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K Illingworth

Publications and source records attributed to K Illingworth.

6 recordsLinked to original sources
PubMed1996

Von Willebrand factor, thrombomodulin, thromboxane, beta-thromboglobulin and markers of fibrinolysis in primary Raynaud's phenomenon and systemic sclerosis.

OBJECTIVE: To determine whether measurement of different markers of endothelial damage, activation of coagulation, and platelet activation might differentiate between patients with primary Raynaud's phenomenon (PRP), limited cutaneous and diffuse systemic sclerosis (lcSSc and dSSc), and healthy control subjects. METHODS: Under carefully controlled conditions, fasting blood was drawn from 19 healthy control subjects, 10 patients with PRP, 17 with lcSSc and nine with dSSc for measurement of the following: von Willebrand factor (VWF) and soluble thrombomodulin as markers of endothelial damage/activation, thromboxane (as thromboxane B2) and beta-thromboglobulin as markers of platelet activation, and tissue plasminogen activator antigen, tissue plasminogen activator activity and plasminogen activator inhibitor-1 (PAI-1) as markers of fibrinolysis. RESULTS: VWF was increased significantly in patients with SSc, and there was also a linear trend for thromboxane and tissue plasminogen activator antigen (in addition to VWF) to differentiate between different subgroups of patients with Raynaud's phenomenon. Patients with dSSc had the highest values. A combined index of VWF and thromboxane showed a highly significant trend across the four groups studied. CONCLUSION: VWF, and to a lesser extent thromboxane and tissue plasminogen activator antigen, are associated with disease severity in patients with Raynaud's phenomenon. Prospective studies are now required to establish if these parameters can be used as markers of disease progression.

Adult↗
PubMed1994

Plasma TGF beta in systemic sclerosis: a cross-sectional study.

OBJECTIVES: To determine whether the active 25 kDa form of the fibrogenic cytokine transforming growth factor beta (TGF beta) can be detected in plasma from patients with systemic sclerosis and to examine the relationship between plasma TGF beta and clinical markers of disease severity and serum concentrations of the aminoterminal peptide of type III procollagen (PIIINP) (a laboratory marker of the fibrotic process). METHODS: A cross sectional study was made of 39 patients with systemic sclerosis (11 diffuse and 28 limited), nine patients with primary Raynaud's disease and 60 healthy controls. TGF beta 1 and TGF beta 2 were measured by enzyme linked immunosorbent assay (ELISA) (sensitivity 100 pg/ml) and PIIINP by radioimmunoassay. RESULTS: TGF beta 1 was detected in plasma from six of 39 patients with systemic sclerosis but not in any patient with primary Raynaud's disease or healthy controls. TGF beta 2 was not detected in plasma from patients or controls. No clear relationship was demonstrated between TGF beta 1, clinical features or PIIINP concentrations. CONCLUSIONS: The 25 kDa form of TGF beta 1 can be detected in the plasma of some patients with systemic sclerosis. This provides limited support for the hypothesis that this cytokine plays a role in the pathogenesis of this disease. However, longitudinal studies, particularly in early diffuse disease, are required to clarify the relationship between circulating TGF beta 1 and disease activity.

Adult↗
PubMed1993

Mechanisms of endothelial cell damage in systemic sclerosis and Raynaud's phenomenon.

OBJECTIVE: To investigate tumor necrosis factor (TNF), circulating immune complexes (CIC) and oxidized lipoproteins [measured as thiobarbituric acid reactive substances (TBARS)] as mediators of damage to endothelial cells (EC) in systemic sclerosis (SSc) and Raynaud's phenomenon (RP). METHODS: In addition to CIC, TBARS and TNF, von Willebrand factor (vWF), angiotensin converting enzyme (ACE) and EC cytotoxicity were measured as markers of EC damage. C-reactive protein (CRP) and rheumatoid factor (RF) were measured as indicators of inflammation. RESULTS: There were increases in TBARS and CIC, vWF and EC cytotoxicity, and CRP, with reduced levels of ACE. There were no correlations between any possible mediator of damage (TNF, TBARS, CIC) and indicators of such injury to the endothelium (vWF, ACE, EC cytotoxicity) except an inverse correlation between vWF and ACE. When patients with SSc were classified into those with limited disease (ISSc) or diffuse disease (dSSc), only wWF was different, being higher in patients with dSSc. In RP, vWF, RF and TBARS were again raised and ACE was lower. The only correlation was inversely between vWF and ACE. CONCLUSION: Our results are suggestive of injury to the endothelium in both SSc and RP, with greater damage in patients with dSSc. Although there were multiple abnormalities in biochemical and immunological indices, there were no consistent correlations to explain the clear damage to the vasculature. We conclude that additional mechanisms other than TNF, CIC and lipid peroxides may be responsible for the insult to the vascular tree so evident in these patients.

Adult↗
PubMed1991

A controlled study of stanozolol in primary Raynaud's phenomenon and systemic sclerosis.

A double blind, crossover study of fibrinolytic enhancement treatment using stanozolol has been performed in primary Raynaud's phenomenon and in systemic sclerosis. The outcome criteria included subjective evaluation, clinical examination, physiological measurements of peripheral blood flow, and fibrinolytic measurements. Nineteen patients entered and 11 completed the study of primary Raynaud's phenomenon. There was nonsignificant evidence of improvement in peripheral blood flow. Twenty four patients entered and 17 completed the study of systemic sclerosis. There was marked objective but not subjective evidence of improvement in the peripheral microcirculation during the stanozolol treatment period. There was also a nonsignificant improvement in dermal sclerosis. There were improvements in fibrinolytic activity during the stanozolol treatment period. There was no alteration in fibrinolytic reserve as measured by 1-desamino-8-D-arginine vasopressin stimulation, however. Although adverse events were common in both treatment periods, withdrawals predominantly occurred during the period of treatment with stanozolol and were principally due to anabolic problems. There does not seem to be any indication for the use of stanozolol in primary Raynaud's phenomenon. Fibrinolytic enhancement with stanozolol does appear useful in treating the microvascular features of systemic sclerosis.

Adult↗