Poison as cure: a clinical review of botulinum toxin as an invaluable drug

Botulinum toxin is the most potent toxin known. It is readily absorbed from mucosal surfaces. If dispersed as an aerosol or mixed in the food or water it can lead to a large outbreak of botulism. The disease presents as a symmetric descending paralysis in an afebrile patient. Cranial nerve involvement with diplopia, dysarthria, dysphonia, dysphagia and respiratory paralysis is seen after a variable incubation period. The treatment is mainly supportive. The source of the toxin is Clostridium botulinum, an anaerobic gram-positive spore-forming organism. Some other species of Clostridium like C. butyricum and C. baratii also produce the toxin. The toxin is heat labile and can be inactivated by heating at 100°C for 10 minutes. The toxin acts at the peripheral cholinergic nerve terminals at the neuromuscular junctions, postganglionic parasympathetic ganglia, etc, and affects neurotransmitter release by inhibiting exocytosis. Clinical uses in various medical fields were found for it.(AU)

Pre-hospital treatment of snake envenomation in patients presented AT a tertiary care hospital in Northwestern India

Snakebite is an important medical emergency. Anti-snake venom along with supportive care is the only specific treatment. However, many people put their faith in non-registered medical practitioners. Where medical aid is available, lack of trained health personnel jeopardizes the situation. This retrospective study, the first of its kind, was aimed at studying the pre-hospital treatment as well as the behavior of patients bitten by snakes and referred to the Postgraduate Institute of Medical Education and Research, Chandigarh, India. A total of 88 cases that occurred between January 1997 and December 2001 were studied. Seventy patients received treatment prior to admission (the majority was treated by non-registered medical practitioners, registered medical practitioners, and MBBS doctors). The various treatment modalities used were: anti-snake venom (ASV), tourniquet, incision and drainage (I&D), tetanus toxoid, injections, and tablets. Non-registered medical practitioners still preferred tourniquet and I&D. The patients who were referred within 24 hours stayed less time in the hospital and spent less money on the treatment compared to those who were referred after 24 hours. Non-registered medical practitioners and inadequately trained health staff are often the first contact of snakebite victims. Their traditional and unscientific methods of treatment lead to unnecessary morbidity and increased treatment cost. It is therefore necessary to train these people adequately so that proper treatment can be instituted at the earliest.

Synthesis and biological activities of some human gastrin analogs

The synthesis of analogs of the C-terminal tridecapeptide of gastrin in described. These pseudopeptide analogs were obtained either by replacing the C-terminal phenylalanine amide with 2-phenylethytalcohol or with 2-phenylethylamine, or by replacing the peptid bond between Trp and Leu, or between Leu and Asp with an aminomethylene (CH2NH). The ability of these compounds to stimulate gastric acid secretion in anesthetized rats and to inhibit binding of labeled CCK-8 to isolated cells from rabbit fundic mucosa was tested. [desPhe13, Leu11]-HG-12-I-beta-phenylethylester 33, [desPhe13, Leu11]-HG-12-II-beta-phenylethylester 38 [desPhe13, Leu11]-HG-12-I-beta-phenylethylamide 32, and [desPhe13, Leu11]-HG-12-II-beta-phenylethylamide 37 acted as gastrin receptor antagonists, while [Trp10-((CH2NH)-Leu11]-HG-13-I 31 and (Trp10-((CH2NH)-Leu11]-HG-13-II 36 acted as agonists. Unexpectedly, [Leu11-((CH2NH)-Asp12]-HG-13-I 30 and [Leu11-((CH2NH)-Asp12]-HG-13-II 35 were almost devoid of affinity for the gastrin receptor.