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Biomedical subjects

J Revuz

Publications and source records attributed to J Revuz.

At least 325 records · Page 18Linked to original sources
PubMed1985

Lymphopenia and abnormal balance of T-lymphocyte subpopulations in toxic epidermal necrolysis.

A lymphopenia (peripheral-blood-lymphocyte count less than 1,000/mm3) was observed in seven out of ten patients with toxic epidermal necrolysis (TEN). The enumeration of T-lymphocyte subsets with monoclonal antibodies showed a decreased number of pan T-lymphocytes (OKT3-positive), which was related to a profound depletion of OKT4-positive cells. In contrast, OKT8-positive cell counts were not significantly changed. This abnormal balance of T-lymphocytes was linked to the acute phase of the disease and was not found after recovery. The pathogenetic mechanisms of such T-lymphocyte abnormalities in TEN remain unclear.

Adolescent↗
PubMed1985

Involvement of macrophages in the pathology of toxic epidermal necrolysis.

In toxic epidermal necrolysis (TEN), as in the 'epidermal type' of erythema multiforme, the necrotic epidermis is infiltrated with mononuclear cells. We studied the epidermal infiltrate in seven cases of TEN. About half the cells obtained from pieces of cleaved epidermis dissociated by trypsin were non-epithelial. On cytologic analysis, 80% of these foreign cells exhibited markers of macrophages, 15% were granulocytes and only 5% were lymphocytes (almost exclusively OKT8 T lymphocytes). Semi-thin sections of early prenecrotic lesions showed exocytosis of mononuclear cells within the epidermis with features of satellite cell necrosis and formation of colloid bodies. Almost all these mononuclear cells were macrophages as evidenced by endogenous peroxidase-positive granules. These findings suggest that some kind of macrophage-mediated cytotoxicity may play a role in the necrosis of epidermal cells during TEN.

Adolescent↗
PubMed1985

Lymphocyte transformation test in drug-induced toxic epidermal necrolysis.

Lymphocyte transformation tests (LTT) to drugs remain widely used in drug reactions, despite controversies about their real usefulness. We tested the lymphocytes of 12 patients recovering from a drug-induced Toxic epidermal necrolysis (TEN). There was no difference between the amounts of thymidine incorporated when patients' lymphocytes were cultivated with culprit or innocent drugs. In both situations the lymphocytes from patients reacted like the lymphocytes from controls cultivated with the same panel of drugs. These negative results do not exclude that a hypersensitivity reaction may play a role in the physiopathology of TEN. Anyhow, they clearly indicate that testing lymphocyte transformation to drugs has no practical value in the diagnosis of TEN.

Adolescent↗
PubMed1985

[Ocular sequelae and sicca syndrome following Lyell's syndrome].

The mucous lesions are customary in toxic epidermal necrolysis. The acute ocular lesions have led to definitive sequelae. 22 out of 32 patients surviving to a Lyell's syndrome lend themselves to an ophthalmological supervision. 13 of these 22 patients (59 p. 100) presented a sicca syndrome with a decrease of the lacrimal secretion (12 cases) and/or salivary secretion (8 cases). The sicca syndrome appeared sometimes from the beginning of the acute phase of the Lyell's syndrome or more often a few weeks later. This decrease of the lacrimal flux went along with objective corneal lesions among 11 patients, and 6 of them had a change of the visual function. A biopsy of the accessory salivary glands was performed on 7 of these patients having a reduction of the salivary flux. 5 of these 7 biopsies showed lymphocytic infiltrates giving in 2 cases a nodular aspect, grade III of Chisholm's classification, held to be pathognomonic of Sjögren syndrome. The 13 patients having presented a sicca syndrome differed from the other 9 patients (without sicca syndrome) by a higher severity of their Lyell's syndrome and by a higher age. None of our patients with dry syndrome had antinuclear antibody detected by immunofluorescence on sections of rat's livers. Sicca syndromes with sometimes lymphocytic infiltrate similar to those of Sjögren's syndrome were occasionally imputed to drug reactions. The occurrence of "Sjögren like's syndrome" after a toxic epidermal necrolysis suggests the intervening of autoimmune phenomena in the pathogenesis of this toxic epidermal necrolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Lyell's syndrome and ectodermosis pluriorificialis during treatment with oxicams: 11 cases].

Piroxicam (Feldene) and isoxicam (Vectren) form a part of a new family of non-steroid anti-inflammatory drugs (NSAID) highly used in France: the oxicams. The cutaneous accidents of all kinds are frequent, estimated from 1 to 3 p. 100 of the patients with piroxicam (16, 20). In addition to the maculo-papular eruptions, there has been reported: lichenoid eruption (21), erythroderma (7), purpuric vasculitis (1, 10, 21), pemphigus (12, 14), bullous dermatosis difficult to classify (15), erythema multiforme and Stevens-Johnson's syndrome (3, 6, 7, 9, 13, 21, 23) and at last many photosensitization accidents (3, 8, 11, 19, 20, 21). We report 11 observations of Lyell's syndrome (8 cases) or Stevens-Johnson's syndrome (3 cases) occurred during treatments by isoxicam or piroxicam. Eight women and 3 men aged from 35 to 80 years begin a Lyell's syndrome or a Stevens-Johnson's syndrome after 9 to 45 days (at an average of 16 days) of a treatment by isoxicam (6 cases) or piroxicam (5 cases). Five patients attacked by a Lyell's syndrome are intubated and ventilated and 2 patients die of a septic shock at the ninth and the thirteenth day of evolution: the duration of hospitalization is from 11 days to 3 and a half months for the Lyell's syndromes survivors and from 7 to 19 days in the cases of Stevens-Johnson's syndrome: 7 surviving patients have ocular sequelae with in 2 cases a complete or partial blindness. A slight hepatic cytolysis is observed 5 times and a neutropenia mainly as a lymphopenia 4 times. In 2 observations, the CMV serology is positive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Silent lupus nephritis among patients with discoid lupus erythematosus.

A kidney biopsy was performed in 7 hypocomplementemic discoid lupus erythematosus patients despite the absence of overt renal involvement. Five patients had glomerular immune deposits and 2 patients with disseminated discoid lupus erythematosus exhibited definite proliferative glomerulonephritis. Those findings show that silent lupus nephritis may be encountered in discoid as well as in systemic lupus erythematosus, providing additional evidence supporting the unity of the disease. We suggest that hypocomplementemic patients with discoid lupus erythematosus must be carefully screened for renal disease by periodic urinalysis examinations.

Complement C3↗
PubMed1984

[Drug eruptions caused by noncorticoid anti-inflammatory agents].

Non-steroidal anti-inflammatory drugs (NSAI) may elicit various kinds of cutaneous side effects. The commonest ones are non-specific erythematous eruptions, sometimes with a phototoxic distribution, and urticaria. Vasculitis and severe bullous eruptions (Stevens-Johnson's syndrome and Toxic Epidermal Necrolysis) are rare but may have severe outcomes. The overall incidence of cutaneous reactions is about the same for all NSAI, 1 to 3 p. 100, during the clinical studies performed before marketing the drug, but this increases afterwards (up to 45 p. 100 for Benoxaprofen). Drugs with long half-lives may carry a higher risk for severe cutaneous reactions. NSAI are now the main cause of drug induced TEN. Urticarial reactions seem related to pharmacological phenomena while the pathogenic events leading to other kinds of skin reactions remain unknown. An hypersensitivity reaction is postulated. The therapeutic value of corticosteroids for the severe cutaneous side effects of drugs is still controversial.

Angioedema↗
PubMed1984

[Acquired immunodeficiency syndrome, Kaposi's disease and cerebral toxoplasmosis in a young man. Review of the literature apropos of a case].

We report a new case of acquired immune-deficiency syndrome (AIDS) in a 43 year-old white homosexual man, characterized by the association of disseminated cutaneo-mucous Kaposi's sarcoma and cerebral toxoplasmosis. This man had Kaposi's sarcoma for about 10 years but evolution became quickly extensive in July 1981. Chlorambucil was prescribed at that time and was the cause of a pancytopenia. Death occurred in July 1982 due to a cerebral mass identified as toxoplasmosis on a left temporal biopsy. This observation is typical of AIDS, a new syndrome which suddenly developed in the last 2 years in the United States in homosexual men, Haitians and hemophiliacs, and is characterized by disseminated Kaposi's sarcoma and/or opportunistic infections, with a very high mortality rate. Severe toxoplasmosis of CNS has been reported in AIDS and appears to result from defects in cellular immunity which permit recrudescence of latent infection. Cerebral biopsy is necessary for the diagnosis of cerebral toxoplasmosis as seroconversion occurs infrequently in immuno-suppressed hosts. AIDS appeared in Western Europe in 1982. Most of the cases were reported in France, Denmark, Belgium and Great Britain. These cases differ from reported cases in the USA: fewer drug or poppers users, fewer homosexual men, an important number of people having lived or travelled in the Kaposi's endemic area (Mediterranean basin and Central Africa). The immunological profile of patients presenting AIDS in Europe doesn't seem to differ from the american profile: serious cellular immunodeficiency and marked increase in the suppressor/cytotoxic cell population. As in the United States, one may suspect, among several hypotheses, that it is caused by one or several transmissible agents now present in France. The nature of these agents, transmissible by sexual contacts and blood, is not yet known: the role of the CMV is now less probable and most of the studies look for the role of other factors such as the HTLV.

Acquired Immunodeficiency Syndrome↗
PubMed1984

[Contact dermatitis from hexamidine].

Twenty patients with contact dermatitis to hexamidine, a commonly used antiseptic solution are reported. They have been collected during a 7 months period, thus suggesting that this contact allergy is not infrequent. Hydroalcoholic solution applied on epidermless skin is most frequently responsible for the contact dermatitis. Clinical features are very peculiar with papular semi-spheric and papulo-vesicular lesions being more frequently seen than classical vesicular eczema lesions. Due to this peculiar aspect, contact dermatitis to hexamidine is frequently misdiagnosed. The delay between onset and diagnosis has been sometimes longer than one year. It is four months as a mean. Pathologic aspect of these lesions is unusual too: dermal vasculitis either lymphocytic or with pycnotic polymorphonuclear is the most frequent aspect (14 out of 23 histological sections). Epidermal spongiosis is infrequent (5 cases). Contact dermatitis has usually a long standing evolution despite removal of the allergen and topical cortico-steroid treatment. Patch-test to hexamidine are frequently followed by a worsening of cutaneous lesions. One case of anaphylaxis following patch-testing has been reported. Clinical and pathological features of this contact dermatitis, suggests that humoral immune mechanisms play a key-role in its pathogenesis.

Anti-Infective Agents, Local↗
PubMed1984

[Melanoma and dysplastic nevus after 8 years of topical Caryolysine].

A 48-year-old woman with poikiloderma atrophicans vasculare was treated with topical mechlorethamine, applied three times weekly, for eight years. After five years treatment she developed nine melanocytic naevi on covered skin. The naevi spread for the next three years and a surgical excision was performed. Pathological examination revealed one level II SSM, one level I SSM and seven junctional naevi with focal dysplasia or melanocytic hyperplasia. The development of melanoma and dysplastic naevi after topical mechlorethamine has not been previously reported. However it seems likely that mechlorethamine was the causative agent. As for the mechlorethamine's imputability in this case, we have used a method combining intrinsic identification of adverse drug responsibility's score, based on the clinical case and on extrinsic identification based on literature evaluation. We suggest that mechlorethamine could act as UV light.

Administration, Topical↗