Occupational contact dermatitis from trans-methyl-3-(4-methoxyphenyl)glycidate.
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Biomedical subjects
Publications and source records attributed to L Vaillant.
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We retrospectively analyzed 63 observations collected in nine French departments of dermatology of an acute pustular dermatosis, recently named in the French literature acute generalized exanthematous pustulosis (AGEP). Even though 11 of these cases occurred in patients with a history of psoriasis, AGEP appeared distinct from pustular psoriasis based on several slight pathologic differences, drug induction in most cases, and a more acute course of fever and pustulosis, with rapid spontaneous healing. We, therefore, suggest that AGEP is a reaction pattern, perhaps favored by a "psoriatic background." The most frequent causes of AGEP seem to be drug reactions, acute infections with enteroviruses, and hypersensitivity to mercury. With 55 (87%) of 63 cases attributed to drugs in this series, AGEP should be added to the list of cutaneous adverse drug reactions. Among drug-induced skin eruptions, AGEP is remarkable by its short time to onset after the administration of the suspected drug (less than 24 hours in half of our cases) and the great predominance (80%) of antibiotics as causative agents. It is suggested that some cases previously reported as "drug-induced pustular psoriasis" were in fact AGEP.
Modifications in the pharmacokinetics of aminoglycosides have been reported among patients with cystic fibrosis. We obtained suction blister fluid (SBF) to study the tissue diffusion of amikacin in cystic fibrosis in 2 children (a 9-year-old boy and a 7-year-old girl) over the course of bronchopulmonary infection. Amikacin was administered intravenously using a single dose of 5 mg/kg. The peak plasma concentrations were 24.5 and 11.2 mg/l, and the peak SBF concentrations were 8.3 and 3.2 mg/l. The ratio of the area under the curve in SBF and plasma was 58 and 60%, respectively. These results suggest a good penetration of amikacin through SBF and a good tissue diffusion of amikacin. The preliminary data suggest that the suction blister method may be useful to assess the tissue diffusion of drugs.
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A 72-year-old woman with chronic renal failure requiring haemodialysis developed acute iododerma twice, after receiving iodide contrast dye for radiological procedures. Iododerma was localized to the face, scalp and elbows and was associated with papular purpura of the legs. Histopathology of the skin lesions showed acute necrotizing vasculitis. During the second skin eruption the patient developed acute respiratory distress, which was treated with corticosteroids. During the first eruption asymptomatic infiltrates were present on chest X-ray which disappeared 2 months later. At the present time iododerma seems more frequent in patients with renal failure. Iodides may also be responsible for pulmonary abnormalities, which are sometimes asymptomatic. All these features may be due to leucocytoclastic vasculitis following iodide ingestion.
Transdermal nitroglycerin is commonly used and may induce contact dermatitis. The frequency of adverse skin reactions is controversial and may vary from 10% to 75%, according to various authors. 33 patients using transdermal nitroglycerin for more than 7 days were examined and patch tested (nitroglycerin 0.5% aq., 2% pet. and TTS in toto). 5 patients (15%) had adverse reactions. The patch tests were all negative in the 33 patients. Contact dermatitis occurs in many cases, about 15% of the cases with the newly available TTS, and even if patients respect the conditions for using TTS. These contact dermatitides are mainly irritant reactions and do not require transdermal nitroglycerin treatment to be stopped. Nevertheless, since some cases of allergic contact dermatitis have been reported, a contact dermatitis from transdermal nitroglycerin should lead to patch testing.
Pruritus is an unpleasant sensation that provokes an urge to scratch. Many stimuli (notably histamine) are able to induce pruritus. The neural conduction of the itch sensation from the free unmyelinated nerve endings to the central nervous system mainly occurs on unmyelinated C fibres and the anterolateral spinothalamic tract. Pruritus is a common symptom in many skin or systemic diseases, but very little is known about the mechanism of the condition. Treatment evaluation is difficult; many methods do not evaluate the pruritus, but only the scratching, which is a consequence of pruritus. A number of asymptomatic treatments are only partially effective and we know little about their mechanism of action. Antihistamines remain the treatment of first choice for pruritus without known cause, but generally give incomplete relief. Whenever possible it is best to treat the underlying disease.
The medial canthus is a surgical entity. The anatomical features are defined from a dissection of eight orbital regions. The pathways of carcinological invasion and the anatomical barriers are considered. The conclusions are discussed in the light of the data reported in the literature.
Sneddon's syndrome consists of livedo reticularis and cerebral vascular accidents with no evidence of systemic disease responsible for the livedo. The syndrome has been assimilated to a subgroup of systemic lupus erythematosus (SLE) with presence of antibodies directed against phospholipids. Recently, a significant increase in the frequency of cardiac valve diseases has been demonstrated in some SLE patients with livedo reticularis, cerebral vascular accidents and antiphospholipid antibodies. We report the case of a 26-year old woman who had been presenting for 6 years with idiopathic livedo reticularis. Her history was remarkable for the occurrence of 2 cerebral ischaemic accidents at the ages of 23 and 26 years, generalized convulsive seizures at 22 years, and hypertension of pregnancy with 2 miscarriages. Biopsy of the livedo showed normal histological patterns, but electron microscopy detected an obliterating endothelial proliferation and endothelial cells with numerous Weibel-Palade bodies. Laboratory signs of SLE, as well as antiphospholipid antibodies were absent. At the age of 26 years, cardiac abnormalities were heard at auscultation for the first time, and echocardiography showed that they were due to a fairly loose mitral stenosis. According to Burton's criteria our patient had all the typical features of Sneddon's syndrome. The finding of mitral stenosis--an emboligenic cardiopathy that is potentially responsible for cerebral vascular accidents--raises the problem of its relationship with Sneddon's syndrome. The association does not seem to be fortuitous, since our case is very similar to the cases of SLE or antiphospholipid antibody syndrome associated with cardiac valve lesions. However, this case is particular in that 6 years after the onset of the disease there was still no sign of SLE and of antiphospholipid antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)