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E Chantelau

Publications and source records attributed to E Chantelau.

At least 19 recordsLinked to original sources
PubMed2007

"Silent" bone stress injuries in the feet of diabetic patients with polyneuropathy: a report on 12 cases.

BACKGROUND: Bone stress injuries are rarely being diagnosed in patients with sensory neuropathy, most likely because they may be silent in terms of pain. Load-related pain is considered a key feature of any bone stress injury, a symptom, which may be partially or completely absent in subjects with sensory neuropathy (loss of protective sensation). We evaluated the clinical course of bone stress injuries in insensitive feet in diabetic patients with polyneuropathy. METHODS: We investigated 12 consecutive diabetic patients with bone stress injuries of the foot (bone marrow edema, bone bruise and microtrabecular fractures, on magnetic resonance imaging MRI), which were undetectable on plain X-ray. All patients suffered from diabetic polyneuropathy, none of them had an active foot ulcer. RESULTS: The patients presented with a swollen foot, which was only mildly painful and did not prevent them from walking. Complaints were related to the swelling, which increased during load-bearing. In seven cases, a traumatic event preceding the onset of symptoms could be ascertained. MRI disclosed stress injuries in 2.5 (1-8) [median (range)] bones per foot. In 11 patients, treatment was started immediately by off-loading with total contact cast for 17 (8-52) weeks, followed by gradual increase in weight bearing. One patient unfortunately received off-loading treatment only after deforming fractures had developed. All bone injuries healed uneventuelly in eight patients, and with residual mild osteoarthrosis in three patients without gross deformities. However, the untreated patient developed severe Charcot foot deformity. CONCLUSIONS: In diabetic patients with polyneuropathy, symptoms of bone stress injuries of the foot are atypical, in that there is load-related swelling rather than load-related pain. Immediate diagnosis, and treatment with off-loading, leads to a restitutio ad integrum like in non-neuropathic patients. Delayed cessation of overuse, however, may cause irreversible joint and bone damage (Charcot foot).

Aged↗
PubMed2006

The diabetic charcot foot: MRI discloses bone stress injury as trigger mechanism of neuroarthropathy.

It is generally accepted that traumatic bone injury contributes to the clinical picture of neuroarthropathy of the foot in diabetes, i.e., of the diabetic Charcot foot. While radiology is capable of visualizing only advanced bone injuries, like complete fractures, magnetic resonance imaging (MRI) discloses bone injuries that precede complete fractures (stress bone injuries). In diabetic polyneuropathy, stress bone injuries are silent in terms of pain, due to the lack of pain sensation. At the foot, their clinical appearance is characterized by inflammatory swelling with little or no pain. The present paper reviews the contribution of MRI to the detection of bone injuries in what is called stage 0 Charcot foot, with emphasis on the bearings for the treatment strategy.

Bone Marrow Diseases↗
PubMed2006

Evaluation of the diabetic charcot foot by MR imaging or plain radiography--an observational study.

Magnetic resonance (MR) images and concomitant plain radiographs of 26 Charcot feet of different stages (stage 0 to III) were reviewed in retrospect for discordant findings. Bone and joint abnormalities were evaluated qualitatively, and quantitatively guided by the AO integral classification of injuries of the foot. MR images revealed traumatic bone and joint injuries (bone oedema, occult fractures, and joint effusion) already in stage 0, when X-ray still showed normal bone and joint anatomy (p = 0.02). Moreover, MR images revealed bone oedema, joint effusion and soft tissue oedema in addition to fractures and calluses in stage I (bone dissolution), stage II (bone coalescence), and stage III (bone remodeling), i.e., in stages with overt radiographic pathology. According to this observational study, MR imaging, in addition to radiography, provides important information as to the extent and the natural course of bone injury in the diabetic Charcot foot. MR imaging, thus, may improve disease staging, as well as treatment monitoring.

Aged↗
PubMed2006

Charcot foot in diabetes: farewell to the neurotrophic theory.

Neuropathic osteoarthropathy is characterised by relatively painless swelling together with extensive damage in bones and joints, predominantly in the feet and ankles. The uncontrolled natural course of the condition leads to gross foot deformity, skin pressure ulceration, spreading infections, and sometimes amputation. Jean-Martin Charcot in 1883 described "Charcot foot" named after him in patients with tabes dorsalis insensitivity. Charcot believed that intrinsic bone weakness was the underlying condition, and was caused by neurogenic deficiencies in bone nutrition. His followers believed such dystrophy to be mediated by sympathetic denervation of the bone vasculature (neurotrophic, or neurovascular theory). Attempts to prove this theory were futile. A neurogenic circulatory disorder potentially relevant to bone nutrition could not be identified. Nowadays, Charcot foot is mostly seen in diabetic neuropathy, which has replaced syphilis as a frequent cause of peripheral nerve dysfunction. Recent studies in the diabetic Charcot foot and bone turnover indicate that the neurotrophic theory is a myth. The assumption of bone resorption due to sympathetic denervation proved to be false--sympathetic activity increases osteoclastic activity and thereby bone loss (sympathomimetic bone resorption). Except for the transient, inflammatory stage of the diabetic Charcot foot, there is no evidence of relevant osteoporosis or demineralisation of the foot skeleton in diabetes.

Arthropathy, Neurogenic↗
PubMed2005

Progression of diabetic retinopathy during improved metabolic control may be treated with reduced insulin dosage and/or somatostatin analogue administration -- a case report.

It is well known that intensified insulin treatment of poorly controlled type 1 diabetic patients may worsen an existing diabetic retinopathy (DR). This observation has been explained by an insulin-induced stimulation of the GH/IGF-I axis. Here, we report on three cases, where the progression of DR during intensified metabolic control was treated with manipulation of insulin therapy and/or by administration of octreotide. Serum concentrations of IGF-I, IGFBP-3, insulin, cystatin C, creatinine, endogenous creatinine clearance and HbA1c-levels were assessed by routine laboratory methods; serum IGF-I bioactivity was estimated by a highly specific kinase receptor activation assay. Visual acuity and retinopathy stage was assessed by established clinical methods including fluorescein angiography. After glycaemic control was improved by intensified insulin therapy, serum IGF-I levels acutely increased. Subsequently, DR progressed to an advanced stage ("florid retinopathy"), with macular edema, and proliferation of new vessels (in two cases). Immediate reduction of insulin dosage and administration of octreotide lowered serum total IGF-I levels (and IGF-I bioactivity as measured in one patient). Subsequently, macular edema resolved partly, and visual acuity improved, allowing laser photocoagulation to be performed. In conclusion, in poorly controlled type 1 diabetic patients, intensified insulin therapy is able to cause florid DR with acute macular edema. These sight-threatening changes may improve by short-term reduction of insulin dosage or by administration of octreotide, and we speculate that this may be related to down-regulation of (serum) IGF-I.

Adult↗
PubMed2005

The perils of procrastination: effects of early vs. delayed detection and treatment of incipient Charcot fracture.

BACKGROUND: At the onset of acute diabetic Charcot foot, therapeutic intervention may be delayed because plain X-rays may not show fractures. AIM OF THE STUDY: To assess the clinical course of acute Charcot foot in 24 patients without evidence of definite fractures on the first X-ray after onset of symptoms, who were referred to the foot clinic for diagnosis and treatment either early or delayed, i.e. before or after definite fractures were detectable on repeat X-rays. PATIENTS AND METHODS: Eleven patients were referred early (incipient Charcot foot, case group), and 13 patients were referred delayed (overt Charcot foot, control group). In the foot clinic, both groups were immediately treated with off-loading and total contact casting. After the healing process of the Charcot foot was complete, the extent of fractures and subsequent deformities were evaluated. RESULTS: Based on X-rays at the onset of symptoms, in 19 of the 24 patients the condition had been misdiagnosed prior to referral (in 11 patients as sprain injury). Additional imaging techniques (MRI, CT scan or bone scintigraphy) had been performed in 10 patients prior to referral. While these techniques had been used more frequently in the cases vs. the controls (P=0.012), misdiagnosis was less frequent in the cases vs. the controls (P=0.013). Only one out of 11 case patients developed extended foot fractures and severe deformity, vs. 12 out of 13 control patients (P<0.001). CONCLUSION: Early detection of incipient Charcot foot is facilitated by imaging techniques other than plain X-rays. Immediate off-loading of incipient Charcot foot appears to minimize fractures and incapacitating deformities.

Acute Disease↗
PubMed2004

Outcome of critical foot ischaemia in longstanding diabetic patients: a retrospective cohort study in a specialised tertiary care centre.

BACKGROUND: We sought to establish risk factors predicting the outcome of foot lesions in longstanding diabetic patients with critical foot ischaemia (CFI). PATIENTS AND METHODS: We investigated retrospectively 98 consecutive diabetic patients with ischaemic foot lesions. The patients (mean age 70 years, duration of diabetes 21 years) were jointly cared for by specialised diabetologists and vascular surgeons; 75 patients were treated by arterial revascularisation. RESULTS: Good outcome (lesions healing) was observed in 53 patients (54%). Bad outcome was observed in 45 patients: not healing lesions (n = 5), major amputation (n = 19), and death in relation to the foot lesion (n = 21). Patients with good and bad outcome did not differ regarding age, sex, smoking status, type, duration and treatment of diabetes mellitus, presence of neuropathy, coronary heart disease, stroke, previous amputations, current revascularization, and localization of the foot lesion. The risk of bad outcome was increased 8.9 times in patients on dialysis for end-stage renal disease; 7.0 times if surgical complications were present; and 5.4 times with C-reactive protein (CRP) above the second quintile (cut-off value 8 mg/dl). CONCLUSION: Management of longstanding diabetic patients with ischaemic foot lesions leaves room for improvement. Dialysis treatment, elevated CRP levels and surgical complications were strongly predictive of non-healing lesions, major amputation and death.

Aged↗
PubMed2004

New insights into the pathogenesis of diabetic retinopathy--hormonal rather than metabolic factors are important.

Diabetic retinopathy has traditionally been viewed as a metabolite-driven, occlusive vasculopathy that affects both retinal microvascular haemodynamics and stricture; analogies to cholesterol-driven occlusive atherosclerosis of the macrovascular circulation were drawn. However this paradigm may no longer be appropriate. Recent evidence suggests that diabetic retinopathy from the beginning is the consequence of a complex hormonal dysfunction, which is related to insulin-dependent up- and downregulation of growth factors, to which metabolic, haemodynamic, endocrine, paracrine, and autocrine mechanisms contribute.

Animals↗
PubMed2003

Effectiveness of a new brand of stock 'diabetic' shoes to protect against diabetic foot ulcer relapse. A prospective cohort study.

AIMS: Diabetic patients with podopathy (diabetic foot syndrome) may need protective footwear, be it customized or industrially produced stock 'diabetic' shoes (SDS). The effectiveness of each type of 'diabetic' shoe needs to be proven clinically, e.g. in terms of prevention of foot ulceration. The following study assesses a new German SDS, the LucRo shoe, which consists of rocker-shaped walking sole, a standardized shock absorption insole, and soft uppers without stiff toe-caps. The LucRo SDS has been registered as a Medicinal Product according to the European Community Guideline 93/42/EC. PATIENTS AND METHODS: A total of 92 high-risk diabetic patients (mean age 63 years, duration of diabetes 13 years) with healed foot ulcer were recruited prospectively over 31 months; 87 patients suffered from polyneuropathy, 24 patients had peripheral ischaemic vessel disease. One group of patients (n = 60) received the LucRo SDS and wore them, while the remaining patients (n = 32) did not receive the SDS and were forced to use their normal footwear. This allocation reflects the haphazard reimbursement policies of the individual patients' health insurance, and is in accordance with the current German legislation. The patients were followed up for up to 42 months until the first foot ulcer relapse, or the end of the study. RESULTS: There were no differences between the groups concerning age, sex, type and duration of diabetes, prevalence of polyneuropathy and peripheral ischaemic vessel disease, frequency of foot care and mortality rate. The first year annual rate of foot ulcer relapse was significantly different between the groups: 60% without SDS vs. 15% with SDS. The overall cumulative ulcer-free survival was significantly greater with SDS (P < 0.0001, log rank test). CONCLUSION: The LucRo stock 'diabetic' shoe appears effective in the prevention of foot re-ulceration in high-risk patients with diabetic podopathy.

Aged↗
PubMed2002

HLA-patterns in patients with multiple sclerosis and type I diabetes mellitus: evidence for possible mutual exclusion of both diseases.

BACKGROUND: Type I diabetes mellitus (T1DM) and multiple sclerosis (MS), both immune-mediated diseases, rarely co-exist in the same individual or co-segregate in families. HLA susceptibility genes for T1DM (DRB1*0401, DRB1*0404, DQB1*0302, DRB1*0301, DQB1*0201) rarely occur in MS patients. HLA genes known to confer "resistance" to T1DM (DRB1*1501, DQB1*0602-DQA1*0102) predispose to MS. To test the hypothesis of mutually exclusive HLA patterns, patients affected by T1DM plus MS were compared to those of patients affected by either of the diseases alone in a case-control study. METHODS: Blood was sampled for analysis of HLA class I and class II alleles from 66 patients of German ancestry, of whom 33 had T1DM plus MS, and 33 had MS-only. For comparison to patients with T1 DM-only we referred to published data. HLA typing was performed using conventional serology (immuno-magnetic beads) and genotyping (SSP-PCR Dynal(R) SSP low/high resolution kits). RESULTS: Individuals with co-existing MS plus T1DM displayed the expected T1DM associated HLA-pattern (75.8% carried DRB1*04, 69.7% carried DQB1*0302, 42% were DR4, DR3 heterozygous), but failed to display the expected MS associated HLA-pattern (0% carried DQB1*0602, 3.1% carried DQA1*0102). The expected MS associated HLA-pattern of Caucasoid patients, however, was found in the MS-only patients (42% carried DRB1*1501-DQB1*0602, 58% carried DQA1*0102), while the prevalence of T1DM susceptibility and 'resistance' alleles was not different from the general population. The allele frequency of DRB1*1501 was 16/66, 24.2% in the 33 MS-only patients, and 0% in the 33 MS plus T1DM patients. The allele frequency of DQB1*0602 was 16/66, 24.2% in the 33 MS-only patients, and 0% in the 33 MS plus T1DM patients. The allele frequency of DQA1*0102 was 18/66, 27.3%, in the 33 MS-only patients, and 1/66 1.5% in the 33 MS plus T1DM patients. CONCLUSION: These data confirm the hypothesis of mutually exclusive HLA-patterns of T1DM and MS, and are consistent with a low rate of co-morbidity of both diseases.

Adolescent↗
PubMed2001

What may be gained from standard photocoagulation during early worsening of diabetic retinopathy? An observational study in type-1 diabetic patients after tightening of glycaemic control.

OBJECTIVE: To assess the outcome of laser photocoagulation treatment for rapidly progressing diabetic retinopathy, socalled early worsening, subsequent to a rapid improvement of glycemic control. For the purpose of this study, early worsening was defined as any incidence or progression of retinopathy that followed a reduction in HbA1c by > 2% within 6 months. MATERIAL AND METHODS: Retrospective observational study in type-1 diabetic patients in a university diabetes center. PATIENTS: 23 patients with early worsening were identfied during a 16-year period, with a mean age of 25 years, duration of diabetes of 12 years, and glycated hemoglobin HbA1c of 12.4%; retinopathy was absent or mild nonproliferative at baseline. Focal, and/or panretinal laser coagulation was performed according to standard ETDRS criteria. Retinal pathology and visual acuity was followed-up for 12-120 months. RESULTS: Improving metabolic control induced mild non-proliferative retinopathy without macular edema in 4 patients, which regressed without treatment. In 19 patients, symptomatic diabetic maculopathy developed with macular edema, resolving by focal coagulation in 3 patients. Of the remaining 16 patients, 14 developed proliferative retinopathy (7 of whom despite focal, grid or scatter coagulation pretreatment), and were treated by full panretinal coagulation. In 7 of the 14 patients with proliferative retinopathy, vitreous hemorrhages occurred requiring pars plana vitrectomy. Proteinuria, polyneuropathy, and impaired vision prior to laser treatment were indicative of poor prognosis. Visual acuity > 0.3 in at least one eye was preserved in 22 of the 23 patients. CONCLUSIONS: In patients with type-1 diabetes mellitus and early worsening of diabetic retinopathy, the benefit of standard laser photocoagulation was limited, and particularly in the presence of symptomatic macular edema.

Adolescent↗