The aim of the study was to evaluate the efficacy of amiodarone used alone or in combination with propranolol in infants and children affected by life-threatening or drug-resistant tachyarrhythmias. The study included 27 children (median age 3 months), affected by life-threatening and/or drug-resistant supraventricular or ventricular tachyarrhythmias. The loading dose of amiodarone was 10-20 mg/kg/day and the maintenance dose ranged between 3 and 20 mg/kg/day. When amiodarone was ineffective, propranolol was added at a dosage of 2-4 mg/kg/day. The study population was divided into two groups: group A was composed of patients <1 year and group B of patients >1 year. The effectiveness of the therapy was assessed by clinical evaluation, Holter monitoring, exercise testing, and, in patients with reentry tachycardias, electrophysiological testing. Amiodarone used alone was effective or partially effective in 4/14 (28%) patients in group A and in 11/13 (85%) patients in group B (p < 0.006). Among amiodarone-resistant patients, the combined therapy with propranolol was effective in 8/10 patients in group A and 2/2 patients in group B. Therefore, amiodarone used alone or in combination with propranolol was effective in 25/27 (93%) patients. During the follow-up (20.5 +/- 13 months) there were no arrhythmic effects but side effects were noted in 5/27 (18.5%) patients. Amiodarone seems to be an effective drug in the control of the life-threatening and/or drug-resistant supraventricular and ventricular tachyarrhythmias in children. The addition of propranolol can significantly enhance the success rate of this class III drug, especially in the treatment of reentry tachycardias due to accessory pathways.

Adolescent↗

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The heliothis virescens 170 kDa aminopeptidase functions as "receptor A" by mediating specific Bacillus thuringiensis Cry1A delta-endotoxin binding and pore formation.

The relationship between Bacillus thuringiensis Cry1Aa, Cry1Ab and Cry1Ac delta-endotoxin binding and pore formation was investigated using a purified 170 kDa aminopeptidase N (APN) from Heliothis virescens brush border membranes. Aminopeptidases with molecular sizes of 110, 140 and 170 kDa were eluted from a Cry1Ac toxin affinity column using N-acetylgalactosamine. The 140 kDa aminopeptidase has a cross-reacting determinant typical of a cleaved glycosyl-phosphatidylinositol anchor. After mild base treatment to de-acylate the glycosyl-phosphatidylinositol linkage and incubation in phosphatidyl inositol phospholipase C, anti-cross-reacting determinant antibody recognized the 170 kDa protein. Kinetic binding characteristics of Cry1A toxins to purified 170 kDa APN were determined using surface plasmon resonance. Cry1Aa, Cry1Ab and Cry1Ac, but not Cry1C and Cry1E toxins recognized 170 kDa APN. Each Cry1A toxin recognized two binding sites: a high affinity site with KD ranging from 41 to 95 nM and a lower affinity site with KD in the 325 to 623 nM range. N-acetylgalactosamine inhibited Cry1Ac but not Cry1Aa and Cry1Ab binding to 170 kDa APN. When reconstituted into phospholipid vesicles, the 170 kDa APN promoted toxin-induced 86Rb+ release for Cry1A toxins, but not Cry1C toxin. Furthermore Cry1Ac, the Cry protein most toxic to H. virescens larvae, caused 86Rb+ release at lower concentrations, and to a greater extent than Cry1Aa and Cry1Ab toxins. The correlation between toxin-binding specificity and 86Rb+ release strongly suggests that the purified 170 kDa APN is the functional receptor A in the H. virescens midgut epithelial cell brush border membranes.

Acetylgalactosamine↗

PubMedDate not supplied

Cardiopulmonary exercise response in patients with left ventricular dysfunction or heart failure: a noninvasive study by gas exchange and impedance cardiography monitoring.

We investigated the upright bicycle exercise cardiopulmonary response in 20 patients with left ventricular dysfunction (LVD, secondary to previous myocardial infarction, left ventricular ejection fraction range 18-44%). Ten patients (48 +/- 7 years) asymptomatic (I NYHA class) without drug treatment (LVD group). The others (n = 10) (50 +/- 1 years) complained of dyspnea and/or fatigue despite therapy (NYHA II-III). They represented the heart failure (HF) group. Eight sedentary men (40 +/- 10 years) served as controls. Controls and patients performed stress testings under drug treatment, when administered. Anaerobic ventilatory threshold (ATge) was considered as an index of submaximal exercise while peak exercise VO2 (Peak VO2) was considered the maximal volitional exercise capacity. The ratio between minute ventilation (VE) to carbon dioxide release (VCO2) (VE/VCO2) was assessed to evaluate the ventilatory response during exercise. We coupled gas exchange assessment (2001, MGC) with noninvasive monitoring of stroke volume (SV) by impedance cardiography (NCCOM3, BOMED) and total systemic vascular resistances (TSVR; by auscultatory blood pressure measurement). In controls VO2 increase during exercise was related to higher heart rate (HR) and SV both from resting to ATge and from this point to the peak. TSVR declined during both steps. In patients with HF VO2 rose from resting to ATge (by faster HR and unchanged SV). VO2 increased slightly from this point to Peak VO2. This result was related to flat HR increase and unchanged SV as well as TSVR. In patients with LVD VO2 increased similarly to controls from resting to ATge and less above the threshold. In these patients both HR and SV increased during submaximal exercise. From ATge to Peak VO2 only HR increased. TSVR declined significantly similarly to controls. The VE/VCO2 ratio was higher at peak exercise in patients with HF compared to controls. Different determinants were demonstrated in patients with left ventricular dysfunction with mild or symptomatic chronic heart failure (CHF). These findings and the increased ventilatory response in patients with CHF can explain different changes of VO2 in these patients during submaximal and maximal voluntary exercise and contribute to explain exercise-induced exertion in these subjects.

Adult↗

PubMedDate not supplied

Tetanus-like syndrome secondary to metoclopramide administration.

A case of metoclopramide-induced pseudotetanus in a 24-year-old woman is described. Symptoms included flexor spasms of the neck muscles, neck pain, left deviation of the lower jaw and tongue protrusion. Tetanus was initially suspected. Mydriasis, hyperhydrosis and clinical observation indicated that this syndrome could be caused by metoclopramide taken for gastrointestinal symptoms. Orphenadrine hydrochloride, diazepam and ketoprofen completely resolved the symptoms. Pseudotetanus presents in many different ways, and it is sometimes very hard to distinguish it from infective tetanus, which is very difficult to diagnose. Physicians using metoclopramide should be aware of its adverse effects and how to treat them.

Adult↗

PubMedDate not supplied