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Biomedical subjects

S H Ibbotson

Publications and source records attributed to S H Ibbotson.

At least 55 records · Page 3Linked to original sources
PubMed1998

Benzoyl peroxide increases UVA-induced plasma membrane damage and lipid oxidation in murine leukemia L1210 cells.

Ultraviolet A radiation induces oxidative stress and cell damage. The purpose of this investigation was to examine whether ultraviolet A-induced cell injury was amplified by the presence of a non-ultraviolet A absorbing molecule capable of generating free radicals. Benzoyl peroxide was used as a lipid soluble potential radical-generating agent. Plasma membrane permeability assessed by trypan blue uptake was used to measure cell damage in murine leukemia L1210 cells. Cells were irradiated with a pulsed Nd/YAG laser at 355 nm using 0-160 J per cm2. The ratio of the fluence-response slope in the presence of 40 microM benzoyl peroxide to that of irradiated controls was 4.3 +/- 2.6. Benzoyl peroxide alone or benzoyl peroxide added after irradiation did not cause increased trypan blue uptake. The ratio of the fluence-response slopes in the presence of 40 microM benzoyl peroxide to that of irradiated controls was 4.7 +/- 1.4 when cells were irradiated (0-43 J per cm2) with a xenon lamp, filtered to remove wavelengths <320 nm. The increased trypan blue uptake in 355 nm-irradiated cells in the presence of benzoyl peroxide was inhibited in a concentration-dependent manner by butylated hydroxytoluene, vitamin E, and trolox, a water-soluble vitamin E derivative. Lipid oxidation, assessed as thiobarbituric acid reactive substances, was significantly increased in samples irradiated with ultraviolet A in the presence of benzoyl peroxide at fluences >34 J per cm2. The increased trypan blue uptake and thiobarbituric acid reactive substances were inhibited by butylated hydroxytoluene. These results suggest that agents not absorbing ultraviolet A radiation may enhance ultraviolet A-initiated oxidative stress in cells.

Absorption↗
PubMed1996

Disseminated superficial porokeratosis: what is the association with ultraviolet radiation?

A female patient is presented who consistently developed lesions of disseminated superficial porokeratosis (DSP) whilst on holiday abroad. The lesions resolved completely within 4-6 weeks of return to the UK. Induction of the lesions by exposure to artificial sources of UVA and UVB was unsuccessful. Disseminated superficial porokeratosis (DSP) is thought to be a clonal disorder of keratinization and the histological hallmark is the cornoid lamella. The aetiology of DSP is unclear although it has been suggested that local or systemic immune suppression may allow the development of mutant clones of keratinocytes. Chernosky and Freeman first proposed an actinic aetiology for DSP in 1967 but the mechanism of induction is unclear.

Adult↗
PubMed1996

The relevance and effect of amalgam replacement in subjects with oral lichenoid reactions.

In this study we examined the prevalence of mercury hypersensitivity in patients with oral lichenoid reactions (OLR) and the effect of amalgam replacement in subjects with amalgams adjacent to OLR irrespective of their mercury sensitivity status. One hundred and ninety-seven patients with oral problems were examined: 109 with OLR, 22 with oral and generalized lichen planus, and 66 with other oral diagnoses, including aphthous ulcers and orofacial granulomatosis. Nineteen per cent of patients with OLR reacted to mercury on patch testing, significantly more than in those with generalized lichen planus (0%) and in those with other oral diagnoses (3%). Twenty-two patients with OLR and adjacent amalgams had amalgam replacement and, in 16 of 17 mercury-positive subjects and three of four mercury-negative subjects, the OLR resolved after amalgam removal. In conclusion, we found a significantly increased prevalence of mercury hypersensitivity in patients with localized OLR in comparison to subjects with other oral problems. Amalgam replacement resulted in resolution of OLR in the majority of patients with amalgams adjacent to OLR irrespective of their mercury sensitivity status.

Adult↗
PubMed1996

The effect of topical indomethacin on ultraviolet-radiation-induced erythema.

Indomethacin inhibits UVB erythema but is thought not to influence UVA erythema. We have examined the wavelength dependence of the effect of indomethacin on ultraviolet radiation (UVR) erythema. Duplicate sites on the back were irradiated with a series of doses at 300 and 320 nm, or single doses at 330, 340, 350 or 370 nm. Indomethacin 1% was applied to sites on one side of the back after irradiation, occluded for 2h and erythema measured at 24h with a reflectance instrument. Indomethacin inhibited 300 and 320 nm (UVB) erythema, had no effect at 330 and 340 nm (UVA2), but augmented 350 and 370 nm (UVA1) erythema. There appears to be a varied response of UVR erythema to cyclo-oxygenase inhibition at different wavelengths across the UVR spectrum. This mechanism may be deranged in certain photosensitive disorders.

Adult↗
PubMed1995

The effect of aspirin on haemostatic activity in the treatment of chronic venous leg ulceration.

An increased rate of venous ulcer healing with the use of oral enteric-coated aspirin (300 mg) daily has been reported. Whether the effect of aspirin in this condition is related to its action on the haemostatic mechanism is unclear, and therefore this study aimed to assess the effect of aspirin on some haemostatic parameters in patients with chronic venous leg ulcers. A double-blind, randomized, placebo-controlled, parallel-group study of haemostatic activity and the effect of aspirin was implemented over a 4-month period. Twenty patients with venous leg ulcers, and 20 age- and sex-matched controls were studied. Patients received enteric-coated aspirin (300 mg) or placebo (one tablet) daily for 4 months, in addition to standardized local compressive bandaging (Setopress). Assessments made at recruitment, and at 2 and 4 months, included measurement of total ulcer surface area, haematological and biochemical screening, measurement of coagulation times, coagulation factor VIII:C (FVIII:C) and von Willebrand factor (vWF), and plasminogen activator inhibitor-1 (PAI-1) levels. Procoagulant activity was assessed by a computer-assisted technique, to determine the rate of thrombin production in vitro. Patients with venous ulcers had increased levels of fibrinogen (P < 0.01), FVIII:C (P < 0.05), vWF (P < 0.05) and PAI-1 antigen (P < 0.01) compared with controls. Shortening of the coagulation rate, shown by a reduction of the time to generate 50% maximal thrombin activity in seconds (T50), was seen in patients, in comparison with control subjects (P < 0.05). T50 was longer in patients receiving aspirin than those receiving placebo, reflecting prolongation of coagulation rate in the aspirin-treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed1995

Acute severe bronchoconstriction precipitated by coal tar bandages.

We report the occurrence of severe symptomatic bronchoconstriction in an atopic asthmatic subject following the application of coal tar bandages. Investigations showed that this was likely to have been caused by inhalation of coal tar vapour. We suggest that coal tar preparations should be used with caution in asthmatic subjects.

Acute Disease↗
PubMed1995

Adhesion molecules in inflammatory bowel disease.

The ability of leucocytes to adhere to endothelium is essential for leucocyte migration into inflammatory sites. Some of these adhesion molecules are released from the cell surface and can be detected in serum. The soluble adhesion molecules intercellular adhesion molecule 1 (ICAM-1), E selectin, and vascular cell adhesion molecule 1 (VCAM-1) were studied in the serum of patients with Crohn's disease, ulcerative colitis, and healthy controls. A second blood sample was taken from patients with active disease after one month of treatment and a third two months after remission was achieved. Tissue expression of the same adhesion molecules was studied by immunohistology. Circulating VCAM-1 concentrations were significantly higher in patients with active ulcerative colitis (n = 11, median = 165 U/ml) compared with patients with inactive ulcerative colitis (n = 10, median = 117 U/ml, p < 0.005), active Crohn's disease (n = 12, median = 124 U/ml, p < 0.02), and controls (n = 90, median = 50 U/ml, p < 0.0001). Within each disease group there were no significant differences in E selectin or ICAM-1 concentrations between the active and inactive states, however, patients with active Crohn's disease had significantly higher ICAM-1 concentrations (n = 12, median = 273 ng/ml) than controls (n = 28, median = 168, p < 0.003). VCAM-1 concentrations fell significantly from pretreatment values to remission in active ulcerative colitis (p < 0.01). In Crohn's disease there was a significant fall in ICAM-1 both during treatment (p < 0.01) and two months after remission (p < 0.02). Vascular expression of ICAM-1 occurred more often and was more intense in inflamed tissue sections from patients with ulcerative colitis and Crohn's disease than from controls. Vascular labelling with antibody to E selectin also occurred more often in patients with active inflammatory bowel disease. In conclusion, increased circulating concentrations of selected adhesion molecules are associated with inflammatory bowel disease. There is also evidence of local upregulation, particularly of ICAM-1. Differential expression of adhesion molecules in tissue may play a part in the initiation of leucocyte migration and local inflammation; the function of circulating adhesion molecules is unknown, but may play a physiological part in blocking adhesion.

Acute Disease↗
PubMed1995

The effect of insulin-induced hypoglycaemia on factor VIII:C concentrations and thrombin activity in subjects with type 1 (insulin-dependent) diabetes.

The effect of insulin-induced hypoglycaemia on plasma coagulant activity was studied in 11 subjects with well-controlled, uncomplicated type 1 diabetes. Thrombin generation was determined in plasma by a computer ex-vivo assisted chromogenic method and by the activated partial thromboplastin time (APTT). In addition, factor VIII:C, thrombin-antithrombin III (TAT) complex and fibrinopeptide A (FPA) levels were measured. Hypoglycaemia induced a rise in mean (SD) factor VIII:C concentrations from a baseline level of 1.13 (0.32) IU/ml to a peak 15 min after onset of symptoms and they remained increased at 90 min [1.54 (0.57) and 1.5 (0.54) IU/ml, p < 0.001 respectively]. A corresponding reduction in time to generate 50% maximal thrombin activity occurred from a pre-insulin value of 56 (6) s to a minimum reading of 46 (7) s at 15 min (p < 0.001) and remained low at 90 min [48 (6) s, p < 0.001]. APTT shortened from 43.3 (4.8) s to 40.1 (4.6) s at 30 min (p < 0.001) but did not fall below the normal range (37.6-42.7 s) and no significant changes in TAT or FPA levels were noted. Factor VIII:C correlated inversely with time to generate 50% maximal thrombin activity and APTT (r = -0.580, p < 0.001; r = -0.673, p < 0.001, n = 66, respectively). The results show that the rise in plasma factor VIII:C levels induced by hypoglycaemia is accompanied by accelerated rates of generation of thrombin in contact-activated plasma, though concentrations of FPA and TAT remain unchanged, although TAT complexes are not a sensitive marker of in vivo thrombin generation.

Acute Disease↗
PubMed1994

Randomised trial of oral aspirin for chronic venous leg ulcers.

The effect of oral aspirin on the healing rate of chronic venous leg ulcers was compared with that of placebo in a double-blind randomised trial. 20 subjects with chronic venous leg ulcers were randomised to daily enteric-coated aspirin 300 mg or placebo, and standardised compression bandaging. 4 months of treatment achieved ulcer healing in 38% of the patients receiving aspirin compared with 0% of those receiving placebo (p < 0.007). 52% of the aspirin-treated group showed significant reduction in ulcer size compared with 26% of placebo recipients (p < 0.007). Reduction in ulcer surface area was significantly better in the aspirin-treated group at 2 (p < 0.01) and 4 months (p < 0.002) compared with that in the placebo group.

Administration, Oral↗
PubMed1994

Follicular keratoses at amputation sites.

We describe two patients with painful follicular keratoses at lower limb amputation sites. Subsequent examination of 31 amputees revealed evidence of keratoses in four of 28 patients with lower limb stumps. Two of the four affected subjects experienced stump pain exacerbated by weight-bearing. This problem is not well documented. Local treatment measures may be ineffective. Painful stump follicular keratoses may be a cause of significant morbidity in lower limb amputees, and may be the result of an ill-fitting prosthesis.

Adult↗
PubMed1993

The effect of short-term exercise on plasma procoagulant activity in patients with type II (non-insulin-dependent) diabetes and healthy volunteers.

The effect of exercise on plasma coagulant activity was studied in 16 subjects with newly-diagnosed type II diabetes without vascular complications and 9 healthy volunteers. Generation of thrombin was determined by a computer-assisted chromogenic method and results expressed as time to generate 50% maximal thrombin activity (T50/s). In addition, APTT, factor VIII and thrombin-antithrombin III (TAT) complex levels were measured. Pre-exercise FVIII:C [mean (+/- SD)] was increased in diabetic compared to control subjects [1.5 (0.4); 0.9 (0.2) IU ml-1; (p < 0.001) respectively]. No significant differences in APTT, TAT or T50 were detected between the groups. Exercise induced a rise in FVIII complex, reduction of APTT [33 (2) s to 31 (2) s; (p = 0.004)] and T50 [58 (6) s to 53 (6) s; (p = 0.01)] in controls and an increase in FVIII complex but no significant changes in APTT or T50 in diabetic patients, with no change in TAT in either group. A greater increase in FVIII:C than vWF levels occurred in controls [0.2 (0.1); 0.1 (0.1) IU ml-1; (p = 0.005)] and patients [0.3 (0.4); 0.2 (0.1) IU ml-1; (p = 0.032)]. In patients, FVIII:C correlated inversely with APTT (r = -0.522, p = 0.038) and T50 (r = -0.592, p = 0.016). The results show that FVIII:C levels are increased at diagnosis in patients with type II diabetes without vascular disease but there is no enhancement of plasma procoagulant activity. In healthy individuals, exercise induced activation of coagulation which was not seen in patients, suggesting that it does not precipitate a state of accelerated thrombogenesis in subjects with uncomplicated type II diabetes.

Blood Coagulation Factors↗
PubMed1993

Thrombin generation and factor VIII:C levels in patients with type 1 diabetes complicated by nephropathy.

The association between plasma coagulant activity and the presence of diabetic nephropathy was investigated in 31 patients with Type 1 diabetes, 12 with and 19 without nephropathy, and in 11 healthy subjects. Thrombin generation was assessed by computer assisted chromogenic method and expressed as time (in seconds) to 50% maximal thrombin activity (T50). Factor VIII:C levels related to thrombin activity, glycaemic control, and renal function. Median (IQ) FVIII:C concentration was increased in patients with nephropathy (1590 (1130-1900) IU l-1) compared to those without renal disease and with controls (960 (750-1090); 1020 (810-1100) IU l-1, p < 0.01, respectively). There were no significant differences in T50 values between the groups. FVIII:C correlated with age in all subjects and in the diabetic group (r = 0.33, p = 0.036; r = 0.39, p = 0.031) and inversely with T50 in all subjects and in controls (r = -0.35, p = 0.02; r = -0.62, p = 0.04). In all subjects and in patients, FVIII:C was related to urinary albumin excretion and creatinine clearance. FVIII:C and T50 were not related to HbA1c. The results show that FVIII:C levels are increased in Type 1 diabetes complicated by nephropathy and are related to degree of renal impairment but not levels of glycaemia. No associated enhancement of plasma procoagulant activity was detected.

Adult↗