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Biomedical subjects

M E Edmonds

Publications and source records attributed to M E Edmonds.

At least 19 recordsLinked to original sources
PubMed2005

Calcaneal bone mineral density in patients with Charcot neuropathic osteoarthropathy: differences between Type 1 and Type 2 diabetes.

AIMS: To measure bone density and neuropathy in both feet in Type 1 and Type 2 patients with unilateral Charcot osteoarthropathy and controls. METHODS: Calcaneal bone density, temperature and vibration thresholds were compared between 17 Type 1 diabetic patients with osteoarthropathy and 47 Type 1 controls and between 18 Type 2 diabetic patients and 48 Type 2 controls. As well as the Charcot foot, the non-Charcot foot was studied to assess osteopenia at onset of osteoarthropathy. RESULTS: In Type 1 diabetes, bone density was reduced in the non-Charcot foot compared with controls [Z-score: -1.7 ({-1.9}-{-1.4}) vs. -0.2 ({-1.1}-{0.5}), P < 0.0001, median (interquartile range)]; but not in Type 2 diabetes [Z-score: 0.15 ({-0.45}-{0.85}) vs. 0.3 ({-0.5}-{0.9}), P = 0.675]. Bone density in the Charcot foot was lower compared with the non-Charcot foot in both Type 1 [Z-score: -2.0 ({-2.8}-{-1.4}) vs. -1.7 ({-1.9}-{-1.4}), P = 0.018] and Type 2 diabetes [Z-score: -0.2 ({-1.4}-{0.1}) vs. 0.3 ({-0.5}-{0.9}), P = 0.001]. In Type 1 diabetes, bone density of the non-Charcot foot was reduced compared with that in Type 2 (P < 0.0001). Body mass index was lower in Type 1 than in Type 2 Charcot patients (P = 0.007). Type 2 patients had high temperature (P = 0.001) and vibration thresholds (P < 0.0001) in the non-Charcot foot compared with Type 2 controls whereas Type 1 patients had a high temperature threshold (P = 0.01) but not vibration threshold compared with Type 1 controls (P = 0.077). CONCLUSION: Bone density was reduced in the non-Charcot foot in Type 1 but not in Type 2 diabetes. Type 2 patients had high temperature and vibration thresholds in contrast to Type 1 patients who had a high temperature threshold only.

Adult↗
PubMed2004

Safety and performance of a new non-adhesive foam dressing for the treatment of diabetic foot ulcers.

OBJECTIVE: This study aimed to document the safety and performance of a new non-adhesive foam dressing (Biatain Non-adhesive Dressing, Coloplast A/S) in the treatment of established foot ulcers in patients with diabetes. METHOD: This was an open non-comparative prospective study. Participants had an ankle brachial pressure index score of over 0.4 (neuro-ischaemic) and an ulcer bigger than 1 cm2 and less than 8 cm2 in any direction. The treatment period was six weeks. RESULTS: Thirty-five out of 37 patients completed the study. The mean wound area reduced from 5.4 cm2 to 2.5 cm2. Relative wound area reduced from 100% at baseline to 40% at week 6. 'Wearing comfort' improved throughout the study (p = 0.039). Maceration remained stable or improved. None of the four reported adverse events were device related. CONCLUSION: This study demonstrates that treatment of diabetic foot ulcers with Biatain Non-adhesive Dressing results in considerable wound area reduction and prevents any deterioration in maceration. The dressing is safe and effective in the management of these ulcers.

Activities of Daily Living↗
PubMed2001

Bisphosphonates in the treatment of Charcot neuroarthropathy: a double-blind randomised controlled trial.

AIMS/HYPOTHESIS: The management of charcot neuroarthropathy, a severe disabling condition in diabetic patients with peripheral neuropathy, is currently inadequate with no specific pharmacological treatment available. We undertook a double-blind randomised controlled trial to study the effect of pamidronate, a bisphosphonate, in the management of acute diabetic Charcot neuroarthropathy. METHODS: Altogether 39 diabetic patients with active Charcot neuroarthropathy from four centres in England were randomised in a double-blind placebo-controlled trial. Patients received a single infusion of 90 mg of pamidronate or placebo (saline). Foot temperatures, symptoms and markers of bone turnover (bone specific alkaline phosphatase and deoxypyridinoline crosslinks) were measured over the 12 months, in 10 visits. All patients also had standard treatment of the Charcot foot. RESULTS: Mean age of the study group (59 % Type II (non-insulin-dependent) diabetes mellitus) was 56.3 +/- 10.2 years. The mean temperature difference between active and control groups was 3.6 +/- 1.7 degrees C and 3.3 +/- 1.4 degrees C, respectively. There was a fall in temperature of the affected foot in both groups after 2 weeks with a further reduction in temperature in the active group at 4 weeks (active and placebo vs baseline; p = 0.001; p = 0.01, respectively), but no difference was seen between groups. An improvement in symptoms was seen in the active group compared with the placebo group (p < 0.001). Reduction in bone turnover (means +/- SEM) was greater in the active than in the control group. Urinary deoxypyridinoline in the pamidronate treated group fell to 4.4 +/- 0.4 nmol/mmol creatinine at 4 weeks compared with 7.1 +/- 1.0 in the placebo group (p = 0.01) and bone-specific alkaline phosphatase fell to 14.1 +/- 1.2 u/l compared with 18.6 +/- 1.6 u/l after 4 weeks, respectively (p = 0.03). CONCLUSION/INTERPRETATION: The bisphosphonate, pamidronate, given as a single dose leads to a reduction in bone turnover, symptoms and disease activity in diabetic patients with active Charcot neuroarthropathy.

Adult↗
PubMed2000

Medial arterial calcification and diabetes mellitus.

Medial arterial calcification (MAC) is a frequent vascular finding in patients with type II diabetes mellitus. Morphologically distinct from focal calcifications of atherosclerosis its radiographically distinct tramline pattern is frequently encountered in the arteries of the lower extremities. MAC is inconsistently related to age, duration and therapy of diabetes. In contrast, a strong association with diabetic polyneuropathy and familial aggregation have been documented. Although initially considered benign MAC is now recognized as a strong predictor of cardiovascular morbidity and mortality in diabetic patients. Investigations into MAC pathogenes and into its role in vascular pathophysiology are underway.

Arteriosclerosis↗
PubMed2000

Infection of foot ulcers with Staphylococcus aureus associated with increased mortality in diabetic patients.

Diabetic patients with foot ulceration have a poorer prognosis than those without ulceration. The reason for this is unclear, but there is considerable interest in the putative links between infection and atherogenesis, and it is notable that diabetic foot ulcers (DFU) are often infected with Staphylococcus aureus and the main cause of death in DFU patients is ischaemic heart disease. We examined the 5 year survival of 71 diabetic patients who presented with foot ulcers that were newly infected (Sa group, n = 56) or not infected at all during the study period (non-Sa group, n = 15) with S. aureus. Twenty-nine patients (52%) infected with S. aureus died compared with three patients (20%) whose foot ulcers were not infected with S. aureus. The patients in the two groups were similar in age and duration of diabetes. The overall five year mortality rate was 10.4% per year for those infected, significantly higher than the average of 4.0% for patients without infection (p = 0.015). None of the patients was bacteraemic or died directly from sepsis. Infection of DFU by S. aureus may increase the risk of death in diabetic patients.

Aged↗
PubMed1999

Medial localization of mineralization-regulating proteins in association with Mönckeberg's sclerosis: evidence for smooth muscle cell-mediated vascular calcification.

BACKGROUND: Calcification of the media of peripheral arteries is referred to as Mönckeberg's sclerosis (MS) and occurs commonly in aged and diabetic individuals. Its pathogenesis is unknown, but its presence predicts risk of cardiovascular events and leg amputation in diabetic patients. Several studies have documented expression of bone-associated genes in association with intimal atherosclerotic calcification, leading to the suggestion that vascular calcification may be a regulated process with similarities to developmental osteogenesis. Therefore, we examined gene expression in vessels with MS to determine whether there was evidence for a regulated calcification process in the vessel media. METHODS AND RESULTS: In situ hybridization, immunohistochemistry, and semiquantitative reverse-transcription polymerase chain reaction were used to examine the expression of mineralization-regulating proteins in human peripheral arteries with and without MS. MS occurred in direct apposition to medial vascular smooth muscle cells (VSMCs) in the absence of macrophages or lipid. These VSMCs expressed the smooth muscle-specific gene SM22alpha and high levels of matrix Gla protein but little osteopontin mRNA. Compared with normal vessels, vessels with MS globally expressed lower levels of matrix Gla protein and osteonectin, whereas alkaline phosphatase, bone sialoprotein, bone Gla protein, and collagen II, all indicators of osteogenesis/chondrogenesis, were upregulated. Furthermore, VSMCs derived from MS lesions exhibited osteoblastic properties and mineralized in vitro. CONCLUSIONS: These data indicate that medial calcification in MS lesions is an active process potentially orchestrated by phenotypically modified VSMCs.

Adult↗
PubMed1999

Why do foot ulcers recur in diabetic patients?

AIM: To investigate factors predisposing to recurrent foot ulceration in patients with diabetes mellitus. METHODS: Two groups of patients who had attended a specialist Diabetes Foot Centre were assessed: relapsers (n = 26), whose foot ulceration had recurred at least twice, and nonrelapsers (n = 25), whose initial ulcer had not recurred for at least 2 years. RESULTS: In the relapser group 10/26 patients waited at least 24 h before reporting symptoms compared with only 2/25 in the nonrelapser group (P < 0.05). Vibration perception threshold (volts) was 38 +/- 12 (mean +/- SD) in relapsers compared with 25 +/- 13 in nonrelapsers (P < 0.005). Cold perception threshold (degrees C) was 9.1 +/- 4.6 in relapsers compared with 5.1 +/- 3.5 in nonrelapsers (P<0.005). HbA1c (%) was significantly raised at 8.5 +/- 1.7 in relapsers compared with 7.6 +/- 1.2 in nonrelapsers (P = 0.03). Alcohol intake was 0.5 (median, interquartile range 0-2) units per day in relapsers compared with 0.0 (median, interquartile range 0-0.25) units in nonrelapsers (P = 0.04). Smoking habits, housing conditions, visual acuity, threshold for warm perception and the Doppler pressure index were not significantly different in the two groups. CONCLUSIONS: Patients who develop recurrent foot ulceration delay in reporting symptoms, when compared with diabetic patients whose foot ulceration does not recur. The relapsers also have evidence of poorer glycaemic control, more neuropathy and increased alcohol intake.

Adult↗
PubMed1999

Novel surgical treatment and gastric pathology in diabetic gastroparesis.

AIMS: Observations are made on four Type 1 diabetic patients with the rare syndrome of intractable vomiting from confirmed gastroparesis, to determine whether radical surgery would alleviate their symptoms and subsequently to examine in detail the gastric histopathology. METHODS: The surgical approach consisted of an approximate 70% resection of the stomach, including the antrum and pylorus, with closure of the duodenum and restoration of gastrointestinal continuity with a 60-cm Roux-en-Y jejunal loop. Four longstanding Type 1 diabetic patients were examined and treated as described. They were all women in the age range 2741 years with grossly abnormal autonomic function tests in whom other causes for gastric paresis had been excluded. RESULTS: Vomiting episodes leading to multiple hospital admissions (6-8) in the year preceding surgery were eliminated in three of the four patients, while in the fourth initial success was followed by the need for dialysis for renal failure. Gastric histopathology showed evidence of smooth muscle degeneration and fibrosis, with eosinophilic inclusion bodies (M-bodies) which appear to be unique to this condition. The findings suggest the presence of a gastromyopathy. CONCLUSIONS: Satisfactory relief of intractable vomiting from diabetic gastroparesis was achieved by a novel radical surgical procedure. Histopathological findings suggest that gastromyopathy may contribute to the production of this syndrome.

Adult↗
PubMed1999

Plantar pressures are elevated in the neuroischemic and the neuropathic diabetic foot.

OBJECTIVE: Clinical observation has noted that diabetic neuropathic ulcers occur frequently on the plantar surface, whereas neuroischemic ulcers seem to occur often on the foot margins. The reason for this difference in the site of ulceration is unknown, but it may be related to differences in pressure loading. The aim of the study was to compare vertical in-shoe foot pressures measured during walking (using the F-SCAN system) in four groups of patients whose degree of neuropathy was measured by vibration perception threshold (VPT). RESEARCH DESIGN AND METHODS: Subjects included 14 neuroischemic diabetic patients (VPT 29.3 +/- 13.5 V) with history of ulceration on the margins of the foot, 18 patients with neuropathy alone (VPT 38.7 +/- 12.7 V) and previous history of ulceration on the plantar surface, 10 diabetic control patients (VPT 9.9 +/- 2.7 V), and 15 nondiabetic control subjects (VPT 7.0 +/- 0.5 V). RESULTS: When compared with the other three groups, neuroischemic patients had higher foot pressures when measured as mean peak pressures and highest peak pressures under four areas of the foot: medial and lateral forefoot, hallux, and heel. Furthermore, when measuring the maximum pressures developed at any point under the plantar surface, the neuroischemic patients also had the most elevated pressures (757.6 +/- 135.9 kPa), significantly higher than those found in the neuropathic group (482.8 +/- 68.6 kPa, P = 0.04) and in both diabetic control patients (310.2 +/- 34.7 kPa, P = 0.008) and nondiabetic controls subjects (365.1 +/- 49.8 kPa, P = 0.007). CONCLUSIONS: Despite having increased plantar pressures and a comparable degree of neuropatny, the neuroischemic patients did not have a history of ulceration on the plantar surface. These observations may have relevance to different mechanisms of ulcer formation in the neuroischemic and neuropathic foot.

Diabetic Angiopathies↗
PubMed1997

Randomised placebo-controlled trial of granulocyte-colony stimulating factor in diabetic foot infection.

BACKGROUND: Diabetic foot infections cause substantial morbidity and mortality. Neutrophil superoxide generation, a crucial part of neutrophil bactericidal activity, is impaired in diabetes. Granulocyte-colony stimulating factor (G-CSF) increases the release of neutrophils from the bone marrow and improves neutrophil function. We assessed G-CSF as adjuvant therapy for the treatment of severe foot infections in diabetic patients. METHODS: 40 diabetic patients with foot infections were enrolled in a double-blind placebo-controlled study. On admission, patients were randomly assigned G-CSF (filgrastim) therapy (n = 20) or placebo (n = 20) for 7 days. Both groups received similar antibiotic and insulin treatment. Neutrophils from the peripheral blood of these participants and from healthy controls were stimulated with opsonised zymosan, and superoxide production was measured by a spectrophotometric assay (reduction of ferricytochrome C). FINDINGS: G-CSF therapy was associated with earlier eradication of pathogens from the infected ulcer (median 4 [range 2-10] vs 8 [2-79] days in the placebo group; p = 0.02), quicker resolution of cellulitis (7 [5-20] vs 12 [5-93] days; p = 0.03), shorter hospital stay (10 [7-31] vs 17.5 [9-100] days; p = 0.02), and a shorter duration of intravenous antibiotic treatment (8.5 [5-30] vs 14.5 [8-63] days; p = 0.02). No G-CSF-treated patient needed surgery, whereas two placebo recipients underwent to amputation and two had extensive debridement under anaesthesia. After 7 days' treatment, neutrophil superoxide production was significantly higher in the G-CSF group than in the placebo group (16.1 [4.2-24.2] vs 7.3 [2.1-11.5] nmol per 10(6) neutrophils in 30 min; p < 0.0001). G-CSF therapy was generally well tolerated. INTERPRETATION: G-CSF treatment was associated with improved clinical outcome of foot infection in diabetic patients. This improvement may be related to an increase in neutrophil superoxide production.

Aged↗
PubMed1997

NO-dependent smooth muscle vasodilatation is reduced in NIDDM patients with peripheral sensory neuropathy.

In order to determine the involvement of denervation in endothelium-independent, nitric oxide (NO)-dependent smooth muscle vasodilation, we have measured vascular endothelial and smooth muscle function in three groups of age- and sex-matched patients: 8 patients with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) with neuropathy; 7 NIDDM patients without neuropathy; and 10 non-diabetic control subjects. Laser Doppler probes were used to measure blood flow in the dorsum of the left foot. Vascular endothelial response was assessed by measuring vasodilatory responses to iontophoretic application of acetylcholine to the dorsum of the foot. Vascular smooth muscle activity was assessed by the response to iontophoresis of sodium nitroprusside (SNP)-a NO donor and direct vasodilator. The vasodilator response to acetylcholine, expressed as the ratio of peak to basal blood flow, was significantly reduced in both diabetic groups when compared to non-diabetic controls (geometric mean x/divided by anti-logged SD 9.81 x/divided by 1.65 versus patients with neuropathy 3.50 x/divided by 2.03, p < 0.005 and diabetic non-neuropathic subjects 3.49 x/divided by 1.67, p < 0.005). The difference between the two groups of diabetic patients was not significant. In contrast, the vasodilatation to nitroprusside was significantly reduced only in the diabetic neuropathic patients, significantly lower than in either the non-neuropathic diabetic controls or the non-diabetic controls (2.1 x/divided by 2.0 versus 6.42 x/divided by 1.56 and 7.02 x/divided by 2.05, p < 0.005). This indicates that neuropathy is important in abnormalities of endothelium-independent vasodilatation.

Acetylcholine↗
PubMed1997

Measurement of markers of osteoclast and osteoblast activity in patients with acute and chronic diabetic Charcot neuroarthropathy.

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 microg 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 microg l(-1), patients with chronic Charcot neuroarthropathy 109 +/- 1.5 microg l(-1), diabetic controls 93.5 +/- 2.3 microg l(-1), and non-diabetic controls 90.1 +/- 1.5 microg 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.

Acute Disease↗
PubMed1996

Time-dependent behaviour of a force-sensitive resistor plantar pressure measurement insole.

Thin pressure-measuring insoles have enabled new clinical studies of in-shoe distribution of plantar pressure. One of these new devices, based on force-sensitive resistor (FSR) technology, exhibits time-varying behaviour due to the mechanical properties of the sensor materials. This has been variously attributed to initial bedding in, wear or time-dependency behaviour. Cyclic and sustained loading were used in laboratory conditions to investigate this phenomenon. The results show that the sensitivity of the sensor varies rapidly over the first minute of loading. There is also a slower long-term effect which reduces over time. From this information, procedures for optimal calibration and use are suggested.

Biomechanical Phenomena↗
PubMed1995

The splanchnic circulation and postural hypotension in diabetic autonomic neuropathy.

Postural hypotension results from sympathetic failure to cause superior peripheral vasoconstriction. The importance of the splanchnic circulation was studied by measuring mesenteric artery blood flow with duplex Doppler scanning. Nine normal and 9 Type 1 diabetic controls were compared to 8 Type 1 patients with autonomic neuropathy whose pressure fell 40-113 mmHg (range) on tilting. Measurements were made supine and after vertical tilt, fasting without insulin and after a 550 kcal meal. Superior mesenteric artery diameter decreased on tilting in normal controls but not in diabetic control or neuropathy groups (supine vs tilted: controls. 6.3 +/- 0.9 to 5 +/- 0.9 mm, p = 0.004, diabetic controls: 6.0 +/- 0.6 to 6.0 +/- 1.0 mm, and neuropathy group: 6.4 +/- 0.9 to 5.6 +/- 0.9 mm), but proportional blood flow changes were similar in all subjects (controls: 407 +/- 154 to 255 +/- 67 ml min-1 (-31%, p = 0.03), diabetic controls: 379 +/- 140 to 306 +/- 149 ml min-1 (-8%, p = 0.28), neuropathy group: 639 +/- 371 to 435 +/- 142 ml min-1 (-23%, p = 0.10). Postprandially supine superior mesenteric artery flow increased in all subjects but this did not affect the degree of systolic blood pressure drop on tilting (fasting vs postprandial blood flow: controls: 407 +/- 154 to 775 +/- 400 ml min-1 (p = 0.04), diabetic controls: 379 +/- 140 to 691 +/- 262 ml min-1 (p = 0.01), neuropathy group: 639 +/- 371 to 943 +/- 468 ml min-1 (p < 0.06)). The similarity of superior mesenteric artery responses to tilting in the three groups, and the lack of exacerbation of postural hypotension in the presence of postprandial hyperaemia indicates that control of splanchnic blood flow is less important in the aetiology of diabetic autonomic postural hypotension than previously thought.

Adult↗