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Biomedical subjects

William J Jeffcoate

Publications and source records attributed to William J Jeffcoate.

12 recordsLinked to original sources
PubMed2006

Temporal association between the incidence of foot ulceration and the start of dialysis in diabetes mellitus.

BACKGROUND: The aim of this study was to seek a temporal association between the start of renal replacement therapy (RRT) and the first recorded foot ulcer in diabetes. METHODS: Details of all patients with diabetes who had received RRT were extracted from the renal database and were cross-checked with the database held in the specialist foot clinic. The date of onset of first registered foot ulcer was taken and compared with the date of onset of RRT. The self-controlled case-series method was used to establish any significant temporal association between the start of RRT and first recorded foot ulcer in diabetes. RESULTS: Of 466 patients with diabetes dialysed at our hospital since 1976, 94 (20.2%) were recorded as having at least one foot ulcer, with 15 of these undergoing major amputation. Incidence ratios (IRs) were calculated for 90 patients in whom complete data were available. A close temporal association was observed between the start of RRT and the first recorded foot ulceration: IR (95% CI) in the first and between the second and fifth years of dialysis were 3.35 (95% CI: 1.59-7.04), and 4.56 (2.19-9.50), respectively, relative to the time before dialysis. The IR for major amputation was 31.98 (2.09-490.3) in the first year and 34.01 (1.74-666.2) in the second to fifth years. CONCLUSION: These results reveal a close relationship between the onset of RRT in diabetes and the onset of foot ulceration, and confirm the high incidence of amputation in those on dialysis. Urgent steps should be taken to coordinate all aspects of diabetes foot care before and after the start of RRT.

Diabetic Foot↗
PubMed2006

Assessing the outcome of the management of diabetic foot ulcers using ulcer-related and person-related measures.

OBJECTIVE: The purpose of this study was to compare different outcome measures in the audit of management of diabetic foot ulcers RESEARCH DESIGN AND METHODS: Data collected prospectively in a consecutive cohort of patients referred to a specialist multidisciplinary foot care clinic between 1 January 2000 and 31 December 2003 were analyzed. A single index ulcer was selected for each patient and classified according to both the Size (Area and Depth), Sepsis, Arteriopathy, and Denervation [S(AD)SAD] and University of Texas (UT) systems. Ulcer-related outcomes (healing, resolution by ipsilateral amputation or by death, and persisting unhealed) were determined at 6 and 12 months and compared with patient-related outcomes (survival, any amputation, and being free from any ulcer) at 12 months. RESULTS: In 449 patients (63.7% male, mean age 66.7 +/- 13.2 years), 352 (78.4%) ulcers were superficial [S(AD)SAD/UT grade 1] and 134 of these (38.1% of 352) were neither ischemic nor infected. A total of 183 (40.8% of 449) ulcers were clinically infected, and peripheral arterial disease was present in 216 patients (48.1%). Seventeen patients (3.8%) were lost to follow-up and were excluded from analysis. Of the ulcers, 247 (55.0% of 449) and 295 (65.7%) healed without amputation by 6 and 12 months, respectively. Median (range) time to healing was 78 (7-364) days. Of all index ulcers, 5.8 and 8.0% were resolved by amputation, and 6.2 and 10.9% by death by the same time points; 27.8 and 11.6% persisted unhealed. In contrast, patient-related outcomes revealed that of 449 patients only 202 (45.0%) were alive, without amputation, and ulcer free at 12 months. This group had had 272 (1-358) days without any ulcer. A total of 48 (10.7%) patients had undergone some form of amputation, and 75 (16.7%) had died. CONCLUSIONS: These data illustrate the extent to which ulcer-related outcomes may underestimate the true morbidity and mortality associated with diabetic foot disease. It is suggested that when attempts are made to compare the effectiveness of management in different centers, greater emphasis should be placed on patient-related outcome measures.

Aged↗
PubMed2005

The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute Charcot foot) in diabetes.

The pathogenesis of the acute Charcot foot of diabetes remains unclear. All patients with this condition have evidence of peripheral neuropathy, with loss of protective sensation and abnormal foot biomechanics. However, the acute Charcot foot is also characterised by a pronounced inflammatory reaction and the pathogenic significance of this inflammation has received little attention. We suggest that an initial insult--which may or may not be detected--is sufficient to trigger an inflammatory cascade through increased expression of proinflammatory cytokines, including TNFalpha and interleukin 1beta. This cascade then leads to increased expression of the nuclear transcription factor, NF-kappaB, which results in increased osteoclastogenesis. Osteoclasts cause progressive bone lysis, leading to further fracture, which in turn potentiates the inflammatory process. The potential role of proinflammatory cytokines suggests the possibility of new treatments for this sometimes devastating complication of diabetes.

Arthropathy, Neurogenic↗
PubMed2005

Theories concerning the pathogenesis of the acute charcot foot suggest future therapy.

The acute Charcot foot is characterized by bone fracture and dislocation, and is a rare complication of distal symmetrical neuropathy in diabetes. The cause is unknown, but it cannot be attributed solely to loss of protective sensation. However, recent advances in understanding the mechanisms of osteoclast activation have suggested that the key abnormality may lie in an enhanced inflammatory response to injury, which is itself linked to increased bone lysis. The recognition that the acute Charcot foot is essentially an inflammatory arthropathy suggests new options for the management of this potentially devastating condition.

Acute Disease↗
PubMed2005

Abnormalities of vasomotor regulation in the pathogenesis of the acute charcot foot of diabetes mellitus.

The acute Charcot foot complicates distal symmetrical neuropathy but is remarkably rare. This article reviews the multiple processes that may complicate both diabetes and neuropathy and might, in turn, explain the association of features that are typical of this disorder: osteolysis, vascular calcification in association with intact lower limb blood flow, and uncontrolled inflammation. Specifically, it is suggested that the disorder arises because of abnormal expression of the nuclear transcription factor, NFkappaB, in diabetic neuropathy and that this is further enhanced at the onset of the acute arthropathy as a result of the release of proinflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-1. These proinflammatory cytokines and RANKL may then enter a cycle of mutual augmentation, and this is a factor that underlies the continuing inflammation that characterizes the disorder. If this hypothesis is confirmed, it would suggest the option of new effective treatments for this sometimes devastating disorder.

Acute Disease↗
PubMed2004

Controversies in diagnosing and managing osteomyelitis of the foot in diabetes.

The optimal approach to diagnosing and managing osteomyelitis of the foot in diabetes is unclear. Diagnosis is based on clinical signs, supplemented by a variety of imaging tests. Bone biopsy is the accepted criterion standard for diagnosis but is not used by many. Management traditionally involves surgical removal of infected bone, combined with antibiotic therapy. However, recent studies have shown that antibiotics alone may apparently eliminate bone infection in many cases. There is also evidence that early amputation of infected digits is frequently noncurative. Agreement on criteria for diagnosing osteomyelitis is required, and randomized trials are urgently needed, to determine the relative benefits of various surgical interventions and the optimal deployment of antibiotics. We review the microbiology of osteomyelitis of the foot in diabetes, the benefits and limitations of various diagnostic procedures, and the evidence for the effectiveness of both surgical and nonsurgical approaches to management.

Clinical Trials as Topic↗
PubMed2003

Diabetic foot ulcers.

Ulceration of the foot in diabetes is common and disabling and frequently leads to amputation of the leg. Mortality is high and healed ulcers often recur. The pathogenesis of foot ulceration is complex, clinical presentation variable, and management requires early expert assessment. Interventions should be directed at infection, peripheral ischaemia, and abnormal pressure loading caused by peripheral neuropathy and limited joint mobility. Despite treatment, ulcers readily become chronic wounds. Diabetic foot ulcers have been neglected in health-care research and planning, and clinical practice is based more on opinion than scientific fact. Furthermore, the pathological processes are poorly understood and poorly taught and communication between the many specialties involved is disjointed and insensitive to the needs of patients.

Diabetic Foot↗
PubMedDate not supplied

Wound healing and treatments for people with diabetic foot ulcers.

The factors that delay wound healing are multiple and relate both to diabetes and to the effect of its complications. Diabetic foot ulcers readily become chronic, and chronic ulcers have biological properties that differ substantially from acute ones. Much of the available information on the biology of wound healing relates to acute and experimental wounds and may not be directly relevant. It follows that there is limited evidence currently available to underpin protocols for the management of diabetic foot ulcers, or to guide choice of applications and dressings 1. Nevertheless, it is possible to define certain principles.GLYCAEMIC CONTROL: The first relates to glycaemic control. While chronic complications of diabetes such as peripheral vascular disease and neuropathy may be largely irreversible, aspects of structure and function of connective tissue and cells may be impaired by hyperglycaemia, and their function should be improved if normoglycaemia is achieved. PROMOTION OF HEALING: The second principle concerns attempts at active promotion of wound healing by (1) surgical revascularization, and (2) specific attempts to correct defined biological abnormalities thought to be hindering the healing process. These include the use of a variety of applications, dressings and technologies, which may stimulate healing by applying, or stimulating the release of, growth factors and cytokines. While this approach holds the greatest promise for the future, it will be dependent on defining defects which need correction in specific individuals, and having technologies available to address them. This field is in its infancy. WOUND CARE: The third broad principle concerns the management of the wound and its surrounding tissue in order to promote healing. This includes regular inspection, cleansing and removal of surface debris, elimination of pathogenic bacteria and creation of an appropriate environment to facilitate endogenous tissue regeneration. There are many applications and dressings that may be chosen to promote healing, but, whichever is selected, wound management has to be integrated into an effective programme of multidisciplinary care.

Debridement↗