Schnitzler's syndrome: A broader clinical spectrum
Identifieur interne : 002F12 ( Main/Exploration ); précédent : 002F11; suivant : 002F13Schnitzler's syndrome: A broader clinical spectrum
Auteurs : Susan S. Berdy [États-Unis] ; Kurt J. Bloch [États-Unis]Source :
- The Journal of Allergy and Clinical Immunology [ 0091-6749 ] ; 1991.
English descriptors
- Teeft :
- Acad dermatol, Allergic rhinitis, Allergy, Allergy units, American board, Angioedema, Appl physiol, Arthralgia, Asthma, Binding activity, Biopsy, Bone marrow, Bone pain, Cell volume, Chronic urticaria, Clinical immunology, Cold urticaria, Complement activation, Complement profile, Complement values, Dermatol syphil, Fibrinoid necrosis, Large amount, Lesion, Leukocytosis, Lymph nodes, Lymphadenopathy, Mast cells, Microcytic anemia, Monoclonal immunoglobulins, Nonpruritic, Normal complement values, Other patient, Platelet count, Presenceof, Recurrent fever, Respir, Rheumatoid factor, Several years, Syndrome, Systemic capillary leak syndrome, Systemic lupus erythematosus, Urticaire chronique, Urticaria, Urticarial, Urticarial lesion, Urticarial lesions, Volume number, White blood cells.
Abstract
Abstract: Schnitzler's syndrome is characterized by chronic urticaria, recurrent fever, bone pain, and lymphadenopathy in conjunction with a serum IgM M component in a concentration that is usually <10,000 mg/L. Complement activation and cryoprecipitation do not appear to be involved. We report two additional patients who share many of the characteristics of this entity. These patients differ from patients previously reported because of the markedly elevated IgM M-component concentration in one patient and the severity of anemia in the second patient. An increased frequency of IgG autoantibodies to interleukin-1-α has been reported by other investigators; it has been suggested that an antibody-mediated prolongation of the half-life of interleukin-1-α might account for some of the symptoms and signs of this disorder. However, neither the mediators involved in the induction of nonpruritic urticaria nor the role of the IgM M component has been established.
Url:
DOI: 10.1016/0091-6749(91)90132-8
Affiliations:
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Berdy</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>From the Department of Medicine, Harvard Medical School, Boston, Mass.</wicri:regionArea><wicri:noRegion>Mass.</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>From the Clinical Immunology and Allergy Units, General Medical Services, Massachusetts General Hospital, Boston, Mass.</wicri:regionArea><wicri:noRegion>Mass.</wicri:noRegion></affiliation></author><author><name sortKey="Bloch, Kurt J" sort="Bloch, Kurt J" uniqKey="Bloch K" first="Kurt J." last="Bloch">Kurt J. Bloch</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Reprint requests: Kurt J. Bloch, MD, Chief, Clinical Immunology and Allergy Units, Massachusetts General Hospital, 55 Fruit St., Bulfinch 422, Boston</wicri:cityArea></affiliation><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>From the Department of Medicine, Harvard Medical School, Boston, Mass.</wicri:regionArea><wicri:noRegion>Mass.</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>From the Clinical Immunology and Allergy Units, General Medical Services, Massachusetts General Hospital, Boston, Mass.</wicri:regionArea><wicri:noRegion>Mass.</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">The Journal of Allergy and Clinical Immunology</title><title level="j" type="abbrev">YMAI</title><idno type="ISSN">0091-6749</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">87</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="849">849</biblScope><biblScope unit="page" to="854">854</biblScope></imprint><idno type="ISSN">0091-6749</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0091-6749</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acad dermatol</term><term>Allergic rhinitis</term><term>Allergy</term><term>Allergy units</term><term>American board</term><term>Angioedema</term><term>Appl physiol</term><term>Arthralgia</term><term>Asthma</term><term>Binding activity</term><term>Biopsy</term><term>Bone marrow</term><term>Bone pain</term><term>Cell volume</term><term>Chronic urticaria</term><term>Clinical immunology</term><term>Cold urticaria</term><term>Complement activation</term><term>Complement profile</term><term>Complement values</term><term>Dermatol syphil</term><term>Fibrinoid necrosis</term><term>Large amount</term><term>Lesion</term><term>Leukocytosis</term><term>Lymph nodes</term><term>Lymphadenopathy</term><term>Mast cells</term><term>Microcytic anemia</term><term>Monoclonal immunoglobulins</term><term>Nonpruritic</term><term>Normal complement values</term><term>Other patient</term><term>Platelet count</term><term>Presenceof</term><term>Recurrent fever</term><term>Respir</term><term>Rheumatoid factor</term><term>Several years</term><term>Syndrome</term><term>Systemic capillary leak syndrome</term><term>Systemic lupus erythematosus</term><term>Urticaire chronique</term><term>Urticaria</term><term>Urticarial</term><term>Urticarial lesion</term><term>Urticarial lesions</term><term>Volume number</term><term>White blood cells</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Schnitzler's syndrome is characterized by chronic urticaria, recurrent fever, bone pain, and lymphadenopathy in conjunction with a serum IgM M component in a concentration that is usually <10,000 mg/L. Complement activation and cryoprecipitation do not appear to be involved. We report two additional patients who share many of the characteristics of this entity. These patients differ from patients previously reported because of the markedly elevated IgM M-component concentration in one patient and the severity of anemia in the second patient. An increased frequency of IgG autoantibodies to interleukin-1-α has been reported by other investigators; it has been suggested that an antibody-mediated prolongation of the half-life of interleukin-1-α might account for some of the symptoms and signs of this disorder. However, neither the mediators involved in the induction of nonpruritic urticaria nor the role of the IgM M component has been established.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><country name="États-Unis"><noRegion><name sortKey="Berdy, Susan S" sort="Berdy, Susan S" uniqKey="Berdy S" first="Susan S." last="Berdy">Susan S. Berdy</name></noRegion><name sortKey="Berdy, Susan S" sort="Berdy, Susan S" uniqKey="Berdy S" first="Susan S." last="Berdy">Susan S. Berdy</name><name sortKey="Bloch, Kurt J" sort="Bloch, Kurt J" uniqKey="Bloch K" first="Kurt J." last="Bloch">Kurt J. Bloch</name><name sortKey="Bloch, Kurt J" sort="Bloch, Kurt J" uniqKey="Bloch K" first="Kurt J." last="Bloch">Kurt J. Bloch</name><name sortKey="Bloch, Kurt J" sort="Bloch, Kurt J" uniqKey="Bloch K" first="Kurt J." last="Bloch">Kurt J. 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