Pati ent with di abetes – internal medicine pati ent

Czech version

Authors: R. Češka ^1,2
Authors‘ workplace: Centrum preventivní kardi ologi e III. interní kliniky 1. lékařské fakulty UK a VFN Praha, přednosta prof. MU Dr. Štěpán Svačina, DrSc., MBA, 2Česká internistická společnost České lékařské společnosti J. E. Purkyně, předseda prof. MU Dr. Richard Češka, CS ¹
Published in: Vnitř Lék 2009; 55(Suppl 1)(Supplementum 1): 34-40

Overview

Pati ents with type 2 di abetes mellitus (DM2T) are a part of all physici ans’, including internal medicine physici ans’, everyday practice. Furthermore, it is possible to presume that the number of pati ents with di abetes mellitus will incre ase consequent to the obesity and metabolic syndrome epidemic as well as deteri orating lifestyle within the populati on. What is the role of an internal medicine physici an, primary or secondary care‑based, in the care of a DM2T pati ent? It first needs to be taken into acco unt that a pati ent with di abetes is a pati ent with polymorbidity who is at risk of cardi ovascular dise ase as well as nephropathy, infecti ons and other T2DM‑related complicati ons. At the same time, DM2T does not usu ally stand alone, as an isolated disorder, but is often fo und in a cluster together with dyslipidemi a (DLP), hypertensi on (HT), visceral obesity and other disorders. This cluster of disorders co uld be called metabolic syndrome, cardi ometabolic risk or we co uld simply accept the fact that these disorders occur frequently, together and that they jo intly le ad to seri o us complicati ons. Who sho uld then take care of such a pati ent? An internal medicine physici an, primary as well as secondary care‑based (for whom this is the basis of professi onal practice) is not only optimally placed for care of such a pati ent but represent a model of how care for a pati ent with polymorbidity sho uld be conducted. Obvi o usly, care for a DM2T pati ent sho uld be comprehensive. We have to optimize the DM2T therapy as well as to provide effective tre atment of DLP, HT, obesity and other complicati ons. Early di agnosis of DM2T as well as di agnosis of subclinical stages of micro‑ and macro angi opathi es are equ ally important. Evidence‑based medicine sho uld always be considered during therape utic decisi on- making and drugs that provide the most significant benefit to the pati ents sho uld be prescribed. Metformin is the mainstay of DM2T tre atment itself and might be given in combinati on with sulphonylure a derivatives or, possibly, pi oglitazone. Incretins, particularly gliptins sitagliptin and vildagliptin, and GLP‑1 analogues, mainly exenatide, are interesting drug gro ups for a combinati on therapy. Hypertensi on tre atment sho uld include metabolically ne utral or positive drugs, ACE- I, calci um channel blockers or sartans – among these, metabolically positive telmisartan is preferred. Statins have the most extensive evidence for use in tre atment of DLP in di abetics. Micro angi opathy is best managed with fibrates. Sibutramine is the le ading agent in the tre atment of obesity. Even tho ugh the therape utic overvi ew above focuses on pharmacotherapy, it needs to be emphasised that lifestyle changes, including di et, are the core of tre atment.

Key words:
type 2 di abetes mellitus – macro angi opathy – micro angi opathy – metformin – pi oglitazone – sitagliptin – statins – fibrates – ACE- I – telmisartan – calci um channel blockers

Sources

1. Haffner SM. Coronary he art dise ase in pati ents with di abetes. N Engl J Med 2000; 342: 1040– 1042.

2. Fruchart JCh, Sacks F, Hermans MP et al. For the Residu al Risk Reducti on Initi ative (R3i): The Residu al Risk Reducti on Initi ative: A Call to Acti on to Reduce Residu al Vascular Risk in Pati ents with Dyslipidemi a. Am J Cardi ol 2008; 102 (Suppl): 1K– 34K.

3. Fruchart JCh, Sacks F, Hermans MP et al. For the Residu al Risk Reducti on Initi ative (R3i): The Residu al Risk Reducti on Initi ative: A Call to Acti on to Reduce Residu al Vascular Risk in Pati ents with Dyslipidemi a. Di abetes and Vasc Dis Res 2008; 5: 319– 325.

4. Keech AC, Mitchell P, Summanen PA et al. Effect of fenofibrate on the need for laser tre atment for di abetic retinopathy (FIELD study): a randomised controlled tri al. Lancet 2007; 370: 1687– 1697.

5. ADA, NHLBI, AHA et al. Di abetes mellitus: A major risk factor for cardi ovascular dise ase. Circulati on 1999; 100: 1132– 1133.

6. O’Keefe JH et al. Improving the adverse cardi ovascular prognosis of type 2 di abetes. Mayo Clin Proc 1999; 74: 171– 180.

7. Češka R. Cholesterol a ateroskleróza. Léčba dyslipidemi í. Praha: Triton 2005.

8. Robins SJ, Collins D, Wittes JT et al. Relati on of gemfibrozil tre atment and lipid levels with major coronary events, VA- HIT: A randomized controlled tri al. JAMA 2001; 285: 1585– 1591.

9. Jones PH, Davidson MH, Stein EA et al. Comparison of the Efficacy and Safety of Rosuvastatin Versus Atorvastatin, Simvastatin and Pravastatin Across Doses (STELLAR Tri al). Am J Cardi ol 2003; 93: 152– 160.

10. Law MR, Wald NJ, Rudnicka AR. Qu antifying effect of statins on low density lipoproteid cholesterol, ischaemic he art dise ase and stroke: systematic revi ew and meta‑analysis, BMJ 2003; 326: 1– 7.

11. Sacks FM. Low- Density Lipoprotein Lowering Therapy: An Analysis of the Opti on. J Am Coll Cardi ol 2002; 40: 2135– 2138.

12. Shepherd J. Combined lipid lowering drug therapy for the effective tre atment of hypercholesterolemi a. Eur He art J 2003; 24: 685– 689.

13. Ridker PM, Dani elson E, Fonseca FAH et al. Rosuvastatin to prevent vascular events in men and women with elevated C‑re active protein. N Engl J Med 2008; 359: 2195– 2207.

14. Ridker PM, Dani elson E, Fonseca FA et al. Reducti on in C‑re active protein and LDL cholesterol and cardi ovascular event rates after initi ati on of rosuvastatin: A prospective study of the JUPITER tri al. Lancet 2009; DOI: 10.1016/ S0140- 6736(09)/ 60447- 5. Available from http:/ / www.thelancet.com/ .

15. Glynn RJ, Dani elson E, Fonseca FA et al. A Randomized Tri al of Rosuvastatin in the Preventi on of Veno us Thromboembolism, www.nejm.org March 29, 2009 (10.1056/ NEJMo a0900241).

16. Nissen S et al. Effect of very high‑intensity statin therapy on regressi on of coronary atherosclerosis. The ASTEROID tri al. JAMA 2006; 295: 1556– 1565.