Input: Iatrogenically induced intractable atrioventricular reentrant tachycardia after verapamil and catheter ablation in a patient with Wolff - Parkinson - White syndrome and idiopathic dilated cardiomyopathy. In a patient with WPW syndrome and idiopathic dilated cardiomyopathy, intractable atrioventricular reentrant tachycardia (AVRT) was iatrogenically induced. QRS without preexcitation, caused by junctional escape beats after verapamil or unidirectional antegrade block of accessory pathway after catheter ablation, established frequent AVRT attack.

atrioventricular reentrant tachycardia

Wolff - Parkinson - White syndrome

idiopathic dilated cardiomyopathy

WPW syndrome

idiopathic dilated cardiomyopathy

atrioventricular reentrant tachycardia

AVRT

AVRT

verapamil

verapamil

verapamil

atrioventricular reentrant tachycardia

verapamil

atrioventricular reentrant tachycardia

verapamil

AVRT

verapamil

AVRT

verapamil

atrioventricular reentrant tachycardia

verapamil

atrioventricular reentrant tachycardia

verapamil

AVRT

verapamil

AVRT


Input: Epidemic of liver disease caused by hydrochlorofluorocarbons used as ozone - sparing substitutes of chlorofluorocarbons. BACKGROUND: Hydrochlorofluorocarbons (HCFCs) are used increasingly in industry as substitutes for ozone - depleting chlorofluorocarbons (CFCs). Limited studies in animals indicate potential hepatotoxicity of some of these compounds. We investigated an epidemic of liver disease in nine industrial workers who had had repeated accidental exposure to a mixture of 1, 1 - dichloro - 2, 2, 2 - trifluoroethane (HCFC 123) and 1 - chloro - 1, 2, 2, 2 - tetrafluoroethane (HCFC 124). All nine exposed workers were affected to various degrees. Both compounds are metabolised in the same way as 1 - bromo - 1 - chloro - 2, 2, 2 - trifluoroethane (halothane) to form reactive trifluoroacetyl halide intermediates, which have been implicated in the hepatotoxicity of halothane. We aimed to test whether HCFCs 123 and 124 can result in serious liver disease. METHODS: For one severely affected worker liver biopsy and immunohistochemical stainings for the presence of trifluoroacetyl protein adducts were done. The serum of six affected workers and five controls was tested for autoantibodies that react with human liver cytochrome - P450 2E1 (P450 2E1) and P58 protein disulphide isomerase isoform (P58). FINDINGS: The liver biopsy sample showed hepatocellular necrosis which was prominent in perivenular zone three and extended focally from portal tracts to portal tracts and centrilobular areas (bridging necrosis). Trifluoroacetyl - adducted proteins were detected in surviving hepatocytes. Autoantibodies against P450 2E1 or P58, previously associated with halothane hepatitis, were detected in the serum of five affected workers. INTERPRETATION: Repeated exposure of human beings to HCFCs 123 and 124 can result in serious liver injury in a large proportion of the exposed population. Although the exact mechanism of hepatotoxicity of these agents is not known, the results suggest that trifluoroacetyl - altered liver proteins are involved. In view of the potentially widespread use of these compounds, there is an urgent need to develop safer alternatives.

liver disease

hepatotoxicity

liver disease

hepatotoxicity

liver disease

necrosis

necrosis

halothane hepatitis

liver injury

hepatotoxicity

hydrochlorofluorocarbons

ozone

chlorofluorocarbons

Hydrochlorofluorocarbons

HCFCs

ozone

chlorofluorocarbons

CFCs

1, 1 - dichloro - 2, 2, 2 - trifluoroethane

HCFC 123

1 - chloro - 1, 2, 2, 2 - tetrafluoroethane

HCFC 124

1 - bromo - 1 - chloro - 2, 2, 2 - trifluoroethane

halothane

trifluoroacetyl

halothane

HCFCs 123 and 124

HCFCs 123

HCFCs 123 and 124

trifluoroacetyl

Trifluoroacetyl

HCFCs 123 and 124

HCFCs 123

HCFCs 123 and 124

trifluoroacetyl

1 - chloro - 1, 2, 2, 2 - tetrafluoroethane

liver disease

1 - chloro - 1, 2, 2, 2 - tetrafluoroethane

liver disease

1 - chloro - 1, 2, 2, 2 - tetrafluoroethane

liver disease

HCFC 124

liver disease

HCFC 124

liver disease

HCFC 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

HCFCs 123 and 124

liver disease

1, 1 - dichloro - 2, 2, 2 - trifluoroethane

liver disease

1, 1 - dichloro - 2, 2, 2 - trifluoroethane

liver disease

1, 1 - dichloro - 2, 2, 2 - trifluoroethane

liver disease

HCFC 123

liver disease

HCFC 123

liver disease

HCFC 123

liver disease

HCFCs 123

liver disease

HCFCs 123

liver disease

HCFCs 123

liver disease

HCFCs 123

liver disease

HCFCs 123

liver disease

HCFCs 123

liver disease


Input: The effect of different anaesthetic agents in hearing loss following spinal anaesthesia. The cause of hearing loss after spinal anaesthesia is unknown. Up until now, the only factor studied has been the effect of the diameter of the spinal needle on post - operative sensorineural hearing loss. The aim of this study was to describe this hearing loss and to investigate other factors influencing the degree of hearing loss. Two groups of 22 similar patients were studied: one group received 6 mL prilocaine 2%; and the other received 3 mL bupivacaine 0. 5%. Patients given prilocaine were more likely to develop hearing loss (10 out of 22) than those given bupivacaine (4 out of 22) (P < 0. 05). The average hearing loss for speech frequencies was about 10 dB after prilocaine and 15 dB after bupivacaine. None of the patients complained of subjective hearing loss. Long - term follow - up of the patients was not possible.

hearing loss

hearing loss

sensorineural hearing loss

hearing loss

hearing loss

hearing loss

hearing loss

hearing loss

prilocaine

bupivacaine

prilocaine

bupivacaine

prilocaine

bupivacaine

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

prilocaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss

bupivacaine

hearing loss


Input: A transient neurological deficit following intrathecal injection of 1% hyperbaric bupivacaine for unilateral spinal anaesthesia. We describe a case of transient neurological deficit that occurred after unilateral spinal anaesthesia with 8 mg of 1% hyperbaric bupivacaine slowly injected through a 25 - gauge pencil - point spinal needle. The surgery and anaesthesia were uneventful, but 3 days after surgery, the patient reported an area of hypoaesthesia over L3 - L4 dermatomes of the leg which had been operated on (loss of pinprick sensation) without reduction in muscular strength. Sensation in this area returned to normal over the following 2 weeks. Prospective multicentre studies with a large population and a long follow - up should be performed in order to evaluate the incidence of this unusual side effect. However, we suggest that a low solution concentration should be preferred for unilateral spinal anaesthesia with a hyperbaric anaesthetic solution (if pencil - point needle and slow injection rate are employed), in order to minimize the risk of a localized high peak anaesthetic concentration, which might lead to a transient neurological deficit.

neurological deficit

neurological deficit

loss of pinprick sensation

neurological deficit

bupivacaine

bupivacaine

bupivacaine

loss of pinprick sensation

bupivacaine

loss of pinprick sensation


Input: Pethidine - associated seizure in a healthy adolescent receiving pethidine for postoperative pain control. A healthy 17 - year - old male received standard intermittent doses of pethidine via a patient - controlled analgesia (PCA) pump for management of postoperative pain control. Twenty - three h postoperatively he developed a brief self - limited seizure. Both plasma pethidine and norpethidine were elevated in the range associated with clinical manifestations of central nervous system excitation. No other risk factors for CNS toxicity were identified. This method allowed frequent self - dosing of pethidine at short time intervals and rapid accumulation of pethidine and norpethidine. The routine use of pethidine via PCA even for a brief postoperative analgesia should be reconsidered.

Pethidine

pethidine

pethidine

pethidine

norpethidine

pethidine

pethidine

norpethidine

pethidine

seizure

postoperative pain

postoperative pain

seizure

toxicity

Pethidine

seizure

Pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure

pethidine

seizure


Input: Drug - associated acute - onset vanishing bile duct and Stevens - Johnson syndromes in a child. Acute vanishing bile duct syndrome is a rare but established cause of progressive cholestasis in adults, is most often drug or toxin related, and is of unknown pathogenesis. It has not been reported previously in children. Stevens - Johnson syndrome is a well - recognized immune complex - mediated hypersensitivity reaction that affects all age groups, is drug or infection induced, and has classic systemic, mucosal, and dermatologic manifestations. A previously healthy child who developed acute, severe, rapidly progressive vanishing bile duct syndrome shortly after Stevens - Johnson syndrome is described; this was temporally associated with ibuprofen use. Despite therapy with ursodeoxycholic acid, prednisone, and then tacrolimus, her cholestatic disease was unrelenting, with cirrhosis shown by biopsy 6 months after presentation. This case documents acute drug - related vanishing bile duct syndrome in the pediatric age group and suggests shared immune mechanisms in the pathogenesis of both Stevens - Johnson syndrome and vanishing bile duct syndrome.

vanishing bile duct

Stevens - Johnson syndromes

vanishing bile duct

cholestasis

Stevens - Johnson syndrome

hypersensitivity

infection

vanishing bile duct syndrome

Stevens - Johnson syndrome

cholestatic disease

cirrhosis

vanishing bile duct syndrome

Stevens - Johnson syndrome

vanishing bile duct syndrome

ibuprofen

ursodeoxycholic acid

prednisone

tacrolimus

ibuprofen

Stevens - Johnson syndromes

ibuprofen

Stevens - Johnson syndrome

ibuprofen

Stevens - Johnson syndrome

ibuprofen

Stevens - Johnson syndrome

ibuprofen

cholestasis

ibuprofen

cholestatic disease


Input: High incidence of primary pulmonary hypertension associated with appetite suppressants in Belgium. Primary pulmonary hypertension is a rare, progressive and incurable disease, which has been associated with the intake of appetite suppressant drugs. The importance of this association was evaluated in Belgium while this country still had no restriction on the prescription of appetite suppressants. Thirty - five patients with primary pulmonary hypertension and 85 matched controls were recruited over 32 months (1992 - 1994) in Belgium. Exposure to appetite - suppressants was assessed on the basis of hospital records and standardized interview. Twenty - three of the patients had previously taken appetite suppressants, mainly fenfluramines, as compared with only 5 of the controls (66 versus 6%, p < 0. 0001). Five patients died before the interview, all of them had taken appetite suppressants. In 8 patients the diagnosis of primary pulmonary hypertension was uncertain, 5 of them had taken appetite suppressants. The patients who had been exposed to appetite suppressants tended to be on average more severely ill, and to have a shorter median delay between onset of symptoms and diagnosis. A policy of unrestricted prescription of appetite suppressants may lead to a high incidence of associated primary pulmonary hypertension. Intake of appetite suppressants may accelerate the progression of the disease.

primary pulmonary hypertension

Primary pulmonary hypertension

primary pulmonary hypertension

primary pulmonary hypertension

primary pulmonary hypertension

appetite suppressants

appetite suppressant

appetite suppressants

appetite - suppressants

appetite suppressants

fenfluramines

appetite suppressants

appetite suppressants

appetite suppressants

appetite suppressants

appetite suppressants

fenfluramines

primary pulmonary hypertension

fenfluramines

Primary pulmonary hypertension

fenfluramines

primary pulmonary hypertension

fenfluramines

primary pulmonary hypertension

fenfluramines

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressant

primary pulmonary hypertension

appetite suppressant

Primary pulmonary hypertension

appetite suppressant

primary pulmonary hypertension

appetite suppressant

primary pulmonary hypertension

appetite suppressant

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite - suppressants

primary pulmonary hypertension

appetite - suppressants

Primary pulmonary hypertension

appetite - suppressants

primary pulmonary hypertension

appetite - suppressants

primary pulmonary hypertension

appetite - suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

Primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension

appetite suppressants

primary pulmonary hypertension


Input: Choreoathetoid movements associated with rapid adjustment to methadone. Choreatiform hyperkinesias are known to be occasional movement abnormalities during intoxications with cocaine but not opiates. This is a case report of euphoria and choreoathetoid movements both transiently induced by rapid adjustment to the selective mu - opioid receptor agonist methadone in an inpatient previously abusing heroine and cocaine. In addition, minor EEG abnormalities occurred. Possible underlying neurobiological phenomena are discussed.

Choreoathetoid movements

Choreatiform hyperkinesias

Choreatiform

hyperkinesias

movement abnormalities

choreoathetoid movements

methadone

cocaine

methadone

heroine

cocaine

methadone

Choreoathetoid movements

methadone

Choreatiform hyperkinesias

methadone

Choreatiform

methadone

choreoathetoid movements

methadone

Choreoathetoid movements

methadone

Choreatiform hyperkinesias

methadone

Choreatiform

methadone

choreoathetoid movements

cocaine

Choreatiform hyperkinesias

cocaine

hyperkinesias

cocaine

Choreatiform hyperkinesias

cocaine

hyperkinesias

cocaine

Choreoathetoid movements

cocaine

Choreatiform

cocaine

choreoathetoid movements

cocaine

Choreoathetoid movements

cocaine

Choreatiform

cocaine

choreoathetoid movements


Input: Cocaine - induced mood disorder: prevalence rates and psychiatric symptoms in an outpatient cocaine - dependent sample. This paper attempts to examine and compare prevalence rates and symptom patterns of DSM substance - induced and other mood disorders. 243 cocaine - dependent outpatients with cocaine - induced mood disorder (CIMD), other mood disorders, or no mood disorder were compared on measures of psychiatric symptoms. The prevalence rate for CIMD was 12% at baseline. Introduction of the DSM - IV diagnosis of CIMD did not substantially affect rates of the other depressive disorders. Patients with CIMD had symptom severity levels between those of patients with and without a mood disorder. These findings suggest some validity for the new DSM - IV diagnosis of CIMD, but also suggest that it requires further specification and replication.

Cocaine

cocaine

cocaine

cocaine

mood disorder

psychiatric

mood disorders

mood disorder

CIMD

mood disorders

mood disorder

psychiatric

CIMD

CIMD

depressive disorders

CIMD

mood disorder

CIMD

Cocaine

mood disorder

Cocaine

mood disorders

Cocaine

mood disorder

Cocaine

mood disorders

Cocaine

mood disorder

Cocaine

mood disorder

cocaine

mood disorder

cocaine

mood disorders

cocaine

mood disorder

cocaine

mood disorders

cocaine

mood disorder

cocaine

mood disorder

cocaine

mood disorder

cocaine

mood disorders

cocaine

mood disorder

cocaine

mood disorders

cocaine

mood disorder

cocaine

mood disorder

cocaine

mood disorder

cocaine

mood disorders

cocaine

mood disorder

cocaine

mood disorders

cocaine

mood disorder

cocaine

mood disorder


Input: Hemolysis of human erythrocytes induced by tamoxifen is related to disruption of membrane structure. Tamoxifen (TAM), the antiestrogenic drug most widely prescribed in the chemotherapy of breast cancer, induces changes in normal discoid shape of erythrocytes and hemolytic anemia. This work evaluates the effects of TAM on isolated human erythrocytes, attempting to identify the underlying mechanisms on TAM - induced hemolytic anemia and the involvement of biomembranes in its cytostatic action mechanisms. TAM induces hemolysis of erythrocytes as a function of concentration. The extension of hemolysis is variable with erythrocyte samples, but 12. 5 microM TAM induces total hemolysis of all tested suspensions. Despite inducing extensive erythrocyte lysis, TAM does not shift the osmotic fragility curves of erythrocytes. The hemolytic effect of TAM is prevented by low concentrations of alpha - tocopherol (alpha - T) and alpha - tocopherol acetate (alpha - TAc) (inactivated functional hydroxyl) indicating that TAM - induced hemolysis is not related to oxidative membrane damage. This was further evidenced by absence of oxygen consumption and hemoglobin oxidation both determined in parallel with TAM - induced hemolysis. Furthermore, it was observed that TAM inhibits the peroxidation of human erythrocytes induced by AAPH, thus ruling out TAM - induced cell oxidative stress. Hemolysis caused by TAM was not preceded by the leakage of K (+) from the cells, also excluding a colloid - osmotic type mechanism of hemolysis, according to the effects on osmotic fragility curves. However, TAM induces release of peripheral proteins of membrane - cytoskeleton and cytosol proteins essentially bound to band 3. Either alpha - T or alpha - TAc increases membrane packing and prevents TAM partition into model membranes. These effects suggest that the protection from hemolysis by tocopherols is related to a decreased TAM incorporation in condensed membranes and the structural damage of the erythrocyte membrane is consequently avoided. Therefore, TAM - induced hemolysis results from a structural perturbation of red cell membrane, leading to changes in the framework of the erythrocyte membrane and its cytoskeleton caused by its high partition in the membrane. These defects explain the abnormal erythrocyte shape and decreased mechanical stability promoted by TAM, resulting in hemolytic anemia. Additionally, since membrane leakage is a final stage of cytotoxicity, the disruption of the structural characteristics of biomembranes by TAM may contribute to the multiple mechanisms of its anticancer action.

Hemolysis

breast cancer

hemolytic anemia

hemolytic anemia

hemolysis

hemolysis

hemolysis

hemolytic

hemolysis

hemolysis

Hemolysis

hemolysis

hemolysis

hemolysis

hemolytic anemia

tamoxifen

Tamoxifen

TAM

TAM

TAM

TAM

TAM

TAM

TAM

alpha - tocopherol

alpha - T

alpha - tocopherol acetate

alpha - TAc

hydroxyl

TAM

oxygen

TAM

TAM

AAPH

TAM

TAM

K

TAM

alpha - T

alpha - TAc

TAM

tocopherols

TAM

TAM

TAM

TAM

tamoxifen

Hemolysis

tamoxifen

hemolysis

tamoxifen

hemolysis

tamoxifen

hemolysis

tamoxifen

hemolytic

tamoxifen

hemolysis

tamoxifen

hemolysis

tamoxifen

Hemolysis

tamoxifen

hemolysis

tamoxifen

hemolysis

tamoxifen

hemolysis

Tamoxifen

Hemolysis

Tamoxifen

hemolysis

Tamoxifen

hemolysis

Tamoxifen

hemolysis

Tamoxifen

hemolytic

Tamoxifen

hemolysis

Tamoxifen

hemolysis

Tamoxifen

Hemolysis

Tamoxifen

hemolysis

Tamoxifen

hemolysis

Tamoxifen

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolytic

TAM

hemolysis

TAM

hemolysis

TAM

Hemolysis

TAM

hemolysis

TAM

hemolysis

TAM

hemolysis

tamoxifen

hemolytic anemia

tamoxifen

hemolytic anemia

tamoxifen

hemolytic anemia

Tamoxifen

hemolytic anemia

Tamoxifen

hemolytic anemia

Tamoxifen

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia

TAM

hemolytic anemia


Input: Changes of sodium and ATP affinities of the cardiac (Na, K) - ATPase during and after nitric oxide deficient hypertension. In the cardiovascular system, NO is involved in the regulation of a variety of functions. Inhibition of NO synthesis induces sustained hypertension. In several models of hypertension, elevation of intracellular sodium level was documented in cardiac tissue. To assess the molecular basis of disturbances in transmembraneous transport of Na +, we studied the response of cardiac (Na, K) - ATPase to NO - deficient hypertension induced in rats by NO - synthase inhibition with 40 mg / kg / day N (G) - nitro - L - arginine methyl ester (L - NAME) for 4 four weeks. After 4 - week administration of L - NAME, the systolic blood pressure (SBP) increased by 36%. Two weeks after terminating the treatment, the SBP recovered to control value. When activating the (Na, K) - ATPase with its substrate ATP, no changes in Km and Vmax values were observed in NO - deficient rats. During activation with Na +, the Vmax remained unchanged, however the K (Na) increased by 50%, indicating a profound decrease in the affinity of the Na + - binding site in NO - deficient rats. After recovery from hypertension, the activity of (Na, K) - ATPase increased, due to higher affinity of the ATP - binding site, as revealed from the lowered Km value for ATP. The K (Na) value for Na + returned to control value. Inhibition of NO - synthase induced a reversible hypertension accompanied by depressed Na + - extrusion from cardiac cells as a consequence of deteriorated Na + - binding properties of the (Na, K) - ATPase. After recovery of blood pressure to control values, the extrusion of Na + from cardiac cells was normalized, as revealed by restoration of the (Na, K) - ATPase activity.

sodium

ATP

K

nitric oxide

NO

NO

sodium

K

NO

NO

N (G) - nitro - L - arginine methyl ester

L - NAME

L - NAME

K

ATP

NO

K

NO

K

ATP

ATP

K

NO

K

K

hypertension

hypertension

hypertension

hypertension

hypertension

hypertension

depressed

nitric oxide

hypertension

nitric oxide

hypertension

nitric oxide

hypertension

nitric oxide

hypertension

nitric oxide

hypertension

nitric oxide

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension

NO

hypertension


Input: Effects of long - term pretreatment with isoproterenol on bromocriptine - induced tachycardia in conscious rats. It has been shown that bromocriptine - induced tachycardia, which persisted after adrenalectomy, is (i) mediated by central dopamine D2 receptor activation and (ii) reduced by 5 - day isoproterenol pretreatment, supporting therefore the hypothesis that this effect is dependent on sympathetic outflow to the heart. This study was conducted to examine whether prolonged pretreatment with isoproterenol could abolish bromocriptine - induced tachycardia in conscious rats. Isoproterenol pretreatment for 15 days caused cardiac hypertrophy without affecting baseline blood pressure and heart rate. In control rats, intravenous bromocriptine (150 microg / kg) induced significant hypotension and tachycardia. Bromocriptine - induced hypotension was unaffected by isoproterenol pretreatment, while tachycardia was reversed to significant bradycardia, an effect that was partly reduced by i. v. domperidone (0. 5 mg / kg). Neither cardiac vagal nor sympathetic tone was altered by isoproterenol pretreatment. In isolated perfused heart preparations from isoproterenol - pretreated rats, the isoproterenol - induced maximal increase in left ventricular systolic pressure was significantly reduced, compared with saline - pretreated rats (the EC50 of the isoproterenol - induced increase in left ventricular systolic pressure was enhanced approximately 22 - fold). These results show that 15 - day isoproterenol pretreatment not only abolished but reversed bromocriptine - induced tachycardia to bradycardia, an effect that is mainly related to further cardiac beta - adrenoceptor desensitization rather than to impairment of autonomic regulation of the heart. They suggest that, in normal conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at peripheral dopamine D2 receptors.

isoproterenol

bromocriptine

bromocriptine

dopamine

isoproterenol

isoproterenol

bromocriptine

Isoproterenol

bromocriptine

Bromocriptine

isoproterenol

domperidone

isoproterenol

isoproterenol

isoproterenol

isoproterenol

isoproterenol

bromocriptine

bromocriptine

dopamine

tachycardia

tachycardia

tachycardia

cardiac hypertrophy

hypotension

tachycardia

hypotension

tachycardia

bradycardia

tachycardia

bradycardia

tachycardia

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

Isoproterenol

bradycardia

Isoproterenol

bradycardia

Isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

isoproterenol

bradycardia

domperidone

bradycardia

domperidone

bradycardia

domperidone

bradycardia

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

Bromocriptine

hypotension

Bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

bromocriptine

hypotension

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

Isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

isoproterenol

cardiac hypertrophy

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

Bromocriptine

tachycardia

Bromocriptine

tachycardia

Bromocriptine

tachycardia

Bromocriptine

tachycardia

Bromocriptine

tachycardia

Bromocriptine

tachycardia

Bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia

bromocriptine

tachycardia


Input: A developmental analysis of clonidine' s effects on cardiac rate and ultrasound production in infant rats. Under controlled conditions, infant rats emit ultrasonic vocalizations during extreme cold exposure and after administration of the alpha (2) adrenoceptor agonist, clonidine. Previous investigations have determined that, in response to clonidine, ultrasound production increases through the 2nd - week postpartum and decreases thereafter. Given that sympathetic neural dominance exhibits a similar developmental pattern, and given that clonidine induces sympathetic withdrawal and bradycardia, we hypothesized that clonidine' s developmental effects on cardiac rate and ultrasound production would mirror each other. Therefore, in the present experiment, the effects of clonidine administration (0. 5 mg / kg) on cardiac rate and ultrasound production were examined in 2 -, 8 -, 15 -, and 20 - day - old rats. Age - related changes in ultrasound production corresponded with changes in cardiovascular variables, including baseline cardiac rate and clonidine - induced bradycardia. This experiment is discussed with regard to the hypothesis that ultrasound production is the acoustic by - product of a physiological maneuver that compensates for clonidine' s detrimental effects on cardiovascular function.

clonidine

clonidine

clonidine

clonidine

clonidine

clonidine

clonidine

clonidine

bradycardia

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia

clonidine

bradycardia


Input: Differential effects of systemically administered ketamine and lidocaine on dynamic and static hyperalgesia induced by intradermal capsaicin in humans. We have examined the effect of systemic administration of ketamine and lidocaine on brush - evoked (dynamic) pain and punctate - evoked (static) hyperalgesia induced by capsaicin. In a randomized, double - blind, placebo - controlled, crossover study, we studied 12 volunteers in three experiments. Capsaicin 100 micrograms was injected intradermally on the volar forearm followed by an i. v. infusion of ketamine (bolus 0. 1 mg kg - 1 over 10 min followed by infusion of 7 micrograms kg - 1 min - 1), lidocaine 5 mg kg - 1 or saline for 50 min. Infusion started 15 min after injection of capsaicin. The following were measured: spontaneous pain, pain evoked by punctate and brush stimuli (VAS), and areas of brush - evoked and punctate - evoked hyperalgesia. Ketamine reduced both the area of brush - evoked and punctate - evoked hyperalgesia significantly and it tended to reduce brush - evoked pain. Lidocaine reduced the area of punctate - evoked hyperalgesia significantly. It tended to reduce VAS scores of spontaneous pain but had no effect on evoked pain. The differential effects of ketamine and lidocaine on static and dynamic hyperalgesia suggest that the two types of hyperalgesia are mediated by separate mechanisms and have a distinct pharmacology.

ketamine

lidocaine

capsaicin

ketamine

lidocaine

capsaicin

Capsaicin

ketamine

lidocaine

capsaicin

Ketamine

Lidocaine

ketamine

lidocaine

hyperalgesia

pain

hyperalgesia

pain

pain

hyperalgesia

hyperalgesia

pain

hyperalgesia

pain

pain

hyperalgesia

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

Capsaicin

hyperalgesia

Capsaicin

hyperalgesia

Capsaicin

hyperalgesia

Capsaicin

hyperalgesia

Capsaicin

hyperalgesia

Capsaicin

hyperalgesia

Capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

hyperalgesia

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

Capsaicin

pain

Capsaicin

pain

Capsaicin

pain

Capsaicin

pain

Capsaicin

pain

Capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain


Input: Cyclosporine and tacrolimus - associated thrombotic microangiopathy. The development of thrombotic microangiopathy (TMA) associated with the use of cyclosporine has been well documented. Treatments have included discontinuation or reduction of cyclosporine dose with or without concurrent plasma exchange, plasma infusion, anticoagulation, and intravenous immunoglobulin G infusion. However, for recipients of organ transplantation, removing the inciting agent is not without the attendant risk of precipitating acute rejection and graft loss. The last decade has seen the emergence of tacrolimus as a potent immunosuppressive agent with mechanisms of action virtually identical to those of cyclosporine. As a result, switching to tacrolimus has been reported to be a viable therapeutic option in the setting of cyclosporine - induced TMA. With the more widespread application of tacrolimus in organ transplantation, tacrolimus - associated TMA has also been recognized. However, literature regarding the incidence of the recurrence of TMA in patients exposed sequentially to cyclosporine and tacrolimus is limited. We report a case of a living donor renal transplant recipient who developed cyclosporine - induced TMA that responded to the withdrawal of cyclosporine in conjunction with plasmapheresis and fresh frozen plasma replacement therapy. Introduction of tacrolimus as an alternative immunosuppressive agent resulted in the recurrence of TMA and the subsequent loss of the renal allograft. Patients who are switched from cyclosporine to tacrolimus or vice versa should be closely monitored for the signs and symptoms of recurrent TMA.

Cyclosporine

tacrolimus

cyclosporine

cyclosporine

tacrolimus

cyclosporine

tacrolimus

cyclosporine

tacrolimus

tacrolimus

cyclosporine

tacrolimus

cyclosporine

cyclosporine

tacrolimus

cyclosporine

tacrolimus

thrombotic microangiopathy

thrombotic microangiopathy

TMA

TMA

TMA

TMA

TMA

TMA

TMA

Cyclosporine

thrombotic microangiopathy

Cyclosporine

thrombotic microangiopathy

Cyclosporine

TMA

Cyclosporine

TMA

Cyclosporine

TMA

Cyclosporine

TMA

Cyclosporine

TMA

Cyclosporine

TMA

Cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

thrombotic microangiopathy

cyclosporine

thrombotic microangiopathy

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

cyclosporine

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

thrombotic microangiopathy

tacrolimus

thrombotic microangiopathy

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA

tacrolimus

TMA


Input: Repeated transient anuria following losartan administration in a patient with a solitary kidney. We report the case of a 70 - year - old hypertensive man with a solitary kidney and chronic renal insufficiency who developed two episodes of transient anuria after losartan administration. He was hospitalized for a myocardial infarction with pulmonary edema, treated with high - dose diuretics. Due to severe systolic dysfunction losartan was prescribed. Surprisingly, the first dose of 50 mg of losartan resulted in a sudden anuria, which lasted eight hours despite high - dose furosemide and amine infusion. One week later, by mistake, losartan was prescribed again and after the second dose of 50 mg, the patient developed a second episode of transient anuria lasting 10 hours. During these two episodes, his blood pressure diminished but no severe hypotension was noted. Ultimately, an arteriography showed a 70 - 80% renal artery stenosis. In this patient, renal artery stenosis combined with heart failure and diuretic therapy certainly resulted in a strong activation of the renin - angiotensin system (RAS). Under such conditions, angiotensin II receptor blockade by losartan probably induced a critical fall in glomerular filtration pressure. This case report highlights the fact that the angiotensin II receptor antagonist losartan can cause serious unexpected complications in patients with renovascular disease and should be used with extreme caution in this setting.

anuria

hypertensive

chronic renal insufficiency

anuria

myocardial infarction

pulmonary edema

systolic dysfunction

anuria

anuria

hypotension

renal artery stenosis

renal artery stenosis

heart failure

renovascular disease

losartan

losartan

losartan

losartan

furosemide

amine

losartan

angiotensin

angiotensin II

losartan

angiotensin II

losartan

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria

losartan

anuria


Input: In vivo protection of dna damage associated apoptotic and necrotic cell deaths during acetaminophen - induced nephrotoxicity, amiodarone - induced lung toxicity and doxorubicin - induced cardiotoxicity by a novel IH636 grape seed proanthocyanidin extract. Grape seed extract, primarily a mixture of proanthocyanidins, has been shown to modulate a wide - range of biological, pharmacological and toxicological effects which are mainly cytoprotective. This study assessed the ability of IH636 grape seed proanthocyanidin extract (GSPE) to prevent acetaminophen (AAP) - induced nephrotoxicity, amiodarone (AMI) - induced lung toxicity, and doxorubicin (DOX) - induced cardiotoxicity in mice. Experimental design consisted of four groups: control (vehicle alone), GSPE alone, drug alone and GSPE + drug. For the cytoprotection study, animals were orally gavaged 100 mg / Kg GSPE for 7 - 10 days followed by i. p. injections of organ specific three drugs (AAP: 500 mg / Kg for 24 h; AMI: 50 mg / Kg / day for four days; DOX: 20 mg / Kg for 48 h). Parameters of study included analysis of serum chemistry (ALT, BUN and CPK), and orderly fragmentation of genomic DNA (both endonuclease - dependent and independent) in addition to microscopic evaluation of damage and / or protection in corresponding PAS stained tissues. Results indicate that GSPE preexposure prior to AAP, AMI and DOX, provided near complete protection in terms of serum chemistry changes (ALT, BUN and CPK), and significantly reduced DNA fragmentation. Histopathological examination of kidney, heart and lung sections revealed moderate to massive tissue damage with a variety of morphological aberrations by all the three drugs in the absence of GSPE preexposure than in its presence. GSPE + drug exposed tissues exhibited minor residual damage or near total recovery. Additionally, histopathological alterations mirrored both serum chemistry changes and the pattern of DNA fragmentation. Interestingly, all the drugs, such as, AAP, AMI and DOX induced apoptotic death in addition to necrosis in the respective organs which was very effectively blocked by GSPE. Since AAP, AMI and DOX undergo biotransformation and are known to produce damaging radicals in vivo, the protection by GSPE may be linked to both inhibition of metabolism and / or detoxification of cytotoxic radicals. In addition, its' presumed contribution to DNA repair may be another important attribute, which played a role in the chemoprevention process. Additionally, this may have been the first report on AMI - induced apoptotic death in the lung tissue. Taken together, these events undoubtedly establish GSPE' s abundant bioavailability, and the power to defend multiple target organs from toxic assaults induced by structurally diverse and functionally different entities in vivo.

necrotic

nephrotoxicity

lung toxicity

cardiotoxicity

nephrotoxicity

lung toxicity

cardiotoxicity

tissue damage

necrosis

acetaminophen

amiodarone

doxorubicin

IH636 grape seed proanthocyanidin extract

Grape seed extract

proanthocyanidins

IH636 grape seed proanthocyanidin extract

GSPE

acetaminophen

AAP

amiodarone

AMI

doxorubicin

DOX

GSPE

GSPE

GSPE

AAP

AMI

DOX

GSPE

AAP

AMI

DOX

GSPE

GSPE

AAP

AMI

DOX

GSPE

AAP

AMI

DOX

GSPE

AMI

GSPE

amiodarone

necrotic

amiodarone

necrosis

amiodarone

necrotic

amiodarone

necrosis

AMI

necrotic

AMI

necrosis

AMI

necrotic

AMI

necrosis

AMI

necrotic

AMI

necrosis

AMI

necrotic

AMI

necrosis

AMI

necrotic

AMI

necrosis

AMI

necrotic

AMI

necrosis

doxorubicin

necrotic

doxorubicin

necrosis

doxorubicin

necrotic

doxorubicin

necrosis

DOX

necrotic

DOX

necrosis

DOX

necrotic

DOX

necrosis

DOX

necrotic

DOX

necrosis

DOX

necrotic

DOX

necrosis

DOX

necrotic

DOX

necrosis

acetaminophen

necrotic

acetaminophen

necrosis

acetaminophen

necrotic

acetaminophen

necrosis

AAP

necrotic

AAP

necrosis

AAP

necrotic

AAP

necrosis

AAP

necrotic

AAP

necrosis

AAP

necrotic

AAP

necrosis

AAP

necrotic

AAP

necrosis

acetaminophen

nephrotoxicity

acetaminophen

nephrotoxicity

acetaminophen

nephrotoxicity

acetaminophen

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

AAP

nephrotoxicity

amiodarone

lung toxicity

amiodarone

lung toxicity

amiodarone

lung toxicity

amiodarone

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

AMI

lung toxicity

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


Input: Palpebral twitching in a depressed adolescent on citalopram. Current estimates suggest that between 0. 4% and 8. 3% of children and adolescents are affected by major depression. We report a favorable response to treatment with citalopram by a 15 - year - old boy with major depression who exhibited palpebral twitching during his first 2 weeks of treatment. This may have been a side effect of citalopram as it remitted with redistribution of doses.

Palpebral twitching

depressed

major depression

major depression

palpebral twitching

citalopram

citalopram

citalopram

citalopram

Palpebral twitching

citalopram

palpebral twitching

citalopram

Palpebral twitching

citalopram

palpebral twitching

citalopram

Palpebral twitching

citalopram

palpebral twitching


Input: Metamizol potentiates morphine antinociception but not constipation after chronic treatment. This work evaluates the antinociceptive and constipating effects of the combination of 3. 2 mg / kg s. c. morphine with 177. 8 mg / kg s. c. metamizol in acutely and chronically treated (once a day for 12 days) rats. On the 13th day, antinociceptive effects were assessed using a model of inflammatory nociception, pain - induced functional impairment model, and the charcoal meal test was used to evaluate the intestinal transit. Simultaneous administration of morphine with metamizol resulted in a markedly antinociceptive potentiation and an increasing of the duration of action after a single (298 + / - 7 vs. 139 + / - 36 units area (ua); P < 0. 001) and repeated administration (280 + / - 17 vs. 131 + / - 22 ua; P < 0. 001). Antinociceptive effect of morphine was reduced in chronically treated rats (39 + / - 10 vs. 18 + / - 5 au) while the combination - induced antinociception was remained similar as an acute treatment (298 + / - 7 vs. 280 + / - 17 au). Acute antinociceptive effects of the combination were partially prevented by 3. 2 mg / kg naloxone s. c. (P < 0. 05), suggesting the partial involvement of the opioidergic system in the synergism observed. In independent groups, morphine inhibited the intestinal transit in 48 + / - 4% and 38 + / - 4% after acute and chronic treatment, respectively, suggesting that tolerance did not develop to the constipating effects. The combination inhibited intestinal transit similar to that produced by morphine regardless of the time of treatment, suggesting that metamizol did not potentiate morphine - induced constipation. These findings show a significant interaction between morphine and metamizol in chronically treated rats, suggesting that this combination could be useful for the treatment of chronic pain.

Metamizol

morphine

morphine

metamizol

charcoal

morphine

metamizol

morphine

naloxone

morphine

morphine

metamizol

morphine

morphine

metamizol

constipation

constipating

pain

constipating

constipation

chronic pain

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation

morphine

constipation

morphine

constipating

morphine

constipating

morphine

constipation


Input: Ifosfamide encephalopathy presenting with asterixis. CNS toxic effects of the antineoplastic agent ifosfamide (IFX) are frequent and include a variety of neurological symptoms that can limit drug use. We report a case of a 51 - year - old man who developed severe, disabling negative myoclonus of the upper and lower extremities after the infusion of ifosfamide for plasmacytoma. He was awake, revealed no changes of mental status and at rest there were no further motor symptoms. Cranial magnetic resonance imaging and extensive laboratory studies failed to reveal structural lesions of the brain and metabolic abnormalities. An electroencephalogram showed continuous, generalized irregular slowing with admixed periodic triphasic waves indicating symptomatic encephalopathy. The administration of ifosfamide was discontinued and within 12 h the asterixis resolved completely. In the patient described, the presence of asterixis during infusion of ifosfamide, normal laboratory findings and imaging studies and the resolution of symptoms following the discontinuation of the drug suggest that negative myoclonus is associated with the use of IFX.

Ifosfamide

ifosfamide

IFX

ifosfamide

ifosfamide

ifosfamide

IFX

encephalopathy

asterixis

myoclonus

plasmacytoma

structural lesions of the brain

metabolic abnormalities

encephalopathy

asterixis

asterixis

myoclonus

Ifosfamide

myoclonus

Ifosfamide

myoclonus

ifosfamide

myoclonus

ifosfamide

myoclonus

IFX

myoclonus

IFX

myoclonus

ifosfamide

myoclonus

ifosfamide

myoclonus

ifosfamide

myoclonus

ifosfamide

myoclonus

ifosfamide

myoclonus

ifosfamide

myoclonus

IFX

myoclonus

IFX

myoclonus

Ifosfamide

encephalopathy

Ifosfamide

structural lesions of the brain

Ifosfamide

encephalopathy

ifosfamide

encephalopathy

ifosfamide

structural lesions of the brain

ifosfamide

encephalopathy

IFX

encephalopathy

IFX

structural lesions of the brain

IFX

encephalopathy

ifosfamide

encephalopathy

ifosfamide

structural lesions of the brain

ifosfamide

encephalopathy

ifosfamide

encephalopathy

ifosfamide

structural lesions of the brain

ifosfamide

encephalopathy

ifosfamide

encephalopathy

ifosfamide

structural lesions of the brain

ifosfamide

encephalopathy

IFX

encephalopathy

IFX

structural lesions of the brain

IFX

encephalopathy


Input: Sub - chronic low dose gamma - vinyl GABA (vigabatrin) inhibits cocaine - induced increases in nucleus accumbens dopamine. RATIONALE: gamma - Vinyl GABA (GVG) irreversibly inhibits GABA - transaminase. This non - receptor mediated inhibition requires de novo synthesis for restoration of functional GABA catabolism. OBJECTIVES: Given its preclinical success for treating substance abuse and the increased risk of visual field defects (VFD) associated with cumulative lifetime exposure, we explored the effects of sub - chronic low dose GVG on cocaine - induced increases in nucleus accumbens (NAcc) dopamine (DA). METHODS: Using in vivo microdialysis, we compared acute exposure (450 mg / kg) to an identical sub - chronic exposure (150 mg / kg per day for 3 days), followed by 1 - or 3 - day washout. Finally, we examined the low dose of 150 mg / kg (50 mg / kg per day) using a similar washout period. RESULTS: Sub - chronic GVG exposure inhibited the effect of cocaine for 3 days, which exceeded in magnitude and duration the identical acute dose. CONCLUSIONS: Sub - chronic low dose GVG potentiates and extends the inhibition of cocaine - induced increases in dopamine, effectively reducing cumulative exposures and the risk for VFDS.

gamma - vinyl GABA

vigabatrin

cocaine

dopamine

gamma - Vinyl GABA

GVG

GABA

GABA

GVG

cocaine

dopamine

DA

GVG

cocaine

GVG

cocaine

dopamine

substance abuse

visual field defects

VFD

gamma - vinyl GABA

visual field defects

gamma - vinyl GABA

VFD

vigabatrin

visual field defects

vigabatrin

VFD

gamma - Vinyl GABA

visual field defects

gamma - Vinyl GABA

VFD

GVG

visual field defects

GVG

VFD

GVG

visual field defects

GVG

VFD

GVG

visual field defects

GVG

VFD

GVG

visual field defects

GVG

VFD


Input: Amount of bleeding and hematoma size in the collagenase - induced intracerebral hemorrhage rat model. The aggravated risk on intracerebral hemorrhage (ICH) with drugs used for stroke patients should be estimated carefully. We therefore established sensitive quantification methods and provided a rat ICH model for detection of ICH deterioration. In ICH intrastriatally induced by 0. 014 - unit, 0. 070 - unit, and 0. 350 - unit collagenase, the amount of bleeding was measured using a hemoglobin assay developed in the present study and was compared with the morphologically determined hematoma volume. The blood amounts and hematoma volumes were significantly correlated, and the hematoma induced by 0. 014 - unit collagenase was adequate to detect ICH deterioration. In ICH induction using 0. 014 - unit collagenase, heparin enhanced the hematoma volume 3. 4 - fold over that seen in control ICH animals and the bleeding 7. 6 - fold. Data suggest that this sensitive hemoglobin assay is useful for ICH detection, and that a model with a small ICH induced with a low - dose collagenase should be used for evaluation of drugs that may affect ICH.

bleeding

hematoma

intracerebral hemorrhage

intracerebral hemorrhage

ICH

stroke

ICH

ICH

ICH

bleeding

hematoma

hematoma

hematoma

ICH

ICH

hematoma

ICH

bleeding

ICH

ICH

ICH

heparin

heparin

hematoma

heparin

hematoma

heparin

hematoma

heparin

hematoma

heparin

hematoma


Input: Estradiol reduces seizure - induced hippocampal injury in ovariectomized female but not in male rats. Estrogens protect ovariectomized rats from hippocampal injury induced by kainic acid - induced status epilepticus (SE). We compared the effects of 17beta - estradiol in adult male and ovariectomized female rats subjected to lithium - pilocarpine - induced SE. Rats received subcutaneous injections of 17beta - estradiol (2 microg / rat) or oil once daily for four consecutive days. SE was induced 20 h following the second injection and terminated 3 h later. The extent of silver - stained CA3 and CA1 hippocampal neurons was evaluated 2 days after SE. 17beta - Estradiol did not alter the onset of first clonus in ovariectomized rats but accelerated it in males. 17beta - Estradiol reduced the argyrophilic neurons in the CA1 and CA3 - C sectors of ovariectomized rats. In males, estradiol increased the total damage score. These findings suggest that the effects of estradiol on seizure threshold and damage may be altered by sex - related differences in the hormonal environment.

Estradiol

kainic acid

17beta - estradiol

lithium

pilocarpine

17beta - estradiol

silver

17beta - Estradiol

17beta - Estradiol

estradiol

estradiol

seizure

hippocampal injury

hippocampal injury

status epilepticus

SE

SE

SE

SE

seizure

lithium

status epilepticus

lithium

SE

lithium

SE

lithium

SE

lithium

SE

lithium

hippocampal injury

lithium

hippocampal injury

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

hippocampal injury

pilocarpine

hippocampal injury


Input: Delirium during clozapine treatment: incidence and associated risk factors. BACKGROUND: Incidence and risk factors for delirium during clozapine treatment require further clarification. METHODS: We used computerized pharmacy records to identify all adult psychiatric inpatients treated with clozapine (1995 - 96), reviewed their medical records to score incidence and severity of delirium, and tested associations with potential risk factors. RESULTS: Subjects (n = 139) were 72 women and 67 men, aged 40. 8 + / - 12. 1 years, hospitalized for 24. 9 + / - 23. 3 days, and given clozapine, gradually increased to an average daily dose of 282 + / - 203 mg (3. 45 + / - 2. 45 mg / kg) for 18. 9 + / - 16. 4 days. Delirium was diagnosed in 14 (10. 1% incidence, or 1. 48 cases / person - years of exposure); 71. 4% of cases were moderate or severe. Associated factors were co - treatment with other centrally antimuscarinic agents, poor clinical outcome, older age, and longer hospitalization (by 17. 5 days, increasing cost); sex, diagnosis or medical co - morbidity, and daily clozapine dose, which fell with age, were unrelated. CONCLUSIONS: Delirium was found in 10% of clozapine - treated inpatients, particularly in older patients exposed to other central anticholinergics. Delirium was inconsistently recognized clinically in milder cases and was associated with increased length - of - stay and higher costs, and inferior clinical outcome.

Delirium

delirium

psychiatric

delirium

Delirium

Delirium

Delirium

clozapine

clozapine

clozapine

clozapine

clozapine

clozapine

clozapine

Delirium

clozapine

delirium

clozapine

delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

delirium

clozapine

delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

delirium

clozapine

delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

delirium

clozapine

delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

delirium

clozapine

delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium

clozapine

delirium

clozapine

delirium

clozapine

Delirium

clozapine

Delirium

clozapine

Delirium


Input: Ketoconazole - induced neurologic sequelae. A 77 - y - old patient developed weakness of extremities, legs paralysis, dysarthria and tremor 1 h after ingestion of 200 mg ketoconazole for the first time in his life. All complaints faded away within 24 h. Few days later, the patient used another 200 mg ketoconazole tablet, and within an hour experienced a similar clinical picture, which resolved again spontaneously within hours. Laboratory evaluations, including head CT scan, were normal. This case illustrates the need for close vigilance in adverse drug reactions, particularly in the elderly.

Ketoconazole

ketoconazole

ketoconazole

neurologic sequelae

weakness of extremities

legs paralysis

dysarthria

tremor

adverse drug reactions

Ketoconazole

dysarthria

ketoconazole

dysarthria

ketoconazole

dysarthria

Ketoconazole

weakness of extremities

ketoconazole

weakness of extremities

ketoconazole

weakness of extremities

Ketoconazole

tremor

ketoconazole

tremor

ketoconazole

tremor

Ketoconazole

legs paralysis

ketoconazole

legs paralysis

ketoconazole

legs paralysis


Input: Noxious chemical stimulation of rat facial mucosa increases intracranial blood flow through a trigemino - parasympathetic reflex - - an experimental model for vascular dysfunctions in cluster headache. Cluster headache is characterized by typical autonomic dysfunctions including facial and intracranial vascular disturbances. Both the trigeminal and the cranial parasympathetic systems may be involved in mediating these dysfunctions. An experimental model was developed in the rat to measure changes in lacrimation and intracranial blood flow following noxious chemical stimulation of facial mucosa. Blood flow was monitored in arteries of the exposed cranial dura mater and the parietal cortex using laser Doppler flowmetry. Capsaicin (0. 01 - 1 mm) applied to oral or nasal mucosa induced increases in dural and cortical blood flow and provoked lacrimation. These responses were blocked by systemic pre - administration of hexamethonium chloride (20 mg / kg). The evoked increases in dural blood flow were also abolished by topical pre - administration of atropine (1 mm) and [Lys1, Pro2, 5, Arg3, 4, Tyr6] - VIP (0. 1 mm), a vasoactive intestinal polypeptide (VIP) antagonist, onto the exposed dura mater. We conclude that noxious stimulation of facial mucosa increases intracranial blood flow and lacrimation via a trigemino - parasympathetic reflex. The blood flow responses seem to be mediated by the release of acetylcholine and VIP within the meninges. Similar mechanisms may be involved in the pathogenesis of cluster headache.

vascular dysfunctions

cluster headache

Cluster headache

intracranial vascular disturbances

increases in dural and cortical blood flow

increases in dural blood flow

cluster headache

Capsaicin

hexamethonium chloride

atropine

acetylcholine

Capsaicin

vascular dysfunctions

Capsaicin

intracranial vascular disturbances

Capsaicin

increases in dural and cortical blood flow

Capsaicin

increases in dural blood flow


Input: Recurrent excitation in the dentate gyrus of a murine model of temporal lobe epilepsy. Similar to rats, systemic pilocarpine injection causes status epilepticus (SE) and the eventual development of spontaneous seizures and mossy fiber sprouting in C57BL / 6 and CD1 mice, but the physiological correlates of these events have not been identified in mice. Population responses in granule cells of the dentate gyrus were examined in transverse slices of the ventral hippocampus from pilocarpine - treated and untreated mice. In Mg (2 +) - free bathing medium containing bicuculline, conditions designed to increase excitability in the slices, electrical stimulation of the hilus resulted in a single population spike in granule cells from control mice and pilocarpine - treated mice that did not experience SE. In SE survivors, similar stimulation resulted in a population spike followed, at a variable latency, by negative DC shifts and repetitive afterdischarges of 3 - 60 s duration, which were blocked by ionotropic glutamate receptor antagonists. Focal glutamate photostimulation of the granule cell layer at sites distant from the recording pipette resulted in population responses of 1 - 30 s duration in slices from SE survivors but not other groups. These data support the hypothesis that SE - induced mossy fiber sprouting and synaptic reorganization are relevant characteristics of seizure development in these murine strains, resembling rat models of human temporal lobe epilepsy.

temporal lobe epilepsy

status epilepticus

SE

seizures

SE

SE

SE

SE

seizure

temporal lobe epilepsy

pilocarpine

pilocarpine

Mg

bicuculline

pilocarpine

glutamate

glutamate

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizure


Input: The alpha3 and beta4 nicotinic acetylcholine receptor subunits are necessary for nicotine - induced seizures and hypolocomotion in mice. Binding of nicotine to nicotinic acetylcholine receptors (nAChRs) elicits a series of dose - dependent behaviors that go from altered exploration, sedation, and tremors, to seizures and death. nAChRs are pentameric ion channels usually composed of alpha and beta subunits. A gene cluster comprises the alpha3, alpha5 and beta4 subunits, which coassemble to form functional receptors. We examined the role of the beta4 subunits in nicotine - induced seizures and hypolocomotion in beta4 homozygous null (beta4 - / -) and alpha3 heterozygous (+ / -) mice. beta4 - / - mice were less sensitive to the effects of nicotine both at low doses, measured as decreased exploration in an open field, and at high doses, measured as sensitivity to nicotine - induced seizures. Using in situ hybridization probes for the alpha3 and alpha5 subunits, we showed that alpha5 mRNA levels are unchanged, whereas alpha3 mRNA levels are selectively decreased in the mitral cell layer of the olfactory bulb, and the inferior and the superior colliculus of beta4 - / - brains. alpha3 + / - mice were partially resistant to nicotine - induced seizures when compared to wild - type littermates. mRNA levels for the alpha5 and the beta4 subunits were unchanged in alpha3 + / - brains. Together, these results suggest that the beta4 and the alpha3 subunits are mediators of nicotine - induced seizures and hypolocomotion.

acetylcholine

nicotine

nicotine

acetylcholine

nicotine

nicotine

nicotine

nicotine

nicotine

seizures

hypolocomotion

tremors

seizures

death

seizures

hypolocomotion

seizures

seizures

seizures

hypolocomotion

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures

nicotine

seizures


Input: Recurrent acute interstitial nephritis induced by azithromycin. A 14 - year - old girl is reported with recurrent, azithromycin - induced, acute interstitial nephritis. The second episode was more severe than the first; and although both were treated with intensive corticosteroid therapy, renal function remained impaired. Although most cases of antibiotic induced acute interstitial nephritis are benign and self - limited, some patients are at risk for permanent renal injury.

interstitial nephritis

interstitial nephritis

interstitial nephritis

renal injury

azithromycin

azithromycin

azithromycin

interstitial nephritis

azithromycin

interstitial nephritis

azithromycin

interstitial nephritis

azithromycin

interstitial nephritis

azithromycin

interstitial nephritis

azithromycin

interstitial nephritis


Input: Valproate - induced encephalopathy. Valproate - induced encephalopathy is a rare syndrome that may manifest in otherwise normal epileptic individuals. It may even present in patients who have tolerated this medicine well in the past. It is usually but not necessarily associated with hyperammonemia. The EEG shows characteristic triphasic waves in most patients with this complication. A case of valproate - induced encephalopathy is presented. The problems in diagnosing this condition are subsequently discussed.

Valproate

Valproate

valproate

encephalopathy

encephalopathy

epileptic

hyperammonemia

encephalopathy

Valproate

encephalopathy

Valproate

encephalopathy

Valproate

encephalopathy

Valproate

encephalopathy

Valproate

encephalopathy

Valproate

encephalopathy

valproate

encephalopathy

valproate

encephalopathy

valproate

encephalopathy


Input: Nitro - L - arginine methyl ester: a potential protector against gentamicin ototoxicity. The nitric oxide (NO) inhibitor nitro - L - arginine methyl ester (L - NAME) may act as an otoprotectant against high - frequency hearing loss caused by gentamicin, but further studies are needed to confirm this. Aminoglycoside antibiotics are still widely used by virtue of their efficacy and low cost. Their ototoxicity is a serious health problem and, as their ototoxic mechanism involves the production of NO, we need to assess the use of NO inhibitors for the prevention of aminoglycoside - induced sensorineural hearing loss. In this experimental study we used 30 Sprague - Dawley rats, 27 of which had gentamicin instilled into the middle ear. The otoprotectant L - NAME was administered topically to 12 / 27 animals. Its effect was determined in terms of attenuation of hearing loss, measured by shifts in the auditory brainstem response threshold. L - NAME reduced gentamicin - induced hearing loss in the high - frequency range, but gave no protection in the middle or low frequencies.

Nitro - L - arginine methyl ester

gentamicin

nitric oxide

NO

nitro - L - arginine methyl ester

L - NAME

gentamicin

Aminoglycoside

NO

NO

aminoglycoside

gentamicin

L - NAME

L - NAME

gentamicin

ototoxicity

high - frequency hearing loss

ototoxicity

ototoxic

sensorineural hearing loss

hearing loss

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss

gentamicin

hearing loss


Input: Cerebral vasculitis following oral methylphenidate intake in an adult: a case report. Methylphenidate is structurally and functionally similar to amphetamine. Cerebral vasculitis associated with amphetamine abuse is well documented, and in rare cases ischaemic stroke has been reported after methylphenidate intake in children. We report the case of a 63 - year - old female who was treated with methylphenidate due to hyperactivity and suffered from multiple ischaemic strokes. We consider drug - induced cerebral vasculitis as the most likely cause of recurrent ischaemic strokes in the absence of any pathological findings during the diagnostic work - up. We conclude that methylphenidate mediated vasculitis should be considered in patients with neurological symptoms and a history of methylphenidate therapy. This potential side - effect, though very rare, represents one more reason to be very restrictive in the use of methylphenidate.

Cerebral vasculitis

Cerebral vasculitis

amphetamine abuse

ischaemic stroke

hyperactivity

ischaemic strokes

cerebral vasculitis

ischaemic strokes

vasculitis

methylphenidate

Methylphenidate

amphetamine

methylphenidate

methylphenidate

methylphenidate

methylphenidate

methylphenidate

methylphenidate

Cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

cerebral vasculitis

Methylphenidate

Cerebral vasculitis

Methylphenidate

Cerebral vasculitis

Methylphenidate

cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

Cerebral vasculitis

methylphenidate

cerebral vasculitis


Input: Cerebral haemorrhage induced by warfarin - the influence of drug - drug interactions. PURPOSE: To evaluate the frequency, severity and preventability of warfarin - induced cerebral haemorrhages due to warfarin and warfarin - drug interactions in patients living in the county of Osterg tland, Sweden. METHODS: All patients with a diagnosed cerebral haemorrhage at three hospitals during the period 2000 - 2002 were identified. Medical records were studied retrospectively to evaluate whether warfarin and warfarin - drug interactions could have caused the cerebral haemorrhage. The proportion of possibly avoidable cases due to drug interactions was estimated. RESULTS: Among 593 patients with cerebral haemorrhage, 59 (10%) were assessed as related to warfarin treatment. This imply an incidence of 1. 7 / 100, 000 treatment years. Of the 59 cases, 26 (44%) had a fatal outcome, compared to 136 (25%) among the non - warfarin patients (p < 0. 01). A warfarin - drug interaction could have contributed to the haemorrhage in 24 (41%) of the warfarin patients and in 7 of these (12%) the bleeding complication was considered being possible to avoid. CONCLUSIONS: Warfarin - induced cerebral haemorrhages are a major clinical problem with a high fatality rate. Almost half of the cases was related to a warfarin - drug interaction. A significant proportion of warfarin - related cerebral haemorrhages might have been prevented if greater caution had been taken when prescribing drugs known to interact with warfarin.

Cerebral haemorrhage

cerebral haemorrhages

cerebral haemorrhage

cerebral haemorrhage

cerebral haemorrhage

haemorrhage

bleeding

cerebral haemorrhages

cerebral haemorrhages

warfarin

warfarin

warfarin

warfarin

warfarin

warfarin

warfarin

warfarin

warfarin

warfarin

Warfarin

warfarin

warfarin

warfarin

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

Warfarin

Cerebral haemorrhage

Warfarin

cerebral haemorrhages

Warfarin

cerebral haemorrhage

Warfarin

cerebral haemorrhage

Warfarin

cerebral haemorrhage

Warfarin

cerebral haemorrhages

Warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages

warfarin

Cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhage

warfarin

cerebral haemorrhages

warfarin

cerebral haemorrhages


Input: Side effects of postoperative administration of methylprednisolone and gentamicin into the posterior sub - Tenon' s space. PURPOSE: To assess the incidence of postoperative emetic side effects after the administration of methylprednisolone and gentamicin into the posterior sub - Tenon' s space at the end of routine cataract surgery. SETTING: St. Luke' s Hospital, Gwardamangia, Malta. METHODS: A double - blind double - armed prospective study comprised 40 patients who had uneventful sutureless phacoemulsification under sub - Tenon' s local infiltration of 3 mL of plain lignocaine. At the end of the procedure, Group A (n = 20) had 20 mg / 0. 5 mL of methylprednisolone and 10 mg / 0. 5 mL of gentamicin injected into the posterior sub - Tenon' s space and Group B (n = 20) had the same combination injected into the anterior sub - Tenon' s space. Postoperatively, all patients were assessed for symptoms of nausea, vomiting, and headache. A chi - square test was used to assess the statistical significance of results. RESULTS: Sixty percent in Group A developed postoperative emetic symptoms, headache, or both; 1 patient in Group B developed symptoms. CONCLUSIONS: The administration of methylprednisolone and gentamicin in the posterior sub - Tenon' s space was related to a high incidence of side effects including nausea, vomiting, and headache. All adverse effects were self - limiting.

methylprednisolone

gentamicin

methylprednisolone

gentamicin

lignocaine

methylprednisolone

gentamicin

methylprednisolone

gentamicin

cataract

nausea, vomiting

headache

postoperative emetic symptoms

headache

nausea, vomiting

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

gentamicin

headache

methylprednisolone

nausea, vomiting

methylprednisolone

postoperative emetic symptoms

methylprednisolone

nausea, vomiting

methylprednisolone

nausea, vomiting

methylprednisolone

postoperative emetic symptoms

methylprednisolone

nausea, vomiting

methylprednisolone

nausea, vomiting

methylprednisolone

postoperative emetic symptoms

methylprednisolone

nausea, vomiting

methylprednisolone

nausea, vomiting

methylprednisolone

postoperative emetic symptoms

methylprednisolone

nausea, vomiting

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

methylprednisolone

headache

gentamicin

nausea, vomiting

gentamicin

postoperative emetic symptoms

gentamicin

nausea, vomiting

gentamicin

nausea, vomiting

gentamicin

postoperative emetic symptoms

gentamicin

nausea, vomiting

gentamicin

nausea, vomiting

gentamicin

postoperative emetic symptoms

gentamicin

nausea, vomiting

gentamicin

nausea, vomiting

gentamicin

postoperative emetic symptoms

gentamicin

nausea, vomiting


Input: Cardiac Angiography in Renally Impaired Patients (CARE) study: a randomized double - blind trial of contrast - induced nephropathy in patients with chronic kidney disease. BACKGROUND: No direct comparisons exist of the renal tolerability of the low - osmolality contrast medium iopamidol with that of the iso - osmolality contrast medium iodixanol in high - risk patients. METHODS AND RESULTS: The present study is a multicenter, randomized, double - blind comparison of iopamidol and iodixanol in patients with chronic kidney disease (estimated glomerular filtration rate, 20 to 59 mL / min) who underwent cardiac angiography or percutaneous coronary interventions. Serum creatinine (SCr) levels and estimated glomerular filtration rate were assessed at baseline and 2 to 5 days after receiving medications. The primary outcome was a postdose SCr increase > or = 0. 5 mg / dL (44. 2 micromol / L) over baseline. Secondary outcomes were a postdose SCr increase > or = 25%, a postdose estimated glomerular filtration rate decrease of > or = 25%, and the mean peak change in SCr. In 414 patients, contrast volume, presence of diabetes mellitus, use of N - acetylcysteine, mean baseline SCr, and estimated glomerular filtration rate were comparable in the 2 groups. SCr increases > or = 0. 5 mg / dL occurred in 4. 4% (9 of 204 patients) after iopamidol and 6. 7% (14 of 210 patients) after iodixanol (P = 0. 39), whereas rates of SCr increases > or = 25% were 9. 8% and 12. 4%, respectively (P = 0. 44). In patients with diabetes, SCr increases > or = 0. 5 mg / dL were 5. 1% (4 of 78 patients) with iopamidol and 13. 0% (12 of 92 patients) with iodixanol (P = 0. 11), whereas SCr increases > or = 25% were 10. 3% and 15. 2%, respectively (P = 0. 37). Mean post - SCr increases were significantly less with iopamidol (all patients: 0. 07 versus 0. 12 mg / dL, 6. 2 versus 10. 6 micromol / L, P = 0. 03; patients with diabetes: 0. 07 versus 0. 16 mg / dL, 6. 2 versus 14. 1 micromol / L, P = 0. 01). CONCLUSIONS: The rate of contrast - induced nephropathy, defined by multiple end points, is not statistically different after the intraarterial administration of iopamidol or iodixanol to high - risk patients, with or without diabetes mellitus. Any true difference between the agents is small and not likely to be clinically significant.

nephropathy

chronic kidney disease

chronic kidney disease

diabetes mellitus

diabetes

diabetes

nephropathy

diabetes mellitus

contrast medium

iopamidol

contrast medium

iodixanol

iopamidol

iodixanol

creatinine

N - acetylcysteine

iopamidol

iodixanol

iopamidol

iodixanol

iopamidol

iopamidol

iodixanol

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

iodixanol

nephropathy

contrast medium

nephropathy

contrast medium

nephropathy

contrast medium

nephropathy

contrast medium

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy

iopamidol

nephropathy


Input: A novel compound, maltolyl p - coumarate, attenuates cognitive deficits and shows neuroprotective effects in vitro and in vivo dementia models. To develop a novel and effective drug that could enhance cognitive function and neuroprotection, we newly synthesized maltolyl p - coumarate by the esterification of maltol and p - coumaric acid. In the present study, we investigated whether maltolyl p - coumarate could improve cognitive decline in scopolamine - injected rats and in amyloid beta peptide (1 - 42) - infused rats. Maltolyl p - coumarate was found to attenuate cognitive deficits in both rat models using passive avoidance test and to reduce apoptotic cell death observed in the hippocampus of the amyloid beta peptide (1 - 42) - infused rats. We also examined the neuroprotective effects of maltolyl p - coumarate in vitro using SH - SY5Y cells. Cells were pretreated with maltolyl p - coumarate, before exposed to amyloid beta peptide (1 - 42), glutamate or H2O2. We found that maltolyl p - coumarate significantly decreased apoptotic cell death and reduced reactive oxygen species, cytochrome c release, and caspase 3 activation. Taking these in vitro and in vivo results together, our study suggests that maltolyl p - coumarate is a potentially effective candidate against Alzheimer' s disease that is characterized by wide spread neuronal death and progressive decline of cognitive function.

maltolyl p - coumarate

maltolyl p - coumarate

maltol

p - coumaric acid

maltolyl p - coumarate

scopolamine

amyloid beta peptide (1 - 42)

Maltolyl p - coumarate

amyloid beta peptide (1 - 42)

maltolyl p - coumarate

maltolyl p - coumarate

amyloid beta peptide (1 - 42)

glutamate

maltolyl p - coumarate

maltolyl p - coumarate

cognitive deficits

dementia

cognitive decline

cognitive deficits

Alzheimer' s disease

neuronal death

decline of cognitive function

scopolamine

cognitive deficits

scopolamine

cognitive decline

scopolamine

cognitive deficits

scopolamine

decline of cognitive function


Input: Interaction between warfarin and levofloxacin: case series. Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram - positive, Gram - negative, and atypical bacteria. While small prospective studies have not revealed any significant drug - drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin.

warfarin

levofloxacin

Warfarin

Levofloxacin

fluoroquinolone

warfarin

levofloxacin

levofloxacin

warfarin

warfarin

levofloxacin

levofloxacin

warfarin

bleeding

warfarin

bleeding

Warfarin

bleeding

warfarin

bleeding

warfarin

bleeding

warfarin

bleeding

warfarin

bleeding

levofloxacin

bleeding

Levofloxacin

bleeding

levofloxacin

bleeding

levofloxacin

bleeding

levofloxacin

bleeding

levofloxacin

bleeding


Input: Mutations associated with lamivudine - resistance in therapy - na ve hepatitis B virus (HBV) infected patients with and without HIV co - infection: implications for antiretroviral therapy in HBV and HIV co - infected South African patients. This was an exploratory study to investigate lamivudine - resistant hepatitis B virus (HBV) strains in selected lamivudine - na ve HBV carriers with and without human immunodeficiency virus (HIV) co - infection in South African patients. Thirty - five lamivudine - na ve HBV infected patients with or without HIV co - infection were studied: 15 chronic HBV mono - infected patients and 20 HBV - HIV co - infected patients. The latter group was further sub - divided into 13 occult HBV (HBsAg - negative) and 7 overt HBV (HBsAg - positive) patients. HBsAg, anti - HBs, anti - HBc, and anti - HIV 1 / 2 were determined as part of routine diagnosis using Axsym assays (Abbott Laboratories, North Chicago, IL). Serum samples were PCR amplified with HBV reverse transcriptase (RT) primers, followed by direct sequencing across the tyrosine - methionine - aspartate - aspartate (YMDD) motif of the major catalytic region in the C domain of the HBV RT enzyme. HBV viral load was performed with Amplicor HBV Monitor test v2. 0 (Roche Diagnostics, Penzberg, Germany). HBV lamivudine - resistant strains were detected in 3 of 15 mono - infected chronic hepatitis B patients and 10 of 20 HBV - HIV co - infected patients. To the best of our knowledge, this constitutes the first report of HBV lamivudine - resistant strains in therapy - na ve HBV - HIV co - infected patients. The HBV viral loads for mono - infected and co - infected patients ranged from 3. 32 x 10 (2) to 3. 82 x 10 (7) and < 200 to 4. 40 x 10 (3) copies / ml, respectively. It remains to be seen whether such pre - existing antiviral mutations could result in widespread emergence of HBV resistant strains when lamivudine - containing highly active antiretroviral (ARV) treatment (HAART) regimens become widely applied in South Africa, as this is likely to have potential implications in the management of HBV - HIV co - infected patients.

lamivudine

lamivudine

lamivudine

lamivudine

HBsAg

HBsAg

HBsAg

tyrosine

methionine

aspartate

aspartate

lamivudine

lamivudine

lamivudine

hepatitis B virus (HBV) infected

HIV co - infection

HBV and HIV co - infected

HBV and HIV co - infected

HIV co - infected

hepatitis B

human immunodeficiency virus (HIV) co - infection

HBV infected

HIV co - infection

HBV mono - infected

HBV - HIV co - infected

HBV - HIV co - infected

HIV co - infected

hepatitis B

HBV - HIV co - infected

HBV - HIV co - infected

HIV co - infected

HBV - HIV co - infected

HBV - HIV co - infected

HIV co - infected

HBV - HIV co - infected

HBV - HIV co - infected

HIV co - infected

HBsAg

hepatitis B virus (HBV) infected

HBsAg

HBV and HIV co - infected

HBsAg

HBV and HIV co - infected

HBsAg

hepatitis B

HBsAg

HBV infected

HBsAg

HBV mono - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

hepatitis B

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

hepatitis B virus (HBV) infected

HBsAg

HBV and HIV co - infected

HBsAg

HBV and HIV co - infected

HBsAg

hepatitis B

HBsAg

HBV infected

HBsAg

HBV mono - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

hepatitis B

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

hepatitis B virus (HBV) infected

HBsAg

HBV and HIV co - infected

HBsAg

HBV and HIV co - infected

HBsAg

hepatitis B

HBsAg

HBV infected

HBsAg

HBV mono - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

hepatitis B

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected

HBsAg

HBV - HIV co - infected