PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PEMPHIGUS ERYTHEMATOSUS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2002

[Alpha-1-antitrypsin deficiency. Role in skin disorders].

Alpha1 antitrypsin (AAT) deficiency is an autosomic codominant inherited disorder characterized by inefficient or non-functional serum AAT. The principal clinical manifestations are panlobular emphysema and cirrhoses. Among cutaneous aspects, about 30 cases of panniculitis have been reported in the literature, likewise rare clinical cases: pemphigus herpetiformis, Muir Torre syndrome, urticaria and angioedema, cutis laxa and Marshall syndrome, lupus erythematosus, psoriasis, vasculitis. Probably because of it's high frequency, numerous others diseases have been reported described in association. Acting on several factors of inflammation, AAT deficiency seems product or modify the expression of some, notably cutaneous diseases.

Humans↗
PubMed1997

The presence of anti-basement membrane zone antibodies in the sera of patients with non-bullous lupus erythematosus.

We performed indirect immunofluorescence (IF) studies using 1 mol/l sodium chloride split skin to determine whether or not a positive IF is specific to patients with bullous lupus erythematosus (LE). We examined the sera from 21 patients with systemic LE (SLE), three of which were obtained from two SLE patients and one subacute cutaneous LE (SCLE) patient with bullous eruptions. As a comparison, we also studied the sera from patients with discoid LE (DLE, n = 7), SCLE (n = 1), systemic sclerosis (SSc, n = 20), bullous pemphigoid (n = 2) and normal individuals (n = 10). Sera from 16 SLE, four DLE and two SSc revealed a linear deposition of IgG isotype antibody at the epidermal side and/or the dermal side on indirect IF of split skin. The sera from three patients with bullous eruption and from 12 patients of SLE, SCLE, DLE without bullous eruption or SSc were further analysed by immunoblotting using five defined antigens, i.e. dermal extract, epidermal extract, three fusion proteins of 230 kDa bullous pemphigoid antigen (BPAG). 180 kDa BPAG, and human epidermolysis bullosa acquisita (EBA) antigen. Two SLE sera as well as one of the SCLE and the DLE serum reacted with 230 kDa BPAG in epidermal extract, and one of the SCLE and the DLE serum also reacted with the fusion protein of 180 kDa BPAG. No serum reacted with the dermal extract or the fusion protein of 230 kDa BPAG or EBA antigen. There was no consistent correlation between split-skin IF results and immunoblotting results. These results may suggest that even non-bullous LE patients often have autoantibodies to the basement membrane zone antigens, most of which are less pathogenic. Although we rarely examine the sera from non-bullous LE patients, we should keep this phenomenon in mind to avoid overestimating the results of split-skin test and immunoblotting.

Adult↗
PubMed1985

Dermatologic diseases of the nail unit other than psoriasis and lichen planus.

Diseases in which involvement of the nails may be helpful in the diagnosis of dermatologic disease elsewhere include psoriasis, lichen planus, Darier's disease, alopecia areata and totalis, keratotic scabies, scleroderma, and lupus erythematosus and dermatomyositis. Dermatologic diseases in which involvement of the nail commonly occurs but is relatively nonspecific and not diagnostic include dermatitis, lichen striatus, parakeratosis pustulosa, pityriasis rubra pilaris, acrokeratosis paraneoplastica, pemphigus vulgaris, epidermolysis bullosa, porokeratosis of Mibelli, and acanthosis nigricans. These entities are described and treatments summarized as appropriate.

Acanthosis Nigricans↗
PubMed1997

Mucocutaneous features of autoimmune blistering diseases.

This review will describe adult onset mucocutaneous/autoimmune diseases that involve defects in cell-to-cell, cell-to-matrix, or cell-to-basement membrane adhesion. Included in this group are pemphigus, cicatricial pemphigoid, linear IgA bullous dermatosis, epidermolysis bullosa acquisita, and bullous systemic lupus erythematous. Detection and treatment of blistering disorders that manifest early in the oral cavity may prevent widespread involvement of skin. During the past few years, targets of autoantibodies have been clarified and new targets have been identified, allowing better understanding of the pathophysiology involved in these diseases. New information about more effective regimens with fewer side effects has also been obtained, presenting new treatment options. Clinical manifestations and management of these disorders will be described as well as histopathologic, ultrastructural, and immunopathologic studies that distinguish each disorder and facilitate diagnosis and treatment.

Adult↗
PubMed1998

The pathophysiological significance of nondesmoglein targets of pemphigus autoimmunity. Development of antibodies against keratinocyte cholinergic receptors in patients with pemphigus vulgaris and pemphigus foliaceus.

OBJECTIVES: To determine whether nondesmoglein (non-Dsg) autoantibodies are pathogenic and whether they recognize keratinocyte cholinergic receptors that control cell adhesion because antikeratinocyte autoimmunity in patients with pemphigus vulgaris is not limited to the development of autoantibodies to Dsg. DESIGN: To determine whether non-DSg autoantibodies are pathogenic, we sought to induce pemphigus in genetically engineered neonatal mice lacking Dsg 3 using pemphigus vulgaris IgGs that did not cross-react with Dsg 1. To determine whether pemphigus autoimmunity involves keratinocyte cholinergic receptors, the latter were separated from cell membranes of human keratinocytes, tagged with the covalent label [3H]propylbenzilylcholine mustard, and used as an antigen in a radioimmunoprecipitation assay of 34 pemphigus vulgaris and 6 pemphigus foliaceus serum samples. SETTING: The dermatologic clinics of the University of Minnesota, Minneapolis; the Mayo Clinic, Rochester, Minn; and the University of California-Davis Medical Center, Sacramento. PATIENTS: Serum samples were collected from 34 patients with pemphigus vulgaris and 6 patients with pemphigus foliaceus (aged 31-89 years) and from 7 age-similar patients of both sexes with nonpemphigus blistering or the following immune-mediated conditions: pemphigoid gestation, bullous drug eruption, lupus erythematosus, erythema nodosum, urticaria, acute contact dermatitis, and skin ulcers. MAIN OUTCOME MEASURES: Clinical, laboratory, and histopathologic findings. RESULTS: Extensive skin blistering accompanied by the Nikolsky sign and suprabasilar acantholysis was induced in the Dsg3null mice that received pemphigus, but not normal human IgGs. In the radioimmunoprecipitation assays for reactivity with cholinergic receptors, the mean radioactivity precipitated by pemphigus serum samples significantly exceeded both normal- and disease-control levels (P = .001-.02). The mean individual levels of radioactivity precipitated by 34 pemphigus vulgaris and pemphigus foliaceus serum samples (85%) exceeded control values by a mean of approximately 2.6 times. CONCLUSIONS: Autoantibodies to keratinocyte cell-surface molecules other than Dsg 1 and Dsg 3 can induce clinical features of pemphigus vulgaris. Patients with pemphigus vulgaris and those with pemphigus foliaceus develop IgG antibodies that precipitate radiolabeled cholinergic receptors. Because these receptors control keratinocyte adhesion and motility, their inactivation by autoantibodies may elicit intracellular signals that cause disassembly of desmosomes, leading to acantholysis and blistering.

Acantholysis↗
PubMed1986

Treatment of common orofacial conditions.

The conditions discussed in this article are those most likely to cause a patient to seek emergency care, primarily for pain. All the characteristics given for the conditions to aid in the diagnosis do not necessarily need to be present and other characteristics not mentioned may in fact be present. A complete differential diagnosis, especially of more obscure lesions, was also not attempted. An attempt was made to provide the practitioner with enough information to develop a working diagnosis from which to alleviate the patient's discomfort. A definitive diagnosis may not be available in an emergency setting. However, it must be emphasized that the final responsibility of the dentist is to make a definitive diagnosis at a later time if one cannot be made when emergency treatment is sought. Alleviating pain without dealing with the underlying cause may be more detrimental to the patient's health in the long run, as palliative therapy may mask a more severe condition.

Antifungal Agents↗