Program Chairmen and Editors:
Gary S. Hoffman, MD, and John H. Stone, MD, MPH

Contents

I. PATHOGENESIS

A. Immune Predisposition and Infectious Etiology of Systemic Vasculitis
Moderators: Coen Stegeman and Herbert Virgin

Keynote Presentation
Host and viral genes that control herpesvirus vasculitis
Herbert W. Virgin IV

Plenary Session Abstracts (1-3)
1-090. Induction of pauci-immune necrotizing and crescentic glomerulonephritis (NCGN) by intravenous administration of anti-myeloperoxidase (anti-MPO) antibodies to recombinase activating gene-2 deficient (RAG-2 -/-) mice
J.C. Jennette, H. Xiao, P. Heeringa, Z. Liu, P. Hu, M. Zhao, Y. Aratani, R.J. Falk

2-091. Induction of necrotizing and crescentic glomerulonephritis (NCGN) and small-vessel vasculitis (SVV) by adoptive transfer of anti-myeloperoxidase (anti-MPO) lymphocytes into recombinase activating gene-2 deficient (RAG-2 -/-) mice
H. Xiao, P. Heeringa, Z. Liu, P. Hu, M. Zhao, Y. Aratani, R.J. Falk, J.C. Jennette

3-049. Contribution of activated neurotrophils and MPO-ANCA to the development of crescentic glomerulonephritis in SCG/KJ mice
A. Ishida-Okawara, T. Ito-Ihara, T. Ono, E. Muso, K. Saiga, K. Nemoto, K. Suzuki

Keynote Presentations
Known causes of vasculitis in man
Stanley J. Naides

HCV and cryoglobulinemic vasculitis
Clodoveo Ferri, A.L. Zignego, D. Giuggioli, M. Sebastiani, M. Cazzato, A. Antonelli, L. La Civita, P. Fadda, G. Longombardo, and S. Pileri

Infections in primary vasculitides
Jan W. Cohen Tervaert

Plenary session Abstracts (4-5)
4-093. Staphylococcal toxic-shock-syndrome-toxin-1 (TSST-1) is a risk factor for disease relapse in Wegener's granulomatosis
E.R. Popa, B. van der Meer, J. Arends, W.M. Manson, N.A. Bos, C.G.M. Kallenberg, J.W. Cohen Tervaert, C.A. Stegeman

5-104.Chlamydia pneumoniae and giant-cell arteritis: Failure to detect Chlamydia pneumoniae in temporal artery biopsies by polymerase chain reaction
M.J. Regan, B.J. Wood, Y.-H. Hsieh, M.L. Theodore, T.C. Quinn, D.B. Hellmann, W.R. Green, C.A. Gaydos, J.H. Stone

B. Patterns of Injury: Implications for Pathogenesis
Moderators: Loïc Guillevin and Cornelia Weyand

Keynote Presentations
Pathogenic mechanisms in giant cell arteritis
Cornelia M. Weyand and Jörg J. Goronzy

Implications for pathogenesis of patterns of injury in small- and medium-sized-vessel vasculitis
J. Charles Jennette

Plenary Session Abstracts (6-7)

6-037. Superantigenic activation of T lymphocytes and endothelial cells: A mechanism for superantigen-induced vasculitis
P.A. Brogan, V. Shah, N. Klein, M.J. Dillon

7-108. Analysis of autoantibody repertoires in small and medium sized vessel vasculitis: Evidence for disease-specific perturbations in classic polyarteritis nodosa (PAN), micropolyangiitis (MPA), Churg-Strauss syndrome (CSS) and Wegener's granulomatosis (WG)
Y. Chanseaud, L. Guillevin, M. Kambouchner, M.C. Boissier, L. Mouthon

Keynote Presentation
Granuloma formation, implications for the pathogenesis of vasculitis
Michael C. Sneller

Plenary Session Abstracts (8-9)
8-052. Chemokine receptor expression on CD4+ and CD8+ memory T-cells and in granulomas in Wegener's granulomatosis
P. Lamprecht, A. Erdmann, A. Mueller, E. Csernok, H. Bruehl, W.L. Gross, M. Mack

9-016. Genetic resistance to Wegener's granulomatosis—a role for CCR5 in patients without antineutrophil cytoplasmic antibodies
Y. Zhou, D. Huang, C. Farver, G. Hoffman

Keynote Presentation
Endothelial cell biology, perivascular inflammation, and vasculitis
Maria C. Cid

Plenary Session Abstract (10)
10-023. Novel effects of inflammatory cell proteases on vascular endothelia
G.A. Preston, W.F. Pendergraft, J.J. Yang, J.C. Jennette, R.J. Falk

C. Possible Role of ANCA and AECA in Select Forms of Systemic Vasculitis
Moderators: Wolfgang Gross and Caroline Savage

Keynote Presentation
Understanding the pathogenesis of ANCA: Where are we today?
Gloria A. Preston, Jia Jin Yang, Hong Xiao, and Ronald J. Falk

Plenary Session Abstracts (11-12)
11-027. TNF-alpha accelerated apoptosis abrogates ANCA-mediated neutrophil respiratory burst by a caspase-dependent mechanism
R. Kettritz, J. Scheumann, Y. Xu, F.C. Luft, H. Haller

12-071. Membrane expression of neurotrophil proteinase 3 (PR3) is associated with relapse in PR3-ANCA related vasculitis
A.A. Rarok, C.A. Stegeman, P.C. Limburg, C.G.M. Kallenberg

Keynote Presentation
ANCA subsets: Influence on disease phenotype
Ulrich Specks

Plenary Session Abstract (13)
13-096. Sequential epitope mapping of the myeloperoxidase antigen
D.M. Wynn, J.A. James

Keynote Presentation
Genetics of ANCA-associated vasculitis
Cees G.M. Kallenberg, Agnieszka Rarok, and Coen A. Stegeman

Plenary Session Abstracts (14-15)
14-028. Membrane expression of proteinase 3 is genetically controlled
A. Schreiber, A. Bushjahn, F.C. Luft, R. Kettritz

15-015. Genetic polymorphisms in TNF, IL-1, IL-6 and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) in Wegener's granulomatosis (WG)
Y. Zhou, D. Huang, G.S. Hoffman

Keynote Presentation
Classification of anti-endothelial cell antibodies into antibodies against microvascular and macrovascular endothelial cells: The pathogenic and diagnostic implications
Yehuda Shoenfeld

Plenary Session Abstract (16)
16-029. HMG-COA reductase inhibitors decrease ANCA-mediated activation of human neutrophils
M. Choi, S. Rolle M. Rane, H. Haller, F.C. Luft, R. Kettritz

II. EPIDEMIOLOGY OF VASCULITIS
Moderators: Miguel Gonzalez-Gay and Gene Hunder

Keynote Presentations
Kawasaki disease: Etiology, pathogenesis, and treatment
Karyl S. Barron

Epidemiology of giant-cell arteritis
Gene G. Hunder

Plenary Session Abstract (17)
17-102. Ethnic disparity in the incidence of temporal arteritis: A 32-year experience at an urban medical center
M.J. Regan, W.R. Green, J.H. Stone

Keynote Presentations
Epidemiology of Wegener's granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome
Richard A. Watts, David G.I. Scott, and Suzanne E. Lane

Epidemiology of Henoch-Schönlein purpura
Frank Saulsbury

Plenary Session Abstract (18)
18-010. Henoch-Schönlein purpura and cutaneous leukocytoclastic angiitis exhibit different HLA-DRB1 associations
M.M. Amoli, W. Thomson, A.H. Hajeer, M.C. Calviño, C. Garcia-Porrua, W.E.R. Ollier, M.A. Gonzalez-Gay

III. DIAGNOSTIC MODALITIES, SURROGATE MARKERS OF DISEASE ACTIVITY, AND TOOLS FOR OUTCOME MEASUREMENTS
Moderators: Carol Langford and Raashid Luqmani

Keynote Presentations
Cytokines in giant-cell arteritis
Jörg J. Goronzy and Cornelia M. Weyand

Utility of imaging studies in assessment of vascular inflammation
Daniël Blockmans

Measuring disease activity and outcomes in clinical studies
Raashid Luqmani

Plenary Session Abstracts (19-21)
19-022. Increases of PR3 and MPO gene transcription in circulating leukocyte of ANCA-associated disease correlate with disease activity
J.J. Yang, G.A. Preston, D.A. Alcorta, B.D. Phillips, R.P. Thomas, S.L. Hogan, J.C. Jennette, R.J. Falk

20-119. Cardiac involvement in Wegener's granulomatosis: Echocardiographic features and clinical outcomes
G.H.M. Oliveira, J.B. Seward, U. Specks

21-041. Endothelial microparticles: Just blood "dust," or a "must" for the diagnosis and monitoring of disease activity in childhood vasculitides?
P.A. Brogan, V. Shah, C. Brachet, N. Klein, M.J. Dillon

Keynote Presentation
Diagnostic strategies in vasculitis affecting the central nervous system
Leonard H. Calabrese

Plenary Session Abstracts (22-23)
Moderator: Leonard Calabrese

22-082. Circulating endothelial cells and vasculitis
A. Woywodt, F. Streiber, K. de Groot, H. Haller, M. Haubitz

23-051. Diffuse endothelial dysfunction is a common feature of SNV
P.A. Bacon, D.M. Carruthers, A.D. Diler, K. Raza, J. Townend

IV. TREATMENT AND OUTCOMES
Moderators: Charles Pusey and Fokko van der Woude

Keynote Presentation
Conventional treatment and outcome of Wegener's granulomatosis and microscopic polyangiitis
David R.W. Jayne

Plenary Session Abstract (24)
24-012. Randomized trial of cyclophosphamide versus methotrexate for induction of remission in "non-renal" ANCA-associated vasculitis
K. de Groot, N. Rasmussen, J.W. Cohen Tervaert, D.R.W. Jayne for EUVAS (European Vasculitis Study Group)

Keynote Presentations
Treatment of giant-cell arteritis: Where we have been and why we must move on
Gary S. Hoffman

Henoch-Schönlein purpura (treatment and outcome)
Michael J. Dillon

Targeted therapies in systemic vasculitis
John H. Stone

Plenary Session Abstract (25)
25-070. Campath 1-H (anti-CD52) for refractory vasculitis: Retrospective Cambridge experience 1989-1999
D.R.W. Jayne

V. TREATING THE PERMANENT SEQUELAE OF VASCULITIS
Moderators: Robert Kimberly and John Stone

Keynote Presentations
Inflammation in acute coronary syndromes
Mark Robbins and Eric J. Topol

Kidney transplantation and ANCA-associated vasculitis
Fokko J. van der Woude

Surgical treatment of Takayasu's disease
Joseph M. Giordano

New approaches to the management of subglottic stenosis in Wegener's granulomatosis
Isaac Eliachar, James Chan, and Lee Akst

Sinonasal complications of vasculitic diseases
Robert S. Lebovics

POSTER PRESENTATIONS (26-120)

Pathogenesis—Immune Predisposition and Infectious Etiology of Systemic Vasculitis

Pathogenesis—Patterns of Injury: Implications for Pathogenesis

Pathogenesis—Possible Role of ANCA and AECA in Selected Forms of Systemic Vasculitis

Epidemiology of Vasculitis

Diagnostic Modalities, Surrogate Markers of Disease Activity, and Tools for Outcome Measurements

Treatment and Outcomes

Treating the Permanent Sequelae of Vasculitis

Program Chairmen and Editors:
Gary S. Hoffman, MD, and John H. Stone, MD, MPH

Contents

I. PATHOGENESIS

A. Immune Predisposition and Infectious Etiology of Systemic Vasculitis
Moderators: Coen Stegeman and Herbert Virgin

Keynote Presentation
Host and viral genes that control herpesvirus vasculitis
Herbert W. Virgin IV

Plenary Session Abstracts (1-3)
1-090. Induction of pauci-immune necrotizing and crescentic glomerulonephritis (NCGN) by intravenous administration of anti-myeloperoxidase (anti-MPO) antibodies to recombinase activating gene-2 deficient (RAG-2 -/-) mice
J.C. Jennette, H. Xiao, P. Heeringa, Z. Liu, P. Hu, M. Zhao, Y. Aratani, R.J. Falk

2-091. Induction of necrotizing and crescentic glomerulonephritis (NCGN) and small-vessel vasculitis (SVV) by adoptive transfer of anti-myeloperoxidase (anti-MPO) lymphocytes into recombinase activating gene-2 deficient (RAG-2 -/-) mice
H. Xiao, P. Heeringa, Z. Liu, P. Hu, M. Zhao, Y. Aratani, R.J. Falk, J.C. Jennette

3-049. Contribution of activated neurotrophils and MPO-ANCA to the development of crescentic glomerulonephritis in SCG/KJ mice
A. Ishida-Okawara, T. Ito-Ihara, T. Ono, E. Muso, K. Saiga, K. Nemoto, K. Suzuki

Keynote Presentations
Known causes of vasculitis in man
Stanley J. Naides

HCV and cryoglobulinemic vasculitis
Clodoveo Ferri, A.L. Zignego, D. Giuggioli, M. Sebastiani, M. Cazzato, A. Antonelli, L. La Civita, P. Fadda, G. Longombardo, and S. Pileri

Infections in primary vasculitides
Jan W. Cohen Tervaert

Plenary session Abstracts (4-5)
4-093. Staphylococcal toxic-shock-syndrome-toxin-1 (TSST-1) is a risk factor for disease relapse in Wegener's granulomatosis
E.R. Popa, B. van der Meer, J. Arends, W.M. Manson, N.A. Bos, C.G.M. Kallenberg, J.W. Cohen Tervaert, C.A. Stegeman

5-104.Chlamydia pneumoniae and giant-cell arteritis: Failure to detect Chlamydia pneumoniae in temporal artery biopsies by polymerase chain reaction
M.J. Regan, B.J. Wood, Y.-H. Hsieh, M.L. Theodore, T.C. Quinn, D.B. Hellmann, W.R. Green, C.A. Gaydos, J.H. Stone

B. Patterns of Injury: Implications for Pathogenesis
Moderators: Loïc Guillevin and Cornelia Weyand

Keynote Presentations
Pathogenic mechanisms in giant cell arteritis
Cornelia M. Weyand and Jörg J. Goronzy

Implications for pathogenesis of patterns of injury in small- and medium-sized-vessel vasculitis
J. Charles Jennette

Plenary Session Abstracts (6-7)

6-037. Superantigenic activation of T lymphocytes and endothelial cells: A mechanism for superantigen-induced vasculitis
P.A. Brogan, V. Shah, N. Klein, M.J. Dillon

7-108. Analysis of autoantibody repertoires in small and medium sized vessel vasculitis: Evidence for disease-specific perturbations in classic polyarteritis nodosa (PAN), micropolyangiitis (MPA), Churg-Strauss syndrome (CSS) and Wegener's granulomatosis (WG)
Y. Chanseaud, L. Guillevin, M. Kambouchner, M.C. Boissier, L. Mouthon

Keynote Presentation
Granuloma formation, implications for the pathogenesis of vasculitis
Michael C. Sneller

Plenary Session Abstracts (8-9)
8-052. Chemokine receptor expression on CD4+ and CD8+ memory T-cells and in granulomas in Wegener's granulomatosis
P. Lamprecht, A. Erdmann, A. Mueller, E. Csernok, H. Bruehl, W.L. Gross, M. Mack

9-016. Genetic resistance to Wegener's granulomatosis—a role for CCR5 in patients without antineutrophil cytoplasmic antibodies
Y. Zhou, D. Huang, C. Farver, G. Hoffman

Keynote Presentation
Endothelial cell biology, perivascular inflammation, and vasculitis
Maria C. Cid

Plenary Session Abstract (10)
10-023. Novel effects of inflammatory cell proteases on vascular endothelia
G.A. Preston, W.F. Pendergraft, J.J. Yang, J.C. Jennette, R.J. Falk

C. Possible Role of ANCA and AECA in Select Forms of Systemic Vasculitis
Moderators: Wolfgang Gross and Caroline Savage

Keynote Presentation
Understanding the pathogenesis of ANCA: Where are we today?
Gloria A. Preston, Jia Jin Yang, Hong Xiao, and Ronald J. Falk

Plenary Session Abstracts (11-12)
11-027. TNF-alpha accelerated apoptosis abrogates ANCA-mediated neutrophil respiratory burst by a caspase-dependent mechanism
R. Kettritz, J. Scheumann, Y. Xu, F.C. Luft, H. Haller

12-071. Membrane expression of neurotrophil proteinase 3 (PR3) is associated with relapse in PR3-ANCA related vasculitis
A.A. Rarok, C.A. Stegeman, P.C. Limburg, C.G.M. Kallenberg

Keynote Presentation
ANCA subsets: Influence on disease phenotype
Ulrich Specks

Plenary Session Abstract (13)
13-096. Sequential epitope mapping of the myeloperoxidase antigen
D.M. Wynn, J.A. James

Keynote Presentation
Genetics of ANCA-associated vasculitis
Cees G.M. Kallenberg, Agnieszka Rarok, and Coen A. Stegeman

Plenary Session Abstracts (14-15)
14-028. Membrane expression of proteinase 3 is genetically controlled
A. Schreiber, A. Bushjahn, F.C. Luft, R. Kettritz

15-015. Genetic polymorphisms in TNF, IL-1, IL-6 and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) in Wegener's granulomatosis (WG)
Y. Zhou, D. Huang, G.S. Hoffman

Keynote Presentation
Classification of anti-endothelial cell antibodies into antibodies against microvascular and macrovascular endothelial cells: The pathogenic and diagnostic implications
Yehuda Shoenfeld

Plenary Session Abstract (16)
16-029. HMG-COA reductase inhibitors decrease ANCA-mediated activation of human neutrophils
M. Choi, S. Rolle M. Rane, H. Haller, F.C. Luft, R. Kettritz

II. EPIDEMIOLOGY OF VASCULITIS
Moderators: Miguel Gonzalez-Gay and Gene Hunder

Keynote Presentations
Kawasaki disease: Etiology, pathogenesis, and treatment
Karyl S. Barron

Epidemiology of giant-cell arteritis
Gene G. Hunder

Plenary Session Abstract (17)
17-102. Ethnic disparity in the incidence of temporal arteritis: A 32-year experience at an urban medical center
M.J. Regan, W.R. Green, J.H. Stone

Keynote Presentations
Epidemiology of Wegener's granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome
Richard A. Watts, David G.I. Scott, and Suzanne E. Lane

Epidemiology of Henoch-Schönlein purpura
Frank Saulsbury

Plenary Session Abstract (18)
18-010. Henoch-Schönlein purpura and cutaneous leukocytoclastic angiitis exhibit different HLA-DRB1 associations
M.M. Amoli, W. Thomson, A.H. Hajeer, M.C. Calviño, C. Garcia-Porrua, W.E.R. Ollier, M.A. Gonzalez-Gay

III. DIAGNOSTIC MODALITIES, SURROGATE MARKERS OF DISEASE ACTIVITY, AND TOOLS FOR OUTCOME MEASUREMENTS
Moderators: Carol Langford and Raashid Luqmani

Keynote Presentations
Cytokines in giant-cell arteritis
Jörg J. Goronzy and Cornelia M. Weyand

Utility of imaging studies in assessment of vascular inflammation
Daniël Blockmans

Measuring disease activity and outcomes in clinical studies
Raashid Luqmani

Plenary Session Abstracts (19-21)
19-022. Increases of PR3 and MPO gene transcription in circulating leukocyte of ANCA-associated disease correlate with disease activity
J.J. Yang, G.A. Preston, D.A. Alcorta, B.D. Phillips, R.P. Thomas, S.L. Hogan, J.C. Jennette, R.J. Falk

20-119. Cardiac involvement in Wegener's granulomatosis: Echocardiographic features and clinical outcomes
G.H.M. Oliveira, J.B. Seward, U. Specks

21-041. Endothelial microparticles: Just blood "dust," or a "must" for the diagnosis and monitoring of disease activity in childhood vasculitides?
P.A. Brogan, V. Shah, C. Brachet, N. Klein, M.J. Dillon

Keynote Presentation
Diagnostic strategies in vasculitis affecting the central nervous system
Leonard H. Calabrese

Plenary Session Abstracts (22-23)
Moderator: Leonard Calabrese

22-082. Circulating endothelial cells and vasculitis
A. Woywodt, F. Streiber, K. de Groot, H. Haller, M. Haubitz

23-051. Diffuse endothelial dysfunction is a common feature of SNV
P.A. Bacon, D.M. Carruthers, A.D. Diler, K. Raza, J. Townend

IV. TREATMENT AND OUTCOMES
Moderators: Charles Pusey and Fokko van der Woude

Keynote Presentation
Conventional treatment and outcome of Wegener's granulomatosis and microscopic polyangiitis
David R.W. Jayne

Plenary Session Abstract (24)
24-012. Randomized trial of cyclophosphamide versus methotrexate for induction of remission in "non-renal" ANCA-associated vasculitis
K. de Groot, N. Rasmussen, J.W. Cohen Tervaert, D.R.W. Jayne for EUVAS (European Vasculitis Study Group)

Keynote Presentations
Treatment of giant-cell arteritis: Where we have been and why we must move on
Gary S. Hoffman

Henoch-Schönlein purpura (treatment and outcome)
Michael J. Dillon

Targeted therapies in systemic vasculitis
John H. Stone

Plenary Session Abstract (25)
25-070. Campath 1-H (anti-CD52) for refractory vasculitis: Retrospective Cambridge experience 1989-1999
D.R.W. Jayne

V. TREATING THE PERMANENT SEQUELAE OF VASCULITIS
Moderators: Robert Kimberly and John Stone

Keynote Presentations
Inflammation in acute coronary syndromes
Mark Robbins and Eric J. Topol

Kidney transplantation and ANCA-associated vasculitis
Fokko J. van der Woude

Surgical treatment of Takayasu's disease
Joseph M. Giordano

New approaches to the management of subglottic stenosis in Wegener's granulomatosis
Isaac Eliachar, James Chan, and Lee Akst

Sinonasal complications of vasculitic diseases
Robert S. Lebovics

POSTER PRESENTATIONS (26-120)

Pathogenesis—Immune Predisposition and Infectious Etiology of Systemic Vasculitis

Pathogenesis—Patterns of Injury: Implications for Pathogenesis

Pathogenesis—Possible Role of ANCA and AECA in Selected Forms of Systemic Vasculitis

Epidemiology of Vasculitis

Diagnostic Modalities, Surrogate Markers of Disease Activity, and Tools for Outcome Measurements

Treatment and Outcomes

Treating the Permanent Sequelae of Vasculitis

Program Chairmen and Editors:
Gary S. Hoffman, MD, and John H. Stone, MD, MPH

Contents

I. PATHOGENESIS

A. Immune Predisposition and Infectious Etiology of Systemic Vasculitis
Moderators: Coen Stegeman and Herbert Virgin

Keynote Presentation
Host and viral genes that control herpesvirus vasculitis
Herbert W. Virgin IV

Plenary Session Abstracts (1-3)
1-090. Induction of pauci-immune necrotizing and crescentic glomerulonephritis (NCGN) by intravenous administration of anti-myeloperoxidase (anti-MPO) antibodies to recombinase activating gene-2 deficient (RAG-2 -/-) mice
J.C. Jennette, H. Xiao, P. Heeringa, Z. Liu, P. Hu, M. Zhao, Y. Aratani, R.J. Falk

2-091. Induction of necrotizing and crescentic glomerulonephritis (NCGN) and small-vessel vasculitis (SVV) by adoptive transfer of anti-myeloperoxidase (anti-MPO) lymphocytes into recombinase activating gene-2 deficient (RAG-2 -/-) mice
H. Xiao, P. Heeringa, Z. Liu, P. Hu, M. Zhao, Y. Aratani, R.J. Falk, J.C. Jennette

3-049. Contribution of activated neurotrophils and MPO-ANCA to the development of crescentic glomerulonephritis in SCG/KJ mice
A. Ishida-Okawara, T. Ito-Ihara, T. Ono, E. Muso, K. Saiga, K. Nemoto, K. Suzuki

Keynote Presentations
Known causes of vasculitis in man
Stanley J. Naides

HCV and cryoglobulinemic vasculitis
Clodoveo Ferri, A.L. Zignego, D. Giuggioli, M. Sebastiani, M. Cazzato, A. Antonelli, L. La Civita, P. Fadda, G. Longombardo, and S. Pileri

Infections in primary vasculitides
Jan W. Cohen Tervaert

Plenary session Abstracts (4-5)
4-093. Staphylococcal toxic-shock-syndrome-toxin-1 (TSST-1) is a risk factor for disease relapse in Wegener's granulomatosis
E.R. Popa, B. van der Meer, J. Arends, W.M. Manson, N.A. Bos, C.G.M. Kallenberg, J.W. Cohen Tervaert, C.A. Stegeman

5-104.Chlamydia pneumoniae and giant-cell arteritis: Failure to detect Chlamydia pneumoniae in temporal artery biopsies by polymerase chain reaction
M.J. Regan, B.J. Wood, Y.-H. Hsieh, M.L. Theodore, T.C. Quinn, D.B. Hellmann, W.R. Green, C.A. Gaydos, J.H. Stone

B. Patterns of Injury: Implications for Pathogenesis
Moderators: Loïc Guillevin and Cornelia Weyand

Keynote Presentations
Pathogenic mechanisms in giant cell arteritis
Cornelia M. Weyand and Jörg J. Goronzy

Implications for pathogenesis of patterns of injury in small- and medium-sized-vessel vasculitis
J. Charles Jennette

Plenary Session Abstracts (6-7)

6-037. Superantigenic activation of T lymphocytes and endothelial cells: A mechanism for superantigen-induced vasculitis
P.A. Brogan, V. Shah, N. Klein, M.J. Dillon

7-108. Analysis of autoantibody repertoires in small and medium sized vessel vasculitis: Evidence for disease-specific perturbations in classic polyarteritis nodosa (PAN), micropolyangiitis (MPA), Churg-Strauss syndrome (CSS) and Wegener's granulomatosis (WG)
Y. Chanseaud, L. Guillevin, M. Kambouchner, M.C. Boissier, L. Mouthon

Keynote Presentation
Granuloma formation, implications for the pathogenesis of vasculitis
Michael C. Sneller

Plenary Session Abstracts (8-9)
8-052. Chemokine receptor expression on CD4+ and CD8+ memory T-cells and in granulomas in Wegener's granulomatosis
P. Lamprecht, A. Erdmann, A. Mueller, E. Csernok, H. Bruehl, W.L. Gross, M. Mack

9-016. Genetic resistance to Wegener's granulomatosis—a role for CCR5 in patients without antineutrophil cytoplasmic antibodies
Y. Zhou, D. Huang, C. Farver, G. Hoffman

Keynote Presentation
Endothelial cell biology, perivascular inflammation, and vasculitis
Maria C. Cid

Plenary Session Abstract (10)
10-023. Novel effects of inflammatory cell proteases on vascular endothelia
G.A. Preston, W.F. Pendergraft, J.J. Yang, J.C. Jennette, R.J. Falk

C. Possible Role of ANCA and AECA in Select Forms of Systemic Vasculitis
Moderators: Wolfgang Gross and Caroline Savage

Keynote Presentation
Understanding the pathogenesis of ANCA: Where are we today?
Gloria A. Preston, Jia Jin Yang, Hong Xiao, and Ronald J. Falk

Plenary Session Abstracts (11-12)
11-027. TNF-alpha accelerated apoptosis abrogates ANCA-mediated neutrophil respiratory burst by a caspase-dependent mechanism
R. Kettritz, J. Scheumann, Y. Xu, F.C. Luft, H. Haller

12-071. Membrane expression of neurotrophil proteinase 3 (PR3) is associated with relapse in PR3-ANCA related vasculitis
A.A. Rarok, C.A. Stegeman, P.C. Limburg, C.G.M. Kallenberg

Keynote Presentation
ANCA subsets: Influence on disease phenotype
Ulrich Specks

Plenary Session Abstract (13)
13-096. Sequential epitope mapping of the myeloperoxidase antigen
D.M. Wynn, J.A. James

Keynote Presentation
Genetics of ANCA-associated vasculitis
Cees G.M. Kallenberg, Agnieszka Rarok, and Coen A. Stegeman

Plenary Session Abstracts (14-15)
14-028. Membrane expression of proteinase 3 is genetically controlled
A. Schreiber, A. Bushjahn, F.C. Luft, R. Kettritz

15-015. Genetic polymorphisms in TNF, IL-1, IL-6 and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) in Wegener's granulomatosis (WG)
Y. Zhou, D. Huang, G.S. Hoffman

Keynote Presentation
Classification of anti-endothelial cell antibodies into antibodies against microvascular and macrovascular endothelial cells: The pathogenic and diagnostic implications
Yehuda Shoenfeld

Plenary Session Abstract (16)
16-029. HMG-COA reductase inhibitors decrease ANCA-mediated activation of human neutrophils
M. Choi, S. Rolle M. Rane, H. Haller, F.C. Luft, R. Kettritz

II. EPIDEMIOLOGY OF VASCULITIS
Moderators: Miguel Gonzalez-Gay and Gene Hunder

Keynote Presentations
Kawasaki disease: Etiology, pathogenesis, and treatment
Karyl S. Barron

Epidemiology of giant-cell arteritis
Gene G. Hunder

Plenary Session Abstract (17)
17-102. Ethnic disparity in the incidence of temporal arteritis: A 32-year experience at an urban medical center
M.J. Regan, W.R. Green, J.H. Stone

Keynote Presentations
Epidemiology of Wegener's granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome
Richard A. Watts, David G.I. Scott, and Suzanne E. Lane

Epidemiology of Henoch-Schönlein purpura
Frank Saulsbury

Plenary Session Abstract (18)
18-010. Henoch-Schönlein purpura and cutaneous leukocytoclastic angiitis exhibit different HLA-DRB1 associations
M.M. Amoli, W. Thomson, A.H. Hajeer, M.C. Calviño, C. Garcia-Porrua, W.E.R. Ollier, M.A. Gonzalez-Gay

III. DIAGNOSTIC MODALITIES, SURROGATE MARKERS OF DISEASE ACTIVITY, AND TOOLS FOR OUTCOME MEASUREMENTS
Moderators: Carol Langford and Raashid Luqmani

Keynote Presentations
Cytokines in giant-cell arteritis
Jörg J. Goronzy and Cornelia M. Weyand

Utility of imaging studies in assessment of vascular inflammation
Daniël Blockmans

Measuring disease activity and outcomes in clinical studies
Raashid Luqmani

Plenary Session Abstracts (19-21)
19-022. Increases of PR3 and MPO gene transcription in circulating leukocyte of ANCA-associated disease correlate with disease activity
J.J. Yang, G.A. Preston, D.A. Alcorta, B.D. Phillips, R.P. Thomas, S.L. Hogan, J.C. Jennette, R.J. Falk

20-119. Cardiac involvement in Wegener's granulomatosis: Echocardiographic features and clinical outcomes
G.H.M. Oliveira, J.B. Seward, U. Specks

21-041. Endothelial microparticles: Just blood "dust," or a "must" for the diagnosis and monitoring of disease activity in childhood vasculitides?
P.A. Brogan, V. Shah, C. Brachet, N. Klein, M.J. Dillon

Keynote Presentation
Diagnostic strategies in vasculitis affecting the central nervous system
Leonard H. Calabrese

Plenary Session Abstracts (22-23)
Moderator: Leonard Calabrese

22-082. Circulating endothelial cells and vasculitis
A. Woywodt, F. Streiber, K. de Groot, H. Haller, M. Haubitz

23-051. Diffuse endothelial dysfunction is a common feature of SNV
P.A. Bacon, D.M. Carruthers, A.D. Diler, K. Raza, J. Townend

IV. TREATMENT AND OUTCOMES
Moderators: Charles Pusey and Fokko van der Woude

Keynote Presentation
Conventional treatment and outcome of Wegener's granulomatosis and microscopic polyangiitis
David R.W. Jayne

Plenary Session Abstract (24)
24-012. Randomized trial of cyclophosphamide versus methotrexate for induction of remission in "non-renal" ANCA-associated vasculitis
K. de Groot, N. Rasmussen, J.W. Cohen Tervaert, D.R.W. Jayne for EUVAS (European Vasculitis Study Group)

Keynote Presentations
Treatment of giant-cell arteritis: Where we have been and why we must move on
Gary S. Hoffman

Henoch-Schönlein purpura (treatment and outcome)
Michael J. Dillon

Targeted therapies in systemic vasculitis
John H. Stone

Plenary Session Abstract (25)
25-070. Campath 1-H (anti-CD52) for refractory vasculitis: Retrospective Cambridge experience 1989-1999
D.R.W. Jayne

V. TREATING THE PERMANENT SEQUELAE OF VASCULITIS
Moderators: Robert Kimberly and John Stone

Keynote Presentations
Inflammation in acute coronary syndromes
Mark Robbins and Eric J. Topol

Kidney transplantation and ANCA-associated vasculitis
Fokko J. van der Woude

Surgical treatment of Takayasu's disease
Joseph M. Giordano

New approaches to the management of subglottic stenosis in Wegener's granulomatosis
Isaac Eliachar, James Chan, and Lee Akst

Sinonasal complications of vasculitic diseases
Robert S. Lebovics

POSTER PRESENTATIONS (26-120)

Pathogenesis—Immune Predisposition and Infectious Etiology of Systemic Vasculitis

Pathogenesis—Patterns of Injury: Implications for Pathogenesis

Pathogenesis—Possible Role of ANCA and AECA in Selected Forms of Systemic Vasculitis

Epidemiology of Vasculitis

Diagnostic Modalities, Surrogate Markers of Disease Activity, and Tools for Outcome Measurements

Treatment and Outcomes

Treating the Permanent Sequelae of Vasculitis

Supplement Editor:
Marc C. Hochberg, MD, MPH

Contents

Preface and Foreword
Marc C. Hochberg, MD, MPH

Development and clinical application of COX-2–selective inhibitors for the treatment of osteoarthritis and rheumatoid arthritis
Clifton G. Bingham III, MD

Cyclooxygenase-2–selective inhibitors: Translating pharmacology into clinical utility
Bruce N. Cronstein, MD

COX-2–selective inhibitors in the treatment of arthritis
Thomas J. Schnitzer, MD, PhD, and Marc C. Hochberg, MD, MPH

Gastrointestinal safety and tolerability of non-selective nonsteroidal anti-inflammatory agents and cyclooxygenase-2–selective inhibitors
David A. Peura, MD

Outcomes studies of the gastrointestinal safety of cyclooxygenase-2 inhibitors
James M. Scheiman, MD

Current perspective on the cardiovascular effects of coxibs
Marvin A. Konstam, MD, and Matthew R. Weir, MD

Renal effects of nonselective NSAIDs and coxibs
Matthew R. Weir, MD

Developing an economic rationale for the use of selective COX-2 inhibitors for patients at risk for NSAID gastropathy
A. Mark Fendrick, MD

Cyclooxygenase-2–selective inhibitors in the management of acute and perioperative pain
Warren A. Katz, MD

Emerging options with coxib therapy
Mark J. Lema, MD, PhD

Supplement Editor:
Marc C. Hochberg, MD, MPH

Contents

Preface and Foreword
Marc C. Hochberg, MD, MPH

Development and clinical application of COX-2–selective inhibitors for the treatment of osteoarthritis and rheumatoid arthritis
Clifton G. Bingham III, MD

Cyclooxygenase-2–selective inhibitors: Translating pharmacology into clinical utility
Bruce N. Cronstein, MD

COX-2–selective inhibitors in the treatment of arthritis
Thomas J. Schnitzer, MD, PhD, and Marc C. Hochberg, MD, MPH

Gastrointestinal safety and tolerability of non-selective nonsteroidal anti-inflammatory agents and cyclooxygenase-2–selective inhibitors
David A. Peura, MD

Outcomes studies of the gastrointestinal safety of cyclooxygenase-2 inhibitors
James M. Scheiman, MD

Current perspective on the cardiovascular effects of coxibs
Marvin A. Konstam, MD, and Matthew R. Weir, MD

Renal effects of nonselective NSAIDs and coxibs
Matthew R. Weir, MD

Developing an economic rationale for the use of selective COX-2 inhibitors for patients at risk for NSAID gastropathy
A. Mark Fendrick, MD

Cyclooxygenase-2–selective inhibitors in the management of acute and perioperative pain
Warren A. Katz, MD

Emerging options with coxib therapy
Mark J. Lema, MD, PhD

Supplement Editor:
Marc C. Hochberg, MD, MPH

Contents

Preface and Foreword
Marc C. Hochberg, MD, MPH

Development and clinical application of COX-2–selective inhibitors for the treatment of osteoarthritis and rheumatoid arthritis
Clifton G. Bingham III, MD

Cyclooxygenase-2–selective inhibitors: Translating pharmacology into clinical utility
Bruce N. Cronstein, MD

COX-2–selective inhibitors in the treatment of arthritis
Thomas J. Schnitzer, MD, PhD, and Marc C. Hochberg, MD, MPH

Gastrointestinal safety and tolerability of non-selective nonsteroidal anti-inflammatory agents and cyclooxygenase-2–selective inhibitors
David A. Peura, MD

Outcomes studies of the gastrointestinal safety of cyclooxygenase-2 inhibitors
James M. Scheiman, MD

Current perspective on the cardiovascular effects of coxibs
Marvin A. Konstam, MD, and Matthew R. Weir, MD

Renal effects of nonselective NSAIDs and coxibs
Matthew R. Weir, MD

Developing an economic rationale for the use of selective COX-2 inhibitors for patients at risk for NSAID gastropathy
A. Mark Fendrick, MD

Cyclooxygenase-2–selective inhibitors in the management of acute and perioperative pain
Warren A. Katz, MD

Emerging options with coxib therapy
Mark J. Lema, MD, PhD

ABSTRACT

BACKGROUND: About 10% of people in the United States develop at least 1 symptomatic kidney stone during their lives. The recurrence rate after 10 years is at least 50%. Many physicians recommend a low-calcium diet in patients with calcium oxalate stones to prevent recurrence. Recent studies suggest that a low-calcium diet may not be effective and that intake of animal protein and salt may influence renal calcium excretion. This study compares the traditional low-calcium diet with a diet that is low in animal protein and salt.

POPULATION STUDIED: This study enrolled 120 men with idiopathic hypercalciuria (urinary calcium excretion of more than 300 mg per day on an unrestricted diet) who had been referred to a nephrology clinic in Parma, Italy, and who had had at least 2 episodes of symptomatic renal stones. Reasons for exclusion included previous visits to any “stone disease center” and conditions associated with calcium stones, such as hyperparathyroidism or inflammatory bowel disease.

STUDY DESIGN AND VALIDITY: The investigators randomly assigned subjects, using concealed allocation, to 1 of 2 diets in this randomized controlled study. The low-calcium diet limited calcium intake to about 400 mg per day. The other diet, which included about 1200 mg per day of calcium, limited sodium chloride to about 3000 mg and animal protein to 93 g (15% of total calories). Both groups were advised to limit intake of high-oxalate foods and encouraged to drink 2 liters of water per day in cold weather and 3 liters in warm weather. Subjects were allowed moderate consumption of beer, wine, coffee, and sodas. (Detailed dietary instructions are available to New England Journal of Medicine subscribers in the supplement to the publication at www.nejm.org.) The study followed the patients for 5 years or until they developed clinical or radiologic evidence of a renal stone. Annual x-ray and ultrasound studies identified asymptomatic stone recurrences.

OUTCOMES MEASURED: The primary outcome was the time to development of the first recurrence of a renal stone, whether or not it was clinically evident. Other outcomes included changes in calcium and oxalate excretion and calcium oxalate saturation in the urine.

RESULTS: After 5 years, the low-protein, low-sodium diet led to fewer recurrences (20% compared with 38% in the low-calcium group, relative risk 0.49, number needed to treat with diet for 5 years = 5.5). The risk of recurrence in the low-calcium group was similar to the 35% to 40% expected in the absence of any intervention. The disease-oriented changes in urine characteristics were predictable: urinary calcium decreased in both groups, but oxalate secretion increased in the low-calcium group, causing greater calcium oxalate saturation.

ABSTRACT

BACKGROUND: About 10% of people in the United States develop at least 1 symptomatic kidney stone during their lives. The recurrence rate after 10 years is at least 50%. Many physicians recommend a low-calcium diet in patients with calcium oxalate stones to prevent recurrence. Recent studies suggest that a low-calcium diet may not be effective and that intake of animal protein and salt may influence renal calcium excretion. This study compares the traditional low-calcium diet with a diet that is low in animal protein and salt.

POPULATION STUDIED: This study enrolled 120 men with idiopathic hypercalciuria (urinary calcium excretion of more than 300 mg per day on an unrestricted diet) who had been referred to a nephrology clinic in Parma, Italy, and who had had at least 2 episodes of symptomatic renal stones. Reasons for exclusion included previous visits to any “stone disease center” and conditions associated with calcium stones, such as hyperparathyroidism or inflammatory bowel disease.

STUDY DESIGN AND VALIDITY: The investigators randomly assigned subjects, using concealed allocation, to 1 of 2 diets in this randomized controlled study. The low-calcium diet limited calcium intake to about 400 mg per day. The other diet, which included about 1200 mg per day of calcium, limited sodium chloride to about 3000 mg and animal protein to 93 g (15% of total calories). Both groups were advised to limit intake of high-oxalate foods and encouraged to drink 2 liters of water per day in cold weather and 3 liters in warm weather. Subjects were allowed moderate consumption of beer, wine, coffee, and sodas. (Detailed dietary instructions are available to New England Journal of Medicine subscribers in the supplement to the publication at www.nejm.org.) The study followed the patients for 5 years or until they developed clinical or radiologic evidence of a renal stone. Annual x-ray and ultrasound studies identified asymptomatic stone recurrences.

OUTCOMES MEASURED: The primary outcome was the time to development of the first recurrence of a renal stone, whether or not it was clinically evident. Other outcomes included changes in calcium and oxalate excretion and calcium oxalate saturation in the urine.

RESULTS: After 5 years, the low-protein, low-sodium diet led to fewer recurrences (20% compared with 38% in the low-calcium group, relative risk 0.49, number needed to treat with diet for 5 years = 5.5). The risk of recurrence in the low-calcium group was similar to the 35% to 40% expected in the absence of any intervention. The disease-oriented changes in urine characteristics were predictable: urinary calcium decreased in both groups, but oxalate secretion increased in the low-calcium group, causing greater calcium oxalate saturation.

ABSTRACT

BACKGROUND: About 10% of people in the United States develop at least 1 symptomatic kidney stone during their lives. The recurrence rate after 10 years is at least 50%. Many physicians recommend a low-calcium diet in patients with calcium oxalate stones to prevent recurrence. Recent studies suggest that a low-calcium diet may not be effective and that intake of animal protein and salt may influence renal calcium excretion. This study compares the traditional low-calcium diet with a diet that is low in animal protein and salt.

POPULATION STUDIED: This study enrolled 120 men with idiopathic hypercalciuria (urinary calcium excretion of more than 300 mg per day on an unrestricted diet) who had been referred to a nephrology clinic in Parma, Italy, and who had had at least 2 episodes of symptomatic renal stones. Reasons for exclusion included previous visits to any “stone disease center” and conditions associated with calcium stones, such as hyperparathyroidism or inflammatory bowel disease.

STUDY DESIGN AND VALIDITY: The investigators randomly assigned subjects, using concealed allocation, to 1 of 2 diets in this randomized controlled study. The low-calcium diet limited calcium intake to about 400 mg per day. The other diet, which included about 1200 mg per day of calcium, limited sodium chloride to about 3000 mg and animal protein to 93 g (15% of total calories). Both groups were advised to limit intake of high-oxalate foods and encouraged to drink 2 liters of water per day in cold weather and 3 liters in warm weather. Subjects were allowed moderate consumption of beer, wine, coffee, and sodas. (Detailed dietary instructions are available to New England Journal of Medicine subscribers in the supplement to the publication at www.nejm.org.) The study followed the patients for 5 years or until they developed clinical or radiologic evidence of a renal stone. Annual x-ray and ultrasound studies identified asymptomatic stone recurrences.

OUTCOMES MEASURED: The primary outcome was the time to development of the first recurrence of a renal stone, whether or not it was clinically evident. Other outcomes included changes in calcium and oxalate excretion and calcium oxalate saturation in the urine.

RESULTS: After 5 years, the low-protein, low-sodium diet led to fewer recurrences (20% compared with 38% in the low-calcium group, relative risk 0.49, number needed to treat with diet for 5 years = 5.5). The risk of recurrence in the low-calcium group was similar to the 35% to 40% expected in the absence of any intervention. The disease-oriented changes in urine characteristics were predictable: urinary calcium decreased in both groups, but oxalate secretion increased in the low-calcium group, causing greater calcium oxalate saturation.

Making a quick diagnosis in a hyperactive, inattentive child is often difficult. The National Institutes of Health concluded in a consensus statement that no independent diagnostic test for attention-deficit/hyperactivity disorder (ADHD) exists.¹ Furthermore, the American Academy of Child & Adolescent Psychiatry (AACAP) issued a treatment guideline classifying ADHD as a clinical diagnosis.

With the time constraints imposed by managed care organizations, questioning and history gathering must be precisely aimed to elicit specific information. Over the years, I have identified the following 5 red flags that help distinguish ADHD from mood problems,² anxiety, psychosis, obsessions, and other psychiatric disorders.

1. Moodiness is not part of ADHD. The DSM-IV criteria for ADHD do not include elevated mood. “Mood swings,” persistent clowning, or angry affect should prompt further questioning about similar features in relatives. Frequently we hear that “his father was never diagnosed with anything, but he was the class clown.”
2. ADHD is not an intermittent condition. By asking if the child has “good days and bad days,” we can obtain valuable information. ADHD has a biological basis and is present every day, like Parkinson’s disease or diabetes. Obviously, some days can be more challenging than others, but if a parent says, “Some days she is a perfect child,” the possibility of ADHD is small.
3. Symptoms are not present in kindergarten. The child with ADHD begins to show signs of this condition very early in life; parents are frequently informed of problems by preschool and kindergarten teachers. The usual complaints are inability to stay with a task and disrupting the class. Start of these symptoms as late as first or second grade is a red flag to question the ADHD diagnosis.
4. More than one diagnosis probably means “none of the above.” When a child has been diagnosed with conduct disorder (CD) and/or oppositional-defiant disorder (ODD) along with ADHD, chances are that we are missing the real diagnosis. I have seen cases of social anxiety disorder that had been diagnosed as ADHD/ODD because the child was inattentive secondary to nervousness. Incidentally, DSM-IV does not allow the diagnosis of ODD in the presence of CD.
5. Worsening of symptoms is not an expected outcome of stimulant medications for ADHD. Lack of response to psychostimulants or only mild improvement may occur in ADHD. Frequently, however, we see children with histories of getting worse after starting medication for presumed ADHD.

Making a quick diagnosis in a hyperactive, inattentive child is often difficult. The National Institutes of Health concluded in a consensus statement that no independent diagnostic test for attention-deficit/hyperactivity disorder (ADHD) exists.¹ Furthermore, the American Academy of Child & Adolescent Psychiatry (AACAP) issued a treatment guideline classifying ADHD as a clinical diagnosis.

With the time constraints imposed by managed care organizations, questioning and history gathering must be precisely aimed to elicit specific information. Over the years, I have identified the following 5 red flags that help distinguish ADHD from mood problems,² anxiety, psychosis, obsessions, and other psychiatric disorders.

1. Moodiness is not part of ADHD. The DSM-IV criteria for ADHD do not include elevated mood. “Mood swings,” persistent clowning, or angry affect should prompt further questioning about similar features in relatives. Frequently we hear that “his father was never diagnosed with anything, but he was the class clown.”
2. ADHD is not an intermittent condition. By asking if the child has “good days and bad days,” we can obtain valuable information. ADHD has a biological basis and is present every day, like Parkinson’s disease or diabetes. Obviously, some days can be more challenging than others, but if a parent says, “Some days she is a perfect child,” the possibility of ADHD is small.
3. Symptoms are not present in kindergarten. The child with ADHD begins to show signs of this condition very early in life; parents are frequently informed of problems by preschool and kindergarten teachers. The usual complaints are inability to stay with a task and disrupting the class. Start of these symptoms as late as first or second grade is a red flag to question the ADHD diagnosis.
4. More than one diagnosis probably means “none of the above.” When a child has been diagnosed with conduct disorder (CD) and/or oppositional-defiant disorder (ODD) along with ADHD, chances are that we are missing the real diagnosis. I have seen cases of social anxiety disorder that had been diagnosed as ADHD/ODD because the child was inattentive secondary to nervousness. Incidentally, DSM-IV does not allow the diagnosis of ODD in the presence of CD.
5. Worsening of symptoms is not an expected outcome of stimulant medications for ADHD. Lack of response to psychostimulants or only mild improvement may occur in ADHD. Frequently, however, we see children with histories of getting worse after starting medication for presumed ADHD.

Making a quick diagnosis in a hyperactive, inattentive child is often difficult. The National Institutes of Health concluded in a consensus statement that no independent diagnostic test for attention-deficit/hyperactivity disorder (ADHD) exists.¹ Furthermore, the American Academy of Child & Adolescent Psychiatry (AACAP) issued a treatment guideline classifying ADHD as a clinical diagnosis.

With the time constraints imposed by managed care organizations, questioning and history gathering must be precisely aimed to elicit specific information. Over the years, I have identified the following 5 red flags that help distinguish ADHD from mood problems,² anxiety, psychosis, obsessions, and other psychiatric disorders.

1. Moodiness is not part of ADHD. The DSM-IV criteria for ADHD do not include elevated mood. “Mood swings,” persistent clowning, or angry affect should prompt further questioning about similar features in relatives. Frequently we hear that “his father was never diagnosed with anything, but he was the class clown.”
2. ADHD is not an intermittent condition. By asking if the child has “good days and bad days,” we can obtain valuable information. ADHD has a biological basis and is present every day, like Parkinson’s disease or diabetes. Obviously, some days can be more challenging than others, but if a parent says, “Some days she is a perfect child,” the possibility of ADHD is small.
3. Symptoms are not present in kindergarten. The child with ADHD begins to show signs of this condition very early in life; parents are frequently informed of problems by preschool and kindergarten teachers. The usual complaints are inability to stay with a task and disrupting the class. Start of these symptoms as late as first or second grade is a red flag to question the ADHD diagnosis.
4. More than one diagnosis probably means “none of the above.” When a child has been diagnosed with conduct disorder (CD) and/or oppositional-defiant disorder (ODD) along with ADHD, chances are that we are missing the real diagnosis. I have seen cases of social anxiety disorder that had been diagnosed as ADHD/ODD because the child was inattentive secondary to nervousness. Incidentally, DSM-IV does not allow the diagnosis of ODD in the presence of CD.
5. Worsening of symptoms is not an expected outcome of stimulant medications for ADHD. Lack of response to psychostimulants or only mild improvement may occur in ADHD. Frequently, however, we see children with histories of getting worse after starting medication for presumed ADHD.