Abstract
Dilated cardiomyopathy (DCM) is an idiopathic heart muscle disorder. The presence of circulating cardiac antibodies and the association with HLA-DR4 are consistent with autoimmune pathogenesis in a subset of patients. Sixty-eight DCM patients and 277 controls were typed for IgG heavy-chain constant region (Gm) and κ light-chain (Km) allotypes. All patients and 210 of the 277 controls were HLA-DR typed. The Gm (1, 3, 17; 23; 5*, 21, 28) phenotype was overrepresented in DCM compared with controls (25% vs 13%, p = 0.0139, Pc = NS, RR = 2.23). The frequency of this phenotype was higher in patients with younger age at onset, shorter symptom duration, and among those who were positive for cardiac as well as for non-organ-specific autoantibodies than in controls. A higher frequency of the Gm (1,± 2, 3, 17; ± 23; 5*, 21, 28) heterozygous phenotypes was also found in DCM compared to controls (40.91% vs 26389%; p = 0.02, pc = 0.04, RR = 1.88). The finding of Gm heterozygosity in DCM was associated with serum positivity for cardiac antibodies. A higher proportion of DCM patients were positive for both the Gm (1, 3, 17; 23; 5*, 21, 28) phenotype and HLA-DR4 compared to normals (3/68 vs 0/210; p = 0.04, RR = 22.50). A potentiating interactive effect in susceptibility to DCM was also found between the Gm (1, ±2, 3, 17; ±23; 5*, 21, 28) heterozygous phenotypes and HLA-DR4 (7/66 vs 2/207, p = 0.0009, RR = 12.16). These Gm phenotypes may be new markers of susceptibility in DCM, associated with positive autoimmune serology. The potentiating interaction of Gm and HLA-DR4 is in keeping with results reported in other autoimmune diseases.
| Original language | English |
|---|---|
| Pages (from-to) | 193-199 |
| Number of pages | 7 |
| Journal | Human Immunology |
| Volume | 35 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1992 |
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ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
HLA and immunoglobulin polymorphisms in idiopathic dilated cardiomyopathy. / Martinetti, Miryam; Dogoujon, Jean Michel; Caforio, Alida L P; Schwarz, Giselle; Gavazzi, Antonello; Graziano, Gabriella; Arbustini, Eloisa; Lorini, Renata; McKenna, William J.; Bottazzo, Gian Franco; Cuccia, Mariaclara.
In: Human Immunology, Vol. 35, No. 3, 1992, p. 193-199.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - HLA and immunoglobulin polymorphisms in idiopathic dilated cardiomyopathy
AU - Martinetti, Miryam
AU - Dogoujon, Jean Michel
AU - Caforio, Alida L P
AU - Schwarz, Giselle
AU - Gavazzi, Antonello
AU - Graziano, Gabriella
AU - Arbustini, Eloisa
AU - Lorini, Renata
AU - McKenna, William J.
AU - Bottazzo, Gian Franco
AU - Cuccia, Mariaclara
PY - 1992
Y1 - 1992
N2 - Dilated cardiomyopathy (DCM) is an idiopathic heart muscle disorder. The presence of circulating cardiac antibodies and the association with HLA-DR4 are consistent with autoimmune pathogenesis in a subset of patients. Sixty-eight DCM patients and 277 controls were typed for IgG heavy-chain constant region (Gm) and κ light-chain (Km) allotypes. All patients and 210 of the 277 controls were HLA-DR typed. The Gm (1, 3, 17; 23; 5*, 21, 28) phenotype was overrepresented in DCM compared with controls (25% vs 13%, p = 0.0139, Pc = NS, RR = 2.23). The frequency of this phenotype was higher in patients with younger age at onset, shorter symptom duration, and among those who were positive for cardiac as well as for non-organ-specific autoantibodies than in controls. A higher frequency of the Gm (1,± 2, 3, 17; ± 23; 5*, 21, 28) heterozygous phenotypes was also found in DCM compared to controls (40.91% vs 26389%; p = 0.02, pc = 0.04, RR = 1.88). The finding of Gm heterozygosity in DCM was associated with serum positivity for cardiac antibodies. A higher proportion of DCM patients were positive for both the Gm (1, 3, 17; 23; 5*, 21, 28) phenotype and HLA-DR4 compared to normals (3/68 vs 0/210; p = 0.04, RR = 22.50). A potentiating interactive effect in susceptibility to DCM was also found between the Gm (1, ±2, 3, 17; ±23; 5*, 21, 28) heterozygous phenotypes and HLA-DR4 (7/66 vs 2/207, p = 0.0009, RR = 12.16). These Gm phenotypes may be new markers of susceptibility in DCM, associated with positive autoimmune serology. The potentiating interaction of Gm and HLA-DR4 is in keeping with results reported in other autoimmune diseases.
AB - Dilated cardiomyopathy (DCM) is an idiopathic heart muscle disorder. The presence of circulating cardiac antibodies and the association with HLA-DR4 are consistent with autoimmune pathogenesis in a subset of patients. Sixty-eight DCM patients and 277 controls were typed for IgG heavy-chain constant region (Gm) and κ light-chain (Km) allotypes. All patients and 210 of the 277 controls were HLA-DR typed. The Gm (1, 3, 17; 23; 5*, 21, 28) phenotype was overrepresented in DCM compared with controls (25% vs 13%, p = 0.0139, Pc = NS, RR = 2.23). The frequency of this phenotype was higher in patients with younger age at onset, shorter symptom duration, and among those who were positive for cardiac as well as for non-organ-specific autoantibodies than in controls. A higher frequency of the Gm (1,± 2, 3, 17; ± 23; 5*, 21, 28) heterozygous phenotypes was also found in DCM compared to controls (40.91% vs 26389%; p = 0.02, pc = 0.04, RR = 1.88). The finding of Gm heterozygosity in DCM was associated with serum positivity for cardiac antibodies. A higher proportion of DCM patients were positive for both the Gm (1, 3, 17; 23; 5*, 21, 28) phenotype and HLA-DR4 compared to normals (3/68 vs 0/210; p = 0.04, RR = 22.50). A potentiating interactive effect in susceptibility to DCM was also found between the Gm (1, ±2, 3, 17; ±23; 5*, 21, 28) heterozygous phenotypes and HLA-DR4 (7/66 vs 2/207, p = 0.0009, RR = 12.16). These Gm phenotypes may be new markers of susceptibility in DCM, associated with positive autoimmune serology. The potentiating interaction of Gm and HLA-DR4 is in keeping with results reported in other autoimmune diseases.
UR - http://www.scopus.com/inward/record.url?scp=0027096779&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027096779&partnerID=8YFLogxK
U2 - 10.1016/0198-8859(92)90105-V
DO - 10.1016/0198-8859(92)90105-V
M3 - Article
C2 - 1293083
AN - SCOPUS:0027096779
VL - 35
SP - 193
EP - 199
JO - Human Immunology
JF - Human Immunology
SN - 0198-8859
IS - 3
ER -