Severity of dependence and route of administration of heroin, cocaine and amphetamines

This study investigates severity of dependence upon heroin, cocaine and amphetamines in a group of 200 heroin users, 75% of whom were not in contact with any treatment agency. For drug takers who were current users of more than one drug, heroin produced more severe dependence than either cocaine or amphetamine and many users of these stimulant drugs reported having experienced no problems of dependence. Severity of dependence was influenced by route of administration as welt as type of drug. Heroin taken by injection was associated with more severe dependence than smoked heroin. For cocaine, injection and smoking were associated with equivalent dependence ratings, and both of these routes were associated with more severe dependence than cocaine used intranasally. For amphetamine, there were no differences in severity of dependence ratings for injection, intranasal or oral use. Severity of dependence was correlated with dose and duration of drug use; it was also associated with previous attendance at a drug treatment agency, though dependence problems were also common among heroin users who had never received treatment. Implications of these findings are discussed.     

A monoclonal antibody directed against a granule membrane glycoprotein (GMP-140/PADGEM, P-selectin, CD62P) inhibits ristocetin-induced platelet aggregation

P-selectin (also called CD62, GMP-140, PADGEM, CD62P) is a recently described member of a family of vascular adhesion receptors expressed by activated platelets and endothelial cells that are involved in leucocyte cell adhesion. The aim of this study was to characterize a new monoclonal antibody (LYP7) directed against activated human blood platelets that inhibits ristocetin-induced platelet aggregation. Immunoadsorbent affinity chromatography and immunoprecipitation studies showed that LYP7 (IgG₁) bound a surface-labelled glycoprotein (GP) which changed its apparent molecular mass (M_r) on reduction from 138 kD (situated below GPIIb) to 148 kD (above GPIIbα). LYP7 and S12, a monoclonal antibody directed against P-selectin immunoprecipitated the same band. Using ELISA assay, purified P-selectin was shown to bind LYP7 and S12 monoclonal antibodies. Binding sites of ¹²⁵I-labelled LYP7, which was greatly increased on thrombin-stimulated (2 U/ml) washed platelets (10825±2886, mean ±SD) (K_d=1.5±0.5 nm ) compared to resting platelets (2801±1278, mean ±SD) (K_d=1.5±0.6 nm ), was found to be normal on thrombin-stimulated platelets taken from a patient with grey platelet syndrome or a patient with Glanzmann thrombasthenia. LYP7 (IgG₁, F(ab′)₂ or Fab fragments) inhibited ristocetin-induced platelet aggregation of platelets in a dose-dependent fashion without affecting the binding of von Willebrand (vWf ) factor. However, agglutination of formaldehyde-fixed platelets induced by ristocetin was not affected by monoclonal antibody LYP7. In addition, the binding of thrombin-activated platelets to neutrophils was inhibited by monoclonal antibody LYP7. These results strongly suggest that P-selectin, by promoting cell–cell contact, may play an active role in platelet–platelet interactions.     

Radiofrequency Catheter Ablation of AtypicalAtrioventricular Nodal Reentrant Tachycardia

Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia, Introduction: Published reports of radiofrequency ablation of atypical atrioventricular nodal reentranttacbycardia (AVNRT) have been limited. We present our experience in 10 consecutive patientswith atypical AVNRT wbo underwent radiofrequency ablation of the "slow" AV nodal pathway.
Methods and Resttlts: there were 9 females and 1 male; their mean age was 44 ± 19 years (± SD), the mean AVNRT cycle length and ventriculoatrial (VA) interval at the His positionduring AVNRT were 340 ± 50 msec and 200 ± 70 msec, respectively. the slow pathway wassuccessfully ablated in all patients with a mean of 10 ± 7 radiofrequency energy applications inthe posteroseptal right atritim near the coronary sinus os. The mean procedure duration was 100 ± 35 minutes. There were no complications. In 4 patients, target sites were identified during sinus rhythm by mapping for possible slow pathway potentials, In the other 6 patients, target sites were identified by mapping retrograde atrial activation during AVNRT or ventricularpacing, The VA times at successful target sites were a mean of 45 ± 30 msec less tban the VAtime at the His cathetcr during AVNRT, There were no differences in success rate, number ofradiofrequency energy applications, or procedure duration between patients in whom mappingwas guided by possible slow pathway potentials or by retrograde atrial activation, During 6 ± 3 months of followup, 1 patient bad a recurrence of atypical AVNRT and underwent a secondablation procedure, which was successful.
Conclusion: Radiofrequency ablation of atypical AVNRT can be safely and effectivelyaccomplisbed when target sites are identified based either on possible slow pathway potentialsduring sinus rbytbm or retrograde atrial activation times during tachycardia.     

Chylous ascites in cirrhosis: A case report and review of the literature

Chylous ascites is an uncommon clinical entity which results from the accumulation of fat, predominantly chylomicrons, in the ascitic fluid. Conventional treatment methods are unsatisfactory. A patient is reported with chylous ascites associated with cirrhosis and portal hypertension in whom the ascites, the renal insufficiency and the fluid and electrolyte disturbances were corrected by the insertion of a Denver peritoneovenous shunt.     

NYCTOHEMERAL VARIATION AND SUPPRESSIBILITY OF PLASMA ACTH IN VARIOUS STAGES OF CUSHING''S DISEASE

In order to define nyctohemeral plasma ACTH secretory patterns, frequency plasma ACTH samples were obtained in seven patients with untreated Cushing's disease (i.e. pituitary-dependent Cushing's syndrome), five Cushing's patients treated by bilateral adrenalectomy, four of whom had Nelson's syndrome, and one patient with 21-hydroxylase deficiency (congenital adrenal hyperplasia). A nyctohemeral rhythm of plasma ACTH concentration was apparent in the one patient with the adrenogenital syndrome but not in those with Nelson's syndrome or Cushing's disease. The effect of graded doses of dexamethasone, 2,8 or 32 mg per 24 h period, on plasma ACTH concentrations was studied in patients with untreated or treated Cushing's disease or Nelson's syndrome. In all of these hypercorticotrophic states, the mean plasma ACTH concentraton was not significantly affected by the smallest dose of dexamethasone, was partially suppressed by the intermediate dose, and further suppressed by the largest dose. In contrst, the patient with congenital adrenal hyperplasia and elevated plasma ACTH concentrations showed complete suppression of plasma ACTH levels following the smallest dose of dexamethasone. These findings indicate that there is resistance to ACTH suppression by dexamethasone in all stages of Cushing's disease and suggest that negative feedback of glucocorticoids may be involved in the pathogenesis of this disease.     

Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices

Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement.
Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N-acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide.
Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration-dependent effect of sodium channel blockade on defibrillation energy requirements in patients.