Mona C. Maryjowski

Northwestern University

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Lauren M. Pachman

Lurie Children's Hospital

Jan M. Friedman

University of British Columbia

James G. Scott

University of Queensland

Virgil Hanson

Children's Hospital of Los Angeles

Carlos M. Arroyave

Universidad de Antioquia

Charles H. Spencer

University of Mississippi Medical Center

R E Partridge

Brigham and Women's Hospital

Caren M. Gundberg

Yale University

Donita B. Sullivan

University of Michigan–Ann Arbor

Patricia Gerber

University of British Columbia

Cooperative Institutions

Lurie Children's Hospital

Northwestern University

Northwestern Memorial Hospital

University of Cincinnati

Memorial Hospital

University of Texas Health Science Center at Dallas

Boston Children's Hospital

University of Michigan–Ann Arbor

University of British Columbia

British Columbia Children's Hospital

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953 IMMUNOGENETICS OF JUVENILE DERMATOMYOSITIS (JDMS), A COLLABORATIVE STUDY

Pediatric Research (1981)

Lauren M. Pachman Mona C. Maryjowski Jan M. Friedman Olga Jonasson Ruta Radvany

Juvenile Dermatomyositis

Ophthalmoparesis

Raji cell

10.1203/00006450-198104001-00978

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Citations (2)

GAMMA‐carboxyglutamate excretion and calcinosis in juvenile dermatomyositis

Arthritis & Rheumatism (1982)

Jane B. Lian Lauren M. Pachman Caren M. Gundberg R E Partridge Mona C. Maryjowski

Abstract Proteins containing gamma‐carboxyglutamic acid (Gla) are present in subcutaneous calcifications of adults with dermatomyositis or scleroderma. Sixteen children with juvenile dermatomyositis, including 7 with subcutaneous calcifications, were studied to determine if abnormal synthesis or turnover of Gla‐containing proteins occurred. All study children had increased excretion of the amino acid that was greater than that of age‐and sex‐matched controls. Patients who had juvenile dermatomyositis with calcifications had a 3‐fold increase in Gla excretion, and those without calcinosis had a 2‐fold increase. Five other children with various connective tissue disorders and subcutaneous calcification had 2‐fold increased Gla excretion. Decreased excretion of this amino acid was associated with salicylate therapy (80 mg/kg/24 hours). The data suggest an abnormal turnover of Gla‐containing proteins in juvenile dermatomyositis. Metabolism of these proteins may be involved in the pathophysiology of soft‐tissue calcification in children.

Juvenile Dermatomyositis

10.1002/art.1780250910

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Citations (50)

Juvenile Dermatomyositis and Polymyositis

Clinics in Rheumatic Diseases (1984)

Lauren M. Pachman Mona C. Maryjowski

Juvenile Dermatomyositis

Pathogenesis

Etiology

10.1016/s0307-742x(21)00486-0

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Citations (27)

ACTIVE JUVENILE DERMATOMYOSITIS (JDMS) IS ASSOCIATED WITH COMPLEMENT AND COAGULATION ACTIVATION, AND INCREASED TITERS TO ANTINUCLEAR (ANA) AND COXSACKIE B VIRAL (COX-B) ANTIGENS

Pediatric Research (1984)

Lauren M. Pachman Mary Christensen James G. Scott Carlos M. Arroyave Jan M. Friedman

10.1203/00006450-198404001-01014

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Evidence for intravascular coagulation in systemic onset, but not polyarticular, juvenile rheumatoid arthritis

Arthritis & Rheumatism (1985)

James G. Scott Patricia Gerber Mona C. Maryjowski Lauren M. Pachman

After observing a child with systemic onset juvenile rheumatoid arthritis (S-JRA) who developed purpura fulminans in association with disseminated intravascular coagulation, with subsequent gangrene and autoamputation, we undertook a prospective study of coagulation parameters in children with JRA. Ten consecutive children with S-JRA, 10 children with rheumatoid factor-negative, polyarticular juvenile rheumatoid arthritis (P-JRA), and 10 age- and sex-matched controls were studied. Routine coagulation screening tests were performed, as were tests for plasma fibrinopeptide A (a sensitive measure of intravascular thrombin generation), factor VIII-related antigen (an endothelial cell protein), and platelet factor 4 (a platelet-secreted protein). Our studies suggest that activation of intravascular coagulation is common in systemic onset JRA, but not in rheumatoid factor-negative, polyarticular disease. The coagulopathy may cause severe morbidity. In addition, marked elevations of plasma factor VIII-related antigen suggest perturbation of endothelial cells and vascular involvement in S-JRA, but not in P-JRA. Normal ranges of platelet factor 4 indicate that intravascular platelet consumption does not occur in either type of JRA, despite the thrombocytosis common in both.

Juvenile rheumatoid arthritis

Thrombocytosis

Purpura fulminans

Rheumatoid factor

10.1002/art.1780280304

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Citations (37)