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糖尿病治療新趨勢 時間: 2009-04-24 (09:00-10:30) 地點:花蓮高中 主講人:三軍總醫院 石光中主任 (MD, PhD) 1.

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Presentation on theme: "糖尿病治療新趨勢 時間: 2009-04-24 (09:00-10:30) 地點:花蓮高中 主講人:三軍總醫院 石光中主任 (MD, PhD) 1."— Presentation transcript:

1 糖尿病治療新趨勢 時間: (09:00-10:30) 地點:花蓮高中 主講人:三軍總醫院 石光中主任 (MD, PhD) 1

2 MANAGEMENT OF TYPE 2 DIABETES ORAL ANTIDIABETIC AGENTS (OAD) INSULIN 2

3 MANAGEMENT OF TYPE 2 DIABETES ORAL ANTIDIABETIC AGENTS (OAD) INSULIN 3

4 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 4

5 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 5

6 INSULIN SECRETAGOGUES: SULFONYLUREAS Mechanism of Action –The major action of sulfonylureas is to increase insulin release from the pancreas. –Two additional mechanisms of action have been proposed - a reduction of serum glucagon levels and closure of potassium channels in extrapancreatic tissues. 6

7 INSULIN SECRETAGOGUES: MEGLITINIDES The meglitinides are a relatively new class of insulin secretagogues. These drugs modulate β-cell insulin release by regulating potassium efflux through the potassium channels previously discussed. Repaglinide has a very fast onset of action, with a peak concentration and peak effect within approximately 1 hour after ingestion, but the duration of action is 5-8 hours. Because of its rapid onset, repaglinide is indicated for use in controlling postprandial glucose excursions. 7

8 INSULIN SECRETAGOGUE: D- PHENYLALANINE DERIVATIVE Nateglinide stimulates very rapid and transient release of insulin from β cells through closure of the ATP-sensitive K+ channel. This may be a significant advantage of the drug because type 2 diabetes is associated with loss of this initial insulin response. The restoration of more normal insulin secretion may suppress glucagon release early in the meal and result in less endogenous or hepatic glucose production. Nateglinide may have a special role in the treatment of individuals with isolated postprandial hyperglycemia, but it has minimal effect on overnight or fasting glucose levels. The incidence of hypoglycemia may be the lowest of all the secretagogues, and it has the advantage of being safe in individuals with very reduced renal function. 8

9 治療糖尿病的藥物( 1 ) 種類治療的建議與考量 促胰島素分泌劑 磺醯脲素 Gliclazide Glimepiride Glibenclamide 非磺醯脲素 Nateglinide Repaglinide 所有促胰島素分泌劑在降低血糖的能 力上大致相似。 所有促胰島素分泌劑都有可能引起低 血糖。 病人具高度低血糖危險性(例如:老 年人,肝、腎功能不全者)時,考慮 使用其他較短效的口服抗糖尿病藥。 Nateglinide 和 Repaglinide 主要用於降 低餐後血糖。 9

10 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 10

11 BIGUANIDES Mechanisms of Action –A full explanation of the biguanides' mechanism of action remains elusive. –Currently proposed mechanisms of action include (1) reduced hepatic and renal gluconeogenesis; (2) slowing of glucose absorption from the gastrointestinal tract, with increased glucose to lactate conversion by enterocytes; (3) direct stimulation of glycolysis in tissues, with increased glucose removal from blood; and (4) reduction of plasma glucagon levels. 11

12 治療糖尿病的藥物( 2 ) 種類治療的建議與考量 雙胍類 Metformin 病人合併肝、腎、心臟功能不全時, 不建議使用。 血清肌酸酐≧ 1.5 mg/dl 或肌酸酐清除 率< 60 ml/min 時,不宜使用 (contrast medium, age>80 Y/O) 。 不易增加體重和發生低血糖。 具有腸胃道的副作用。 12

13 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 13

14 THIAZOLIDINEDIONES Thiazolidinediones (TZDs) act to decrease insulin resistance. Their primary action is the regulation of genes involved in glucose and lipid metabolism and adipocyte differentiation. TZDs are ligands of peroxisome proliferator-activated receptor-gamma (PPAR-γ), part of the steroid and thyroid superfamily of nuclear receptors. Two thiazolidinediones are currently available: pioglitazone and rosiglitazone. 14

15 治療糖尿病的藥物( 3 ) 種類治療的建議與考量 胰島素增敏劑 Pioglitazone Rosiglitazone 病人肝功能不全(血清轉胺酶超過上 限的 2.5 倍)或紐約心臟學會分類第 III 級及第 IV 級心臟衰竭時不應使用。 發揮最大療效約 6-12 週。 可能會出現體液滯留,水腫和體重增 加的現象。 合併使用胰島素,可能會增加水腫和 鬱血性心臟衰竭的危險。 15

16 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 16

17 ALPHA-GLUCOSIDASE INHIBITORS Acarbose and miglitol are competitive inhibitors of the intestinal α-glucosidases and reduce the postprandial digestion and absorption of starch and disaccharides. Miglitol differs structurally from acarbose and is six times more potent in inhibiting sucrase. Acarbose has been associated with reversible hepatic enzyme elevation and should be used with caution in the presence of hepatic disease. 17

18 治療糖尿病的藥物( 4 ) 種類治療的建議與考量 阿爾發葡萄糖苷 酶抑制劑 Glucobay 可降低餐後血糖。 具有腸胃道的副作用。 不易增加體重和發生低血糖。 發生低血糖時,必需使用葡萄糖來治 療。 18

19 Pharmacologic targets of current drugs used in the treatment of T2DM  -Glucosidase inhibitors Delay intestinal carbohydrate absorption Thiazolidinediones Increase glucose uptake in skeletal muscle and decrease lipolysis in adipose tissue Sulfonylureas Increase insulin secretion from pancreatic  -cells Adapted from Cheng and Fantus. CMAJ. 2005;172:213–226. Meglitinides Increase insulin secretion from pancreatic  -cells Biguanide (metformin) Decreases hepatic glucose production and increases uptake

20 Traditional Type 2 Diabetes Management: A “Treat-to-Fail Approach” OAD=oral anti-hyperglycaemic drug. Adapted from Campbell IW. Need for intensive, early glycaemic control in patients with type 2 diabetes. Br J Cardiol. 2000;7(10):625–631. Del Prato S et al. Int J Clin Pract. 2005;59:1345– OAD monotherapy Diet and exercise OAD combination OAD up-titration OAD plus multiple daily insulin injections OAD plus basal insulin HbA 1c, % Mean HbA 1c of patients Duration of Diabetes Published Conceptual Approach Time 12 20

21 Major Side Effects of oral anti- diabetes drugs Sulfonylureas, Meglitinides MetforminAGITZD Hypoglycemia+ Weight Gain++ Edema+ GI upset++

22 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 22

23 PRAMLINTIDE Pramlintide, a synthetic analog of amylin, is an injectable antihyperglycemic that modulates postprandial glucose levels and is approved for preprandial use in individuals with type 1 and type 2 diabetes. Pramlintide suppresses glucagon release via undetermined mechanisms, delays gastric emptying, and has central nervous system-mediated anorectic effects. It is rapidly absorbed after subcutaneous administration; levels peak within 20 minutes, and the duration of action is not more than 150 minutes. Pramlintide should be injected immediately before eating; doses range from 15 mcg to 120 mcg subcutaneously.

24 PRAMLINTIDE Therapy with this agent should be initiated with the lowest dose and titrated upward. Because of the risk of hypoglycemia, concurrent rapid- or short-acting mealtime insulin doses should be decreased by 50% or more. Pramlintide should always be injected by itself with a separate syringe; it cannot be mixed with insulin. The major side effects of pramlintide are hypoglycemia and gastrointestinal symptoms including nausea, vomiting, and anorexia.

25 ORAL ANTIDIABETIC AGENTS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor) 25

26 The Incretin Approach

27 Glucagon-like peptide-1 (GLP- 1): a new approach for type 2 diabetes therapy 27

28 GLP-1 and GIP Are the Two Major Incretins GLP-1GIP Secreted by L-cells in the distal gut (ileum and colon) Stimulates glucose-dependent insulin release Secreted by K-cells in the proximal gut (duodenum) Stimulates glucose-dependent insulin release Suppresses hepatic glucose output by inhibiting glucagon secretion in a glucose-dependent manner Enhances beta-cell proliferation and survival in animal models and isolated human islets Enhances beta-cell proliferation and survival in islet cell lines GLP-1=glucagon-like peptide 1; GIP=glucose-dependent insulinotropic polypeptide Adapted from Drucker DJ Diabetes Care 2003;26:2929–2940; Ahrén B Curr Diab Rep 2003;3:365–372; Drucker DJ Gastroenterology 2002;122: 531–544; Farilla L et al Endocrinology 2003;144:5149–5158; Trümper A et al Mol Endocrinol 2001;15:1559–1570; Trümper A et al J Endocrinol 2002;174:233–246.

29 Adapted from Nauck MA, et al. J Clin Endocrinol Metab. 1986;63: Oral Glucose Tolerance Test Insulin (pmol/L) Time (min) Insulin Secretion Increases Dramatically in Response to Oral Glucose Ingestion Glucose (mg/dL) 50 g glucose Time (min) 29

30 Adapted from Nauck MA, et al. J Clin Endocrinol Metab. 1986;63: Glucose (mg/dL) Time (min) Insulin (pmol/L) Time (min) Proof of a Gastrointestinal ‘Incretin Effect’: Different Responses to Oral vs. IV Glucose OralIV 30

31 What is GLP-1? Nauck et al. Diabetologia 1986;29:46–52 31

32 Type 2 diabetes patients have impaired GLP-1 secretion n=54 n =33 Toft-Nielsen et al. J Clin Endocrinol Metab 2001;86:3717–

33 *P <.05 GLP-1 = glucagon-like peptide–1; T2DM= type 2 diabetes mellitus Adapted from Nauck MA, et al. Diabetologia. 1993;36:741 – 744. GLP-1 Restores Islet Cell Glucose Sensing in T2DM – Time (min) C-peptide (nmol/L) Glucose (mg/dL) – Time (min) Saline GLP-1 GLP-1 infusion * * * * Glucagon (pmol/L) – Time (min) GLP-1 infusion * * * * * * * * * * * *

34 GLP-1 has multiple desirable effects Stimulates insulin secretion Preserves or increases β-cell mass in animal models Decreases glucagon secretion Delays gastric emptying Induces satiety and decreases food intake Beneficial effects on memory and learning in animal models 34

35 GLP-1 is Rapidly Degraded by DPP-4 A E  DPP-4 H T F T S D V S S Y L E G Q A A K E F I A W L V K G R G G T ½ = 1–2 minutes *Amino acids shown in gold are homologous with the structure of glucagon. 35

36 Native GLP-1 is rapidly degraded by DPP-IV Hansen et al. Endocrinology 1999;140:5356–

37 GLP-1 related agents 1.NN2211(Liraglutide) : long-acting GLP-1 derivative 2.Exenatide: synthetic exendin 4 compound 3.DPP-4 inhibitors 37

38 GLP-1 related agents 1.NN2211(Liraglutide) : long-acting GLP-1 derivative 2.Exenatide: synthetic exendin 4 compound 3.DPP-4 inhibitors 38

39 NN2211(Liraglutide) is a long- acting GLP-1 analogue Knudsen et al. J Med Chem 2000;43:1664–

40 GLP-1 related agents 1.NN2211(Liraglutide) long-acting GLP-1 derivative 2.Exenatide synthetic exendin 4 compound 3.DPP-4 inhibitors 40

41 EXENATIDE As a synthetic analog of glucagon-like-polypeptide 1 (GLP-1), exenatide is the first incretin therapy to become available for the treatment of diabetes. In clinical studies, exenatide therapy is shown to have multiple actions such as potentiation of glucose- mediated insulin secretion, suppression of postprandial glucagon release through as-yet unknown mechanisms, slowed gastric emptying and a central loss of appetite. Exenatide is absorbed equally from arm, abdomen, or thigh injection sites, reaching a peak concentration in approximately 2 hours with a duration of up to 10 hours. 41

42 EXENATIDE Exenatide is injected subcutaneously within 60 minutes before a meal; therapy is initiated at 5 mcg twice daily, with a maximum dosage of 10 mcg twice daily. When exenatide is added to preexisting sulfonylurea therapy, the oral hypoglycemic dosage may need to be decreased to prevent hypoglycemia. The major side effects are nausea (about 44% of users) and vomiting and diarrhea. The nausea decreases with ongoing exenatide usage. 42

43 GLP-1 related agents 1.NN2211(Liraglutide) long-acting GLP-1 derivative 2.Exenatide synthetic exendin 4 compound 3.DPP-4 inhibitors 43

44 Pancreatic Islet Cells are Targets for Incretin Hormones GLP-1=Glucagon-Like Peptide-1 Adapted from Drucker D. Diabetes Care. 2003;26: Wang Q, et al. Diabetologia. 2004;47: Incretin Response Food intake α-Cell β-Cell Pancreatic Islet Incretin 44

45 Mechanism of Action of DPP-4 Inhibitors GLP-1 Inactive GLP-1 Inactive GLP-1 Actions Mixed meal Plasma Intestinal GLP-1 release DPP-IV Rapid inactivation (>80% of pool) Excreted by kidneys GLP-1 Active GLP-1 Active DPP-4 Inhibitors Improvement of glucose metabolic profile Improvement of glucose metabolic profile Primary actions of GLP-1 - Promote insulin secretion (β- cell) - Reduce glucagon secretion/hepatic glucose production (α- cell) 45

46 Synthesis, Secretion, and Metabolism of GLP-1 and GIP Capillary K-Cell L-Cell GIP [3-42] INACTIVE DPP-4 GIP [1-42] ACTIVE GLP-1[7-36NH 2 ] ACTIVE GLP-1 [9-36NH 2 ] INACTIVE DPP-4 Proglucagon GLP-1 [7-37] GLP-1 [7-36NH 2 ] ProGIP GIP [1-42] Dipeptidyl peptidase-4 (DPP-4) Ubiquitous, specific protease Cleaves N-terminal dipeptide Inactivates > 50% of GLP-1 in ~ 1 min > 50% of GIP in ~ 7 min 46

47 *P <.05 Adapted from Nauck M, et al. Diabetologia. 1986;29: The Incretin Effect is Impaired in T2DM Leading to Reduced Insulin Production NGTT2DM (n=8)(n=14) IV Glucose Oral Glucose Plasma Glucose (mg/dL) Plasma Glucose (mg/dL) * * * * * * * * C-Peptide (nmol/L) Time (min) C-Peptide (nmol/L) Time (min)

48 *Observed in animal models Adapted from Holst JJ. Diabetes Metab Res Rev. 2002;18: GLP-1 Acts at Many Levels to Promote Insulin Secretion –Potentiates glucose-dependent insulin secretion –Enhances all steps of insulin biosynthesis –Upregulates insulin gene expression –Upregulates expression of genes essential for β-cell function –Promotes β-cell neogenesis and progenitor cell differentiation* –Inhibits apoptosis*

49 1. Dunning BE et al. Diabetologica. 2005;48: Degn KB, et al. Diabetes. 2004; 54: Gromada J and Rorsman P Horm Metab Res 2004; 36: GLP-1 Also Controls Glucagon Secretion –Suppresses glucagon release in glucose- dependent manner 1 –Enhances glucagon release in response to hypoglycemia 2 –Improves α-cell glucose sensing 1 –Acts on specific G-protein coupled receptors on alpha-cells 3

50 Endocrine and neural pathways for GLP-1-mediated actions

51 The Need for a More Comprehensive Approach for Treating Type 2 Diabetes 51

52 ORAL ANTIDIABETIC DRUGS Insulin secretagogues (sulfonylureas, meglitinides, D-phenylalanine derivatives) Biguanides Thiazolidinediones α-glucosidase inhibitors Pramlintide (Amylin) Exenatide (GLP-1) Sitagliptin (DPP-4 inhibitor)

53 Glucose dependent  Insulin from beta cells (GLP-1 and GIP) Adapted from Brubaker PL, Drucker DJ Endocrinology 2004;145:2653–2659; Zander M et al Lancet 2002;359:824–830; Ahrén B Curr Diab Rep 2003;3:365–372; Buse JB et al. In Williams Textbook of Endocrinology. 10th ed. Philadelphia, Saunders, 2003:1427–1483. Hyperglycemia DPP-4 Inhibitors Improve Glucose Control by Increasing Incretin Levels in Type 2 Diabetes  Glucagon from alpha cells (GLP-1) Glucose dependent Release of incretins from the gut Pancreas α-cells β-cells Insulin increases peripheral glucose uptake Ingestion of food GI tract ↑insulin and ↓glucagon reduce hepatic glucose output Inactive incretins Improved Physiologic Glucose Control DPP-4 Inhibitor X DPP-4 = dipeptidyl peptidase 4

54 SITAGLIPTIN Sitagliptin is an inhibitor of dipeptidyl peptidase- 4 (DPP-4), the enzyme that degrades incretin and other GLP-1-like molecules. Control of hyperglycemia and reductions in HbA1c were documented at doses of 100 mg orally once daily. Dosage should be reduced in patients with renal impairment. Hypoglycemic episodes were rare and the drug facilitated weight loss. Sitagliptin therapy can be combined with metformin, TZDs, or sulfonylureas.

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56 Characteristics of an Ideal Therapy Characteristics of an ideal oral antidiabetic agent –Lowers HbA 1c to normal levels –Decreases insulin resistance and hepatic glucose production and increases or preserves β-cell mass while restoring first-phase insulin response –Does not cause weight gain –Does not increase risk of hypoglycemia –Does not cause edema or congestive heart failure 56

57 Combination Therapy Offers Advantages Over Monotherapy Combination therapy may provide more glycemic control than the individual monotherapies Combination therapy may provide more comprehensive coverage of the key pathophysiologies of type 2 diabetes than monotherapy An appropriately chosen combination therapy may help more patients achieve their HbA 1c goal without increasing side effects 1 Adapted from Del Prato Int J Clin Pract 2005;59:

58 MANAGEMENT OF TYPE 2 DIABETES ORAL ANTIDIABETIC AGENTS (OAD) INSULIN 58

59 胰島素製劑發揮效力 時間 高峰時間全程作用時 間 超短效胰島素 Lispro 5-15 分 1-2 小時 4-6 小時 Aspart 5-15 分 1-2 小時 4-6 小時 短效胰島素 Human regular 分 2-4 小時 6-10 小時 中效胰島素 Human NPH 1-2 小時 4-8 小時 小時 Lente 1-2 小時 4-8 小時 小時 胰島素種類( 1 ) 59

60 胰島素製劑發揮效力 時間 高峰時間全程作用時 間 長效胰島素 Ultralente 2-4 小時無法預測 小時 超長效胰島素 Glargine 1-2 小時穩定無高峰期 24 小時 預混型胰島素 Novomix 分 1-4 小時 24 小時 Mixtard 0.5 小時 2-8 小時 24 小時 胰島素種類( 2 ) 60

61 Introduction Insulin replacement consists of 1. Prandial (bolus) insulin : mimic the response of endogenous insulin to food intake, but only the first phase of insulin secretion 2. The basal-insulin : mimics the relatively small but constant release of insulin 3. Correction-dose insulin supplement : addresses pre-meal or between-meal hyperglycemia, independently of the prandial insulin. 61

62 傳統人類胰島素 Time of day Plasma insulin (pmol/l) Normal free insulin levels (Mean) Human insulin DinnerNPHBreakfastLunch 需餐前 30 分鐘注射 Meals 餐後血糖控制不足 易產生餐後低血糖 62

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65 NovoRapid 可於餐前或餐後立即注射 顯著改善餐後血糖控制 有助於改善長期血糖控制 大幅降低 hypoglycemia 發生率 第一個獲得 FDA 核准使用於 pump 的 insulin analogue 提升患者生活品質 (Quality of life) 劑量給予 / 轉換容易 65

66 Long-Acting Analogues Insulin glargine The first of the long-acting insulin analogues, insulin glargine, was introduced in the USA in the spring of This analogue is produced by the substitution of glycine for asparagine at position A21 of the insulin molecule and by the addition of two arginine molecules at position B30. These changes lead to a shift in the isoelectric point toward a neutral pH, which results in an insulin molecule that is less soluble at the injection site and that precipitates in the subcutaneous tissue to form a depot from which insulin is slowly released. 66

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69 New analogues Insulin detemir : Long acting, neurtral PH, acylated derivative of human insulin, requires bid injection in type 1 DM, less variability than NPH Insulin glulisine : Rapidly acting analogue, similar to aspart/lispro Inhaled insulin Oral insulin 69

70 胰島素治療的適應症 1. 第 1 型糖尿病患者。 2. 第 2 型糖尿病患者,空腹血糖超過 300 mg/dL 和合併酮酸血症或酮酸尿症。 3. 第 2 型糖尿病患者,持續性出現空腹血糖超過 300 mg/dL 和出現多尿、多喝及體重減輕的症狀 。 4. 願意接受胰島素做為第一線治療的患者。 5. 妊娠型糖尿病患者無法以飲食控制者。 6. 第 2 型糖尿病婦女懷孕時。 70

71 胰島素合併口服抗糖尿病藥治療 (1) 一般而言,此種情形是使用中效胰島 素,於睡前注射,使空腹能維持於理 想範圍內。它的好處在於: 1. 容易衛教。 2. 門診時容易使用。 3. 病患配合度高。 4. 心理調適容易。 5. 較少胰島素劑量。 71

72 胰島素治療:每日兩次注射胰島素 (2) 以一天注射兩次 ( 早餐前、晚餐前 ) 為 例,這種方式目前最常使用於第 2 型 糖尿病的病患和第 1 型糖尿病的幼童 。 1. 計算劑量:一般建議,身體質量指數小於 25 kg/m 2 者,以每公斤 0.4 至 0.6 單位計算起始 劑量;而體重超過 25 kg/m 2 者以 0.6 至 1.0 單位計算。 2. 劑量調整:需要根據相對應的血糖來調整胰 島素劑量。 72

73 胰島素治療:多次注射胰島素 (3) 每日早晚兩次注射胰島素時,有些人發現 清晨空腹血糖居高不下,這時不妨晚餐前 只注射短效胰島素,把中效胰島素移到睡 前注射。第 1 型糖尿病病患,如果每日注 射兩次,可能會出現午餐後血糖偏高,此 時需要午餐前注射短效胰島素。對於多數 第 1 型糖尿病病患和晚期第 2 型糖尿病病 患而言,比較接近生理需求的注射方法可 能是睡前注射中效胰島素來滿足基本需要 量,白天每餐前半小時注射短效胰島素。 73

74 胰島素治療:連續性皮下胰島素輸注 (4) 1. 連續性皮下胰島素輸注:利用幫浦,將裝置 在注射筒內的胰島素,以軟管和注射針頭連 接後置入皮下組織,並將注射針頭固定於皮 下組織以提供胰島素連續注射的一種方法。 2. 胰島素幫浦能夠達到良好控制病患血糖的目 的。 3. 開始劑量常用原來每日總量的 40-60% ,一半 作為基礎量胰島素,另一半則作為追加量胰 島素。 74

75 胰島素治療:連續性皮下胰島素輸注 (4) 優點: 1. 注射一次可維持 3 天。 2. 改進血糖的控制。 3. 飲食、運動及作息較具彈性。 4. 減少嚴重低血糖的發生。 5. 發生低血糖時較易處理。 75

76 胰島素治療:連續性皮下胰島素輸注 (4) 缺點: 1. 幫浦機器。 2. 機械故障、輸注管阻塞。 3. 發炎或感染。 4. 酮酸血症。 5. 花費昂貴。 76

77 胰島素治療的優點與缺點 ( 一 ) 胰島素治療的優點: ( 1 )對口服抗糖尿病藥無效的病人,可以 迅速改善血糖的控制。 ( 二 ) 胰島素治療的缺點: ( 1 )低血糖。 ( 2 )體重增加。 ( 3 )配合度差。 77

78 結語 1. 血糖濃度越接近正常範圍,越容易發 生嚴重的低血糖。因此越需要加強血 糖自我監測,營養及護理衛教。 2. 速效及長效胰島素類似物的出現,讓 我們能以更接近正常生理方式控制血 糖。 3. 多次注射胰島素能夠達到良好控制病 患血糖的目的。 78

79 高血糖的治療 一般飲食控制和運動治療未達治療目標則加上口 服抗糖尿病藥 。 – 須依照個別病人的特性,採用不同的治療方式 。 – 治療目標是儘快和儘可能的將血糖控制在接近正常範 圍內。 開始治療時合併使用較低劑量之多種口服藥物 。 – 較單一高劑量口服藥物快速改善血糖 。 – 不增加副作用 。 依照病人不同特性選擇種治療藥物,適當調整劑 量,使糖化血色素 6-12 個月內達到治療的目標 。 79

80 胰島素療法 當口服抗糖尿病藥無法控制血糖,可考慮停用 口服藥,改一天注射多次胰島素 。 或續用口服藥,加睡前注射中、長效胰島素 。 此時胰島素需要劑量較低,體重增加較少或低血 糖。 睡前胰島素合併 metformin ,體重增加較胰島素 合併磺醯脲素或一天注射二次中效胰島素為少。 嚴重高血糖時(糖化血色素≧ 9.0 %)可使用胰 島素作為第一線的治療。 當生病、懷孕、有壓力、開刀或使用影響血糖 的藥物時可改以胰島素作短期治療 。 80

81 第 2 型糖尿病人高血糖的處理 81

82 Thanks for your attention 82

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