Diabetic Skin Care

Epidemiology
Diabetes mellitus is characterized by high blood glucose (hyperglycemia) which may be due to: decrease) in the production of insulin (called type I diabetes mellitus) due to the destruction of the pancreas in an autoimmune or b) decreased sensitivity peripheral insulin (type II, which also drew some decrease in the production of insulin by the pancreas) associated with obesity and physical inactivity. Only about 5-10% of type I disease, the rest of type II.

The most recent statistics available (2005) show 20.8 million people (7% of the population) have diabetes, including 14.6 million were actually diagnosed, leaving 6.2 million unaware of the presence of this serious disease. In addition, its prevalence has increased by 40% in the last ten years and should increase 165% between 2000 and 2005 (Figure 1). An estimated one third of the population born in the year 2000 will develop diabetes. Beyond the suffering of patients and disability, the economic impact on direct and indirect costs is enormous, amounting to 132 billion dollars in 2002, 1/10th of all health care costs.

There were 224 092 deaths attributable to diabetes in the United States in 2002 (probably a underestimate). The risk of dying patients with diabetes is twice that for persons of the same age without diabetes, and this longevity is due to a reduction in cardiovascular disease. Diabetes increases the risk of heart disease and stroke 2-4 times more than for people without diabetes. The microvascular retinopathy, nephropathy, neuropathy diabetes and the leading cause of blindness, end stage renal disease and nontraumatic lower limb amputations in a USA2 The last complication rate is increasing (Figure 2).

Pathogenesis

The microvascular and macrovascular diabetes are closely associated with hyperglycemia and oxidative stress that is when cells are to detoxify reactive oxygen species (ROS) produced during metabolism. Four hypotheses have been proposed to explain how hyperglycemia leads to complications: 1) increased flow of the polyol pathway, 2) increased intracellular formation of advanced glycation end products (AGEs), 3) activation of protein kinase C (PKC) isoforms, and 4) increased flux through the hexosamine.

A unifying concept is that hyperglycemia superoxide induced mitochondrial overproduction activates these four channels. excess superoxide partially inhibits glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase (GAPDH), thereby diverting metabolites of glycolysis upstream of the pathways of glucose in the over-use. superoxide anion does this type of fracture DNA strands that lead to the activation of poly ADP ribose polymerase (PARP), which in turn disables ribosylation and GAPDH. The prevention of their metabolism, a process increases energy substrates flow consequent increase of dihydroxyacetone phosphate (DHAP) diacylglycerol (DAG), an activator of PKC and methylglyoxol triose phosphate, which is the main intracellular precursor of age. increased flow of fructose-6-phosphate from UDP-N-acetylglucosamine in the modified protein increases in hexosamine path ON-acetylglucosamine and increased glucose flux through the polyol pathway consumes the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) and depletes GSH (reduced glutathione, a powerful natural anti-oxidant).

Several mechanisms have been proposed to explain why the increase in the flow of the polyol pathway is harmful. These are the sorbitol-induced osmotic stress, a decrease of (Na + + K +) ATPase, increased cytosolic NADH / NAD + and decreased Cytosolic NADPH.

Activation of the hexosamine path results in the intracellular glycosylation and the gift of the N-acetylglucosamine to serine and threonine residues Sp1 transcription factors such as increased production resulting from factors such as plasminogen activator inhibitor-1 (PAI-1) and transforming growth factor beta 1 (TGF-beta 1) 0.5

The production of intracellular AGE target cell damage by three mechanisms. intracellular proteins are modified by age failure (Eg neurotropism, axonal transport and gene expression). Second, extracellular matrix components precursors modified by age abnormally with other components of the receiver array and matrix proteins (integrins) on cells. Third, bind to plasma proteins modified by AGE precursors of AGE receptor (RAGE) in endothelial cells, mesangial cells and macrophages, inducing receptor-mediated production of ROS as second messenger to activate the nuclear factor kappa B (NF-kappa B), a transcription factor that leads to pathological changes in the gene expression.5

Hyperglycemia-induced PKC activation has a number of pathogenic consequences, affecting the expression of endothelial NO synthase (ENSO), endothelin-1 (ET-1) oxidase of vascular endothelial growth factor (VEGF), TGF-beta 1 and PAI-1, and activation of NF-kappa B and NAD (P) H. eNOS and decreased ET-1 decreases blood flow causing hypoxia. The increase in VEGF increases vascular permeability and angiogenesis. The increase in TGF-beta leads to increased collagen, fibronectin, matrix membrane extracellular and basement resulting in capillary occlusion. Increased fibrinolytic PAI-1, leads to decreased vascular occlusion. B Increased NF-kappa leads to an increase in the expression of proinflammatory genes. Oxidase increased NAD (P) H causes increased ROS (causing DNA damage, oxidation of fatty acids lipids polydesaturated and oxidation of amino acids in proteins). These pathogenic mechanisms may be characterized as a consequence of effects on genes and ROS proteins.5

Diabetic skin

The skin of diabetics with age and is subject to the problems of neuropathy, macrovascular and microvascular disease. In addition, diabetes is associated with wound healing, susceptibility to infections and decreased cell-mediated immunity. This battle may take a glance and unrecognized require a survey prepared by the doctor and patient to prevent complications of this dreaded disease. The fight is against the oxidative stress and inflammation, ischemia and necrosis.

The clinic

1. Diabetic dermopathy is the most common manifestation of diabetes and the skin is due to microvascular changes. Because it is associated with, but not diabetes specific sweet, which serves as a marker of the disease. This skin disease is more common in diabetic men over 50 years, but it can also be seen in euglycemic diabetics and healthy people. The injury is so named because of characteristic changes in the microvasculature. Irregular-shaped patches of skin with a depressed area is mainly in the front legs, but can occur in the arms and legs and bone prominences. The lesions are light brown due to extravasation of red blood cells and hemosiderin deposits in histiocytes. They appear in the cultures and resolve over 12-18 months. Given that lesions are asymptomatic, with no special treatment is required, except to protect the area of trauma and secondary infections.

2. The skin of the foot diabetes is usually dry due to decreased sweating in the wake of Self neuropathy of diabetes. Sweat is normal stratum corneum and moisturize Dry skin is prone to callus formation with fissures and cracks.

3. The Diabetic Foot "is due to neurovascular and ischemic changes. It is a complication very serious disease. The loss of sensitivity means that the diabetic patient is not able to detect and prevent injuries to environmental agents. injury heat can have horrible results. Even minor mechanical trauma to the skin of the diabetic foot can cause blisters, sores and ulcers. This situation exacerbated by the loss of engine intrinsic foot muscles leads to malformations, including a high arch and "hammer toes." bony created in the heel, toes and metatarsal heads become pressure points on the skin that may crack. This can lead to ulceration, infection skin, soft tissue and bone (osteomyelitis), gangrene (which may be "wet" due to necrosis with an infection or "dry" due to necrosis without infection), and finally amputation. Skin pressure points may become thickened as a corn or callus, or develop blisters that may become infected. The skin between the toes can become macerated that promotes infection by bacteria and fungi. The bones of the feet can degenerate Production fractures (Charcot foot). A terrible complication of this foot is a "swing", which often results in skin lesions and infections. A foot "Diabetic" is usually asymptomatic until the final whistle. requires special attention: the patient should inspect your feet daily to avoid complications and a physician with expertise in this area is necessary for optimal results.

Treatment:

The control of hyperglycemia: The first stage in the control of hyperglycemia in diabetics Type II is diet and exercise. Then, oral hypoglycemic agents are added, of which there are many. Ultimately, insulin injection may be required. Insulin is the first therapeutic step in patients with type I diabetes Unfortunately, glycemic control is difficult, especially in patients with type II, probably related to poor adherence. At this level the patient can be very useful. Make sure the patient takes control of their blood sugar, exercise, diet, care your skin, and proper medication use. Patients should check their blood glucose frequently and feet every day. The best results are obtained with treatment Based on the pathogenesis and prevention is the name of the game.

Pharmacology

Corneotherapy is made possible by what is known as Rule 500 Dalton. The 500 Dalton rule is used in the development of topical medications and trans-dermal systems. skin barrier is effective in blocking molecules with an atomic weight more than 500 Daltons, but lower weight molecules through the skin barrier. Topical medications such as cyclosporine, tacrolimus and ascomycin can be effectively through the skin because the molecules of these drugs are less than 500 Daltons.

Despite the physical and chemical barrier of the horny layer resists penetration of large molecules, small molecules with a molecular weight below 500 daltons pass through the skin. molecular size is an important factor regulates passage of substances through the skin, the healthy properties of the substance of higher molecular weight self-limiting. Passive release of substances due to their low molecular weight provides opportunities for the delivery of the novel. Included in these low molecular weight substances are vitamins, amino acids,? -3? -6 Essential fatty acids and antioxidants such as hydroxytyrosol.

Instructions for patients to prevent diabetic foot problems
You should start caring for your feet. Set a time each day for review. Now is the time for you to play an active role in their care of these 10 steps:

1.Test their level of blood sugar. Work with your health care team doctor to keep your blood glucose within your target range with a good diet and exercise.
2.Avoid foot problems through early detection of changes before they become serious. Look at your bare feet daily for red spots, cuts, swelling and blisters. If you can not see the bottoms of your feet, use a mirror or ask someone.
3.Get active. Plan your exercise program with your health care team.
4.Get knowingly. Talk to your doctor about Medicare coverage for special shoes (orthotics).
5.Wash (not soak) the feet daily with warm water and dry thoroughly, especially between toes.
6.Keep your skin soft and smooth. Apply a thin layer of skin cream on the tops and bottoms of the feet, but not between the toes.
7.Si they can see and reach the nails, cut them if necessary. Cut toenails straight across and file the edges with sandpaper or a nail file.
8.We shoes and socks at all times. Never walk barefoot. Wear comfortable shoes that fit well and protect your feet. Check inside your shoes before using them. Make sure the surface is smooth and there are no objects in the interior.
9.Protect hot and cold feet. Wear shoes at the beach or on hot pavement. Do not put your feet in warm water. Test water before putting your foot in it like you before to bathe the baby. Never use hot water bottles, heating pads or electric blankets. You can seriously burn your feet without realizing it.
Blood 10.Keep flows at his feet. Put your feet while sitting. Stir the toes and ankles up under 5 minutes, two (2) or three (3) times per day. Do not cross your legs during long periods of time. Do not smoke!

Remedy ® Description:

Clinical Pharmacology: The active ingredient in these preparations are 1.5% dimethicone to protect the skin. Olivamine ® is a patented ingredients mix of antioxidants and anti-inflammatory that helps repair cell membranes and restore cells of a healthy state. Olivamine ® contains the following elements:

Hydroxytyrosol

3,4-dihdroxyphenylethanol (hydroxytyrosol: DOPET) is the main component in the phenolic fraction of olive oil. It is a molecule of water soluble and fat soluble, which is a treasure effective peroxyl radical. The DOPET experiments show that effectively neutralizes the cytotoxic effects of reactive oxygen species (ROS) in several human cell systems. In studies with cells DOPET pre-incubated, it was found that the damage caused by oxidative stress such as lipid peroxidation and alterations in cell permeability, can be avoided, DOPET has a protective effect against H2O2-induced oxidative hemolysis.

Wistaria

Edit a statement hyperosmotic cell osmolality decreased adenosine triphosphate (ATP), in combination with necrosis and necrosis. Glycine is a cytoprotective against injury by ATP depletion. Glycine protects cells ATP-depleted by low affinity interactions by multimeric channel protein, stabilization of which can otherwise cause pore formation pathological. These defects porous membranes in ATP depleted cells have been characterized recently, showing the limits defined by the exclusion of molecules increasing size. Glycine provided during ATP depletion blocked the development of membrane pores completely. The relationship between necrosis and a decrease extracellular ATP makes its protection and restoration of key stages during the early necrosis or necrosis prelethal.

L-Taurine

L-taurine can act as a direct antioxidant clean oxygen radicals or free block intracellular ROS-mediated cell death. Beneficial effects of scavenging capacity of ROS-L-Taurine include the attenuation of lipid peroxidation, reducing the permeability of the membrane, and inhibition of intracellular oxidation in different cells. Taurine prevents apoptosis induced by high glucose in endothelial cells through inhibition of ROS and stabilization of intracellular calcium. In addition to its effects in the antioxidant, L-taurine also functions as a modulator of intracellular Ca2 + homeostasis principle.

N-acetyl-L-cysteine

In a study by the Department of Microbiology and Immunology, Faculty of Medicine, SUNY Buffalo, Buffalo, NY, and Department of Radiation Oncology and Free Radical Agenda Radiation Biology, University of Iowa, Iowa City, Iowa, investigated the hypothesis that NAC-induced free radical signaling progression for delays S phase G0/G1 cells by regulating cell cycle protein cyclin D1 and the regulation of free radical-scavenging superoxide dismutase manganese enzyme (MnSOD). NAC treatment resulted in increased cellular levels of glutathione, indicating a shift towards a more reduced. This change in the redox environment cells has been associated with delayed progression of G0/G1 to S. NAC treatment resulted in a decrease of cyclin D1 and increased MnSOD protein levels. The absence of NAC-induced G1 arrest in fibroblasts that overexpress cyclin D1 (or a nondegradable mutant of cyclin D1-T286A) indicates cyclin D1 regulates the delay in progression S. G0/G1 These results support the hypothesis that the cellular redox environment regulates cell proliferation by regulating cellular protein levels regulatory cycle. In addition, our results also suggest that inclusion of NAC in the formulations of skin care can help in healing wounds proliferation of appropriate control and prevention of scars.

L-proline

DNA synthesis is an essential element of cellular life. In studies in vivo and in vitro, L-proline was the only amino acid that has been implicated in the stimulation of DNA synthesis. In addition, factor epidermal growth (EGF) received any response without the addition of L-proline. Media proline-deficient, and Leibovitz L-15, Eagle minimal modification essential and minimum essential Dulebecco did not induce DNA synthesis. But using the media as Williams E McCoy 5A and Ham F-12, which are rich with L-proline, was DNA synthesis and proliferation significantly. L-proline is essential for the induction of cell proliferation in vivo and in vitro through its effect on intracellular synthesis of collagen.

Vitamin B6 (pyridoxine)

The term vitamin B6 is used to describe all forms biologically things convertible pridoxine including pyridoxine, pyridoxal, pyridoxal 5-phosphate, and pyridoxamine. Vitamin B6 is an essential cofactor in many enzymatic reactions mainly involved in the metabolism of amino acids. In addition, vitamin B6 acts as an antioxidant, interacting with singlet molecular oxygen during oxidative stress.

Vitamin B3 (niacinamide)

Niacinamide is a precursor of coenzyme nicotinamide adenine dinucleotide (NAD +) used to generate ATP in mitochondria chain electron transport. Niacinamide is involved in DNA integrity and maintains phosphatidylserine membrane asymmetry to prevent cellular inflammation and phagocytosis. Current research shows that niacinamide prevents the induction of caspase-8, caspase-1 and caspase-2 activities in cell damage. Cytoprotective effects of niacinamide are involved in the maintenance and preservation of cell membranes.

Methylsulfonylmethane (MSM)

Methylsulfonylmethane (MSM) is a natural organic compound that contains 34% sulfur shipments. Sulfur is essential in the formation of collagen. flexible link between cells, including skin depends on sulfur. MSM provides bioavailable sulfur and supports the body's ability to produce N-acetyl-L-cysteine and taurine-L, which are sulfur-containing amino acids. MSM is an important element in the volatile sulfur cycle. Topical keratolytic MSM is the formation of hydrogen sulfide. MSM helps wound healing through of keratin. Sulfur-containing compounds are found in all body cells and are essential for life. Low levels of MSM are involved in the process healing.

Indications and Usage

Olivamine ® Remedy ® to protect and help temporarily relieve chapped or cracking skin in patients with skin dry or diabetes. It is useful in preventing skin complications of diabetes.

Contra-indications

Do not use on deep or puncture wounds, bites animal or burns.

Disclaimer

These products are recommended for external use.

Precautions

When using this product is not in the eyes. Stop use and consult a doctor if your condition worsens, symptoms last longer than seven days, or symptoms disappear and then come back in a few days. Keep out of reach of children. If swallowed, get medical help or contact a poison control center immediately. The product protection against cold and heat.

Adverse

An allergic rash are possible with a component. If redness, cause itching or hives, stop the product and seek medical attention.

Dosage and Administration

Apply lotion, skin cleansing wet or dry and rub gently. Rinse or wipe with a damp cloth. Foam Cleaner without taking action. Apply cream liberally until entire area is covered. Both cleansing lotion and cream can be used to repair if necessary.

About the Author

Dr. Darlene McCord is one of the two founders of McCord Research. As senior researcher, she brings a unique blend of scientific credentials to the position. Through her leadership, the company has achieved worldwide recognition in the OTC Drug and Medical Device categories. Her field of specialty is corneotherapy, focusing on the transport of small molecules across the stratum corneum for treatment of skin disorders associated with distressed and wounded skin. Dr. Darlene E McCord is widely published on subjects related to immunodermatology and corneotherapy.

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