In normotensive patients with diabetes mellitus type II, the institution of angiotensin-converting enzyme inhibition during early stages of diabetic nephropathy results in long-term stabilization of plasma creatinine levels and of the degree of urinary loss of albumin. These effects are probably independent of the antihypertensive action of these agents.

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SUMMARY Late progressive polyneuropathy followed by pyramidal findings in a 20 year old agricultural labourer who ingested Isofenphos solution during his work, is presented. The patient was confined to a wheelchair within 6 weeks, regained walking ability within 6 months, and a 23 months' follow up revealed slight additional clinical improvement with minimal progression of the pyramidal signs. The neuropathic clinical manifestations, the EMG and the nerve conduction studies were compatible with a pathology of a distal, mainly axonal, mainly motor neuropathy.Organo-phosphorus compounds have a well known immediate muscarinic neurotoxic effect precipitated by the acute inhibition of acetylcholinesterase. Late onset non-muscarinic neurological effects of these compounds have been reported as well.`4 A case of ascending, mainly motor, neuropathy which appeared 2 weeks after ingestion of Isofenphos and which was followed up for 23 months is presented. To the best of our knowledge, this is the first description of a case of late onset Isofenphos neurotoxicity in man.Case report A 20 year old healthy agriculture worker accidently ingested a few millilitres of diluted insecticide solution which was thrown off into his face while he was using it for spraying flowers. The solution contained 0 75 mg/ml Isofenphos (0-ethyl-0 (2-isopropoxy-carbonyl) phenyl isopropyl phosphoramidothioate) and 2 mg/ml Maneb (manganese ethylene-1,2-bis-dithiocarbamate). He was first attended to by a local physician who gave him an atropine injection, then taken to the emergency unit of a general hospital, where no clinical signs of organophosphorus poisoning were found, and serum cholinesterase level was 24 units/ml (normal laboratory values: 3-6). Several hours later he experienced weakness, dyspnoea and vomiting from which he recovered about 16 hours after the exposure. Two weeks later, while at home, he contracted pain in the calves, followed by gait impairment and weakness in the hands. Readmitted to hospital 3 weeks after the initial event, his general physical examination was normal and no recent history of a febrile disease was disclosed. However, neurological examination revealed hypotonia of the hand flexors, Achilles hyporeflexia and a mild sensory deficit in a "gloves and stockings" distribution. Blood, urine and CSF laboratory tests for screening possible neuropathic aetiologies produced normal findings. Pulmonary function tests and radiographs were normal. Serum cholinesterase level was 6 3 units/ml.

A patient is reported in whom an intravenous bolus injection of 50 mg lignocaine produced extreme sinus bradycardia (rate 14 to 20/min). Only 2 patients with such a response to a similarly small dose have been previously reported, but these reports indicate clearly that careful electrocardiographic monitoring is advisable when lignocaine is administered.

The analgesic effect of ceruletide in biliary and renal colic was evaluated by a randomized, double-blind study in 82 patients. Ceruletide was compared with pentazocine, a well-established analgetic agent. Rapid and effective analgesia was obtained by intramuscular injection of ceruletide 0.5 micrograms/kg in 56 patients with biliary colic. The analgesic effect of ceruletide compared well with pentazocine 0.5 mg/kg im, and was associated with remarkably fewer side effects. In 26 patients with renal colic, ceruletide was significantly inferior to pentazocine. These data support the recommendation of ceruletide as a first-choice analgetic agent for biliary colic.