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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review examines several of the recently introduced wound care products that have been put forward as treatment modalities for the diabetic foot ulcer. Discussed are the results of clinical trials with the platelet-derived growth factor, becaplermin, the tissue-engineered products Dermagraft and Apligraf, and Hyaff which is an ester of hyaluronic acid. In patients with an infected foot ulcer, encouraging results were obtained with the granulocyte-colony stimulating factor, Filgrastim.
Diabetes Metab Res Rev
PMID:New treatments in ulcer healing and wound infection. 1105 89

Patients with diabetes have an impaired wound healing process that contributes to the pathophysiology that may lead to amputation. In this case study, an extensive (103.49 cm2) full-thickness cutaneous wound with exposure of a necrotic Achilles' tendon in a patient with diabetes, neuropathy, and infrapopliteal vascular disease of the lower limbs was healed using a two-stage autologous skin substitute technique. The scaffolds on which the autologous fibroblasts and keratinocytes were grown comprised an ester derivative of hyaluronic acid. Two applications of the cultured autologous fibroblasts and one of the cultured autologous keratinocytes were placed on the wound at 7-day intervals. The ulcer healed completely 60 days following the first fibroblast graft application. After 16 months of follow-up, no recurrence was noted and the patient can walk without ancillary support. This novel tissue engineering technique is a promising treatment for wound healing.
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PMID:Using hyaluronic acid derivatives and cultured autologous fibroblasts and keratinocytes in a lower limb wound in a patient with diabetes: a case report. 1227 33

The wound healing process in the patient with diabetes can be adversely affected by many factors, including unrelieved pressure, infection, and concurrent underlying conditions. In addition, a static wound may exacerbate patient anxiety or depression and indirectly further delay the healing process while increasing the risk of complications. The polysaccharide hyaluronic acid has long been known to be an integral component of the extracellular matrix in the dermis and other tissues and is implicated in the process of wound healing and tissue repair. Research has shown the benefit of using a novel ester of hyaluronic acid to accelerate the healing process and effectively treat diabetic foot ulceration and other difficult-to-heal chronic wounds. The effects of care using hyaluronic acid on three patients with challenging wounds are presented.
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PMID:Treating recalcitrant diabetic wounds with hyaluronic acid: a review of patients. 1273 39

Diabetic foot complications are the most common cause of nontraumatic lower extremity amputations in the industrialised world. Unsatisfactory healing requires advanced therapeutic strategies, such as the use of skin grafts, which may represent a helpful option for wound coverage. Alternatively, a method using autologous keratinocytes grown to thin sheet grafts is available. The purpose of this pilot study was to investigate the application of autologous human keratinocytes cultured on membranes composed of benzyl ester of hyaluronic acid (Laserskin autograft) to diabetic foot ulcers. We studied 14 patients with type 2 diabetes mellitus and a nonhealing diabetic foot lesion, defined as existing longer than 6 months or with no wound healing apparent for 12 weeks. Between 7 and 64 days after the transplantation (depending on the size of the ulceration), 11/14 of the lesions were completely healed. The transplantation of autologous keratinocytes may allow faster closure of diabetic foot lesions and subsequently reduce length of hospitalization. This method can easily be planned with regard to logistics and time, and furthermore, this therapy option can be carried out by the diabetologist.
J Diabetes Complications
PMID:Autologous human keratinocytes cultured on membranes composed of benzyl ester of hyaluronic acid for grafting in nonhealing diabetic foot lesions: a pilot study. 1281 Feb 43

Biocompatibility issues such as protein deposition and fibrous capsule formation significantly reduce the sensitivity of implanted glucose sensors. One of the approaches to improve the sensor biocompatibility is to disguise the sensors with coatings that mimic body conditions. We anticipate that a biomimetic coating based on hyaluronic acid (HA) would minimize the problems related to protein deposition and fibrous tissue formation. Diffusion experiments were conducted to assess the transport properties of HA coating on a polyvinyl alcohol (PVA) membrane using a classic diffusion cell. HA was coated on PVA membranes, as cross-linked HA membranes alone have poor mechanical strength. The effective diffusivities of glucose and oxygen in a HA/PVA membrane (95% confidence interval) are 1 +/- 0.26 x 10(-4) and 1.42 +/- 0.34 x 10(-4) cm(2)/min, respectively. The effective diffusivities of glucose and oxygen in HA/PVA membranes were approximately two-thirds when compared with the diffusivities of glucose and oxygen (7.29 x 10(-5) and 2.34 x 10(-4) cm(2)/min, respectively) in pure PVA membranes. The results indicate that the HA/PVA membranes have transport properties similar to the commonly used pure PVA membranes, and thus may find usefulness as a coating for implantable glucose sensors.
Diabetes Technol Ther 2003
PMID:Novel hyaluronic acid coating for potential use in glucose sensor design. 1282 23

It has long been recognized that the symptom complex of fibromyalgia can be seen with hypothyroidism. Hypothyroidism may been categorized, like diabetes, into type I (hormone deficient) and type II (hormone resistant). Most cases of fibromyalgia fall into the latter category. The syndrome is reversible with treatment, and is usually of late onset. It is likely more often acquired than due to mutated receptors. Now that there is evidence to support the hypothesis that fibromyalgia may be due to thyroid hormone resistance, four major questions appear addressable. First, can a simple biomarker be found to help diagnose it? Second, what other syndromes similar to Fibromyalgia may share a thyroid-resistant nature? Third, in non-genetic cases, how is resistance acquired? Fourth, what other methods of treatment become available through this new understanding? Preliminary evidence suggests that serum hyaluronic acid is a simple, inexpensive, sensitive, and specific test that identifies fibromyalgia. Overlapping symptom complexes suggest that chronic fatigue syndrome, Gulf war syndrome, premenstrual syndrome, post traumatic stress disorder, breast implant silicone sensitivity syndrome, bipolar affective disorder, systemic candidiasis, myofascial pain syndrome, and idiopathic environmental intolerance are similar enough to fibromyalgia to merit investigation for possible thyroid resistance. Acquired resistance may be due most often to a recently recognized chronic consumptive coagulopathy, which itself may be most often associated with chronic infections with mycoplasmids and related microbes or parasites. Other precipitants of thyroid resistance may use this or other paths as well. In addition to experimentally proven treatment with supraphysiologic doses of thyroid hormone, the thyroid-resistant disorders might be treatable with anti-hypercoagulant, anti-infective, insulin-sensitizing, and hyaluronolytic strategies.
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PMID:A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone. 1288

Elevated glucose level is the main cause of extracellular matrix (ECM) derangement in various tissues in diabetes mellitus. The development of diabetic nephropathy is considered to be dependent on profibrotic cytokine, transforming growth factor-beta1 (TGFbeta1). Its excessive activation due to the up-regulation of thrombospondin-1 (TSP-1) in mesangial cells exposed to high glucose contributes to ECM accumulation. However, the role of TSP-1-TGFbeta1 pathway in the development of glucose-induced imbalance of ECM homeostasis in skin connective tissue is not studied. We investigated the response of human skin fibroblasts to elevated glucose level (11.0 and 30.0 mM) in terms of: (1) the expression and secretion of fibronectin (FN) and plasminogen activator inhibitor-1 (PAI-1); (2) the accumulation of hyaluronic acid (HA) in pericellular matrix and in the conditioned medium; (3) TGFbeta1 expression, secretion and activation; (4) TSP-1 expression and secretion. We demonstrated the up-regulation of FN and PAI-1 by elevated glucose and the stimulation of HA accumulation in both cellular compartments. However, we failed to demonstrate the increase of expression, secretion and activation of TGFbeta1, and the increase of TSP-1 expression and secretion in fibroblasts exposed to high glucose. These results show that ECM derangement in skin fibroblasts due to high glucose is not determined by TGFbeta1 and its activation by TSP-1.
J Diabetes Complications
PMID:High glucose-induced alterations of extracellular matrix of human skin fibroblasts are not dependent on TSP-1-TGFbeta1 pathway. 1458 81

High glucose-induced endothelial cell dysfunction is considered to be the main cause of the development of vascular diabetes complications. Cultured endothelial cells exposed to high glucose in vitro demonstrate a variety of alterations, including extracellular matrix (ECM) deposition, growth inhibition, and changes in cell motility. Some of these effects were shown to be mediated by the up-regulation of endothelial transforming growth factor-beta1 (TGFbeta1) secretion and activation. We investigated the influence of high glucose on human immortalized endothelial cell line ECV304. According to our data, confluent cells exposed to 30 mM glucose for 48 h secrete the increased amount of total and active TGFbeta1 ( approximately 1.4-fold), and accumulate more chondroitin sulphate (CS) in their conditioned medium, pericellular matrix, and cell layer ( approximately 1.6- to 2.0-fold). By blocking the coupling of CS chains to the core protein with p-nitrophenyl-beta-D-xyloside and by chondroitinase ABC treatment, we demonstrated that the increased accumulation of pericellular CS is accompanied by increased cell attachment to immobilized hyaluronic acid (HA), while the expression of cell surface CD44 remains unaltered. Since the exogenous TGFbeta1 affects ECV304 cells in a similar manner, and anti-TGFbeta1-neutralizing antibody cancels the effect of high glucose, we suggest the involvement of TGFbeta1 in the development of endothelial cell response to high glucose in terms of CS accumulation and cell binding to HA.
J Diabetes Complications
PMID:TGFbeta1 is involved in high glucose-induced accumulation of pericellular chondroitin sulphate in human endothelial cells. 1533 4

It is well known that hyaluronic acid and its principal receptor, CD44, are implicated in the regulation of the tissue repair process, but their role in the formation of chronic diabetic ulcers has not been studied. Hyaluronic acid metabolism and CD44 expression are regulated by lactate, where their increased production is considered to affect the properties of fibroblasts in non-insulin-dependent diabetes mellitus. The aim of our work was to investigate the possible role of hyaluronic acid and CD44, and their regulation by lactate, in the abnormal wound healing of diabetes. Fibroblasts were derived from uninjured skin from four non-insulin-dependent diabetic patients with ulcers and four without ulcers; and from four healthy age-matched volunteers. We observed that diabetic fibroblasts of both groups produced more L-lactate ( approximately 30%) and incorporated more (3)H-glucosamine into the medium hyaluronic acid ( approximately 28%) than controls. Fibroblasts of the diabetic group with ulcers, unlike those of the group without ulcers, showed significant increases in the high molecular weight hyaluronic acid accumulation in the pericellular matrix (30.5%, p < 0.01) and CD44 expression (27.0%, p < 0.05). Exogenous L-lactate dose-dependently, and equally for all fibroblasts lines, stimulated the accumulation of medium hyaluronic acid (3.7-fold) and CD44 expression (1.5-fold). However, fibroblasts from diabetic patients with ulcers were more (1.4-fold) sensitive to L-lactate in terms of CD44 expression, and responded to L-lactate by the increased accumulation of high molecular weight hyaluronic acid in the pericellular matrix (32.1%, p < 0.01). We propose that specific properties of fibroblasts from diabetic patients with ulcers may be involved in the increased susceptibility of these patients to chronic ulceration.
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PMID:Hyaluronic acid production and CD44 expression in cultured dermal fibroblasts of patients with non-insulin-dependent diabetes mellitus with and without chronic ulcers on the lower extremity. 1582 43

The transplantation of bioartificial pancreas has the potential to restore endogenous insulin secretion in type I diabetes. The bioartificial pancreas is constructed in vitro from cells and a support matrix. Hyaluronic acid (HA) is an extremely ubiquitous polysaccharide of extracellular matrix in the body and plays various biological roles. It has been suggested that high molecular weight (HMW) HA increases in the function of gap-junctional intercellular communications (GJIC) and the expression of connexin-43 (Cx43). To determine whether the function of pancreatic beta-cells is affected by gap junctions after HMW HA-treatment, we exposed HIT-T15, a clonal pancreatic beta-cell line, in various concentrations of HA for 24h, and then detected the insulin secretion and content, using an insulin assay kit by ELISA technique. The cellular functions of GJIC were assayed by dye-transfer method using the dye solution of Lucifer yellow. HA-treatment resulted in the enhancement of GJIC function, the increase of insulin release and insulin content. The results obtained in this study suggest that HA-coating increases the insulin secretion of HIT-T15 cells by the enhancement of Cx43-mediated GJIC. The results give useful information on design biocompatibility of HA when is used as a biomaterial for bioartificial pancreas.
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PMID:The effect of hyaluronic acid on insulin secretion in HIT-T15 cells through the enhancement of gap-junctional intercellular communications. 1617 59


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