PubMed Health⌕ Search

Biomedical subjects

G Lorette

Publications and source records attributed to G Lorette.

At least 127 records · Page 7Linked to original sources
PubMed1991

Suction blisters technique in amikacin diffusion through interstitial fluid in cystic fibrosis.

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.

Amikacin↗
PubMed1990

Familial occurrence of KID (keratitis, ichthyosis, deafness) syndrome. Case reports of a mother and daughter.

Keratitis, ichthyosis, and deafness (KID) syndrome in a mother and her daughter is reported. Both patients showed the typical cutaneous abnormality of papillomatous hyperkeratosis, which gave the skin a grainy, rugose, spiculated appearance, together with keratitis with corneal neovascularization and a neurosensory hearing defect. Treatment with etretinate did not benefit the daughter. The mother had marked keratitis with progressive corneal opacification that required repeated bilateral corneal grafts, which were unsuccessful. This is the second report of hereditary transmission of this disorder. An autosomal dominant mode of inheritance is probable.

Adult↗
PubMed1990

Iododerma and acute respiratory distress with leucocytoclastic vasculitis following the intravenous injection of contrast medium.

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.

Acute Disease↗
PubMed1990

Pruritus. Current concepts in pathogenesis and treatment.

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.

Antipruritics↗
PubMed1990

[Livedo reticularis, cerebrovascular disorders and mitral disease: a new cause of Sneddon's syndrome?].

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)

Adult↗