Novdec07 P243-254 CME2-BG

MedicalContinuing Education Objectives 1) To clarify the main mechanisms that un- derlie all complications of diabetes mellitus. TTowardsowards BetterBetter 2) To understand the role that hyperglycemia plays in the development of diabetic complications. ManagementManagement ofof 3) To appreciate other mechanisms in the development of diabetic complications besides hyperglycemia. DiabeticDiabetic FootFoot 4) To delineate the role of microan- giopathy vs. macroangiopathy in complications relating to diabetes mellitus. ComplicationsComplications 5) To identify the relationship between systemic complications and those found in the foot of the patient with diabetes. The search for the common 6) To empower the podiatric physi- denominator continues. cian to evaluate the whole patient when treating a problem in the foot. Welcome to Podiatry Management’s CME Instructional program. Our journal has been approved as a sponsor of Contin- uing Medical Education by the Council on Podiatric Medical Education. You may enroll: 1) on a per issue basis (at $20.00 per topic) or 2) per year, for the special introductory rate of $139 (you save $61). You may submit the answer sheet, along with the other information requested, via mail, fax, or phone. In the near future, you may be able to submit via the Internet. If you correctly answer seventy (70%) of the questions correctly, you will receive a certificate attesting to your earned credits. You will also receive a record of any incorrectly answered questions. If you score less than 70%, you can retake the test at no additional cost. A list of states currently honoring CPME approved credits is listed on pg. 252. Other than those entities currently accepting CPME-approved credit, Podiatry Management cannot guarantee that these CME credits will be acceptable by any state licensing agency, hospital, managed care organization or other entity. PM will, however, use its best efforts to ensure the widest acceptance of this program possible. This instructional CME program is designed to supplement, NOT replace, existing CME seminars. The goal of this program is to advance the knowledge of practicing podiatrists. We will endeavor to publish high quality manuscripts by noted authors and researchers. If you have any questions or comments about this program, you can write or call us at: Podiatry Management, P.O. Box 490, East Islip, NY 11730, (631) 563-1604 or e-mail us at [email protected]. Following this article, an answer sheet and full set of instructions are provided (p. 252).—Editor By Kenneth Rehm, DPM for devastating effects on the body. ment and most importantly, the pre- Pedal complications seen by DPM’s vention of these devastating sequellae. iabetes mellitus, a condition demonstrate these areas of pathology, characterized, for the most each of which plays a decisive role in Terms of Art Dpart, by a deficiency in insulin the disease’s occurrence, chronic na- Terms such as “carbonyl stress”, secretion or a resistance to insulin ac- ture, and eventual recovery, or loss of “oxidative stress”, “glycoxidation”, tion, is estimated to afflict approxi- limb, if left untreated. “lipoxidation”, “non-enzymatic glyco- mately 8% of the population.22 The complexity of these diabetic sylation”, “glycation”, “Maillard reac- Complications of this systemic dis- foot complications creates a huge clini- tion” and “cross-linking of collagen” ease, which are basically either macro- cal and financial challenge to their are repetitively used in the literature to or microangiopathic in nature, encom- management; but the additional describe the chemical reactions that passing the neurologic, vascular, mus- knowledge gained as a result of our may be at the root of the common culoskeletal, dermatologic and im- search for a common thread will facili- thread with which science is seeking to munologic systems, can be responsible tate the diagnosis, treatment, manage- Continued on page 244 www.podiatrym.com NOVEMBER/DECEMBER 2007 • PODIATRY MANAGEMENT 243 CME 2... holm Diabetes Interven- tion Study, any improved Continuingtie in all diabetic or lowering of blood glu- complications. These cose delayed the onset and Medical Education terms will be defined in slowed the progression of this article as part of our all microvascular complica- discussion of the search for tions in all categories of pa- these common links. tients who had Type-1 diabetes. Although the DCCT Hyperglycemia and was not designed to evalu- Diabetic Complications ate the effects of glycemic The evolution of the control on macrovascular numerous long-term com- disease, some of its indica- plications of diabetes melli- tors were evaluated. Inten- tus has been shown to cor- sive insulin therapy was as- relate well with the severity sociated with a significant and duration of hyper- relative reduction (34%) (p glycemia. For instance, it < 0.02) in the development has been consistently of hypercholesterolemia demonstrated22 that post- (serum low-density- prandial glucose levels lipoprotein [LDL] choles- above 200 mg/dL have a Figure 1: Factors Promoting Diabetic Complications terol concentrations of strong association with >160 mg/dL). Targeted LDL renal, retinal, and neurologic compli- address the glycemic hypothesis (that cholesterol levels have been revised for cations that could show up five to ten retinopathy, nephropathy and neu- all populations, including patients years after the onset of the disease. ropathy are each related to hyper- with diabetes. It is important to note that many glycemia). The National Cholesterol Educa- patients demonstrate postprandial The study demonstrated a 60% re- tion Program recommends that pa- glucose at or above these critical lev- duction in risk involved in the develop- tients with diabetes achieve LDL els when first diagnosed and already ment and/or progression of nephropa- cholesterol concentrations of <100 demonstrate a degree of diabetic thy, neuropathy and retinopathy be- mg/dL. Intensive insulin therapy also complications. In addition, recent tween a standard treatment group and reduced the relative risk of actual epidemiologic studies23 revealed that an intensive treatment group that fo- macrovascular disease (peripheral and poorly controlled diabetic patients cused on very strict control of hyper- cardiovascular disease) by 41%. have a greater risk for cardiovascular glycemia. The outcome established disease than those with well-con- that reduction of the HgA1C from 9% UKPDS trolled glucose levels. to approximately 7% reduced the pro- In another landmark study, The gression and/or development of all mi- United Kingdom Prospective Diabetes DCCT crovascular complications. Study (UKPDS) compared intensive Three large prospective random- In fact, according to the Stock- glycemic control in Type II diabetic ized trials and one large subjects with conventional epidemiologic trial found a treatments to determine correlation between HYPERGLYCEMIA whether intensive glycemic glycemic control and re- control could reduce the duction in the progression frequency of diabetes-relat- of chronic complications ed microvascular and associated with diabetes. macrovascular complica- Subsequent studies have tions. These subjects were confirmed these findings. followed for an average of The Diabetes Control and ten years. Complications Trial Researchers soon became (DCCT) was designed to aware that high blood pres- determine if there was a re- sure may be an even lationship between hyper- stronger risk factor than glycemia and diabetic vas- hyperglycemia; and blood cular complications. This pressure treatment was study evaluated intensive added to the study. Con- insulin replacement and firming the DCCT data, the self-monitoring of blood UKPDS showed that tightly glucose in subjects who controlling blood glucose had type-1 diabetes for a concentration reduced the known duration; and used risk of complications in well-established goals to Figure 2: Mechanisms By Which Hyperglycemia Creates Damage Continued on page 245 244 PODIATRY MANAGEMENT • NOVEMBER/DECEMBER 2007 www.podiatrym.com MedicalContinuing Education CME 2... A consensual type-2 diabetes. The framework has overall microvascular not been estab- complications rate was lished which encom- decreased by 25% in passes all that is those receiving inten- known about the link sive therapy versus con- between hyper- ventional therapy. A Figure 3: Efforts of The Pharmaceutical Industry Geared Toward Decreasing glycemia and compli- Effects of AGEs. continuous relationship cations, but over the between the risk of microvascular The Wisconsin Epidemiologic last 30 years, four seemingly indepen- complications and glycemia was The Wisconsin Epidemiologic dent major mechanisms of hyper- shown to exist. In fact, for every per- Study of Diabetes Retinopathy glycemia-induced damage have been centage point decrease in HbA1c, there (WESDR) studied the relationship be- discovered: was a 35% reduction in the risk of mi- tween hyperglycemia and the fre- 1) Polyol/sorbitol pathway activa- crovascular complications. quency and progression of diabetes- tion The UKPDS results confirm that it related microvascular and macrovas- 2) Advanced glycation endproduct is glucose itself that is toxic in type-2 cular complications. The initial trial (AGE) formation diabetes and extend the previous evi- focused on diabetic retinopathy, but a 3) Protein kinase C (PKC) activa- dence that hyperglycemia and its se- follow-up trial examined the frequen- tion quelae are a major cause of microvas- cy and

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