigated. RESULTS: CIN was detected in 18 / 90 (20%) patients. CIN developed in 25. 5% patients who underwent chemotherapy and in 11% patients who did not (P = 0. 1). CIN more frequently developed in patients who had undergone CT within 45 days after the last chemotherapy (P = 0. 005); it was also an independent risk factor (P = 0. 017). CIN was significantly more after treatment with bevacizumab / irinotecan (P = 0. 021) and in patients with hypertension (P = 0. 044). CONCLUSIONS: The incidence of CIN after CT in hospitalised oncological patients was 20%. CIN developed 4. 5 - times more frequently in patients with cancer who had undergone recent chemotherapy. Hypertension and the combination of bevacizumab / irinotecan may be additional risk factors for CIN development. KEY POINTS:. Contrast - induced nephropathy (CIN) is a concern for oncological patients undergoing CT.. CIN occurs more often when CT is performed < 45 days after chemotherapy.. Hypertension and treatment with bevacizumab appear to be additional risk factors.

contrast

contrast

contrast

creatinine

Cr

Cr

bevacizumab

irinotecan

bevacizumab

irinotecan

Contrast

bevacizumab

nephropathy

cancer

nephropathy

cancer

acute renal failure

hypertension

cancer

Hypertension

nephropathy

Hypertension

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

contrast

nephropathy

Contrast

nephropathy

Contrast

nephropathy

Contrast

nephropathy

irinotecan

nephropathy

irinotecan

nephropathy

irinotecan

nephropathy

irinotecan

nephropathy

irinotecan

nephropathy

irinotecan

nephropathy


Input: Syndrome of inappropriate antidiuretic hormone secretion associated with desvenlafaxine. OBJECTIVE: To report a case of syndrome of inappropriate anti - diuretic hormone (SIADH) secretion associated with desvenlafaxine. CASE SUMMARY: A 57 - year old female with hyponatraemia. Her medications included desvenlafaxine, and symptoms included nausea, anxiety and confusion. The serum sodium at this time was 120 mmol / L, serum osmolality was 263 mosmol / kg, urine osmolality 410 mosmol / kg and urine sodium 63 mmol / L, consistent with a diagnosis of SIADH. Desvenlafaxine was ceased and fluid restriction implemented. After 4 days the sodium increased to 128 mmol / L and fluid restriction was relaxed. During her further 3 weeks inpatient admission the serum sodium ranged from 134 to 137 mmol / L during treatment with mirtazapine. DISCUSSION: SIADH has been widely reported with a range of antidepressants. This case report suggests that desvenlafaxine might cause clinically significant hyponatremia. CONCLUSIONS: Clinicians should be aware of the potential for antidepressants to cause hyponatremia, and take appropriate corrective action where necessary.

Syndrome of inappropriate antidiuretic hormone

syndrome of inappropriate anti - diuretic hormone

SIADH

hyponatraemia

nausea

anxiety

confusion

SIADH

SIADH

hyponatremia

hyponatremia

desvenlafaxine

desvenlafaxine

desvenlafaxine

sodium

sodium

Desvenlafaxine

sodium

sodium

mirtazapine

desvenlafaxine

desvenlafaxine

Syndrome of inappropriate antidiuretic hormone

desvenlafaxine

syndrome of inappropriate anti - diuretic hormone

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

Syndrome of inappropriate antidiuretic hormone

desvenlafaxine

syndrome of inappropriate anti - diuretic hormone

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

Syndrome of inappropriate antidiuretic hormone

desvenlafaxine

syndrome of inappropriate anti - diuretic hormone

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

SIADH

Desvenlafaxine

Syndrome of inappropriate antidiuretic hormone

Desvenlafaxine

syndrome of inappropriate anti - diuretic hormone

Desvenlafaxine

SIADH

Desvenlafaxine

SIADH

Desvenlafaxine

SIADH

desvenlafaxine

Syndrome of inappropriate antidiuretic hormone

desvenlafaxine

syndrome of inappropriate anti - diuretic hormone

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

SIADH

desvenlafaxine

anxiety

desvenlafaxine

anxiety

desvenlafaxine

anxiety

Desvenlafaxine

anxiety

desvenlafaxine

anxiety

desvenlafaxine

hyponatraemia

desvenlafaxine

hyponatremia

desvenlafaxine

hyponatremia

desvenlafaxine

hyponatraemia

desvenlafaxine

hyponatremia

desvenlafaxine

hyponatremia

desvenlafaxine

hyponatraemia

desvenlafaxine

hyponatremia

desvenlafaxine

hyponatremia

Desvenlafaxine

hyponatraemia

Desvenlafaxine

hyponatremia

Desvenlafaxine

hyponatremia

desvenlafaxine

hyponatraemia

desvenlafaxine

hyponatremia

desvenlafaxine

hyponatremia

desvenlafaxine

confusion

desvenlafaxine

confusion

desvenlafaxine

confusion

Desvenlafaxine

confusion

desvenlafaxine

confusion

desvenlafaxine

nausea

desvenlafaxine

nausea

desvenlafaxine

nausea

Desvenlafaxine

nausea

desvenlafaxine

nausea


Input: Oxidative stress on cardiotoxicity after treatment with single and multiple doses of doxorubicin. The mechanism of doxorubicin (DOX) - induced cardiotoxicity remains controversial. Wistar rats (n = 66) received DOX injections intraperitoneally and were randomly assigned to 2 experimental protocols: (1) rats were killed before (- 24 h, n = 8) and 24 h after (+ 24 h, n = 8) a single dose of DOX (4 mg / kg body weight) to determine the DOX acute effect and (2) rats (n = 58) received 4 injections of DOX (4 mg / kg body weight / week) and were killed before the first injection (M0) and 1 week after each injection (M1, M2, M3, and M4) to determine the chronological effects. Animals used at M0 (n = 8) were also used at moment - 24 h of acute study. Cardiac total antioxidant performance (TAP), DNA damage, and morphology analyses were carried out at each time point. Single dose of DOX was associated with increased cardiac disarrangement, necrosis, and DNA damage (strand breaks (SBs) and oxidized pyrimidines) and decreased TAP. The chronological study showed an effect of a cumulative dose on body weight (R = - 0. 99, p = 0. 011), necrosis (R = 1. 00, p = 0. 004), TAP (R = 0. 95, p = 0. 049), and DNA SBs (R = - 0. 95, p = 0. 049). DNA SBs damage was negatively associated with TAP (R = - 0. 98, p = 0. 018), and necrosis (R = - 0. 97, p = 0. 027). Our results suggest that oxidative damage is associated with acute cardiotoxicity induced by a single dose of DOX only. Increased resistance to the oxidative stress is plausible for the multiple dose of DOX. Thus, different mechanisms may be involved in acute toxicity versus chronic toxicity.

cardiotoxicity

cardiotoxicity

cardiac disarrangement

necrosis

necrosis

necrosis

cardiotoxicity

toxicity

toxicity

doxorubicin

doxorubicin

DOX

DOX

DOX

DOX

DOX

DOX

DOX

DOX

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

doxorubicin

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

DOX

cardiotoxicity

doxorubicin

necrosis

doxorubicin

necrosis

doxorubicin

necrosis

doxorubicin

necrosis

doxorubicin

necrosis

doxorubicin

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis

DOX

necrosis


Input: Tacrolimus - related seizure after pediatric liver transplantation - - a single - center experience. To identify the risk factors for new - onset seizures after pediatric LT and to assess their clinical implications and long - term prognosis. The clinical and laboratory data of 27 consecutive children who underwent LT from January 2007 to December 2010 in our center were analyzed retrospectively. Patients were divided into seizures group and a non - seizures group. Pre - operative, intra - operative, and post - operative data were collected. Seizures occurred in four children, an incidence of 14. 8%. All exhibited generalized tonic - clonic seizures within the first two wk after LT. Univariate analysis showed that the risk factors associated with seizures after pediatric LT included gender, pediatric end - stage liver disease score before surgery, Child - Pugh score before surgery, serum total bilirubin after surgery, and trough TAC level. Multivariate analysis showed that trough TAC level was the only independent risk factor associated with the seizures. All children who experienced seizures survived with good graft function and remained seizure - free without anti - epileptic drugs over a mean follow - up period of 33. 7 + 14. 6 months. High trough TAC level was the predominant factor that contributed to seizures in the early post - operative period after pediatric LT. High PELD and Child - Pugh scores before LT and high post - operative serum Tbil may be contributory risk factors for TAC - related seizures.

Tacrolimus

bilirubin

TAC

TAC

TAC

TAC

seizure

seizures

seizures

seizures

Seizures

tonic - clonic seizures

seizures

end - stage liver disease

seizures

seizures

seizure

epileptic

seizures

seizures

Tacrolimus

seizure

Tacrolimus

seizures

Tacrolimus

seizures

Tacrolimus

seizures

Tacrolimus

Seizures

Tacrolimus

seizures

Tacrolimus

seizures

Tacrolimus

seizures

Tacrolimus

seizure

Tacrolimus

seizures

Tacrolimus

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizures

TAC

Seizures

TAC

seizures

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizures

TAC

Seizures

TAC

seizures

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizures

TAC

Seizures

TAC

seizures

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures

TAC

seizures

TAC

Seizures

TAC

seizures

TAC

seizures

TAC

seizures

TAC

seizure

TAC

seizures

TAC

seizures


Input: The flavonoid apigenin delays forgetting of passive avoidance conditioning in rats. The present experiments were performed to study the effect of the flavonoid apigenin (20 mg / kg intraperitoneally (i. p.), 1 h before acquisition), on 24 h retention performance and forgetting of a step - through passive avoidance task, in young male Wistar rats. There were no differences between saline - and apigenin - treated groups in the 24 h retention trial. Furthermore, apigenin did not prevent the amnesia induced by scopolamine (1mg / kg, i. p., 30 min before the acquisition). The saline - and apigenin - treated rats that did not step through into the dark compartment during the cut - off time (540 s) were retested weekly for up to eight weeks. In the saline treated group, the first significant decline in passive avoidance response was observed at four weeks, and complete memory loss was found five weeks after the acquisition of the passive avoidance task. At the end of the experimental period, 60% of the animals treated with apigenin still did not step through. These data suggest that 1) apigenin delays the long - term forgetting but did not modulate the 24 h retention of fear memory and 2) the obtained beneficial effect of apigenin on the passive avoidance conditioning is mediated by mechanisms that do not implicate its action on the muscarinic cholinergic system.

flavonoid

apigenin

flavonoid

apigenin

apigenin

apigenin

scopolamine

apigenin

apigenin

apigenin

apigenin

amnesia

memory loss

scopolamine

amnesia


Input: Cholecystokinin - octapeptide restored morphine - induced hippocampal long - term potentiation impairment in rats. Cholecystokinin - octapeptide (CCK - 8), which is a typical brain - gut peptide, exerts a wide range of biological activities on the central nervous system. We have previously reported that CCK - 8 significantly alleviated morphine - induced amnesia and reversed spine density decreases in the CA1 region of the hippocampus in morphine - treated animals. Here, we investigated the effects of CCK - 8 on long - term potentiation (LTP) in the lateral perforant path (LPP) - granule cell synapse of rat dentate gyrus (DG) in acute saline or morphine - treated rats. Population spikes (PS), which were evoked by stimulation of the LPP, were recorded in the DG region. Acute morphine (30mg / kg, s. c.) treatment significantly attenuated hippocampal LTP and CCK - 8 (1ug, i. c. v.) restored the amplitude of PS that was attenuated by morphine injection. Furthermore, microinjection of CCK - 8 (0. 1 and 1ug, i. c. v.) also significantly augmented hippocampal LTP in saline - treated (1ml / kg, s. c.) rats. Pre - treatment of the CCK2 receptor antagonist L - 365, 260 (10ug, i. c. v) reversed the effects of CCK - 8, but the CCK1 receptor antagonist L - 364, 718 (10ug, i. c. v) did not. The present results demonstrate that CCK - 8 attenuates the effect of morphine on hippocampal LTP through CCK2 receptors and suggest an ameliorative function of CCK - 8 on morphine - induced memory impairment.

Cholecystokinin - octapeptide

morphine

Cholecystokinin - octapeptide

CCK - 8

CCK - 8

morphine

morphine

CCK - 8

morphine

morphine

CCK - 8

morphine

CCK - 8

CCK - 8

CCK - 8

morphine

CCK - 8

morphine

amnesia

memory impairment

morphine

amnesia

morphine

amnesia

morphine

amnesia

morphine

amnesia

morphine

amnesia

morphine

amnesia

morphine

amnesia

morphine

amnesia


Input: Glial activation and post - synaptic neurotoxicity: the key events in Streptozotocin (ICV) induced memory impairment in rats. In the present study the role of glial activation and post synaptic toxicity in ICV Streptozotocin (STZ) induced memory impaired rats was explored. In experiment set up 1: Memory deficit was found in Morris water maze test on 14 - 16 days after STZ (ICV; 3mg / Kg) administration. STZ causes increased expression of GFAP, CD11b and TNF - a indicating glial activation and neuroinflammation. STZ also significantly increased the level of ROS, nitrite, Ca (2 +) and reduced the mitochondrial activity in synaptosomal preparation illustrating free radical generation and excitotoxicity. Increased expression and activity of Caspase - 3 was also observed in STZ treated rat which specify apoptotic cell death in hippocampus and cortex. STZ treatment showed decrease expression of post synaptic markers CaMKIIa and PSD - 95, while, expression of pre synaptic markers (synaptophysin and SNAP - 25) remains unaltered indicating selective post synaptic neurotoxicity. Oral treatment with Memantine (10mg / kg) and Ibuprofen (50 mg / kg) daily for 13 days attenuated STZ induced glial activation, apoptotic cell death and post synaptic neurotoxicity in rat brain. Further, in experiment set up 2: where memory function was not affected i. e. 7 - 9 days after STZ treatment. The level of GFAP, CD11b, TNF - a, ROS and nitrite levels were increased. On the other hand, apoptotic marker, synaptic markers, mitochondrial activity and Ca (2 +) levels remained unaffected. Collective data indicates that neuroinflammatory process and oxidative stress occurs earlier to apoptosis and does not affect memory function. Present study clearly suggests that glial activation and post synaptic neurotoxicity are the key factors in STZ induced memory impairment and neuronal cell death.

neurotoxicity

memory impairment

toxicity

memory impaired

Memory deficit

neuroinflammation

excitotoxicity

neurotoxicity

neurotoxicity

neuroinflammatory

neurotoxicity

memory impairment

Streptozotocin

Streptozotocin

STZ

STZ

STZ

STZ

nitrite

Ca

STZ

STZ

Memantine

Ibuprofen

STZ

STZ

nitrite

Ca

STZ

Streptozotocin

neuroinflammation

Streptozotocin

neuroinflammatory

Streptozotocin

neuroinflammation

Streptozotocin

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

STZ

neuroinflammation

STZ

neuroinflammatory

Streptozotocin

memory impairment

Streptozotocin

memory impaired

Streptozotocin

Memory deficit

Streptozotocin

memory impairment

Streptozotocin

memory impairment

Streptozotocin

memory impaired

Streptozotocin

Memory deficit

Streptozotocin

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment

STZ

memory impairment

STZ

memory impaired

STZ

Memory deficit

STZ

memory impairment


Input: Comparison of effects of isotonic sodium chloride with diltiazem in prevention of contrast - induced nephropathy. INTRODUCTION AND OBJECTIVE: Contrast - induced nephropathy (CIN) significantly increases the morbidity and mortality of patients. The aim of this study is to investigate and compare the protective effects of isotonic sodium chloride with sodium bicarbonate infusion and isotonic sodium chloride infusion with diltiazem, a calcium channel blocker, in preventing CIN. MATERIALS AND METHODS: Our study included patients who were administered 30 - 60 mL of iodinated contrast agent for percutaneous coronary angiography (PCAG), all with creatinine values between 1. 1 and 3. 1 mg / dL. Patients were divided into three groups and each group had 20 patients. The first group of patients was administered isotonic sodium chloride; the second group was administered a solution that of 5% dextrose and sodium bicarbonate, while the third group was administered isotonic sodium chloride before and after the contrast injection. The third group received an additional injection of diltiazem the day before and first 2 days after the contrast injection. All of the patients' plasma blood urea nitrogen (BUN) and creatinine levels were measured on the second and seventh day after the administration of intravenous contrast material. RESULTS: The basal creatinine levels were similar for all three groups (p > 0. 05). Among a total of 60 patients included in the study, 16 patients developed acute renal failure (ARF) on the second day after contrast material was injected (26. 6%). The number of patients who developed ARF on the second day after the injection in the first group was five (25%), in the second group was six (30%) and the third group was five (25%) (p > 0. 05). CONCLUSION: There was no significant difference between isotonic sodium chloride, sodium bicarbonate and isotonic sodium chloride with diltiazem application in prevention of CIN.

sodium chloride

diltiazem

contrast

Contrast

sodium chloride

sodium bicarbonate

sodium chloride

diltiazem

calcium

contrast

creatinine

sodium chloride

dextrose

sodium bicarbonate

sodium chloride

contrast

diltiazem

contrast

blood urea nitrogen

BUN

creatinine

contrast

creatinine

contrast

sodium chloride

sodium bicarbonate

sodium chloride

diltiazem

nephropathy

nephropathy

acute renal failure

ARF

ARF

contrast

acute renal failure

contrast

ARF

contrast

ARF

Contrast

acute renal failure

Contrast

ARF

Contrast

ARF

contrast

acute renal failure

contrast

ARF

contrast

ARF

contrast

acute renal failure

contrast

ARF

contrast

ARF

contrast

acute renal failure

contrast

ARF

contrast

ARF

contrast

acute renal failure

contrast

ARF

contrast

ARF

contrast

acute renal failure

contrast

ARF

contrast

ARF


Input: Neurocognitive and neuroradiologic central nervous system late effects in children treated on Pediatric Oncology Group (POG) P9605 (standard risk) and P9201 (lesser risk) acute lymphoblastic leukemia protocols (ACCL0131): a methotrexate consequence? A report from the Children' s Oncology Group. Concerns about long - term methotrexate (MTX) neurotoxicity in the 1990s led to modifications in intrathecal (IT) therapy, leucovorin rescue, and frequency of systemic MTX administration in children with acute lymphoblastic leukemia. In this study, neurocognitive outcomes and neuroradiologic evidence of leukoencephalopathy were compared in children treated with intense central nervous system (CNS) - directed therapy (P9605) versus those receiving fewer CNS - directed treatment days during intensive consolidation (P9201). A total of 66 children from 16 Pediatric Oncology Group institutions with " standard - risk " acute lymphoblastic leukemia, 1. 00 to 9. 99 years at diagnosis, without evidence of CNS leukemia at diagnosis were enrolled on ACCL0131: 28 from P9201 and 38 from P9605. Magnetic resonance imaging scans and standard neuropsychological tests were performed > 2. 6 years after the end of treatment. Significantly more P9605 patients developed leukoencephalopathy compared with P9201 patients (68%, 95% confidence interval 49% - 83% vs. 22%, 95% confidence interval 5% - 44%; P = 0. 001) identified as late as 7. 7 years after the end of treatment. Overall, 40% of patients scored < 85 on either Verbal or Performance IQ. Children on both studies had significant attention problems, but P9605 children scored below average on more neurocognitive measures than those treated on P9201 (82%, 14 / 17 measures vs. 24%, 4 / 17 measures). This supports ongoing concerns about intensive MTX exposure as a major contributor to CNS late effects.

acute lymphoblastic leukemia

neurotoxicity

acute lymphoblastic leukemia

leukoencephalopathy

acute lymphoblastic leukemia

leukemia

leukoencephalopathy

attention problems

methotrexate

methotrexate

MTX

MTX

MTX

methotrexate

attention problems

methotrexate

attention problems

MTX

attention problems

MTX

attention problems

MTX

attention problems

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

MTX

leukoencephalopathy

MTX

leukoencephalopathy

MTX

leukoencephalopathy

MTX

leukoencephalopathy

MTX

leukoencephalopathy

MTX

leukoencephalopathy


Input: Tranexamic acid overdosage - induced generalized seizure in renal failure. We report a 45 - year - old lady with chronic kidney disease stage 4 due to chronic tubulointerstial disease. She was admitted to our center for severe anemia due to menorrhagia and deterioration of renal function. She was infused three units of packed cells during a session of hemodialysis. Tranexamic acid (TNA) 1 g 8 - hourly was administered to her to control bleeding per vaginum. Two hours after the sixth dose of TNA, she had an episode of generalized tonic clonic convulsions. TNA was discontinued. Investigations of the patient revealed no biochemical or structural central nervous system abnormalities that could have provoked the convulsions. She did not require any further dialytic support. She had no further episodes of convulsion till dis - charge and during the two months of follow - up. Thus, the precipitating cause of convulsions was believed to be an overdose of TNA.

Tranexamic acid

Tranexamic acid

TNA

TNA

TNA

TNA

seizure

renal failure

chronic kidney disease

tubulointerstial disease

anemia

menorrhagia

deterioration of renal function

bleeding

tonic clonic convulsions

nervous system abnormalities

convulsions

convulsion

convulsions

overdose

Tranexamic acid

tonic clonic convulsions

Tranexamic acid

tonic clonic convulsions

TNA

tonic clonic convulsions

TNA

tonic clonic convulsions

TNA

tonic clonic convulsions

TNA

tonic clonic convulsions