糖尿病肾病合并神经营养性关节病1例报告并文献复习

神经营养性关节病(即Charcot关节病)在临床上发生率很低,即使在其首发疾病糖尿病中也非常少见,因此,临床上易漏诊或误诊该病。本文报道1例糖尿病肾病患者合并Charcot关节病,并做文献复习。1病历资料患者男,46岁,因"血糖升高10年,反复下肢水肿2年余,加重1个月"于2010年3月入院。30年来从事蹼泳运动(入院4个月前停止)。患者于10年前多次化验发现空     

炎症在糖尿病夏科足发病机制中的作用

夏科足又称为夏科神经关节病(Charcot neuroarthropathy),是一种累及足和踝部骨、关节及软组织的炎症性病变,常伴有不同程度的骨质破坏、关节半脱位或脱位,足中部塌陷呈“舟状”畸形为其特征性改变[1];1868年该病首次被报道后以Charcot命名,麻风、中毒（乙醇、药物）、脊椎和神经根病等合并神经损害的疾病均可致病。1936年Jordan首先发现糖尿病与其密切相关。目前糖尿病神经病变已成为夏科足最常见的病因,夏科足亦被称为糖尿病夏科神经关节病（diabetic Charcot neuroarthropathy）。因其发病率不高,且早期仅表现为局部红肿,临床极易误诊漏诊,因此加强对夏科足的认识,对于减少溃疡发生及保全下肢有着重要意义。     

糖尿病足部神经性溃疡与神经性骨关节病

糖尿病足是糖尿病最常见的并发症之一,突出表现为足部溃疡,糖尿病神经病变为其主要病因,无知觉足、畸形足、足底压力异常增高和Charcot关节是发生足溃疡的主要危险因素。及早识别高危人群并对危险足进行特别护理是预防足溃疡的关键。     

Charcot关节病2例报告

Charcot关节病是各种感觉神经系统病变所致关节病变的统称，临床少见。2006～2009年，我们共收治Charcot关节病患者2例。现报告如下。     

糖尿病骨质疏松的诊治及预防

糖尿病患者常伴有各种骨骼疾病,包括骨量减少、骨质疏松、Charcot关节病等。骨质疏松症德特点为低骨量、骨组织微结构破坏、可导致骨脆性增加和易于骨折。现对T1DM、T2DM患者骨质疏松的临床特点、危险因素、发病机制和临床建议进行介绍。     

糖尿病足的诊治进展

糖尿病足是指与下肢远端神经病变和血管病变相关的足部感染、溃疡和／或深层组织破坏，包括神经营养不良和外伤共同作用引起的神经性骨关节病（Charcot氏关节），是糖尿病患者致残、致死的主要原因。据报道，全世界每年估计有超过100万的糖尿病患者需要截肢，大约每30s就有一个大的截肢事件，因此早期诊断、早期干预是降低截肢事件的关键。     

糖尿病合并Charcot关节病1例临床分析

糖尿病合并Charcot关节病在临床中并不少见,在疾病早期通常没有主诉,至出现疼痛、局部红肿等症状来就诊时,往往已到了晚期.现就本科室收治的1例糖尿病合并Charcot关节病的病例分析如下.     

足部的需要

糖尿病足是指因糖尿病血管病变和（或）神经病变和感染等因素，糖尿病患者足或下肢组织破坏的一种病变，是糖尿病患者截肢、致残的主要原因之一。通过对糖尿病足部溃疡的预防，对糖尿病足病的早期诊断和积极管理，90％以上的截肢是可以预防的，减轻患者经济负担，提高生活质量。     

糖尿病足部溃疡研究进展及新型冠状病毒肺炎疫情期间管理原则

世界卫生组织和国际糖尿病联合会将糖尿病足定义为糖尿病的一种严重的慢性并发症.糖尿病足是指因糖尿病神经病变,包括末梢神经感觉障碍及自主神经损害,下肢动脉硬化引起周围小动脉闭塞症,或皮肤微血管病变以及细菌感染所导致的足部疼痛、足部溃疡及足坏疽等病变.常常由于缺血、神经病变和感染三种因素协同发生作用.据报道,糖尿病足部溃疡患...     

糖尿病足病外科治疗应注意三点

糖尿病足是指因糖尿病神经病变（周围神经感觉障碍、运动神经病变所致局部畸形及自主神经损害）、下肢血管病变（如动脉硬化引起的周围小动脉闭塞症,或皮肤微血管病变）以及细菌感染所致的足部疼痛、溃疡及足坏疽等,常常由于缺血、神经病变和感染三种因素协同发生作用。糖尿病足是常见的糖尿病慢性并发症之一,     

A review of bone metabolism and developments in medical treatment of the diabetic Charcot foot

Charcot foot is a rare but severe, and possibly limb-threatening, complication to neuropathy and diabetes mellitus. The current treatment consists of long-term off-loading, and has a large negative impact on the patient's life. Much research has gone into understanding the condition and its biochemical mechanisms, however, the underlying pathogenesis of a Charcot foot is not yet fully understood.In the recent decades several key advances in our understanding of the Charcot foot have been made, both in regards to the changes in bone metabolism and structure an acute Charcot foot can cause, and to the molecular pathways involved in this.This review summerizes the available research into the bone metabolism around a Charcot foot, with an emphasis on the biochemical profile. The existing data regarding attempts at medical treatment is also reviewed, including novel trials targetting specific inflammatory pathways upregulated in the acute diabetic Charcot foot.     

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

Diabetic foot ulceration represents a major medical, social and economic problem all over the world. While more than 5% of diabetic patients have a history of foot ulceration, the cumulative lifetime incidence may be as high as 15%. Ethnic differences exist in both ulcer and amputation incidences, with both being less common in patients of Indian subcontinent origin living in the UK. Foot ulceration results from the interaction of several contributory factors, the most important of which is neuropathy. With respect to the management of acute Charcot neuroarthropathy in diabetes, recent studies suggest that bisphosphonates reduce disease activity as judged not only by differences in skin temperature, but also by assessing markers of bone turnover. The use of the total-contact cast is demonstrated in the treatment of acute Charcot feet and of plantar neuropathic ulcers. Histological evidence suggests that pressure relief results in chronic foot ulcers changing their morphological appearance by displaying some features of an acute wound. Thus, repetitive stresses on the insensate foot appear to play a major role in maintaining ulcer chronicity. It is hoped that increasing research activity in foot disease will ultimately result in fewer ulcers and less amputation in diabetes.Abbreviations BSAP bone-specific alkaline phosphatase - CN Charcot neuroarthropathy - RCW removable cast walker - TCC total-contact cast     

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 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.     

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.     

Mortality in patients with diabetic neuropathic osteoarthropathy (Charcot foot).

OBJECTIVE: To determine the mortality of a population of patients diagnosed with Charcot neuropathic osteoarthropathy managed by a single specialist unit and to compare the results with a control population. METHODS: We have undertaken a retrospective analysis of all cases of Charcot foot on the comprehensive database which has been maintained at the specialist diabetic foot clinic at the City Hospital, Nottingham since 1982. Survival and the incidence of amputation (major and minor) was compared with a control population referred with uncomplicated neuropathic ulceration. Controls were individually matched for gender, age (+/-2 years), disease type, disease duration (+/-2 years) and year of referral (+/-3 years). RESULTS: Forty-seven cases (21 female, 26 male) of Charcot foot were identified, of whom 18 (38.3%) had Type 1 diabetes. Mean age and disease duration at presentation were 59.2 +/- 13.4 (sd) and 16.2 +/- 11.2 years, compared with 59.7 +/- 12.6 and 16.3 +/- 11.2 years, respectively, in the controls. Twenty-one (44.7%) of those with Charcot had died, after a mean interval of 3.7 +/- 2.8 years. This compared with 16 (34.0%) after a mean 3.1 +/- 2.7 years in the control group. Mean duration of follow-up in the survivors was 4.7 +/- 4.9 years (Charcot) and 5.3 +/- 3.9 years (controls). A total of 11 (23.4%) Charcot patients had had a major amputation on the side of the index lesion, compared with five (10.6%) controls. There was no difference between the two groups (P > 0.05, Chi-square). CONCLUSIONS: The mortality in this group of patients with Charcot foot was higher than expected. Nevertheless, there was no difference between those with Charcot and those with uncomplicated neuropathic ulceration. It is possible that it is neuropathy, rather than Charcot osteoarthropathy, which is independently associated with increased mortality in diabetes. The mechanism underlying any such association is not known. There is a need for a formal, prospective, multicentre study to investigate the life expectancy and cardiovascular risk of those with Charcot osteoarthropathy.     

Calcaneal ultrasonometry in patients with Charcot osteoarthropathy and its relationship with densitometry in the lumbar spine and femoral neck and with markers of bone turnover.

AIMS: To assess calcaneal ultrasonometry in Charcot osteoarthropathy (CO) and to compare it with densitometry measured by dual energy X-ray absorptiometry (DEXA) and with bone remodelling markers. PATIENTS AND METHODS: A group of 16 diabetic patients in the acute stage of CO with a mean age (+/- SD) of 51 +/- 13 years was compared with 26 sex- and age-matched control subjects. Both calcaneal quantitative ultrasound (QUS) parameter stiffness and bone mineral density (BMD) measured in lumbar spine and femoral neck by DEXA were compared. Collagen type I cross-linked C-telopeptides (ICTP) were used for assessment of bone resorption. RESULTS: Patients with acute CO had significantly lower stiffness of the calcaneus in the Charcot and non-Charcot foot (both P < 0.001) and significantly lower femoral neck BMD (P < 0.05) in comparison with the control group. The T-score of stiffness was significantly lower in the Charcot foot compared with the non-Charcot foot (-3.00 +/- 1.39 vs. -2.36 +/- 1.12; P < 0.01) and significantly lower than the mean T-score of BMD in the lumbar spine (-0.57 +/- 1.28; P < 0.001) and femoral neck (-1.58 +/- 1.24; P < 0.05). A significant difference in ICTP (8.49 +/- 4.37 vs. 3.92 +/- 2.55 ng/ml; P < 0.001) between patients with CO and the control group was found, and a significant correlation was demonstrated between ICTP and the T-score of stiffness (r = -0.73; P < 0.01). CONCLUSION: The lower calcaneal QUS parameter stiffness in the Charcot foot in comparison with the control group, with the non-Charcot foot and with BMD in the lumbar spine and femoral neck, and its association with increased bone resorption indicate that calcaneal ultrasonometry may be useful in diagnosing the acute stage of CO and in assessing the risk of foot fracture. Diabet. Med. 18, 495-500 (2001)     

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.     

Is this bone infected or not? Differentiating neuro-osteoarthropathy from osteomyelitis in the diabetic foot

Osteomyelitis (bone infection) and neuro-osteoarthropathy (Charcot arthropathy) are limb-threatening complications of diabetic neuropathy with very different therapies. Distinguishing between them may be difficult, but it is important. In Charcot arthropathy, noninfectious soft tissue inflammation accompanies rapidly progressive destruction, first of joints, then of bone. This occurs in a well-vascularized and severely neuropathic, but nonulcerated, foot. In osteomyelitis, chronic soft tissue ulceration precedes infection of bone, which may be physically exposed. Magnetic resonance imaging and bone biopsy are the preferred diagnostic tests, provided adequate technical and interpretive skills are available.     

Charcot neuroarthropathy triggered by osteomyelitis and/or surgery

Introduction Charcot neuroarthropathy (CN) is a rare but devastating complication of diabetic neuropathy. Osteomyelitis is also a complication of the diabetic foot and it may be difficult to differentiate from CN. Patients and methods A patient with Type 1 diabetes and peripheral neuropathy developed a foot ulcer complicated by osteomyelitis of the first proximal phalanx. He was successfully treated with antibiotics and surgical excision of the infected bone. Six months later, he developed a hot, swollen, red foot and X‐ray showed destruction of the second and third metatarsal heads. At the second presentation, it was difficult to determine whether this was a recurrence of osteomyelitis or a new onset of CN. Thus, to obtain a definitive diagnosis, recourse was made to more sophisticated imaging techniques. Results ^99mTc methylenediphosphonate (MDP) bone scans and magnetic resonance imaging proved inconclusive to differentiate between osteomyelitis and CN. Subsequently, an indium‐labelled white cell scan confirmed the absence of osteomyelitis and the patient was successfully treated for CN. Discussion Infection and/or surgery may be predisposing factors in the development of diabetic CN but the combination of the two could accelerate the onset of the Charcot process in people with diabetes and neuropathy.     

Selective neuropathy and preserved vascular responses in the diabetic Charcot foot

Summary Charcot arthropathy is a disabling complication of diabetic neuropathy. It is however, unclear why it occurs in only a small number of neuropathic patients. We have studied 12 diabetic patients (10 insulin-dependent) with an acute Charcot arthropathy, and compared their neuropathy and vascular responsiveness with 12 diabetic patients (10 insulin-dependent) with recurrent neuropathic foot ulceration, 12 diabetic control subjects (9 insulin-dependent) and 10 normal non-diabetic subjects. The Charcot arthropathy patients demonstrated a preservation of warm perception, 6 (5.5) °C, but complete loss of peripheral cold perception, 10 (0) °C, p<0.001 (median (interquartile range)). This contrasted with the ulcerated neuropathy patients, who had equally severe impairment of both warm and cold sensory thresholds, 10 (0.5) °C vs 10 (1) °C, respectively, the diabetic control subjects who were able to detect a 2 (1.3) °C warm stimulus and 3 (3.5) °C cold stimulus and the normal subjects, whose warm threshold was 2 (1) °C and cold was 2 (1) °C. Light touch perception at the foot was preserved in the Charcot patients 4 (4) g vs 100 (50) g, p<0.0002, in the ulcerated neuropathy patients. Vibration perception at the great toe and cardiovascular autonomic function tests (heart rate variability, Valsalva ratio and postural systolic blood pressure fall) were abnormal in both the Charcot patients and ulcerated neuropathy group, with no differences seen between the two groups. Peak skin blood flow at the great toe in response to local heating was preserved in the Charcot arthropathy patients, 63.36 (28.72) flow units when compared to the diabetic and normal subjects, 62.72 (47) flow units and 76.3 (33.92) flow units, respectively and much greater than in the ulcerated neuropathy patients 28.94 (37.39) flow units, p<0.0002. The diabetic patients developing Charcot arthropathy thus have a neuropathy and vascular responsiveness which distinguishes them from diabetic subjects developing neuropathic ulceration. This may be important in the pathogenesis of the Charcot foot.