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Biomedical subjects

M I Jayson

Publications and source records attributed to M I Jayson.

At least 73 records · Page 4Linked to original sources
PubMed1994

Vasculitis in patients with systemic sclerosis and severe digital ischaemia requiring amputation.

OBJECTIVES: To document the incidence of histological vasculitis in amputation specimens from patients with severe digital ischaemia secondary to systemic sclerosis (SSc), and to look for an association between anticardiolipin (aCL) antibodies and severe digital ischaemia in SSc. METHODS: This was a retrospective review of patients with SSc who underwent amputation for digital ischaemia over a three year period. RESULTS: Five of nine patients had histological vasculitis, four of whom had aCL antibodies, although these were not present in high titre. CONCLUSION: Vasculitis does occur in SSc, at least in that subgroup with severe peripheral ischaemia. These findings could have implications for treatment of this subgroup of patients with SSc.

Adult↗
PubMed1994

Anticardiolipin, anticentromere and anti-Scl-70 antibodies in patients with systemic sclerosis and severe digital ischaemia.

OBJECTIVE: Following observation of weakly positive anticardiolipin (aCL) antibodies in four of eight patients with systemic sclerosis (SSc) and severe digital ischaemia requiring amputation, the association between the presence of these and other antibodies and severe peripheral ischaemia in patients with SSc was examined. METHODS: ACL antibodies (IgG and IgM), anticentromere and anti-Scl-70 antibodies were measured in a further 60 patients with SSc over a one year period. Thirty one of the 68 patients in whom aCL antibodies were assayed had 'severe ischaemia', having suffered digital ischaemia severe enough to warrant amputation (13 patients), surgical debridement or admission for intravenous vasodilator therapy. RESULTS: There was no difference in aCL positivity between those with severe ischaemia and those without, nor between those who had amputations and those who had not. Three of the 31 patients (10%) with severe ischaemia had IgG and eight (26%) IgM aCL antibodies in weak to moderate titre compared to 10 (27%) and 6 (16%) respectively of the remaining patients (p = 0.06 for IgG and p = 0.25 for IgM, Fisher's exact test). Seventeen of the 31 patients (55%) with severe ischaemia were anticentromere antibody positive compared with nine of 37 (24%) without ischaemia (p = 0.01). Six patients with severe ischaemia had anti-Scl-70 antibodies compared with two of the 37 without ischaemia (p = 0.08). CONCLUSIONS: The findings do not support an association between aCL antibodies and severe ischaemia in SSc, but confirm the previously reported association between anticentromere antibodies and severe peripheral ischaemia. Although anti-Scl-70 antibodies were present only in a small number of patients, there was also a tendency for these to be associated with severe ischaemia, suggesting that patients with either anticentromere or anti-Scl-70 antibodies should be considered at risk of digital loss.

Adult↗
PubMed1994

Micronutrient antioxidant status in patients with primary Raynaud's phenomenon and systemic sclerosis.

OBJECTIVE: To investigate the possibility that micronutrient antioxidant status is an important factor in determining the severity of Raynaud's phenomenon (RP) and in differentiating between patients with primary Raynaud's phenomenon (PRP) and those in whom Raynaud's is secondary to systemic sclerosis (SSc). METHODS: Four micronutrient antioxidants (selenium, vitamin E, beta-carotene and ascorbic acid) and 2 "markers" of free radical associated activity were assayed in peripheral blood from 10 patients with PRP, 9 with limited cutaneous SSc (ISSc), 9 with diffuse SSc (dSSc) and 15 healthy control subjects. RESULTS: Plasma ascorbic acid was reduced in all 3 groups of patients: median level 10.6 mg/l in controls, 4.8 mg/l in PRP (p < 0.01), 2.5 mg/l in ISSc (p < 0.01) and 6.8 mg/l in dSSc (p < 0.05). A reduction in serum selenium was especially found in dSSc (median 75 micrograms/l compared to 100 micrograms/l in controls, p < 0.05). In keeping with these deficiencies, the serum concentration of 9, 11, linoleic acid was elevated in RP patients: median values for the molar ratio of the isomer to the parent fatty acid were 1.91% in controls, 3.70% in ISSc (p < 0.05) and 3.85% in dSSc (p < 0.01). Smoking patients showed lower levels of ascorbic acid and higher levels of the linoleic isomer than nonsmokers. CONCLUSION: Deficiencies of ascorbic acid and selenium may predispose towards irreversible tissue injury in RP patients and cigarette smoke may be an independent risk factor. Micronutrient antioxidant supplements may be of therapeutic value.

Aging↗
PubMed1993

Increased central drive during fatiguing contractions of the paraspinal muscles in patients with chronic low back pain.

In low back pain patients the paraspinal muscles demonstrate excess fatigability. Whether the cause is "central" as could result from impaired motor unit recruitment due to poor motivation or fear of pain, or "peripheral", and caused by defects in the contractile apparatus, is unknown. Using surface electromyography in conjunction with a standardized isometric fatigue test, this study investigates the mechanisms causing paraspinal muscle dysfunction in patients with both nonsurgical and postsurgical chronic low back pain. During the fatigue test normal subjects and both patient groups exhibited electromyographic increases. These were significantly greater in both patient groups, indicating increased central drive to their muscles. These findings may suggest that patients' excess fatigue is peripheral in origin, with increased central drive arising secondary to muscle wasting or denervation, although a central activation defect has not been excluded. Impaired physical performance in low back pain patients does not seem to be caused by lack of central drive.

Adult↗
PubMed1993

The vascular basement membrane in systemic sclerosis skin: heterogeneity of type IV collagen.

In systemic sclerosis (SS) changes in the dermal microvasculature include endothelial cell damage, a reduction in the number of vessels, and vascular basement membrane thickening. The basement membrane is a critical component of the vessel, and alterations in its structure may lead to changes in the surrounding tissue. In SS the altered basement membrane is associated with the subsequent development of fibrosis. To investigate the relationship between vascular basement membrane changes in affected skin and disease progression, immunohistochemical analyses were performed using both polyclonal and monoclonal antibodies against type IV collagen, the major basement membrane collagen. Using two monoclonal antibodies directed against different conformational epitopes within the (alpha 1)2 (alpha 2) helical domain, type IV collagen was detected in normal skin, and uninvolved SS skin, but not in later grades of disease. Identical results were obtained using a monoclonal antibody against a sequential determinant on the denatured alpha 1 (IV) chain. The use of a polyclonal antibody, however, showed that type IV collagen was present in all grades of disease, suggesting an alteration in the composition of type IV collagen with disease progression.

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↗
PubMed1992

Radiographic demonstration of paraspinal muscle wasting in patients with chronic low back pain.

This study investigated whether paraspinal muscle wasting occurs in association with chronic low back pain (LBP). Cross-sectional areas (CSA) of spinal and paraspinal structures were measured radiographically, at the level of L4, in 43 patients with recent and 44 with chronic LBP. Crude anthropometry demonstrated no differences between the groups with regard to L4 and paraspinal and psoas muscle CSAs, but inter-individual differences were large. Since body weight correlated significantly with L4 CSA this dimension was used as an 'internal standard' and further inter-individual comparisons were made using paraspinal: L4 and psoas: L4 (i.e. muscle to bone) CSA ratios. Muscle assessments made in this 'relative' fashion revealed significant reductions in paraspinal and psoas dimensions in patients with chronic compared to recent onset LBP. These changes could cause paraspinal and psoas muscle weakness and thereby predispose to spinal instability and progressive dysfunction.

Adult↗
PubMed1992

Abnormal temperature control suggesting sympathetic dysfunction in the shoulder skin of patients with frozen shoulder.

In view of the possibility that sympathetically mediated pain could be responsible for frozen shoulder symptoms we compared shoulder skin vasomotor control in 11 patients with frozen shoulder and 17 similarly aged normal subjects without shoulder pain. Using computer-assisted thermography the shoulder skin temperature was assessed before and following a 'cold challenge' which consisted of a 15 degrees C cold pack being held against the skin for 60 sec. Both prior to and immediately following the cold challenge shoulder skin temperatures tended to be lower in the patients. During a 10-min rewarming phase, however, the between-group temperature difference increased and became significant at the 0.05 level. These abnormalities of temperature control in patients clearly suggest sympathetic dysfunction in the dermatome subserving pain sensation from the affected shoulder. Whether these abnormalities are primary or secondary remains unresolved.

Adult↗
PubMed1992

Studies of the microvascular endothelium in uninvolved skin of patients with systemic sclerosis: direct evidence for a generalized microangiopathy.

Various parameters for assessing endothelial cell (EC) metabolism, including immunohistochemistry and adenosine uptake, have been compared in the clinically uninvolved skin of patients with diffuse systemic sclerosis (DSS), CREST, incomplete CREST syndrome (ICREST), primary Raynaud's disease (1 degree RD) and normal controls. Evidence of platelet adhesion to EC, decreased EC storage of factor VII-related antigen, changes in EC morphology and decreased adenosine uptake by EC, were found in the dermal microvasculature of normal skin of patients with DSS, CREST and ICREST, but not in 1 degree RD. These data indicate that a generalized microvascular endothelial dysfunction is present in the skin of patients with the systemic forms of scleroderma.

Adult↗
PubMed1992

Measurement of cold challenge responses in primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis.

Using computed thermography continuous temperature recordings were made before and after cold challenge of the fingers of control subjects and patients with primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis. Basal skin temperature measurements (Tpre) were significantly lower in patients with primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis than in the controls. Temperatures immediately after cold challenge (T0) were significantly lower in patients with primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis than in controls. The lag phase before the start of temperature recovery (Tlag) was significantly greater in patients with primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis than in control subjects. The maximum recovery index (R%) was significantly less in patients with primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis than in controls. The maximum rate of change of temperature during the rapid phase of rewarming (Gmax) was significantly greater in controls than in patients with primary Raynaud's phenomenon and Raynaud's phenomenon associated with systemic sclerosis. Discriminant analysis showed that the dynamic parameters of rewarming (Tlag, Gmax, and R%) showed greater variation between the patients with primary Raynaud's phenomenon and those with Raynaud's phenomenon associated with systemic sclerosis than did Tpre or T0. This method of analysis of cold challenge will be used in studies of the effects of treatment of Raynaud's phenomenon.

Adult↗