Abstract
The role of polymorphonuclear cells (PMNs) in the pathophysiology of ischaemic vascular disease has been increasingly recognized in recent years. Activated PMNs may physically obstruct blood flow. Subsequent release of reactive oxygen radicals and lytic enzymes lead to continued damage. Previous studies have shown increased white cell activity in patients with secondary Raynaud's syndrome (RS). However, whether this is related to the underlying condition or to digital vasospasm is not clear. Using a more physiological whole blood PMN aggregation assay, we assessed PMN activity in 38 patients with severe Raynaud's phenomenon (RP) [16 had systemic sclerosis (SSc) and secondary RS; 22 had RP alone and no other features of a connective tissue disease]. Additionally, plasma levels of malondialdehyde (MDA), an indicator of free radical activity, were measured. Results were compared with those obtained from 56 matched volunteers. In order to assess if changes in PMN activity was directly related to digital vasospasm, patients were asked to record the duration and frequency of their Raynaud's attacks during a 2-week period using a pocket sized diary. Correlation between these clinical variables of Raynaud's severity and white cell activity was assessed.
Patients with RP both with and without SSc, showed a significantly greater fall in single PMN count when compared with control subjects [SSc associated RS 48.2 (41.4–56)% versus control, P = 0.04; RP alone 49.3 (46.8–52.1)% versus control, P = 0.01 (Mann-Whitney U-test)]. MDA levels were significantly higher in both groups of patients when compared with control subjects [SSc associated RS 8.35 (7.35–9.6) µmol/1 versus control, P = 0.000006; RP alone 7.5 (6.4–8.8) µmol/1 versus control, P = 0.003 (Mann-Whitney U-test)]. There were no significant differences in PMN aggregation and MDA levels between the two groups of patients. There were no significant correlations between PMN aggregation and MDA levels and duration and frequency of Raynaud's attacks in either group of patients.
In conclusion, we have shown increased PMN activity in patients with RP The role of polymorphonuclear cells (PMNs) in the pathophysiology of ischaemic vascular disease has been increasingly recognized in recent years. Activated PMNs may physically obstruct blood flow. Subsequent release of reactive oxygen radicals and lytic enzymes lead to continued damage. Previous studies have shown increased white cell activity in patients with secondary Raynaud's syndrome (RS). However, whether this is related to the underlying condition or to digital vasospasm is not clear. Using a more physiological whole blood PMN aggregation assay, we assessed PMN activity in 38 patients with severe Raynaud's phenomenon (RP) [16 had systemic sclerosis (SSc) and secondary RS; 22 had RP alone and no other features of a connective tissue disease]. Additionally, plasma levels of malondialdehyde (MDA), an indicator of free radical activity, were measured. Results were compared with those obtained from 56 matched volunteers. In order to assess if changes in PMN activity was directly related to digital vasospasm, patients were asked to record the duration and frequency of their Raynaud's attacks during a 2-week period using a pocket sized diary. Correlation between these clinical variables of Raynaud's severity and white cell activity was assessed.
Patients with RP both with and without SSc, showed a significantly greater fall in single PMN count when compared with control subjects [SSc associated RS 48.2 (41.4–56)% versus control, P = 0.04; RP alone 49.3 (46.8–52.1)% versus control, P = 0.01 (Mann-Whitney U-test)]. MDA levels were significantly higher in both groups of patients when compared with control subjects [SSc associated RS 8.35 (7.35–9.6) µmol/1 versus control, P = 0.000006; RP alone 7.5 (6.4–8.8) µmol/1 versus control, P = 0.003 (Mann-Whitney U-test)]. There were no significant differences in PMN aggregation and MDA levels between the two groups of patients. There were no significant correlations between PMN aggregation and MDA levels and duration and frequency of Raynaud's attacks in either group of patients.
In conclusion, we have shown increased PMN activity in patients with RP The role of polymorphonuclear cells (PMNs) in the pathophysiology of ischaemic vascular disease has been increasingly recognized in recent years. Activated PMNs may physically obstruct blood flow. Subsequent release of reactive oxygen radicals and lytic enzymes lead to continued damage. Previous studies have shown increased white cell activity in patients with secondary Raynaud's syndrome (RS). However, whether this is related to the underlying condition or to digital vasospasm is not clear. Using a more physiological whole blood PMN aggregation assay, we assessed PMN activity in 38 patients with severe Raynaud's phenomenon (RP) [16 had systemic sclerosis (SSc) and secondary RS; 22 had RP alone and no other features of a connective tissue disease]. Additionally, plasma levels of malondialdehyde (MDA), an indicator of free radical activity, were measured. Results were compared with those obtained from 56 matched volunteers. In order to assess if changes in PMN activity was directly related to digital vasospasm, patients were asked to record the duration and frequency of their Raynaud's attacks during a 2-week period using a pocket sized diary. Correlation between these clinical variables of Raynaud's severity and white cell activity was assessed.
Patients with RP both with and without SSc, showed a significantly greater fall in single PMN count when compared with control subjects [SSc associated RS 48.2 (41.4–56)% versus control, P = 0.04; RP alone 49.3 (46.8–52.1)% versus control, P = 0.01 (Mann-Whitney U-test)]. MDA levels were significantly higher in both groups of patients when compared with control subjects [SSc associated RS 8.35 (7.35–9.6) µmol/1 versus control, P = 0.000006; RP alone 7.5 (6.4–8.8) µmol/1 versus control, P = 0.003 (Mann-Whitney U-test)]. There were no significant differences in PMN aggregation and MDA levels between the two groups of patients. There were no significant correlations between PMN aggregation and MDA levels and duration and frequency of Raynaud's attacks in either group of patients.
In conclusion, we have shown increased PMN activity in patients with RP alone as well as those with SSc associated RS. Such abnormal PMN function may be related to digital vasospasm and not the underlying connective tissue disease. However, no correlation between PMN activity and Raynaud's severity was found. A follow-up study is being planned.
Patients with RP both with and without SSc, showed a significantly greater fall in single PMN count when compared with control subjects [SSc associated RS 48.2 (41.4–56)% versus control, P = 0.04; RP alone 49.3 (46.8–52.1)% versus control, P = 0.01 (Mann-Whitney U-test)]. MDA levels were significantly higher in both groups of patients when compared with control subjects [SSc associated RS 8.35 (7.35–9.6) µmol/1 versus control, P = 0.000006; RP alone 7.5 (6.4–8.8) µmol/1 versus control, P = 0.003 (Mann-Whitney U-test)]. There were no significant differences in PMN aggregation and MDA levels between the two groups of patients. There were no significant correlations between PMN aggregation and MDA levels and duration and frequency of Raynaud's attacks in either group of patients.
In conclusion, we have shown increased PMN activity in patients with RP The role of polymorphonuclear cells (PMNs) in the pathophysiology of ischaemic vascular disease has been increasingly recognized in recent years. Activated PMNs may physically obstruct blood flow. Subsequent release of reactive oxygen radicals and lytic enzymes lead to continued damage. Previous studies have shown increased white cell activity in patients with secondary Raynaud's syndrome (RS). However, whether this is related to the underlying condition or to digital vasospasm is not clear. Using a more physiological whole blood PMN aggregation assay, we assessed PMN activity in 38 patients with severe Raynaud's phenomenon (RP) [16 had systemic sclerosis (SSc) and secondary RS; 22 had RP alone and no other features of a connective tissue disease]. Additionally, plasma levels of malondialdehyde (MDA), an indicator of free radical activity, were measured. Results were compared with those obtained from 56 matched volunteers. In order to assess if changes in PMN activity was directly related to digital vasospasm, patients were asked to record the duration and frequency of their Raynaud's attacks during a 2-week period using a pocket sized diary. Correlation between these clinical variables of Raynaud's severity and white cell activity was assessed.
Patients with RP both with and without SSc, showed a significantly greater fall in single PMN count when compared with control subjects [SSc associated RS 48.2 (41.4–56)% versus control, P = 0.04; RP alone 49.3 (46.8–52.1)% versus control, P = 0.01 (Mann-Whitney U-test)]. MDA levels were significantly higher in both groups of patients when compared with control subjects [SSc associated RS 8.35 (7.35–9.6) µmol/1 versus control, P = 0.000006; RP alone 7.5 (6.4–8.8) µmol/1 versus control, P = 0.003 (Mann-Whitney U-test)]. There were no significant differences in PMN aggregation and MDA levels between the two groups of patients. There were no significant correlations between PMN aggregation and MDA levels and duration and frequency of Raynaud's attacks in either group of patients.
In conclusion, we have shown increased PMN activity in patients with RP The role of polymorphonuclear cells (PMNs) in the pathophysiology of ischaemic vascular disease has been increasingly recognized in recent years. Activated PMNs may physically obstruct blood flow. Subsequent release of reactive oxygen radicals and lytic enzymes lead to continued damage. Previous studies have shown increased white cell activity in patients with secondary Raynaud's syndrome (RS). However, whether this is related to the underlying condition or to digital vasospasm is not clear. Using a more physiological whole blood PMN aggregation assay, we assessed PMN activity in 38 patients with severe Raynaud's phenomenon (RP) [16 had systemic sclerosis (SSc) and secondary RS; 22 had RP alone and no other features of a connective tissue disease]. Additionally, plasma levels of malondialdehyde (MDA), an indicator of free radical activity, were measured. Results were compared with those obtained from 56 matched volunteers. In order to assess if changes in PMN activity was directly related to digital vasospasm, patients were asked to record the duration and frequency of their Raynaud's attacks during a 2-week period using a pocket sized diary. Correlation between these clinical variables of Raynaud's severity and white cell activity was assessed.
Patients with RP both with and without SSc, showed a significantly greater fall in single PMN count when compared with control subjects [SSc associated RS 48.2 (41.4–56)% versus control, P = 0.04; RP alone 49.3 (46.8–52.1)% versus control, P = 0.01 (Mann-Whitney U-test)]. MDA levels were significantly higher in both groups of patients when compared with control subjects [SSc associated RS 8.35 (7.35–9.6) µmol/1 versus control, P = 0.000006; RP alone 7.5 (6.4–8.8) µmol/1 versus control, P = 0.003 (Mann-Whitney U-test)]. There were no significant differences in PMN aggregation and MDA levels between the two groups of patients. There were no significant correlations between PMN aggregation and MDA levels and duration and frequency of Raynaud's attacks in either group of patients.
In conclusion, we have shown increased PMN activity in patients with RP alone as well as those with SSc associated RS. Such abnormal PMN function may be related to digital vasospasm and not the underlying connective tissue disease. However, no correlation between PMN activity and Raynaud's severity was found. A follow-up study is being planned.
Original language | English |
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Pages (from-to) | 375-380 |
Number of pages | 6 |
Journal | Rheumatology |
Volume | 31 |
Issue number | 6 |
DOIs | |
Publication status | Published - Jun 1992 |
Keywords
- Raynaud's syndrome
- Systemic sclerosis
- Polymorphonuclear cell aggregation
- Free radicals