Immunological adverse effects of anticonvulsants. What is their clinical relevance?

Long term administration of anticonvulsants is sometimes associated with impairment of the humoral and/or cellular immune response. Furthermore, certain well known adverse reactions to antiepileptics may have an immunotoxicological origin e.g. lymphadenopathy, pseudolymphoma and systemic lupus erythematosus. However, two important questions remain unresolved. First, the possibility that epilepsy per se might be primarily associated with immune alterations makes it difficult to assess the pathogenetic role of a specific drug, especially in a patient population usually on multiple drug therapy. Secondly, the clinical relevance of some of the observed immunological abnormalities is still highly controversial. This review is intended to give an outline of the present state of knowledge on the effects of anticonvulsants on humoral, cellular and nonspecific immunity, with particular regard to some of the major clinical conditions that have been ascribed to drug-induced immune dysregulation, such as pseudolymphoma and systemic autoimmune diseases. The immunotoxic potential of anticonvulsants appears to be low, and immunological monitoring is not usually required except in patients with known immune defects.

Inhibition of endogenous acetylcholine release by blockade of voltage-dependent calcium channels in enteric neurons of the guinea-pig colon.

The effects on acetylcholine release from the guinea-pig colon of the N-type calcium channel blocker omega-conotoxin GVIA (omega-conotoxin), the L-type calcium channel blocker nifedipine and the putative blocker of T-type channels, flunarizine, have been investigated. Endogenous basal acetylcholine release and electrically (1 Hz, 1 ms, 450 mA)-evoked overflow in the presence of cholinesterase inhibitor were studied. omega-Conotoxin (1-10 nM) and nifedipine (0.03-3 microM) dose-dependently inhibited basal and electrically-evoked acetylcholine release. Maximal inhibition of basal or electrically-evoked acetylcholine release was about 40% for nifedipine and about 75% for omega-conotoxin. The potency of nifedipine was inversely related to the external calcium concentration: its EC50 value in low-calcium medium (0.5 mM) was as low as 12 nM. Flunarizine inhibited acetylcholine release only at concentrations higher than 0.2 microM. Our results are consistent with an involvement of N- and L-type calcium channels in the control of the endogenous acetylcholine release from the guinea-pig colon.

[Utility of angiography in the diagnosis and localization of hepatic carcinomas]. / L'utilita' dell'angiografia nella diagnosi e nell'inquadramento dei carcinomi epatici.

In the field of malignant primitive hepatic tumours, the use of ultrasonic methods and C.A.T. has made a considerable contribution to diagnosis and topographical localisation of such tumours. In addition, hepatic biopsy supplies the histological diagnosis. However it is only by angiography that it is possible to evaluate the involvement of the lobes and segments, supplying the character of invasiveness or otherwise of the lesion through demonstration of the arterial peduncle, and thus giving the surgeon the essential elements for a therapeutic approach. Furthermore, in the case of a monofocal lesion, it is only angiography that can establish the usefulness or otherwise of surgical therapy (William M. - Richard P. J. - Philip C. G. - Robert C. Lim, 1979). The purpose of the work is to examine the angiographic readings, which allow: 1) a diagnosis of hepatic expansive formation to be made, with definition of its nature (bening or malignant); 2) the growth character of the lesion to be characterised through evaluation of the involvement of the vascular structures.

[Indications for cerebral revascularization surgery (author's transl)]. / Indicazioni agli interventi di rivascolarizzazione cerebrale.

Cerebrovascular diseases are among the most widespread. In the USA alone there is at any time a population of 1.6 million people with current stroke syndrome or the sequelae thereof. The most effective weapon to combat this disease is prevention, and here reference is made in particular to surgical prevention, especially through endoarterectomy of the extracranial internal carotid, and to vertebrobasilar circulatory failure.