Patients with hypercortisolism may experience cutaneous atrophy, weakened cutaneous barrier function, decreased immunity, opportunistic bacteria or fungal infections, which hinder the healing of cutaneous wounds, and even the ulcers will not heal for a long time, and may progress to chronic ulcers, which are difficult and expensive to treat. It affects the quality of life of patients, and can lead to the spread of infection and life-threatening in severe cases. The pathological mechanism of cutaneous ulcers and delayed healing caused by hypercortisolism is complicated, which is a clinical problem that needs to be solved urgently. This article explains the possible mechanism of hypercortisolism hindering the healing of cutaneous ulcers from the aspects of leading to cutaneous atrophy, pathophysiological abnormalities affecting wound healing, hyperglycemia inhibiting wound healing, and infection and hypercoagulable state, and discusses the possible mechanisms of hypercortisolism hindering the healing of cutaneous ulcers, and its treatment methods, aiming to provide a basis for more in-depth mechanism research and clinical prevention and treatment.
ObjectiveTo review the regulatory effect of microRNA (miRNA) in wound heal ing, which abnormal expression associates with diabetes. MethodsThe literature on miRNA associating with wound heal ing was reviewed and summarized. ResultsmiRNA plays a key role in wound heal ing, including regulating inflammation, angiogenesis, granulation tissue formation, and re-epithel ization. ConclusionAbnormal expression of miRNA may be related to delayed healing of the diabetic wound, but further research is needed to confirm it.
Objective To evaluate the effectiveness of diabetic patient education on glycemic control for diabeties. Methods Fifty cases of type 2 diabetic patients with educational interventions from the Diabetic Educational Center of West China Hospital and 50 type 2 diabetic patients without educational intervention were selected randomly. All the patients completed the same questionnaire. The data were analyzed by SPSS 10.0. Results The age of patients in educational group was older and the duration of sickness was longer than those in the control group, but their blood glucoses were better controlled. Conclusions Diabetic patient education is important to improve their glycemic control and decrease the risks and deterioration of diabetic chronic complications.
Diabetic foot ulcer is the most serious complication of diabetes. In addition to diabetic peripheral neuropathy and lower extremity vascular disease, diabetic foot pressure abnormality is an independent risk factor for diabetic foot ulcers. This review summarizes the relationship between plantar pressure and diabetes, including the concept of the plantar pressure and its measurement methods, as well as the abnormal changes in the plantar pressure of diabetic patients. In addition, through the explanation of the mechanism of diabetic patients’ plantar pressure changes, the methods of releasing the abnormal plantar pressure are discussed, so as to prevent and treat the diabetic foot ulcers, and improve our understanding of it.
ObjectiveTo investigate the clinical heterogeneity and auto-immunologic state in patients with diabetic ketosis (DK) or diabetic ketoacidosis (DKA). MethodsDiabetic patients who presented with DK/DKA were recruited from West China Hospital of Sichuan University from January 1, 2000, to December 31, 2008. We analyzed the clinical classification, biochemical profiles, and auto-immunologic state of the patients. ResultsAmong them, 257 (15.0%) patients had type 1 diabetes, while 883 (51.6%) with type 2 diabetes, and 515 (30.1%) could be typed as "atypical diabetes" or "untying diabetes". The average age of hospitalized patients with type 1 diabetes was (31.1±13.5) years, which was significantly lower than that of the type 2 diabetes patients [(58.1±13.2) years] (P＜0.001). The most common contributing factor for DK/DKA was infection, followed by noncompliance with therapy. Glutamic acid decarboxylase antibody positive rate was 4.37% in patients with "atypical diabetes", which was similar with type 2 diabetes group (2.69%, P=0.79), but lower than that of the patients with type 1 diabetes (13.79%, P＜0.001). ConclusionsWe conclude that DK or DKA can occur not only in type 1 diabetic patients but also in patients with type 2 diabetes under infection or stress condition. DK/DKA patients have a high clinical heterogeneity. The auto-immunologic state and β-cell function have significant implications for the diagnosis and classification of diabetes.
To compare the platelet enrichment ratio of platelet-rich plasma (PRP) prepared by different centrifuge methods and to compare the concentration of growth factors released from autologous platelet-rich gel (APG) with the whole blood. Methods Thirteen diabetic patients with refractory skin lesions were enrolled in APG treatment. ① Three kinds of centrifuge methods were selected for PRP by 11 diabetic patients: A(n=6): 529 × g for 4 minutes in the first centrifugeand 854 × g for 6 minutes in the second centrifuge; B (n=5): 313 × g for 4 minutes in the first centrifuge and 1 252 × g for 6 minutes in the second centrifuge; C (n=5): 176 × g for 5 minutes in the first centrifuge and 1 252 × g for 5 minutes in the second centrifuge. Platelet counted on the whole blood and PRP was determined. The APG, produced by combining the PRPwith thrombin and calcium gluconate (10 ∶ 1) was used by patients. ② PDGF-BB, TGF-β1, VEGF, EGF, and IGF-1 were measured in the APG and the whole blood using the enzyme-l inked immunosorbent assay method. Results ① The average platelet concentration was higher in group B [(1 363.80 ± 919.74) × 109/ L] than in groups A[(779.67 ± 352.39) × 109/ L)] and C[(765.00 ± 278.78) × 109/ L] and the platelet recovery rate was 75.2% ± 21.0% in group B. ② The concentration of growth factors all increased with the increasing platelet number. On average, for the whole blood as compared with APG, the PDGF-BB concentration increased from (145.94 ± 133.24) pg/mL to (503.81 ± 197.86) pg/mL (P lt; 0.05); TGF-β1 concentration increased from (3.31 ± 2.27) ng/mL to (5.67 ± 4.80) ng/mL (P lt; 0.05); IGF-1concentration increased from (14.54 ± 35.34) ng/mL to (110.56 ± 84.36) ng/mL (P lt; 0.05); and EGF concentration increased from (160.73 ± 71.10) pg/mL to (265.95 ± 138.43) pg/mL (P lt; 0.05). No increase was found for VEGF(P gt; 0.05). ③ There was positive correlation between the platelet concentration and PDGF-BB and TGF-β1 (r = 0.627, r = 0.437, P lt; 0.05). ④ Thirteen diabetic repractory dermal ulcers received APG treatment for 18 times, 9 ulcers (69.2%) and 10 sinuses (88.3%) were cured at the end of 12-week treatment. Conclusion The method ofgroup B is the best centrifuge method. A variety of growth factors are detected and released from the platelets at significant levels in APG. There is positive correlation between the platelet concentration and PDGF-BB and TGF-β1 .
目的 探讨表现为足溃疡的恶性黑色素瘤临床特点。 方法 回顾性分析2002年1月－2010年12月收治的46例表现为足溃疡的恶性黑色素瘤患者。 结果 46例均病理组织活检确诊，男29例，女17例，平均年龄57岁。溃疡形成前多表现为包块、黑素斑、痣、水泡、灰指甲、鸡眼、疣等；溃疡形成后表现为外伤不愈或反复复发、溃疡中央或边缘破溃、不规则、表面凹凸不平、颗粒状或呈瘢痕状态、焦痂、菜花样新生物等；溃疡好发部位为足底、足跟、足趾；3例患者无色素沉着；确诊前溃疡存在时间为（10.74 ± 10.94）个月，38例患者（82.6%）在确诊前误诊，中位误诊时间为6个月（2.75～48个月），分别被误诊为黑色素斑、痣、慢性溃疡、黑色包块等。确诊时18例存在远处转移；35例进行手术治疗，3例采用单纯化学治疗，8例放弃治疗。 结论 恶性黑色素瘤早期表现不典型，常被误诊，由于其高度侵袭性，对表现不典型的足溃疡应提高警惕，尽早行病理组织学检查，以减少其误诊。
Objective To identify the best therapy regimen for a patient with rare hypoglycemia due to insulin autoantibody (IAA). Methods We searched The Cochrane Library (Issue 3, 2008), PubMed (1966-July 2009), EMbase (1974-July 2009) and CBM (1978-July 2009) to identify relevant evidence. The quality of the retrieved studies was critically assessed. Results A total of 291 records were retrieved. No clinical guidelines, systematic reviews or clinical randomized studies were identified. Thirty treatment-related studies involving 6 interventions showed that insulin combined with Prednisone was relatively more effective and safer than conventional therapies. Conclusion The steroid treatment might be useful for the improvement of glycamic control in patients with high IAA levels and severe hypoglycemia and hyperglycemia due to insulin antibodies raised against subcutaneously-injected human insulin.