Organophosphate-induced delayed neuropathy: case report.

Organophosphate induced delayed neuropathy (OPIDN) is an uncommon clinical condition. It occurs in association with the ingestion of great amounts of organophosphate after the stimulation of cholinergic receptor. The clinical picture is characterized by a distal paresis in lower limbs associated with sensitive symptoms. Electrodiagnostic studies show a motor axonal neuropathy. Involvement of the central nervous system may occur. We describe a 39 years-old female patient who developed hyperesthesia associated with lower limbs paresis, fourteen days after she had ingested a Dichlorvos-based insecticide. Electrophysiological study was characterized by an axonal polyneuropathy pattern. Pyramidal tract dysfunction was observed later in upper limbs. Considering that both peripheral and central nervous systems are involved we believe that the more appropriated term would be organophosphate induced delayed neuropathy (OPIDN) instead of organophosphate induced delayed polyneuropathy (OPIDP).

Ranunculus bulbosus: 1ra. parte / Ranunculus bulbosus: 1fts. part

Se resalta el tropismo tisular del medicamento, como así también los principales síntomas característicos y los diversos síndromes para los cuales se adapta. Se hacen resaltar las modalidades de las algias las cuales darán el diagnóstico medicamentoso con exactitud y se traen a consideración cuadros clínicos para los cuales el medicamento es muy útil y poco tenido en cuenta

Ranunculus bulbosus: 1ra. parte / Ranunculus bulbosus: 1fts. part

Se resalta el tropismo tisular del medicamento, como así también los principales síntomas característicos y los diversos síndromes para los cuales se adapta. Se hacen resaltar las modalidades de las algias las cuales darán el diagnóstico medicamentoso con exactitud y se traen a consideración cuadros clínicos para los cuales el medicamento es muy útil y poco tenido en cuenta (AU)

Interleukin-1 beta as a potent hyperalgesic agent antagonized by a tripeptide analogue.

Interleukin-1 (IL-1) describes two inflammatory proteins, IL-1 alpha and IL-1 beta, produced by activated macrophages and other cell types and encoded by two genes. Their amino acid sequences have only 26% similarity, but their biological activities are comparable, with a few exceptions; indeed, both molecules appear to act at the same receptor. As IL-1 release prostaglandins which sensitize nociceptors in man and in experimental animals, we tested IL-1 alpha and IL-1 beta in rats for hyperalgesic (nociceptive) activity. Our results show that IL-1 beta given systemically is an extremely potent hyperalgesic agent with a probable peripheral site of action; IL-1 alpha is approximately 3,000 times less active than IL-1 beta. We have delineated the region of IL-1 beta mediating the hyperalgesic effect and developed an analgesic tripeptide analogue of IL-1 beta which antagonizes hyperalgesia evoked by IL-1 beta and by the inflammatory agent carrageenan.

Interleukin-1 mimics the hyperalgesia induced by a factor obtained by macrophage lysis.

1. Lysis of rat thioglycolate-stimulated peritoneal macrophages releases a low molecular weight factor (0.5 less than MW less than 10 kD) into the supernatant. Bilateral hyperalgesia was observed when this factor, denoted macrophage hyperalgesic factor (MHF), was injected into one hind paw or into the peritoneal cavity of the rat. 2. Similar activity was detected in stimulated peritoneal and tumoral mouse macrophages (J774G8) but not in lysates of rat exudate neutrophils or in peritoneal resident (non-stimulated) macrophages. 3. The hyperalgesia induced by MHF was abolished by local intraplantar injection of indomethacin, thus suggesting a peripheral release of cyclo-oxygenase products. This suggestion was supported by the ability of MHF to release prostaglandin-like material when added to a guinea pig lung perfusate. 4. Peritonitis induced by the administration of carrageenin caused concomitant bilateral rat paw hyperalgesia and an MHF-like activity was demonstrable in peritoneal exudate 30 min after the carrageenin insult. 5. Purified human interleukin-1 (IL-1) given locally or systemically also produced bilateral hind paw hyperalgesia which was abolished by local administration of indomethacin. The possibility that MHF may be a fragment of IL-1 is discussed.