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Biomedical subjects

G Lorette

Publications and source records attributed to G Lorette.

At least 91 records · Page 5Linked to original sources

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

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

[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

[Cicatricial pemphigoid disclosed by superficial desquamative gingivitis. Clinical and immuno-electron microscopic study of a case].

Six months before consulting, a 71-year old man developed buccal and genital erosions which gradually became worse. Physical examination showed signs of superficial desquamative gingivitis, wide erosions on the bony palate, erythemato-erosive balanoposthitis and 7 bullae or skin erosions on the upper part of the back. At histopathological examination of a cutaneous bulla there was dermoepidermal cleavage and an inflammatory infiltrate without eosinophils. At direct immunofluorescence, linear deposits of IgG and C3 were present along the basement membrane. A search for anti-skin autoantibodies was negative at indirect immunofluorescence but positive at immunoblotting (240 Kd band). The cicatricial pemphigoid was treated with dapsone alone in doses of 100 mg/day. Treatment was continued for 6 months, resulting in complete cure of the mucosal and cutaneous lesions. An immunoelectromicroscopic study, performed according to the technique described by Prost et al., on a fragment of skin from around the bullae, showed deposits of granular IgG in the lamina lucida and the lamina densa and deposits of C3 in the lamina densa. This case of cicatricial pemphigoid exhibited 3 features which are not usually found in bullous pemphigoid. Clinically, the buccal lesions were located on the gums and on the hard palate, i.e. where the mucosa adheres to the underlying bone through the periosteum. This location is habitual in cicatricial pemphigoid and differs from that of the bullous pemphigoid lesions which affect the free mucosa lining the cheeks and the soft palate. Treatment with dapsone was dramatically successful in our patient whose lesions disappeared in 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Cutaneous cryptococcosis resembling molluscum contagiosum: a first manifestation of AIDS.

A 30-year-old homosexual man developed multiple skin umbilicated lesions resembling molluscum contagiosum. Initially the lesions were on his face but they rapidly spread. Histopathology and mycologic cultures of a skin biopsy revealed cryptococcus neoformans which was also identified in cerebrospinal fluid and in bronchoalveolar washings. The patient had fever, weight loss, generalized lymph node enlargement, depletion of the T helper subpopulation and positive HIV-1 serology. During treatment with flucytosine and amphotericin B, the skin lesions regressed in 3 months (cryptococcus neoformans disappeared in the cerebrospinal fluid and skin within one and five weeks, respectively). Our case demonstrates that molluscum contagiosum-like skin manifestations may be caused by cryptococcal infections. So it is necessary to perform skin biopsy in HIV seropositive patients with skin lesions resembling molluscum contagiosum, to diagnose mycotic infections, and especially cryptococcosis. Cutaneous cryptococcosis was, in this case, the first symptom of AIDS.

Acquired Immunodeficiency Syndrome