Occupational allergic contact dermatitis and contact urticaria caused by polyfunctional aziridine hardener.

Polyfunctional aziridine (PFA) is increasingly used as a water-based cross-linker in 2-component paints, paint primers, lacquers, topcoats and other protective coatings. The cross-linker (PFA hardener) is made by reacting multifunctional acrylic monomer with a highly reactive aziridine compound. During 1992-1993, we came across 2 patients with allergic patch test reactions provoked by PFA hardener. One of the patients was a parquet layer, and the other a printer. Allergic contact dermatitis (ACD) was diagnosed by positive allergic patch test reactions to PFA hardener in a dilution series in pet.:0.3%-1% gave ++ to allergic reactions in both patients, whereas 0.1% gave a weak (+) or questionable reaction (?+), respectively. The methacrylate patch test series was negative in both patients, although gas chromatography/mass spectrometry analysis showed that PFA hardener contained 0.3% of trimethylolpropane triacrylate (TMPTA), a multifunctional acrylic monomer. One of the patients also had symptoms of contact urticaria, and a prick test with PFA hardener (1% aq.) induced a histamine-sized prick test reaction. The positive reactions with the PFA hardener and the negative reactions with the starting chemicals and additives in PFA, namely acrylates, propyleneimine and dimethylethanolamine, indicate that PFA caused ACD. This is in accordance with our previous observations, but differs from the reports of others, whose patients had been sensitized to acrylates present as remnants in the PFA hardener. As test substance, 0.5% PFA hardener in pet. is recommended for patch testing. Testing should be performed in patients with contact dermatitis if exposure to PFA has occurred. Skin prick tests may be of help to detect contact urticaria.

Orofacial and respiratory tardive dyskinesia: potential side effects of 2-dimethylaminoethanol (deanol)?

A case of essential tremor since early adultness is presented, which has been treated successfully with the acetylcholine precursor 2-dimethylaminoethanol (deanol) for 10 years. Development of a marked dyskinesia syndrome affecting predominantly orofacial and respiratory musculature has been noticed with this medication. Partial remission after discontinuation and a favorable response to anticholinergics are suggestive of an adverse drug effect.

Acción del propel-oxifenil-mandelato de dimetilamino-etano sobre la motilidad esofágica: estudio manométrico en diversas afecciones esofágicas / Action of the dimetyl-ameno-etane propin-oxyphenyl-mandelate on esophageal motility: manometric study in various esophageal lesions

Se estudia la acción del Propin-oxifenil-mandelato de dimetilamino-etano (Sertal [r]) sobre la motilidad del esófago mediante electromanometría intraluminal, demostrando que esta droga no tiene acción sobre la motilidad normal (peristalsis, zona de alta presión del esfínter inferior), pero sí produce reducción en la amplitud y el número de ondas disquinéticas en dosis de 25 mg administradas en forma endovenosa

Double-blind trial of 2-dimethylaminoethanol in Alzheimer's disease.

A double-blind, placebo-controlled trial of 2-dimethylaminoethanol was undertaken in 27 patients with moderately severe or severe Alzheimer's disease. Of 13 patients in the drug group, 6 were withdrawn in the first 5 weeks of the trial because of side effects, which included drowsiness and retardation, with an increase of confusion and mild elevation of blood pressure. No significant benefit appeared from the drug treatment.

Ineffectiveness of deanol in tardive dyskinesia: a placebo controlled study.

In a double-blind placebo-controlled study, deanol acetamidobenzoate, administered in doses up to 1.5 g q.d. for three weeks to chronic schizophrenic patients presenting moderate to severe tardive dyskinesia, failed to alleviate the dyskinetic movements. However, there was a tendency for a significant increase in the schizophrenic symptoms of the deanol-treated group relative to the control group. The ineffectiveness of deanol in alleviating tardive dyskinesia is consistent with its inability to enhance brain acetylcholine synthesis. The worsening of the schizophrenic symptoms may possibly result from an interference by deanol with central cholinergic function.

Mood alterations during deanol therapy.

An imbalance between central cholinergic and adrenergic influences may affect mood disorders. Of 38 patients taking high doses of deanol, a putative acetylcholine precursor, eight developed changes in mood: five became depressed and three became hypomanic. A predisposition is suggested as seven of these eight patients had histories of affective symptoms. There was no relationship between the changes in dyskinesias and mood. These observations have both practical and heuristic implications for the management of patients and for further research into the pharmacology of affective disorders and deanol.

The effects of deanol on cognitive performance and electrophysiology in elderly humans.

Deanol (900 mg/day for 21 days) had no effect on learning a list of words when tested at weekly intervals. Tests of simple and complex reaction time and a test of continuous serial decoding of digits showed no enhancement with the drug. Several components of evoked potentials recorded from several scalp sites did show enhanced amplitude under drug treatment. These changes were not accompanied by changes in the EEG spectrum as are seen with some other psychoactive drugs. Deanol seems to be an ineffective treatment for the normal slowing of cognitive function seen in the normal elderly person or those elderly with only minimal cognitive decline and free of symptoms of dementia. Contrary to earlier reports, elderly persons were found to be able to benefit from warning signals in a complex reaction time task.

Deanol acetamidobenzoate treatment in choreiform movement disorders.

Deanol acetamidobenzoate was administered in double-blind, crossover fashion with placebo to five patients with tardive dyskinesia, three patients with Huntington's chorea, and one patient with posthemiplegic chorea. No significant effect on dyskinesia was observed. Preliminary administration of physostigmine salicylate to patients with tardive dyskinesia had a variable effect, while benztropine mesylate produced no change. Since the status of deanol as an effective precursor of acetylcholine is uncertain, further trials with putative cholinergic agents remain warranted in choreiform syndromes.

Hemiballismus-hemichorea treated with dimethylaminoethanol.

An elderly lady with subacute onset of disabling hemiballismus experienced sustained remission on dimethylaminoethanol 150 mg/day. Two exacerbations followed interruption of therapy. Remission followed resumption of therapy. No undesirable side effects occurred with this treatment. A lady age 85 experienced a very favorable sustained reduction of hemiballismus when treated with dimethylaminoethanol (DMAE or Deanol). Her age and hypertension made the risk of thalamotomy unacceptably high. DMAE was tried because of reports of reduction of chorea, and other dyskinesias with this drug.

Deanol in the treatment of tardive dyskinesia.

Ten hospitalized chronic psychotic patients with symptoms of tardive dyskinesia were given deanol and placebo, each for 8 weeks following a double-bline, crossover design. No psychotropic agents were administered during the trial. Improvement occurred in all patients during the first treatment phase regardless of which drug the patients received; seven patients were on deanol and three on placebo during this time. The possible reasons for this decrease were discussed. It was concluded that deanol may have contributed to the decline but that its effect on the disorder was not dramatic.