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P Tréchot

Publications and source records attributed to P Tréchot.

At least 19 recordsLinked to original sources
PubMed2005

["Iodine allergy": point of view].

OBJECTIVE: The aim of this literature review is to suggest a diagnostic and a preventive attitude in patients having presented an immediate hypersensitivity reaction due to an iodinated drug. DATA SOURCES: Literature review. Data were searched in the Medline database from 1967 to 2004 in English and French language. Complementary references were selected from the bibliography of selected references or from authors' personal databases. The following key-words were used separately or combined: Hypersensitivity, Immediate; Allergy; Contrast Media; Povidone-Iodine; Iodine; Iodine Compounds; Iodides; Amiodarone; Seafood, Parvalbumins; Tropomyosin. STUDY SELECTION: Randomized studies, epidemiological studies, original articles, clinical cases, and letters to the editor were selected. DATA SYNTHESIS: The implication of iodine has never been demonstrated during allergic hypersensitivity reactions due to iodinated drugs. However, IgE-mediated allergic hypersensitivity reactions have been published with contrast media or iodinated antiseptics and will be described in this development. In a wider sense, allergic hypersensitivity reactions due to seafood are evoked because often improperly considered as a risk factor of allergic reaction to iodinated drugs. The allergenic determinant responsible of patient sensitization is not known for iodinated contrast media, but is probably due to povidone in case of iodine povidone. In fish, the allergen is described as the protein M. There has also been strong immunological evidence that tropomyosin is a cross-reactive allergen among crustaceans and molluscs (shellfishs). In case of hypersensitivity reaction occurring with iodinated drug, an allergological assessment is required to confirm the immune mechanism, to identify the culprit drug or substance and to identify cross-reactivity especially with iodinated contrast media. CONCLUSION: Asking a patient if he/she is "allergic to iodine" is a question that should be avoided because its significance is null. A diagnosis of drug allergy, essentially relying on clinical symptoms, biological tests and cutaneous tests, is required to take adequate preventive measures.

Anti-Infective Agents, Local↗
PubMed2004

[Paroxysmal atrioventricular block due to anticholinesterase therapy].

The authors report a case of paroxysmal syncopal complete atrioventricular block due to anticholinesterase therapy occurring after the first administration. The block was reversible. It is therefore important to exclude this cause of atrioventricular block in the elderly in view of the increasing indications of this therapy.

Aged↗
PubMed2001

[Prevalence of hyperhidrosis in a population treated by beta-blocker].

INTRODUCTION: Some cases of hyperhidrosis with beta-blocker therapy have been reported in the literature. We studied the prevalence of hyperhidrosis in a population treated by beta-blockers compared with an untreated control group. PATIENTS AND METHODS: Patients attending the cardiologic consultation of the Nancy hospital were included. Past medical history and medication were collected. Interrogation assessed whether the patient felt hyperhidrosis, and defined a hyperhidrosis score. RESULTS: Sixty-five subjects treated by beta-blocker and 100 controls were included. 36.9 p. 100 of treated patients and 38 p. 100 of controls experienced hyperhidrosis (p=0.88). 23.07 and 23 p. 100, respectively, had hyperhidrosis defined by a high score of sweating (p=0.99). Retrospectively, 8 of 24 patients experienced hyperhidrosis after the beginning of beta-blocker therapy. DISCUSSION: We observed the same prevalence of hyperhidrosis in the two groups. However sweat gland innervation involved both cholinergic and adrenergic stimulations. Furthermore, experimental studies showed an increase in sweating on efforts with beta-blocker therapy.

Adrenergic beta-Antagonists↗
PubMed2000

[The role of drugs in falls in the elderly. Epidemiologic aspects].

FALLS AND POST-FALL SYNDROME: Falls are a major health problem among the elderly because of the resulting psychological sequelae (sometimes termed "post-fall syndrome") and in a few cases serious injury, particularly hip fractures. DRUGS AND FALLS: The scientific literature on the link between medications and falls and fractures suggests that psychotropic drugs used in about 50% of residents of nursing homes and in 20% in the community cause around 30% of falls in nursing homes and 20% of falls in the community. PSYCHOTROPS: The relative effect of selective serotonin reuptake inhibitors and tricyclic antidepressors and the relative effect of short/long acting or sedative/hypnotic benzodiazepines are not well established. CARDIOVASCULAR DRUGS: Appropriate use of cardiovascular medications and analgesics does not increase the risk of falls. PREVENTION: These data reinforce the concept that reducing the use of psychotrops, especially benzodiazepines, is probably one of the most effective means of reducing serious falls in older people.

Accidental Falls↗
PubMed2000

[Non-steroidal anti-inflammatory drugs with selectivity for cyclooxygenase-2 in Alzheimer's disease. Rationale and perspectives].

POSSIBLE INFLAMMATORY MECHANISMS: Alzheimer's disease (AD) is a degenerative disease of the brain including possibly inflammatory mechanisms, as illustrated by the presence of activated microglial cells in the periphery of senile plaques and neurofibrillary tangles and the subsequent release of proinflammatory mediators with neurotoxic potency. RATIONALE FOR NSAID USE: Although not firmly demonstrated, the rationale for the prescription of non steroidal anti-inflammatory drugs (NSAIDS) as neuroprotective agents in AD lies on epidemiological data having shown a reduced risk of developing AD in patients on long-term therapy with NSAIDs (non selective cyclo-oxygenase [COX] inhibitors). RATIONALE FOR THE USE OF SELECTIVE COX-2 INHIBITORS: The rationale for the prescription of selective COX-2 inhibitors as neuroprotective drugs in AD lies on: Epidemiological data having shown a reduced risk of developing AD in patients treated with anti-inflammatory doses of classical NSAIDs (inhibition of COX-1 and COX-2) but not with antithrombotic doses of aspirin (selective inhibition of COX-1), Cellular experiments, Demonstration of a better gastro-intestinal (GI) safety profile with selective COX-2 inhibitors than with classical NSAIDs in short-term studies, allowing a possible long-term use in AD. BEFORE PRESCRIBING: COX-2 may have an ambivalent functionality in the brain since the basal production of prostaglandins through COX-2 may participate in neuronal homeostasis whereas the expression of COX-2 is associated with brain development. Classical NSAIDs are ineffective in reducing the formation of senile plaque and neurofibrillary tangles in AD, which is consistent with an ability to reduce inflammation associated with activation of microglia but illustrates their failure to suppress the degenerative process. Prophylactic use of selective COX-2 NSAIDs can be considered on the basis of their good GI safety after 6 months of marketing in United States but need to be confirmed for a longer time. CURRENT TRIALS: Clinical studies focusing on both the prevention and the slowing down of early AD are under way with two recently launched selective COX-2 inhibitors, celecoxib and rofecoxib.

Adult↗