Input: Minor neurological dysfunction, cognitive development, and somatic development at the age of 3 to 7 years after dexamethasone treatment in very - low birth - weight infants. The objective of this study was to assess minor neurological dysfunction, cognitive development, and somatic development after dexamethasone therapy in very - low - birthweight infants. Thirty - three children after dexamethasone treatment were matched to 33 children without dexamethasone treatment. Data were assessed at the age of 3 - 7 years. Dexamethasone was started between the 7th and the 28th day of life over 7 days with a total dose of 2. 35 mg / kg / day. Exclusion criteria were asphyxia, malformations, major surgical interventions, small for gestational age, intraventricular haemorrhage grades III and IV, periventricular leukomalacia, and severe psychomotor retardation. Each child was examined by a neuropediatrician for minor neurological dysfunctions and tested by a psychologist for cognitive development with a Kaufman Assessment Battery for Children and a Draw - a - Man Test. There were no differences in demographic data, growth, and socio - economic status between the two groups. Fine motor skills and gross motor function were significantly better in the control group (p < 0. 01). In the Draw - a - Man Test, the control group showed better results (p < 0. 001). There were no differences in development of speech, social development, and the Kaufman Assessment Battery for Children. After dexamethasone treatment, children showed a higher rate of minor neurological dysfunctions. Neurological development was affected even without neurological diagnosis. Further long - term follow - up studies will be necessary to fully evaluate the impact of dexamethasone on neurological and cognitive development.

neurological dysfunction

neurological dysfunction

asphyxia

malformations

haemorrhage

periventricular leukomalacia

psychomotor retardation

neurological dysfunctions

neurological dysfunctions

dexamethasone

dexamethasone

dexamethasone

dexamethasone

Dexamethasone

dexamethasone

dexamethasone

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunctions

Dexamethasone

neurological dysfunction

Dexamethasone

neurological dysfunction

Dexamethasone

neurological dysfunctions

Dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunction

dexamethasone

neurological dysfunctions

dexamethasone

neurological dysfunctions


Input: Force overflow and levodopa - induced dyskinesias in Parkinson' s disease. We assessed force coordination of the hand in Parkinson' s disease and its relationship to motor complications of levodopa therapy, particularly to levodopa - induced dyskinesias (LID). We studied two groups of Parkinson' s disease patients with (Parkinson' s disease + LID, n = 23) and without levodopa - induced dyskinesias (Parkinson' s disease - LID, n = 10), and age - matched healthy controls. The motor score of the Unified Parkinson' s Disease Rating Scale, a dyskinesia score and force in a grip - lift paradigm were assessed ON and OFF levodopa. A pathological increase of forces was seen in ON - state in Parkinson' s disease + LID only. In Parkinson' s disease + LID, the force involved in pressing down the object before lifting was significantly increased by levodopa (by 61%, P < 0. 05). An overshooting of peak grip force by 51% (P < 0. 05) and of static grip force by 45% (P < 0. 01) was observed in the ON - compared with the OFF - drug condition. In contrast, no excessive force was found in Parkinson' s disease - LID. Peak grip force in ON - state was 140% (P < 0. 05) higher in Parkinson' s disease + LID than in Parkinson' s disease - LID, while static grip force was increased by 138% (P < 0. 01) between groups. Severity of peak - dose dyskinesias was strongly correlated with grip force in ON - state (r = 0. 79 with peak force, P < 0. 01). No correlation was observed between forces and the motor score as well as with the daily dose of dopaminergic medication. Force excess was only observed in patients with LID and motor fluctuations. A close relationship was seen between the overshooting of forces and dyskinesias in the ON - drug condition. We postulate that both LID and grip force excess share common pathophysiological mechanisms related to motor fluctuations.

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

dyskinesias

Parkinson' s disease

Parkinson' s disease

dyskinesias

LID

Parkinson' s disease

Parkinson' s disease

LID

dyskinesias

Parkinson' s disease

LID

Parkinson' s Disease

dyskinesia

Parkinson' s disease

LID

Parkinson' s disease

LID

Parkinson' s disease

LID

Parkinson' s disease

LID

Parkinson' s disease

LID

dyskinesias

LID

dyskinesias

LID

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesia

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesia

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesia

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesia

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesia

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesia

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

LID

levodopa

dyskinesias

levodopa

LID

levodopa

dyskinesias

levodopa

LID


Input: Postinfarction ventricular septal defect associated with long - term steroid therapy. Two cases of postinfarction ventricular septal rupture in patients on long - term steroid therapy are presented and the favourable outcome in both cases described. A possible association between steroid therapy and subsequent postinfarction septal rupture is discussed.

ventricular septal defect

ventricular septal rupture

septal rupture

steroid

steroid

steroid

steroid

ventricular septal defect

steroid

ventricular septal rupture

steroid

septal rupture

steroid

ventricular septal defect

steroid

ventricular septal rupture

steroid

septal rupture

steroid

ventricular septal defect

steroid

ventricular septal rupture

steroid

septal rupture


Input: Angioedema associated with droperidol administration. Angioedema, also known as angioneurotic edema or Quincke' s disease, is a well - demarcated, localized edema involving the subcutaneous tissues that may cause upper - airway obstruction. We report the case of a previously healthy 19 - year - old man with no known drug allergies in whom angioedema with significant tongue swelling and protrusion developed within 10 minutes of the administration of a single IV dose of droperidol.

Angioedema

Angioedema

angioneurotic edema

Quincke' s disease

edema

upper - airway obstruction

drug allergies

angioedema

tongue swelling

tongue swelling

swelling

droperidol

droperidol

droperidol

Angioedema

droperidol

Angioedema

droperidol

angioneurotic edema

droperidol

Quincke' s disease

droperidol

angioedema

droperidol

Angioedema

droperidol

Angioedema

droperidol

angioneurotic edema

droperidol

Quincke' s disease

droperidol

angioedema


Input: Clarithromycin - associated visual hallucinations in a patient with chronic renal failure on continuous ambulatory peritoneal dialysis. Visual hallucinations are a rare event in chronic renal failure and not related to uremia per se. Unreported in the literature is visual hallucinations occurring in association with the new macrolide antibiotic, clarithromycin. We describe such a case in a patient with end - stage renal disease (ESRD) maintained on continuous ambulatory peritoneal dialysis (CAPD). The combination of a relatively high dose of clarithromycin in face of chronic renal failure in a functionally anephric patient, with underlying aluminum intoxication, may have facilitated the appearance of this neurotoxic side effect. It is important to understand the pharmacokinetics of medications in face of chronic renal failure, the possibility of drug interactions, and how these factors should help guide medication therapy in the ESRD patient.

Clarithromycin

macrolide

clarithromycin

clarithromycin

aluminum

visual hallucinations

chronic renal failure

Visual hallucinations

chronic renal failure

uremia

visual hallucinations

end - stage renal disease

ESRD

chronic renal failure

neurotoxic

chronic renal failure

ESRD

Clarithromycin

visual hallucinations

Clarithromycin

Visual hallucinations

Clarithromycin

visual hallucinations

clarithromycin

visual hallucinations

clarithromycin

Visual hallucinations

clarithromycin

visual hallucinations

clarithromycin

visual hallucinations

clarithromycin

Visual hallucinations

clarithromycin

visual hallucinations


Input: Acute renal toxicity of doxorubicin (adriamycin) - loaded cyanoacrylate nanoparticles. Acute doxorubicin - loaded nanoparticle (DXNP) renal toxicity was explored in both normal rats and rats with experimental glomerulonephritis. In normal rats, 2 / 6 rats given free doxorubicin (DX) (5 mg / kg) died within one week, whereas all control animals and all rats having received free NP or DXNP survived. A 3 times higher proteinuria appeared in animals treated with DXNP than in those treated with DX. Free NP did not provoke any proteinuria. Two hr post - injection, DXNP was 2. 7 times more concentrated in kidneys than free DX (p < 0. 025). In rats with immune experimental glomerulonephritis, 5 / 6 rats given DX died within 7 days, in contrast to animals treated by DXNP, NP, or untreated, which all survived. Proteinuria appeared in all series, but was 2 - 5 times more intense (p > 0. 001) and prolonged after doxorubicin treatment (400 - 700 mg / day), without significant difference between DXNP and DX. Rats treated by unloaded NP behaved as controls. These results demonstrate that, in these experimental conditions, DXNP killed less animals than free DX, despite of an enhanced renal toxicity of the former. Both effects (better survival and nephrosis) are most probably related to an enhanced capture of DXNP by cells of the mononuclear phagocyte system, including mesangial cells.

renal toxicity

renal toxicity

glomerulonephritis

proteinuria

proteinuria

glomerulonephritis

Proteinuria

renal toxicity

nephrosis

doxorubicin

adriamycin

cyanoacrylate

doxorubicin

doxorubicin

DX

DX

DX

DX

doxorubicin

DX

DX

doxorubicin

proteinuria

doxorubicin

proteinuria

doxorubicin

Proteinuria

adriamycin

proteinuria

adriamycin

proteinuria

adriamycin

Proteinuria

doxorubicin

proteinuria

doxorubicin

proteinuria

doxorubicin

Proteinuria

doxorubicin

proteinuria

doxorubicin

proteinuria

doxorubicin

Proteinuria

DX

proteinuria

DX

proteinuria

DX

Proteinuria

DX

proteinuria

DX

proteinuria

DX

Proteinuria

DX

proteinuria

DX

proteinuria

DX

Proteinuria

DX

proteinuria

DX

proteinuria

DX

Proteinuria

doxorubicin

proteinuria

doxorubicin

proteinuria

doxorubicin

Proteinuria

DX

proteinuria

DX

proteinuria

DX

Proteinuria

DX

proteinuria

DX

proteinuria

DX

Proteinuria


Input: Etoposide - related myocardial infarction. The occurrence of a myocardial infarction is reported after chemotherapy containing etoposide, in a man with no risk factors for coronary heart disease. Possible causal mechanisms are discussed.

Etoposide

etoposide

myocardial infarction

myocardial infarction

coronary heart disease

Etoposide

myocardial infarction

Etoposide

myocardial infarction

etoposide

myocardial infarction

etoposide

myocardial infarction


Input: Subjective assessment of sexual dysfunction of patients on long - term administration of digoxin. Various data suggest that male patients who have received digoxin on a longterm basis have increased levels of serum estrogen and decreased levels of plasma testosterone and luteinizing hormone (LH). This study was undertaken to investigate the links between the long - term administration of digoxin therapy and sexual behavior, and the effect of digoxin on plasma levels of estradiol, testosterone, and LH. The patients of the study and control group (without digoxin) were of similar cardiac functional capacity and age (25 - 40 years) and were randomly selected from the rheumatic heart disease patients. A subjective assessment of sexual behavior in the study and control groups was carried out, using parameters such as sexual desire, sexual excitement, and frequency of sexual relations. Personal interviews and a questionnaire were also used for the evaluation of sexual behavior. The findings support the reports concerning digoxin effect on plasma estradiol, testosterone, and LH. The differences in the means were significant. Tests used to evaluate the changes in sexual behavior showed a significant decrease in sexual desire, sexual excitement phase (erection), and frequency of sexual relations in the study group.

sexual dysfunction

rheumatic heart disease

decrease in sexual desire

digoxin

digoxin

estrogen

testosterone

digoxin

digoxin

estradiol

testosterone

digoxin

digoxin

estradiol

testosterone

digoxin

sexual dysfunction

digoxin

decrease in sexual desire

digoxin

sexual dysfunction

digoxin

decrease in sexual desire

digoxin

sexual dysfunction

digoxin

decrease in sexual desire

digoxin

sexual dysfunction

digoxin

decrease in sexual desire

digoxin

sexual dysfunction

digoxin

decrease in sexual desire

digoxin

sexual dysfunction

digoxin

decrease in sexual desire


Input: Fatal aplastic anemia due to indomethacin - - lymphocyte transformation tests in vitro. Although indomethacin has been implicated as a possible cause of aplastic anemia on the basis of a few clinical observations, its role has not been definitely established. A case of fatal aplastic anemia is described in which no drugs other than allopurinol and indomethacin were given. Indomethacin was first given four weeks prior to the onset of symptoms. A positive lymphocyte transformation test with indomethacin in vitro further substantiates the potential role of this drug in causing aplastic anemia in a susceptible patient. Fortunately, this seems to be a very rare complication.

aplastic anemia

aplastic anemia

aplastic anemia

aplastic anemia

indomethacin

indomethacin

allopurinol

indomethacin

Indomethacin

indomethacin

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

Indomethacin

aplastic anemia

Indomethacin

aplastic anemia

Indomethacin

aplastic anemia

Indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia

indomethacin

aplastic anemia


Input: Plasma and urinary lipids and lipoproteins during the development of nephrotic syndrome induced in the rat by puromycin aminonucleoside. This study was undertaken to ascertain whether the alterations of plasma lipoproteins found in nephrotic syndrome induced by puromycin aminonucleoside were due to nephrotic syndrome per se, or, at least in part, to the aminonucleoside. The purpose of the present study was to investigate the changes in plasma and urinary lipoproteins during the administration of puromycin aminonucleoside (20 mg / kg for 7 days) and the subsequent development of nephrotic syndrome. Since massive albuminuria occurred after 6 days of treatment, the time - course study was divided into two stages: pre - nephrotic stage (day 1 - 5) and nephrotic stage (day 6 - 11). In pre - nephrotic stage the plasma level of fatty acids, triacylglycerol and VLDL decreased while that of phospholipid, cholesteryl esters and HDL remained constant. Plasma apolipoprotein A - I tended to increase (40% increase at day 5). At the beginning of nephrotic stage (day 6) the concentration of plasma albumin dropped to a very low level, while that of apolipoprotein A - I increased abruptly (4 - fold increase) and continued to rise, although less steeply, in the following days. The plasma concentration of HDL followed the same pattern. Plasma VLDL and LDL increased at a later stage (day 9). Plasma apolipoprotein A - I was found not only in HDL (1. 063 - 1. 210 g / ml) but also in the LDL density class (1. 025 - 1. 050 g / ml). In the pre - nephrotic stage lipoproteinuria was negligible, while in the early nephrotic stage the urinary loss of plasma lipoproteins consisted mainly of HDL. These observations indicate that puromycin aminonucleoside alters plasma lipoproteins by lowering VLDL and increasing HDL. It is likely that the early and striking increase of plasma HDL found in nephrotic rats is related to a direct effect of the drug on HDL metabolism.

nephrotic syndrome

nephrotic syndrome

nephrotic syndrome

nephrotic syndrome

albuminuria

nephrotic

nephrotic

nephrotic

nephrotic

nephrotic

nephrotic

nephrotic

puromycin aminonucleoside

puromycin aminonucleoside

aminonucleoside

puromycin aminonucleoside

fatty acids

triacylglycerol

cholesteryl esters

puromycin aminonucleoside

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

aminonucleoside

nephrotic syndrome

aminonucleoside

nephrotic syndrome

aminonucleoside

nephrotic syndrome

aminonucleoside

nephrotic syndrome

aminonucleoside

nephrotic

aminonucleoside

nephrotic

aminonucleoside

nephrotic

aminonucleoside

nephrotic

aminonucleoside

nephrotic

aminonucleoside

nephrotic

aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic

puromycin aminonucleoside

nephrotic


Input: Circulating lysosomal enzymes and acute hepatic necrosis. The activities of the lysosomal enzymes acid and neutral protease, N - acetylglucosaminidase, and acid phosphatase were measured in the serum of patients with fulminant hepatic failure. Acid protease (cathepsin D) activity was increased about tenfold in patients who died and nearly fourfold in those who survived fulminant hepatic failure after paracetamol overdose, whereas activities were increased equally in patients with fulminant hepatic failure due to viral hepatitis whether or not they survived. A correlation was found between serum acid protease activity and prothrombin time, and the increase in cathepsin D activity was sustained over several days compared with aspartate aminotransferase, which showed a sharp early peak and then a fall. Circulating lysosomal proteases can damage other organs, and measurement of their activity may therefore be of added value in assessing prognosis in this condition.

acute hepatic necrosis

fulminant hepatic failure

fulminant hepatic failure

overdose

fulminant hepatic failure

viral hepatitis

paracetamol

aspartate

paracetamol

acute hepatic necrosis

paracetamol

fulminant hepatic failure

paracetamol

fulminant hepatic failure

paracetamol

fulminant hepatic failure


Input: Transketolase abnormality in tolazamide - induced Wernicke' s encephalopathy. We studied a thiamine - dependent enzyme, transketolase, from fibroblasts of a diabetic patient who developed Wernicke' s encephalopathy when treated with tolazamide, in order to delineate if this patient also had transketolase abnormality [high Km for thiamine pyrophosphate (TPP)], as previously reported in postalcoholic Wernicke - Korsakoff syndrome. In addition to this patient, we also studied this enzyme from three diabetic kindreds without any history of Wernicke' s encephalopathy and from four normal controls. We found that the above - mentioned patient and one of the diabetic kindreds with no history of Wernicke' s encephalopathy had abnormal transketolase as determined by its Km for TPP. These data suggest a similarity between postalcoholic Wernicke - Korsakoff syndrome and the patient with tolazamide - induced Wernicke' s encephalopathy from the standpoint of transketolase abnormality.

tolazamide

thiamine

tolazamide

thiamine pyrophosphate

TPP

TPP

tolazamide

Wernicke' s encephalopathy

diabetic

Wernicke' s encephalopathy

Wernicke - Korsakoff syndrome

diabetic

Wernicke' s encephalopathy

diabetic

Wernicke' s encephalopathy

Wernicke - Korsakoff syndrome

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy

tolazamide

Wernicke' s encephalopathy


Input: Mechanisms of myocardial ischemia induced by epinephrine: comparison with exercise - induced ischemia. The role of epinephrine in eliciting myocardial ischemia was examined in patients with coronary artery disease. Objective signs of ischemia and factors increasing myocardial oxygen consumption were compared during epinephrine infusion and supine bicycle exercise. Both epinephrine and exercise produced myocardial ischemia as evidenced by ST segment depression and angina. However, the mechanisms of myocardial ischemia induced by epinephrine were significantly different from those of exercise. Exercise - induced myocardial ischemia was marked predominantly by increased heart rate and rate - pressure product with a minor contribution of end - diastolic volume, while epinephrine - induced ischemia was characterized by a marked increase in contractility and a less pronounced increase in heart rate and rate - pressure product. These findings indicate that ischemia produced by epinephrine, as may occur during states of emotional distress, has a mechanism distinct from that due to physical exertion.

myocardial ischemia

ischemia

myocardial ischemia

coronary artery disease

ischemia

myocardial ischemia

depression

angina

myocardial ischemia

myocardial ischemia

ischemia

ischemia

epinephrine

epinephrine

oxygen

epinephrine

epinephrine

epinephrine

epinephrine

epinephrine

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia

epinephrine

myocardial ischemia


Input: Transient contralateral rotation following unilateral substantia nigra lesion reflects susceptibility of the nigrostriatal system to exhaustion by amphetamine. Following unilateral 6 - OHDA induced SN lesion, a transient period of contralateral rotation has been reported to precede the predominant ipsilateral circling. In order to clarify the nature of this initial contralateral rotation we examined the effect of the duration of recovery period after the lesion, on amphetamine - induced rotational behavior. Three days post lesion, most rats circled predominantly contralaterally to the lesion. Such contralateral rotation may result from either degeneration - induced breakdown of the DA pool, or lesion - induced increase of DA turnover in the spared neurons. A substantial degree of contralateral preference was still evident when amphetamine was administered for the first time 24 days after lesioning, indicating involvement of spared cells in the contralateral rotation. However, regardless of the duration of recovery (and irrespective of either lesion volume, amphetamine dose, or post - lesion motor exercise), amphetamine - induced rotation tended to become gradually more ipsilateral as the observation session progressed, and all rats circled ipsilaterally to the lesion in response to further amphetamine injections. These findings suggest that amphetamine has an irreversible effect on the post - lesion DA pool contributing to contralateral rotation.

contralateral rotation

substantia nigra lesion

SN lesion

contralateral rotation

ipsilateral circling

contralateral rotation

rotational behavior

contralateral rotation

contralateral rotation

rotation

contralateral rotation

amphetamine

6 - OHDA

amphetamine

amphetamine

amphetamine

amphetamine

amphetamine

amphetamine

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

ipsilateral circling

amphetamine

contralateral rotation

amphetamine

rotational behavior

amphetamine

contralateral rotation

amphetamine

contralateral rotation

amphetamine

rotation

amphetamine

contralateral rotation


Input: Thyroid function and urine - concentrating ability during lithium treatment. It has been suggested that adenylate cyclase inhibition may be important in the development of both nephrogenic diabetes insipidus and hypothyroidism during lithium treatment. We measured serum thyroxine and urine - concentrating ability (Umax) in response to desmopressin (DDAVP) in 85 patients receiving lithium. Hypothyroidism developed in eight patients while they were taking lithium. Impaired Umax was found in both euthyroid and hypothyroid patients while some hypothyroid patients concentrated their urine well. It is concluded that the dominant mechanisms by which lithium exerts these two effects are different.

lithium

lithium

thyroxine

lithium

lithium

lithium

nephrogenic diabetes insipidus

hypothyroidism

Hypothyroidism

hypothyroid

hypothyroid

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroid

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroid

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroid

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroid

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroid


Input: Sensitivity of erythroid progenitor colonies to erythropoietin in azidothymidine treated immunodeficient mice. The anaemia induced by 3' - azido - 3' dideoxythymidine (AZT) is poorly understood. We have used a murine model of AIDS, infection of female C57BL / 6 mice with LP - BM5 murine leukaemia (MuLV) virus, to determine if AZT - induced anaemia is due, in part, to decreased responsiveness of erythropoietic precursors (BFU - e) to erythropoietin (EPO). Mice in the early stage of LP - BM5 MuLV disease were given AZT in their drinking water at 1. 0 and 2. 5 mg / ml. AZT produced anaemia in both groups, in a dose - dependent fashion. Despite the anaemia, the number of splenic and bone marrow BFU - e in AZT treated mice increased up to five - fold over levels observed in infected untreated animals after 15 d of treatment. Colony formation by splenic and bone marrow BFUe was stimulated at lower concentrations of EPO in mice receiving AZT for 15 d than for infected, untreated mice. By day 30, sensitivity of both splenic and bone marrow BFU - e of treated animals returned to that observed from cells of infected untreated animals. The mean plasma levels of EPO observed in AZT treated mice were appropriate for the degree of anaemia observed when compared with phenylhydrazine (PHZ) treated mice. The numbers of BFU - e and the percentage of bone marrow erythroblasts observed were comparable in AZT and PHZ treated mice with similar degrees of anaemia. However, reticulocytosis was inappropriate for the degree of anaemia observed in AZT treated infected mice. AZT - induced peripheral anaemia in the face of increased numbers of BFU - e and increased levels of plasma EPO suggest a lesion in terminal differentiation.

azidothymidine

3' - azido - 3' dideoxythymidine

AZT

AZT

AZT

AZT

AZT

AZT

AZT

phenylhydrazine

PHZ

AZT

PHZ

AZT

AZT

immunodeficient

anaemia

AIDS

infection

leukaemia

anaemia

anaemia

anaemia

anaemia

anaemia

reticulocytosis

anaemia

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

azidothymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

3' - azido - 3' dideoxythymidine

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia

AZT

anaemia


Input: Detection of abnormal cardiac adrenergic neuron activity in adriamycin - induced cardiomyopathy with iodine - 125 - metaiodobenzylguanidine. Radiolabeled metaiodobenzylguanidine (MIBG), an analog of norepinephrine (NE), serves as an index of adrenergic neuron integrity and function. Using a rat model of adriamycin - induced cardiomyopathy, we tested the hypothesis that abnormal cardiac adrenergic neuron activity may appear and be exacerbated dose - dependently in adriamycin cardiomyopathy. The degree of vacuolar degeneration of myocardial cells was analyzed in relation to the duration of adriamycin treatment (2 mg / kg, once a week). There were no abnormalities or only isolated degeneration in the 1 - or 2 - wk treatment groups, isolated or scattered degeneration in half of the 3 - wk group, frequent scattered degeneration in the 4 - wk group, scattered or focal degeneration in the 5 - wk group, and extensive degeneration in the 8 - wk group. Myocardial accumulation of [125I] MIBG 4 hr after intravenous injection did not differ between the controls and the groups treated 3 wk or less. However, the 4 - wk group had a slightly lower accumulation in the right ventricular wall (82% of the control) and significantly lower accumulation in the left ventricular wall (about 66% of the control: p less than 0. 05). In the 5 - wk group, MIBG accumulation in the right and left ventricular wall was 35% and 27% of that in controls, respectively (p less than 0. 001). In the 8 - wk group, MIBG accumulation in the right and left ventricular wall was 18% and 14% of that in controls, respectively (p less than 0. 001). Thus, MIBG accumulation in the myocardium decreased in an adriamycin dose - dependent manner. The appearance of impaired cardiac adrenergic neuron activity in the presence of slight myocardial impairment (scattered or focal vacuolar degeneration) indicates that MIBG scintigraphy may be a useful method for detection of adriamycin - induced cardiomyopathy.

adriamycin

iodine - 125 - metaiodobenzylguanidine

Radiolabeled metaiodobenzylguanidine

MIBG

norepinephrine

NE

adriamycin

adriamycin

adriamycin

MIBG

MIBG

MIBG

MIBG

adriamycin

MIBG

adriamycin

cardiomyopathy

cardiomyopathy

cardiomyopathy

vacuolar degeneration of myocardial cells

myocardial impairment

vacuolar degeneration

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

myocardial impairment

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

myocardial impairment

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

myocardial impairment

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

myocardial impairment

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

myocardial impairment

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

cardiomyopathy

adriamycin

myocardial impairment

adriamycin

cardiomyopathy


Input: Amnestic syndrome associated with propranolol toxicity: a case report. An elderly woman developed an Alzheimer - like subacute dementia as a result of propranolol toxicity. Analysis of the manifestations showed that severe impairment of memory accounted for virtually all of the abnormalities. There is evidence that cerebral reactions to drug toxicity can exhibit patterns that suggest highly selective involvement of functional subdivisions of the brain.

Amnestic syndrome

toxicity

Alzheimer

dementia

toxicity

toxicity

propranolol

propranolol

propranolol

Amnestic syndrome

propranolol

Amnestic syndrome


Input: Biphasic response of the SA node of the dog heart in vivo to selective administration of ketamine. Effect of ketamine on the SA node of the dog heart was studied in vivo using a selective perfusion technique of the SA node artery. Injections of ketamine in doses from 100 microgram to 3 mg into the artery produced a depression of the SA nodal activity by a direct action. This depression was followed by the sudden appearance of a stimulatory phase. Bilateral vagotomy and sympathectomy or prior administration of a ganglion blocker failed to inhibit the occurrence of the ketamine - induced tachycardia, while it was completely abolished in the reserpinized dogs or by a prior injection of a beta - blocking agent into the SA node artery. This may indicate that an activation of the peripheral adrenergic mechanism plays an important role in the induction of the excitatory effect of ketamine injected in the SA node artery.

ketamine

ketamine

ketamine

ketamine

ketamine

depression

depression

tachycardia

ketamine

tachycardia

ketamine

tachycardia

ketamine

tachycardia

ketamine

tachycardia

ketamine

tachycardia


Input: The use of serum cholinesterase in succinylcholine apnoea. Fifteen patients demonstrating unexpected prolonged apnoea lasting several hours after succinylcholine have been treated by a new preparation of human serum cholinesterase. Adequate spontaneous respiration was re - established in an average period of ten minutes after the injection. In 12 patients biochemical genetic examinations confirmed the presence of an atypical serum cholinesterase. In three patients none of the usual variants were found. It is therefore supposed that other unknown variants of serum cholinesterase exist which cannot hydrolyze succinylcholine. The use of serum cholinesterase in succinylcholine apnoea provided considerable relief to both patient and anaesthetist.

succinylcholine

succinylcholine

succinylcholine

succinylcholine

apnoea

apnoea

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea

succinylcholine

apnoea


Input: Orthostatic hypotension occurs following alpha 2 - adrenoceptor blockade in chronic prazosin - pretreated conscious spontaneously hypertensive rats. 1. Studies were performed to evaluate whether chronic prazosin treatment alters the alpha 2 - adrenoceptor function for orthostatic control of arterial blood pressure in conscious spontaneously hypertensive rats (SHR). 2. Conscious SHR (male 300 - 350 g) were subjected to 90 degrees head - up tilts for 60 s following acute administration of prazosin (0. 1 mg kg - 1 i. p.) or rauwolscine (3 mg kg - 1 i. v.). Orthostatic hypotension was determined by the average decrease (%) in mean arterial pressure (MAP femoral) over the 60 - s tilt period. The basal MAP of conscious SHR was reduced to a similar extent by prazosin (- 23% (-) - 26% MAP) and rauwolscine (- 16% (-) - 33% MAP). However, the head - up tilt induced orthostatic hypotension in the SHR treated with prazosin (- 16% MAP, n = 6), but not in the SHR treated with rauwolscine (less than + 2% MAP, n = 6). 3. Conscious SHR were treated for 4 days with prazosin at 2 mg kg - 1 day - 1 i. p. for chronic alpha 1 - adrenoceptor blockade. MAP in conscious SHR after chronic prazosin treatment was 14% lower than in the untreated SHR (n = 8). Head - up tilts in these rats did not produce orthostatic hypotension when performed either prior to or after acute dosing of prazosin (0. 1 mg kg - 1 i. p.). Conversely, administration of rauwolscine (3 mg kg - 1 i. v.) in chronic prazosin treated SHR decreased the basal MAP by 12 - 31% (n = 4), and subsequent tilts induced further drops of MAP by 19 - 23% in these rats. 4. The pressor responses and bradycardia to the alpha 1 - agonist cirazoline (0. 6 and 2 micrograms kg - 1 i. v.), the alpha 2 - agonist Abbott - 53693 (1 and 3 micrograms kg - 1 i. v.), and noradrenaline (0. 1 and 1. 0 micrograms kg - 1 i. v.) were determined in conscious SHR with and without chronic prazosin pretreatment. Both the pressor and bradycardia effects of cirazoline were abolished in chronic prazosin treated SHR (n = 4) as compared to the untreated SHR (n = 4). On the other hand, the pressor effects of Abbott - 53693 were similar in both groups of SHR, but the accompanying bradycardia was greater in SHR with chronic prazosin treatment than without such treatment. Furthermore, the bradycardia that accompanied the noradrenaline - induced pressor effect in SHR was similar with and without chronic prazosin treatment despite a 47 - 71% reduction of the pressor effect in chronic alpha 1 - receptor blocked SHR. (ABSTRACT TRUNCATED AT 400 WORDS)

Orthostatic hypotension

hypertensive

hypertensive

Orthostatic hypotension

orthostatic hypotension

orthostatic hypotension

bradycardia

bradycardia

bradycardia

bradycardia

prazosin

prazosin

prazosin

rauwolscine

prazosin

rauwolscine

prazosin

rauwolscine

prazosin

prazosin

prazosin

rauwolscine

prazosin

cirazoline

Abbott - 53693

noradrenaline

prazosin

cirazoline

prazosin

Abbott - 53693

prazosin

noradrenaline

prazosin

noradrenaline

bradycardia

noradrenaline

bradycardia

noradrenaline

bradycardia

noradrenaline

bradycardia

noradrenaline

bradycardia

noradrenaline

bradycardia

noradrenaline

bradycardia

noradrenaline

bradycardia

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

Orthostatic hypotension

prazosin

orthostatic hypotension

prazosin

orthostatic hypotension

cirazoline

bradycardia

cirazoline

bradycardia

cirazoline

bradycardia

cirazoline

bradycardia

cirazoline

bradycardia

cirazoline

bradycardia

cirazoline

bradycardia

cirazoline

bradycardia

Abbott - 53693

hypertensive

Abbott - 53693

hypertensive

Abbott - 53693

hypertensive

Abbott - 53693

hypertensive

noradrenaline

hypertensive

noradrenaline

hypertensive

noradrenaline

hypertensive

noradrenaline

hypertensive

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

Abbott - 53693

bradycardia

cirazoline

hypertensive

cirazoline

hypertensive

cirazoline

hypertensive

cirazoline

hypertensive


Input: Coexistence of cerebral venous sinus and internal carotid artery thrombosis associated with exogenous sex hormones. A case report. A forty - six year - old premenopausal woman developed headache, nausea and vomiting, left hemiparesis and seizure two days after parenteral use of progesterone and estradiol. Diabetes mellitus (DM) was found during admission. Computed tomography showed a hemorrhagic infarct in the right frontal lobe and increased density in the superior sagittal sinus (SSS). Left carotid angiography found occlusion of the left internal carotid artery (ICA). Right carotid angiograms failed to show the SSS and inferior sagittal sinus, suggestive of venous sinus thrombosis. Coexistence of the cerebral artery and the venous sinus occlusion has been described infrequently. In this case, the authors postulate that the use of estradiol and progesterone and the underlying DM increased vascular thrombogenicity, which provided a common denominator for thrombosis of both the ICA and the venous sinus.

cerebral venous sinus and internal carotid artery thrombosis

cerebral venous sinus and internal carotid artery thrombosis

internal carotid artery thrombosis

headache

nausea

vomiting

hemiparesis

seizure

Diabetes mellitus

DM

hemorrhagic infarct

hemorrhagic

infarct

occlusion of the left internal carotid artery

venous sinus thrombosis

cerebral artery and the venous sinus occlusion

cerebral artery and the venous sinus occlusion

the venous sinus occlusion

DM

thrombosis of both the ICA and the venous sinus

thrombosis of both the ICA

thrombosis of both the ICA and the venous sinus

progesterone

estradiol

estradiol

progesterone

estradiol

cerebral venous sinus and internal carotid artery thrombosis

estradiol

internal carotid artery thrombosis

estradiol

thrombosis of both the ICA and the venous sinus

estradiol

thrombosis of both the ICA

estradiol

cerebral venous sinus and internal carotid artery thrombosis

estradiol

internal carotid artery thrombosis

estradiol

thrombosis of both the ICA and the venous sinus

estradiol

thrombosis of both the ICA

estradiol

hemorrhagic infarct

estradiol

infarct

estradiol

cerebral artery and the venous sinus occlusion

estradiol

cerebral artery and the venous sinus occlusion

estradiol

hemorrhagic infarct

estradiol

infarct

estradiol

cerebral artery and the venous sinus occlusion

estradiol

cerebral artery and the venous sinus occlusion

progesterone

hemorrhagic infarct

progesterone

hemorrhagic

progesterone

hemorrhagic infarct

progesterone

hemorrhagic

progesterone

cerebral venous sinus and internal carotid artery thrombosis

progesterone

cerebral venous sinus and internal carotid artery thrombosis

progesterone

venous sinus thrombosis

progesterone

thrombosis of both the ICA and the venous sinus

progesterone

thrombosis of both the ICA and the venous sinus

progesterone

cerebral venous sinus and internal carotid artery thrombosis

progesterone

cerebral venous sinus and internal carotid artery thrombosis

progesterone

venous sinus thrombosis

progesterone

thrombosis of both the ICA and the venous sinus

progesterone

thrombosis of both the ICA and the venous sinus

estradiol

cerebral venous sinus and internal carotid artery thrombosis

estradiol

venous sinus thrombosis

estradiol

thrombosis of both the ICA and the venous sinus

estradiol

cerebral venous sinus and internal carotid artery thrombosis

estradiol

venous sinus thrombosis

estradiol

thrombosis of both the ICA and the venous sinus

progesterone

infarct

progesterone

cerebral artery and the venous sinus occlusion

progesterone

cerebral artery and the venous sinus occlusion

progesterone

infarct

progesterone

cerebral artery and the venous sinus occlusion

progesterone

cerebral artery and the venous sinus occlusion

estradiol

hemorrhagic

estradiol

hemorrhagic

progesterone

internal carotid artery thrombosis

progesterone

thrombosis of both the ICA

progesterone

internal carotid artery thrombosis

progesterone

thrombosis of both the ICA


Input: Chloroquine related complete heart block with blindness: case report. A 27 - year old African woman with history of regular chloroquine ingestion presented with progressive deterioration of vision, easy fatiguability, dyspnoea, dizziness progressing to syncopal attacks. Ophthalmological assessment revealed features of chloroquine retinopathy, cardiac assessment revealed features of heart failure and a complete heart block with right bundle branch block pattern. The heart block was treated by pacemaker insertion and the heart failure resolved spontaneously following chloroquine discontinuation. She however remains blind.

Chloroquine

chloroquine

chloroquine

chloroquine

heart block

blindness

deterioration of vision

fatiguability

dyspnoea

dizziness

syncopal attacks

retinopathy

heart failure

heart block

right bundle branch block

heart block

heart failure

blind

Chloroquine

fatiguability

chloroquine

fatiguability

chloroquine

fatiguability

chloroquine

fatiguability

Chloroquine

heart failure

Chloroquine

heart failure

chloroquine

heart failure

chloroquine

heart failure

chloroquine

heart failure

chloroquine

heart failure

chloroquine

heart failure

chloroquine

heart failure

Chloroquine

dyspnoea

chloroquine

dyspnoea

chloroquine

dyspnoea

chloroquine

dyspnoea

Chloroquine

syncopal attacks

chloroquine

syncopal attacks

chloroquine

syncopal attacks

chloroquine

syncopal attacks

Chloroquine

right bundle branch block

chloroquine

right bundle branch block

chloroquine

right bundle branch block

chloroquine

right bundle branch block

Chloroquine

blindness

Chloroquine

blind

chloroquine

blindness

chloroquine

blind

chloroquine

blindness

chloroquine

blind

chloroquine

blindness

chloroquine

blind

Chloroquine

retinopathy

chloroquine

retinopathy

chloroquine

retinopathy

chloroquine

retinopathy

Chloroquine

dizziness

chloroquine

dizziness

chloroquine

dizziness

chloroquine

dizziness


Input: Systemic toxicity and resuscitation in bupivacaine -, levobupivacaine -, or ropivacaine - infused rats. We compared the systemic toxicity of bupivacaine, levobupivacaine, and ropivacaine in anesthetized rats. We also compared the ability to resuscitate rats after lethal doses of these local anesthetics. Bupivacaine, levobupivacaine, or ropivacaine was infused at a rate of 2 mg. kg (- 1). min (- 1) while electrocardiogram, electroencephalogram, and arterial pressure were continuously monitored. When asystole was recorded, drug infusion was stopped and a resuscitation sequence was begun. Epinephrine 0. 01 mg / kg was administered at 1 - min intervals while external cardiac compressions were applied. Resuscitation was considered successful when a systolic arterial pressure > or = 100 mm Hg was achieved within 5 min. The cumulative doses of levobupivacaine and ropivacaine that produced seizures were similar and were larger than those of bupivacaine. The cumulative doses of levobupivacaine that produced dysrhythmias and asystole were smaller than the corresponding doses of ropivacaine, but they were larger than those of bupivacaine. The number of successful resuscitations did not differ among groups. However, a smaller dose of epinephrine was required in the Ropivacaine group than in the other groups. We conclude that the systemic toxicity of levobupivacaine is intermediate between that of ropivacaine and bupivacaine when administered at the same rate and that ropivacaine - induced cardiac arrest appears to be more susceptible to treatment than that induced by bupivacaine or levobupivacaine.

toxicity

toxicity

asystole

seizures

dysrhythmias

asystole

toxicity

cardiac arrest

bupivacaine

levobupivacaine

ropivacaine

bupivacaine

levobupivacaine

ropivacaine

Bupivacaine

levobupivacaine

ropivacaine

Epinephrine

levobupivacaine

ropivacaine

bupivacaine

levobupivacaine

ropivacaine

bupivacaine

epinephrine

Ropivacaine

levobupivacaine

ropivacaine

bupivacaine

ropivacaine

bupivacaine

levobupivacaine

levobupivacaine

dysrhythmias

levobupivacaine

dysrhythmias

levobupivacaine

dysrhythmias

levobupivacaine

dysrhythmias

levobupivacaine

dysrhythmias

levobupivacaine

dysrhythmias

levobupivacaine

dysrhythmias

ropivacaine

seizures

ropivacaine

seizures

ropivacaine

seizures

ropivacaine

seizures

ropivacaine

seizures

Ropivacaine

seizures

ropivacaine

seizures

ropivacaine

seizures

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

Ropivacaine

asystole

Ropivacaine

asystole

Ropivacaine

cardiac arrest

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

ropivacaine

asystole

ropivacaine

asystole

ropivacaine

cardiac arrest

levobupivacaine

seizures

levobupivacaine

seizures

levobupivacaine

seizures

levobupivacaine

seizures

levobupivacaine

seizures

levobupivacaine

seizures

levobupivacaine

seizures

ropivacaine

dysrhythmias

ropivacaine

dysrhythmias

ropivacaine

dysrhythmias

ropivacaine

dysrhythmias

ropivacaine

dysrhythmias

Ropivacaine

dysrhythmias

ropivacaine

dysrhythmias

ropivacaine

dysrhythmias

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest

levobupivacaine

asystole

levobupivacaine

asystole

levobupivacaine

cardiac arrest


Input: 22 - oxacalcitriol suppresses secondary hyperparathyroidism without inducing low bone turnover in dogs with renal failure. BACKGROUND: Calcitriol therapy suppresses serum levels of parathyroid hormone (PTH) in patients with renal failure but has several drawbacks, including hypercalcemia and / or marked suppression of bone turnover, which may lead to adynamic bone disease. A new vitamin D analogue, 22 - oxacalcitriol (OCT), has been shown to have promising characteristics. This study was undertaken to determine the effects of OCT on serum PTH levels and bone turnover in states of normal or impaired renal function. METHODS: Sixty dogs were either nephrectomized (Nx, N = 38) or sham - operated (Sham, N = 22). The animals received supplemental phosphate to enhance PTH secretion. Fourteen weeks after the start of phosphate supplementation, half of the Nx and Sham dogs received doses of OCT (three times per week); the other half were given vehicle for 60 weeks. Thereafter, the treatment modalities for a subset of animals were crossed over for an additional eight months. Biochemical and hormonal indices of calcium and bone metabolism were measured throughout the study, and bone biopsies were done at baseline, 60 weeks after OCT or vehicle treatment, and at the end of the crossover period. RESULTS: In Nx dogs, OCT significantly decreased serum PTH levels soon after the induction of renal insufficiency. In long - standing secondary hyperparathyroidism, OCT (0. 03 microg / kg) stabilized serum PTH levels during the first months. Serum PTH levels rose thereafter, but the rise was less pronounced compared with baseline than the rise seen in Nx control. These effects were accompanied by episodes of hypercalcemia and hyperphosphatemia. In animals with normal renal function, OCT induced a transient decrease in serum PTH levels at a dose of 0. 1 microg / kg, which was not sustained with lowering of the doses. In Nx dogs, OCT reversed abnormal bone formation, such as woven osteoid and fibrosis, but did not significantly alter the level of bone turnover. In addition, OCT improved mineralization lag time, (that is, the rate at which osteoid mineralizes) in both Nx and Sham dogs. CONCLUSIONS: These results indicate that even though OCT does not completely prevent the occurrence of hypercalcemia in experimental dogs with renal insufficiency, it may be of use in the management of secondary hyperparathyroidism because it does not induce low bone turnover and, therefore, does not increase the risk of adynamic bone disease.

22 - oxacalcitriol

Calcitriol

vitamin D

22 - oxacalcitriol

OCT

OCT

phosphate

phosphate

OCT

calcium

OCT

OCT

OCT

OCT

OCT

OCT

OCT

secondary hyperparathyroidism

low bone turnover

renal failure

renal failure

hypercalcemia

suppression of bone turnover

adynamic bone disease

impaired renal function

renal insufficiency

secondary hyperparathyroidism

hypercalcemia

hyperphosphatemia

woven osteoid

fibrosis

hypercalcemia

renal insufficiency

secondary hyperparathyroidism

low bone turnover

adynamic bone disease

22 - oxacalcitriol

hypercalcemia

22 - oxacalcitriol

hypercalcemia

22 - oxacalcitriol

hypercalcemia

22 - oxacalcitriol

hypercalcemia

22 - oxacalcitriol

hypercalcemia

22 - oxacalcitriol

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

OCT

hypercalcemia

22 - oxacalcitriol

hyperphosphatemia

22 - oxacalcitriol

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

OCT

hyperphosphatemia

Calcitriol

low bone turnover

Calcitriol

suppression of bone turnover

Calcitriol

adynamic bone disease

Calcitriol

low bone turnover

Calcitriol

adynamic bone disease

Calcitriol

hypercalcemia

Calcitriol

hypercalcemia

Calcitriol

hypercalcemia


Input: Chemotherapy of advanced inoperable non - small cell lung cancer with paclitaxel: a phase II trial. Paclitaxel (Taxol; Bristol - Myers Squibb Company, Princeton, NJ) has demonstrated significant antineoplastic activity against different tumor types, notably ovarian and breast carcinoma. Two phase II trials of 24 - hour paclitaxel infusions in chemotherapy - naive patients with stage IIIB or IV non - small cell lung cancer (NSCLC) reported response rates of 21% and 24%. Leukopenia was dose limiting: as many as 62. 5% of patients experienced grade 4 leukopenia. We investigated the efficacy and toxicity of a 3 - hour paclitaxel infusion in a phase II trial in patients with inoperable stage IIIB or IV NSCLC. The 58 patients treated (41 men and 17 women) had a median age of 59 years (age range, 25 to 75) and a performance status of 0 through 2. Most patients (72. 4%) had stage IV NSCLC. Paclitaxel 225 mg / m2 was infused over 3 hours every 3 weeks with standard prophylactic premedication. Of 50 patients evaluable for response, 12 (24%) had partial remission, 26 (52%) had no change, and 12 had disease progression (24%). Hematologic toxicities were mild: only one patient (2%) developed grade 3 or 4 neutropenia, while 29% had grade 1 or 2. Grade 1 or 2 polyneuropathy affected 56% of patients while only one (2%) experienced severe polyneuropathy. Similarly, grade 1 or 2 myalgia / arthralgia was observed in 63. 2% of patients, but only 14. 3% experienced grade 3 or 4. Nausea and vomiting were infrequent, with 14% of patients experiencing grade 1 or 2 and only 2% experiencing grade 3 or 4. Paclitaxel is thus an active single agent in this patient population, with a 3 - hour infusion proving comparably effective to a 24 - hour infusion and superior in terms of the incidence of hematologic and nonhematologic toxicity. Further phase II studies with paclitaxel combined with other drugs active against NSCLC are indicated, and phase III studies comparing paclitaxel with standard chemotherapy remain to be completed.

non - small cell lung cancer

tumor

ovarian and breast carcinoma

ovarian and breast carcinoma

breast carcinoma

non - small cell lung cancer

NSCLC

Leukopenia

leukopenia

toxicity

NSCLC

NSCLC

toxicities

neutropenia

polyneuropathy

polyneuropathy

myalgia

arthralgia

Nausea

vomiting

toxicity

NSCLC

paclitaxel

Paclitaxel

Taxol

paclitaxel

paclitaxel

Paclitaxel

Paclitaxel

paclitaxel

paclitaxel

paclitaxel

Nausea

Paclitaxel

Nausea

Taxol

Nausea

paclitaxel

Nausea

paclitaxel

Nausea

Paclitaxel

Nausea

Paclitaxel

Nausea

paclitaxel

Nausea

paclitaxel

Nausea

paclitaxel

vomiting

Paclitaxel

vomiting

Taxol

vomiting

paclitaxel

vomiting

paclitaxel

vomiting

Paclitaxel

vomiting

Paclitaxel

vomiting

paclitaxel

vomiting

paclitaxel

vomiting

paclitaxel

arthralgia

Paclitaxel

arthralgia

Taxol

arthralgia

paclitaxel

arthralgia

paclitaxel

arthralgia

Paclitaxel

arthralgia

Paclitaxel

arthralgia

paclitaxel

arthralgia

paclitaxel

arthralgia

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

Paclitaxel

polyneuropathy

Paclitaxel

polyneuropathy

Taxol

polyneuropathy

Taxol

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

Paclitaxel

polyneuropathy

Paclitaxel

polyneuropathy

Paclitaxel

polyneuropathy

Paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

polyneuropathy

paclitaxel

neutropenia

Paclitaxel

neutropenia

Taxol

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

Paclitaxel

neutropenia

Paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

myalgia

Paclitaxel

myalgia

Taxol

myalgia

paclitaxel

myalgia

paclitaxel

myalgia

Paclitaxel

myalgia

Paclitaxel

myalgia

paclitaxel

myalgia

paclitaxel

myalgia


Input: Cerebral hemorrhage associated with phenylpropanolamine in combination with caffeine. Phenylpropanolamine (PPA) is a drug that has been associated with serious side effects including stroke. It is often combined with caffeine in diet preparations and " look - alike " pills. In order to determine if PPA / caffeine can lead to stroke in normotensive and / or hypertensive rats, we administered the combination in six times the allowed human dose calculated on a per weight basis for the rats two times per day for five days. Subarachnoid and cerebral hemorrhage was noted in 18% of the hypertensive rats. A single PPA / caffeine administration (same dose) lead to acute hypertension in both the normotensive and hypertensive animals. These results suggest that PPA / caffeine can lead to cerebral hemorrhage in previously hypertensive animals when administered in greater than the allowed dosage. An acute elevation in blood pressure may be a contributing factor.

Cerebral hemorrhage

stroke

stroke

hypertensive

Subarachnoid and cerebral hemorrhage

Subarachnoid and cerebral hemorrhage

cerebral hemorrhage

hypertensive

hypertension

hypertensive

cerebral hemorrhage

hypertensive

phenylpropanolamine

caffeine

Phenylpropanolamine

PPA

caffeine

PPA

caffeine

PPA

caffeine

PPA

caffeine

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

caffeine

Subarachnoid and cerebral hemorrhage

phenylpropanolamine

Subarachnoid and cerebral hemorrhage

phenylpropanolamine

Subarachnoid and cerebral hemorrhage

Phenylpropanolamine

Subarachnoid and cerebral hemorrhage

Phenylpropanolamine

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

PPA

Subarachnoid and cerebral hemorrhage

caffeine

Cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

Cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

Cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

Cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

Cerebral hemorrhage

caffeine

cerebral hemorrhage

caffeine

cerebral hemorrhage

phenylpropanolamine

hypertensive

phenylpropanolamine

hypertensive

phenylpropanolamine

hypertension

phenylpropanolamine

hypertensive

phenylpropanolamine

hypertensive

Phenylpropanolamine

hypertensive

Phenylpropanolamine

hypertensive

Phenylpropanolamine

hypertension

Phenylpropanolamine

hypertensive

Phenylpropanolamine

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertension

PPA

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertension

PPA

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertension

PPA

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertensive

PPA

hypertension

PPA

hypertensive

PPA

hypertensive

phenylpropanolamine

Cerebral hemorrhage

phenylpropanolamine

cerebral hemorrhage

phenylpropanolamine

cerebral hemorrhage

Phenylpropanolamine

Cerebral hemorrhage

Phenylpropanolamine

cerebral hemorrhage

Phenylpropanolamine

cerebral hemorrhage

PPA

Cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

Cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

Cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

Cerebral hemorrhage

PPA

cerebral hemorrhage

PPA

cerebral hemorrhage

phenylpropanolamine

stroke

phenylpropanolamine

stroke

Phenylpropanolamine

stroke

Phenylpropanolamine

stroke

PPA

stroke

PPA

stroke

PPA

stroke

PPA

stroke

PPA

stroke

PPA

stroke

PPA

stroke

PPA

stroke


Input: Long - term efficacy and toxicity of high - dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation. Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg / day for 6 weeks and the maintenance dose was 600 mg / day. Sixty - nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow - up of 6 to 52 months (mean + / - standard deviation 14. 2 + / - 8. 2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large - dose amiodarone is highly effective in the long - term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.

toxicity

ventricular tachycardia

ventricular fibrillation

ventricular tachycardia

VT

cardiac arrest

VT

ventricular fibrillation

VF

VT

tremor

ataxia

nausea

anorexia

visual halos or blurring

thyroid function abnormalities

pulmonary interstitial infiltrates

VT

VF

toxicity

VT

VF

amiodarone

Amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

amiodarone

ataxia

Amiodarone

ataxia

amiodarone

ataxia

amiodarone

ataxia

amiodarone

ataxia

amiodarone

ataxia

amiodarone

ataxia

amiodarone

ataxia

amiodarone

anorexia

Amiodarone

anorexia

amiodarone

anorexia

amiodarone

anorexia

amiodarone

anorexia

amiodarone

anorexia

amiodarone

anorexia

amiodarone

anorexia

amiodarone

nausea

Amiodarone

nausea

amiodarone

nausea

amiodarone

nausea

amiodarone

nausea

amiodarone

nausea

amiodarone

nausea

amiodarone

nausea

amiodarone

thyroid function abnormalities

Amiodarone

thyroid function abnormalities

amiodarone

thyroid function abnormalities

amiodarone

thyroid function abnormalities

amiodarone

thyroid function abnormalities

amiodarone

thyroid function abnormalities

amiodarone

thyroid function abnormalities

amiodarone

thyroid function abnormalities

amiodarone

visual halos or blurring

Amiodarone

visual halos or blurring

amiodarone

visual halos or blurring

amiodarone

visual halos or blurring

amiodarone

visual halos or blurring

amiodarone

visual halos or blurring

amiodarone

visual halos or blurring

amiodarone

visual halos or blurring


Input: Effect of calcium chloride and 4 - aminopyridine therapy on desipramine toxicity in rats. BACKGROUND: Hypotension is a major contributor to mortality in tricyclic antidepressant overdose. Recent data suggest that tricyclic antidepressants inhibit calcium influx in some tissues. This study addressed the potential role of calcium channel blockade in tricyclic antidepressant - induced hypotension. METHODS: Two interventions were studied that have been shown previously to improve blood pressure with calcium channel blocker overdose. CaCl2 and 4 - aminopyridine. Anesthetized rats received the tricyclic antidepressant desipramine IP to produce hypotension, QRS prolongation, and bradycardia. Fifteen min later, animals received CaCl2, NaHCO3, or saline. In a second experiment, rats received tricyclic antidepressant desipramine IP followed in 15 min by 4 - aminopyridine or saline. RESULTS: NaHCO3 briefly (5 min) reversed hypotension and QRS prolongation. CaCl2 and 4 - aminopyridine failed to improve blood pressure. The incidence of ventricular arrhythmias (p = 0. 004) and seizures (p = 0. 03) in the CaCl2 group was higher than the other groups. CONCLUSION: The administration of CaCl2 or 4 - aminopyridine did not reverse tricyclic antidepressant - induced hypotension in rats. CaCl2 therapy may possibly worsen both cardiovascular and central nervous system toxicity. These findings do not support a role for calcium channel inhibition in the pathogenesis of tricyclic antidepressant - induced hypotension.

calcium chloride

4 - aminopyridine

desipramine

calcium

calcium

calcium

4 - aminopyridine

desipramine

desipramine

4 - aminopyridine

4 - aminopyridine

4 - aminopyridine

calcium

toxicity

Hypotension

overdose

hypotension

overdose

hypotension

bradycardia

hypotension

ventricular arrhythmias

seizures

hypotension

cardiovascular and central nervous system toxicity

cardiovascular and central nervous system toxicity

central nervous system toxicity

hypotension

desipramine

Hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

Hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

Hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

hypotension

desipramine

ventricular arrhythmias

desipramine

ventricular arrhythmias

desipramine

ventricular arrhythmias

desipramine

bradycardia

desipramine

bradycardia

desipramine

bradycardia

calcium chloride

ventricular arrhythmias

ventricular arrhythmias

ventricular arrhythmias

ventricular arrhythmias

ventricular arrhythmias

ventricular arrhythmias

ventricular arrhythmias


Input: Phase I trial of 13 - cis - retinoic acid in children with neuroblastoma following bone marrow transplantation. PURPOSE: Treatment of neuroblastoma cell lines with 13 - cis - retinoic acid (cis - RA) can cause sustained inhibition of proliferation. Since cis - RA has demonstrated clinical responses in neuroblastoma patients, it may be effective in preventing relapse after cytotoxic therapy. This phase I trial was designed to determine the maximal - tolerated dosage (MTD), toxicities, and pharmacokinetics of cis - RA administered on an intermittent schedule in children with neuroblastoma following bone marrow transplantation (BMT). PATIENTS AND METHODS: Fifty - one assessable patients, 2 to 12 years of age, were treated with oral cis - RA administered in two equally divided doses daily for 2 weeks, followed by a 2 - week rest period, for up to 12 courses. The dose was escalated from 100 to 200 mg / m2 / d until dose - limiting toxicity (DLT) was observed. A single intrapatient dose escalation was permitted. RESULTS: The MTD of cis - RA was 160 mg / m2 / d. Dose - limiting toxicities in six of nine patients at 200 mg / m2 / d included hypercalcemia (n = 3), rash (n = 2), and anemia / thrombocytopenia / emesis / rash (n = 1). All toxicities resolved after cis - RA was discontinued. Three complete responses were observed in marrow metastases. Serum levels of 7. 4 + / - 3. 0 mumol / L (peak) and 4. 0 + / - 2. 8 mumol / L (trough) at the MTD were maintained during 14 days of therapy. The DLT correlated with serum levels > or = 10 mumol / L. CONCLUSION: The MTD of cis - RA given on this intermittent schedule was 160 mg / m2 / d. Serum levels known to be effective against neuroblastoma in vitro were achieved at this dose. The DLT included hypercalcemia, and may be predicted by serum cis - RA levels. Monitoring of serum calcium and cis - RA levels is indicated in future trials.

13 - cis - retinoic acid

13 - cis - retinoic acid

cis - RA

cis - RA

cis - RA

cis - RA

cis - RA

cis - RA

cis - RA

cis - RA

calcium

cis - RA

neuroblastoma

neuroblastoma

neuroblastoma

toxicities

neuroblastoma

toxicity

toxicities

hypercalcemia

rash

anemia

thrombocytopenia

emesis

rash

toxicities

metastases

neuroblastoma

hypercalcemia

13 - cis - retinoic acid

thrombocytopenia

13 - cis - retinoic acid

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

cis - RA

thrombocytopenia

13 - cis - retinoic acid

rash

13 - cis - retinoic acid

rash

13 - cis - retinoic acid

rash

13 - cis - retinoic acid

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

cis - RA

rash

13 - cis - retinoic acid

anemia

13 - cis - retinoic acid

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

cis - RA

anemia

13 - cis - retinoic acid

hypercalcemia

13 - cis - retinoic acid

hypercalcemia

13 - cis - retinoic acid

hypercalcemia

13 - cis - retinoic acid

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

cis - RA

hypercalcemia

13 - cis - retinoic acid

emesis

13 - cis - retinoic acid

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis

cis - RA

emesis


Input: Effect of calcium chloride on gross behavioural changes produced by carbachol and eserine in cats. The effect of calcium chloride injected into the cerebral ventricles of group - housed unanaesthetized cats upon vocalization (rage, hissing and snarling), fighting (attack with paws and claws, defense with paws and claws and biting), mydriasis, tremor and clonic - tonic convulsions produced by carbachol and eserine injected similarly was investigated. Calcium chloride depressed or almost completely abolished the vocalization and fighting due to carbachol and eserine. On the other hand, mydriasis, tremor and clonic - tonic convulsions evoked by carbachol and eserine were not significantly changed by calcium chloride. It is apparent that calcium chloride can " dissociate " vocalization and fighting from autonomic and motor phenomena such as mydriasis, tremor and clonic - tonic convulsions caused by carbachol and eserine. Calcium chloride inhibited the vocalization and fighting produced by carbachol and eserine most probably by a nonspecific stabilizing action on central muscarinic cholinoceptive sites. These results further support the view that calcium ions in excess have an atropine - like action also in the central nervous system.

calcium chloride

carbachol

eserine

calcium chloride

carbachol

eserine

Calcium chloride

carbachol

eserine

carbachol

eserine

calcium chloride

calcium chloride

carbachol

eserine

Calcium chloride

carbachol

eserine

calcium

atropine

mydriasis

tremor

clonic - tonic convulsions

mydriasis

tremor

clonic - tonic convulsions

mydriasis

tremor

clonic - tonic convulsions

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

carbachol

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

mydriasis

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

eserine

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

carbachol

tremor

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

eserine

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions

carbachol

clonic - tonic convulsions


Input: Multiple side effects of penicillamine therapy in one patient with rheumatoid arthritis. Skin rashes, proteinuria, systemic lupus erythematosus, polymyositis and myasthenia gravis have all been recorded as complications of penicillamine therapy in patients with rheumatoid arthritis. A patient who had developed all 5 is now described. The skin lesion resembled elastosis perforans serpiginosa, which has been reported as a rare side effect in patients with Wilson' s disease but not in patients with rheumatoid arthritis treated with penicillamine.

penicillamine

penicillamine

penicillamine

rheumatoid arthritis

Skin rashes

proteinuria

systemic lupus erythematosus

polymyositis

myasthenia gravis

rheumatoid arthritis

skin lesion

elastosis perforans serpiginosa

Wilson' s disease

rheumatoid arthritis

penicillamine

myasthenia gravis

penicillamine

myasthenia gravis

penicillamine

myasthenia gravis

penicillamine

proteinuria

penicillamine

proteinuria

penicillamine

proteinuria

penicillamine

Skin rashes

penicillamine

Skin rashes

penicillamine

Skin rashes

penicillamine

polymyositis

penicillamine

polymyositis

penicillamine

polymyositis

penicillamine

systemic lupus erythematosus

penicillamine

systemic lupus erythematosus

penicillamine

systemic lupus erythematosus


Input: Electrocardiographic changes and cardiac arrhythmias in patients receiving psychotropic drugs. Eight patients had cardiac manifestations that were life - threatening in five while taking psychotropic drugs, either phenothiazines or tricyclic antidepressants. Although most patients were receiving several drugs, Mellaril (thioridazine) appeared to be responsible for five cases of ventricular tachycardia, one of which was fatal in a 35 year old woman. Supraventricular tachycardia developed in one patient receiving Thorazine (chlorpromazine). Aventyl (nortriptyline) and Elavil (amitriptyline) each produced left bundle branch block in a 73 year old woman. Electrocardiographic T and U wave abnormalities were present in most patients. The ventricular arrhythmias responded to intravenous administration of lidocaine and to direct current electric shock; ventricular pacing was required in some instances and intravenous administration of propranolol combined with ventricular pacing in one. The tachyarrhythmias generally subsided within 48 hours after administration of the drugs was stopped. Five of the eight patients were 50 years of age or younger; only one clearly had antecedent heart disease. Major cardiac arrhythmias are a potential hazard in patients without heart disease who are receiving customary therapeutic doses of psychotropic drugs. A prospective clinical trial is suggested to quantify the risk of cardiac complications to patients receiving phenothiazines or tricyclic antidepressant drugs.

cardiac arrhythmias

ventricular tachycardia

Supraventricular tachycardia

left bundle branch block

ventricular arrhythmias

tachyarrhythmias

heart disease

cardiac arrhythmias

heart disease

cardiac complications

phenothiazines

Mellaril

thioridazine

Thorazine

chlorpromazine

Aventyl

nortriptyline

Elavil

amitriptyline

lidocaine

propranolol

phenothiazines

Mellaril

Supraventricular tachycardia

thioridazine

Supraventricular tachycardia

Aventyl

left bundle branch block

nortriptyline

left bundle branch block

Mellaril

ventricular tachycardia

thioridazine

ventricular tachycardia

Elavil

left bundle branch block

amitriptyline

left bundle branch block


Input: Serotonergic drugs, benzodiazepines and baclofen block muscimol - induced myoclonic jerks in a strain of mice. In male Swiss mice, muscimol produced myoclonic jerks. A 3 mg / kg (i. p.) dose induced this response in all of the mice tested and the peak response of 73 jerks per min was observed between 27 and 45 min. Increasing the brain serotonin levels by the administration of 5 - hydroxytryptophan (80 - 160 mg / kg) in combination with a peripheral decarboxylase inhibitor resulted in an inhibition of the muscimol effect. However, in a similar experiment l - dopa (80 - 160 mg / kg) was without effect. In doses of 3 - 10 mg / kg, the serotonin receptor agonist MK - 212 caused a dose - dependent blockade of the response of muscimol. Of the benzodiazepines, clonazepam (0. 1 - 0. 3 mg / kg) was found to be several fold more potent than diazepam (0. 3 - 3 mg / kg) in blocking the myoclonic jerks. While (-) - baclofen (1 - 3 mg / kg) proved to be an effective antagonist of muscimol, its (+) - isomer (5 - 20 mg / kg) lacked this property. Considering the fact that 5 - HTP and the benzodiazepines have been found to be beneficial in the management of clinical myoclonus, the muscimol - induced myoclonus seems to be a satisfactory animal model that may prove useful for the development of new drug treatments for this condition. Our present study indicated the possible value of MK - 212 and (-) - baclofen in the management of clinical myoclonus.

benzodiazepines

baclofen

muscimol

muscimol

serotonin

5 - hydroxytryptophan

muscimol

l - dopa

serotonin

MK - 212

muscimol

benzodiazepines

clonazepam

diazepam

baclofen

muscimol

5 - HTP

benzodiazepines

muscimol

MK - 212

baclofen

myoclonic jerks

myoclonic jerks

myoclonic jerks

myoclonus

myoclonus

myoclonus

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonic jerks

muscimol

myoclonus

muscimol

myoclonus

muscimol

myoclonus


Input: Hyperglycemic acidotic coma and death in Kearns - Sayre syndrome. This paper presents the clinical and metabolic findings in two young boys with long - standing Kearns - Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic - endocrine failure in the Kearns - Sayre syndrome.

Hyperglycemic acidotic coma

Hyperglycemic

acidotic

coma

Kearns - Sayre syndrome

Kearns - Sayre syndrome

lethargy

somnolence

polydipsia

polyphagia

polyuria

coma

hypotension

hyperglycemia

acidosis

lactic acidosis

ketosis

Respiratory failure

metabolic - endocrine failure

Kearns - Sayre syndrome

prednisone

lactate

prednisone

ketosis

prednisone

hypotension

prednisone

Hyperglycemic acidotic coma

prednisone

coma

prednisone

coma

prednisone

acidotic

prednisone

lactic acidosis

prednisone

Hyperglycemic

prednisone

hyperglycemia


Input: Effects of active constituents of Crocus sativus L., crocin on streptozocin - induced model of sporadic Alzheimer' s disease in male rats. BACKGROUND: The involvement of water - soluble carotenoids, crocins, as the main and active components of Crocus sativus L. extract in learning and memory processes has been proposed. In the present study, the effect of crocins on sporadic Alzheimer' s disease induced by intracerebroventricular (icv) streptozocin (STZ) in male rats was investigated. METHODS: Male adult Wistar rats (n = 90 and 260 - 290 g) were divided into 1, control; 2 and 3, crocins (15 and 30 mg / kg); 4, STZ; 5 and 6, STZ + crocins (15 and 30 mg / kg) groups. In Alzheimer' s disease groups, rats were injected with STZ - icv bilaterally (3 mg / kg) in first day and 3 days later, a similar STZ - icv application was repeated. In STZ + crocin animal groups, crocin was applied in doses of 15 and 30 mg / kg, i. p., one day pre - surgery and continued for three weeks. Prescription of crocin in each dose was repeated once for two days. However, the learning and memory performance was assessed using passive avoidance paradigm, and for spatial cognition evaluation, Y - maze task was used. RESULTS: It was found out that crocin (30 mg / kg) - treated STZ - injected rats show higher correct choices and lower errors in Y - maze than vehicle - treated STZ - injected rats. In addition, crocin in the mentioned dose could significantly attenuated learning and memory impairment in treated STZ - injected group in passive avoidance test. CONCLUSION: Therefore, these results demonstrate the effectiveness of crocin (30 mg / kg) in antagonizing the cognitive deficits caused by STZ - icv in rats and its potential in the treatment of neurodegenerative diseases such as Alzheimer' s disease.

crocin

streptozocin

carotenoids

crocins

crocins

streptozocin

STZ

crocins

STZ

STZ

crocins

STZ

STZ

STZ

crocin

crocin

crocin

crocin

STZ

STZ

crocin

STZ

crocin

STZ

Alzheimer' s disease

Alzheimer' s disease

Alzheimer' s disease

learning and memory impairment

learning and memory impairment

memory impairment

cognitive deficits

neurodegenerative diseases

Alzheimer' s disease

streptozocin

cognitive deficits

streptozocin

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

streptozocin

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease

STZ

Alzheimer' s disease


Input: Rosaceiform dermatitis associated with topical tacrolimus treatment. We describe herein 3 patients who developed rosacea - like dermatitis eruptions while using 0. 03% or 0. 1% tacrolimus ointment for facial dermatitis. Skin biopsy specimens showed telangiectasia and noncaseating epithelioid granulomatous tissue formation in the papillary to mid dermis. Continuous topical use of immunomodulators such as tacrolimus or pimecrolimus should be regarded as a potential cause of rosaceiform dermatitis, although many cases have not been reported.

dermatitis

rosacea

dermatitis

eruptions

facial dermatitis

telangiectasia

dermatitis

tacrolimus

tacrolimus

tacrolimus

pimecrolimus

pimecrolimus

dermatitis

pimecrolimus

dermatitis

pimecrolimus

dermatitis

pimecrolimus

eruptions

pimecrolimus

telangiectasia