A.V.M. Foster
University of Cambridge
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by A.V.M. Foster.
Diabetic Medicine | 1997
A. Gough; Hagosa D. Abraha; F. Li; T.S. Purewal; A.V.M. Foster; P.J. Watkins; C. Moniz; Michael Edmonds
Excess osteoclast activity is believed to be responsible for the early bone changes associated with Charcot neuroarthropathy in diabetes mellitus. Markers of osteoclast and osteoblast activity were measured in four groups of patients: 16 with an acute Charcot foot, 16 with a chronic Charcot foot, 10 diabetic controls, and 10 non‐diabetic controls. Serum carboxyterminal telopeptide of type 1 collagen (1CTP), a marker of osteoclastic bone resorption, was significantly raised in the dorsal venous arch of the acute Charcot foot, 6.1 ± 1.5 μg l−1 (mean ± SD) compared with the chronic Charcot foot 4.1 ± 1.4, diabetic controls 3.3 ± 1.4, and non‐diabetic controls 2.8 ± 1.4, p < 0.0001. This local increase in 1CTP was also reflected systemically in a study subgroup of 6 patients with acute Charcot neuroarthropathy, in whom peripheral antecubital vein 1CTP was 9.2 ± 2.6 compared with 9.0 ± 3.1 in the foot. In 6 chronic Charcot neuroarthropathy patients, foot (3.8 ± 1.3) and systemic (4.0 ± 1.5) 1CTP values were similar. Serum procollagen carboxyterminal propeptide (P1CP), an indicator of osteoblastic bone formation, was not significantly different between the feet of patients with acute Charcot neuroarthropathy 112 ± 1.5 μg l−1, patients with chronic Charcot neuroarthropathy 109 ± 1.5 μg l−1, diabetic controls 93.5 ± 2.3 μg l−1, and non‐diabetic controls 90.1 ± 1.5 μg l−1. These results suggest that the acute Charcot foot demonstrates excess osteoclastic activity without concomitant increase in osteoblastic function. This may be important in its pathogenesis. © 1997 John Wiley & Sons, Ltd.
Diabetes-metabolism Research and Reviews | 2000
Michael Edmonds; M. Bates; M. Doxford; Andrew Gough; A.V.M. Foster
This review examines several of the recently introduced wound care products that have been put forward as treatment modalities for the diabetic foot ulcer. Discussed are the results of clinical trials with the platelet‐derived growth factor, becaplermin, the tissue‐engineered products Dermagraft and Apligraf, and Hyaff which is an ester of hyaluronic acid. In patients with an infected foot ulcer, encouraging results were obtained with the granulocyte‐colony stimulating factor, Filgrastim. Copyright
Diabetic Medicine | 1995
A.V.M. Foster; S. Snowden; A. Grenfell; P.J. Watkins; Michael Edmonds
This 4‐year prospective study investigated the reasons for high levels of gangrene and major amputation in diabetic renal transplant patients and whether regular mutli‐disciplinary foot care could reduce morbidity. All foot lesions were documented and investigated in 50 diabetic patients, mean age 49.2 ± 11.0 (SD) years, duration of diabetes 25.3 ± 9.0 years, time since renal transplantation 60.2 ± 35.1 months, who attended a special foot clinic monthly for education, vascular and neurological assessment, podiatry and footwear. Foot lesions included: neuropathic ulcers, ischaemic ulcers, traumatic lesions, Charcots arthropathy, pathological fracture. Treatment included antibiotics, podiatry, footwear, and angioplasty or distal bypass where appropriate. Only 13 patients were deemed ischaemic but peripheral neuropathy was a very common finding (mean VPT 24.8 ± 12.9 V). Gangrene and major amputations showed a decrease on previous years and healing times for lesions were similar to those previously reported in diabetic patients without renal transplants. The majority of foot lesions, both in soft tissue and bone, were related to neuropathy and trauma and responded well to optimal foot care within the renal unit. Gangrene and major amputations were usually preventable.
Diabetic Medicine | 2005
Nina L. Petrova; A.V.M. Foster; Michael Edmonds
Aims To measure bone density and neuropathy in both feet in Type 1 and Type 2 patients with unilateral Charcot osteoarthropathy and controls.
Diabetic Medicine | 1992
Martin J. Stevens; Michael Edmonds; A.V.M. Foster; S.L.E. Douglas; P.J. Watkins
Blood flow is abnormal in the diabetic neuropathic foot, and this may be of importance in the pathogenesis of complications. Arteriovenous shunting is increased, and blood flow through these channels may paradoxically decrease in response to local heating. Peak skin blood flow is also reduced in these patients. It is not known whether these blood flow abnormalities may reflect diabetic microangiopathy, or whether they simply reflect vascular denervation. The skin blood flow response to a local thermal stimulus was studied in four non‐diabetic patients with a unilateral traumatic neuropathy and foot ulceration. All showed a decrease in skin blood flow (to 68% of basal) at the great toe during local heating in the neuropathic limb, in contrast to the normal limb, in which blood flow increased to 180% of basal. Peak skin blood flow was also greatly reduced in the neuropathic limb, being only 29% of the normal limb. Neuropathy alone can be responsible for abnormal skin blood flow responses in the neuropathic foot.
American Journal of Surgery | 2004
Michael Edmonds; A.V.M. Foster
BMJ | 2006
Michael Edmonds; A.V.M. Foster
Diabetic Medicine | 1994
A.V.M. Foster; C. Eaton; D.O. McConville; Michael Edmonds
Diabetic Medicine | 1997
Michael Edmonds; A.V.M. Foster; M McColgan
Diabetic Medicine | 1989
A.V.M. Foster; Michael Edmonds; A.K. Das; P. J. Watkins