Cómo, cuando, iniciar terapia con insulina
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Dosis basal de insulina, mezclas o dosis pre-prandial, cual es más efectiva, causa menos hipoglicemia y no afecta el peso
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Cómo, cuando, iniciar terapia con insulina
- 1. Cómo y Cuando Iniciar Terapia Cómo y Cuando Iniciar Terapia con Insulina? con Insulina? VII CONGRESO PERUANO XXXIV CURSO INTERNACIONAL DE MEDICINA INTERNA-2012 Dra. Olga Núñez Chávez
- 2. DIABETES MELLITUS PROBLEMA DE SALUD PUBLICA Estudio A1chieve • 66,726 DM 2 de 28 países: Africa, Europa y América Latina previos a ser insulinizados el promedio Hb A1c: 9.5% • 75% presentó enfermedad cardiovascular • 84% tenía nefropatía, retinopatía y neuropatía • 9% no recibian medicación alguna a pesar Hb A1 10% • Tiempo de la DM en pacientes ADO fué de 5.9 años Asia S y 10.4 en Latinoamérica, retrazo de la insulinización • Pacientes insulinizados recibían dosis bajas y fijas 71 Congreso ADA, San Antonio , 2011
- 3. Preservación del Beneficio: Memoria Metabólica Progresión EDIC de Retinopatía Convencional Intensivo P<0.001 60 P<0.001 Pacientes (%) 40 ↓ 75% 20 ↓ 76% 0 9.1% 7.2% 8.2% 7.9% Basal 4 años A1c DCCT/EDIC Research Group N Engl J Med 2000;342-381
- 4. DCCT-EDIC: Riesgo de Complicaciones Macrovasculares Largo Plazo Any Cardiovascular Outcome 12% Conventional 42% risk reduction 0.12 P = 0.02 Intensive Hemoglobin A1C 0.10 Cumulative Incidence 10% Conventional 0.08 0.06 8% 0.04 0.02 Intensive 6% P < 0.001 P < 0.001 P = 0.61 0.00 DCCT EDIC EDIC 0 2 4 6 8 10 12 14 16 18 20 End of Year 1 Year 7 Randomized Years Since Entry* Treatment *Diabetes Control and Complications Trial (DCCT) ended and Epidemiology of Diabetes Interventions and Complications (EDIC) began in year 10 (1993). Mean follow-up: 17 years. DCCT/EDIC Research Group. JAMA. 2002;287:2563-2569. Copyright © 2002 American Medical Association. All rights reserved. | Nathan DM, et al. N Engl J Med. 2005;353:2643-2653. Copyright © 2005 Massachusetts Medical Society. All rights reserved.
- 5. Resistencia Adquirida a la Insulina: Glucotoxicidad 400 Utilización de la Glucosa 300 (mg/min/m2) 200 100 0 Normal Diabetes Diabetes (Control Inadecuado) (Buen Control) Garvey TW et al. Diabetes. 1985;34:222-234
- 6. Tratamiento Intensivo con Insulina a Corto plazo (2 semanas) en Diabetes Tipo 2 (Memoria Metabólica) Basal Inmediatamente después de la Rx Insulina 1 año 25 500 Glucosa (mmol/l) Insulina (pmol/l) 20 400 15 300 10 200 5 100 0 0 0 15 30 60 90 120 150 180 0 15 30 60 90 120 150 180 Tiempo (min) • n=16, IMC promedio 30.8 ± 1.9 kg/m2 • Todos los sujetos fueron tratados con MDI por sólo dos semanas y observados durante 1 año Ryan et al. Diabetes Care 27:1028-1032, 2004
- 7. Historia Natural de Diabetes Tipo II0 5 10 15 -10 -5 Years from diagnosis Onset Diagnosis Insulin resistance Insulin secretion Postprandial glucose Fasting glucose Microvascular complications Macrovascular complications Pre-diabetes Type 2 diabetes Adapted from Ramlo-Halsted BA, Edelman SV. Prim Care. 1999;26:771-789; Nathan DM. NEJM. 2002;347:1342-1349
- 8. INSULINOTERAPIA DM 2 Indicaciones - Falla en medicación oral (sóla y/o combinada) si HbA1C >7 % - Embarazo o DM gestacional no controlada - Disminución importante de peso, toxicidad de la glucosa - DM2 insulino requiriente (por historia clínica, medición del péptido C) - LADA, anticuerpos GAD
- 9. AVAILABLE INSULIN PREPARATIONS Product (Manufacturer) Form Product (Manufacturer) Form Rapid Acting (Onset 15-30 min, duration hrs 3-4) Analog Mix Humalog 75/25 Mix Analog** Insulin Analog Novolog Mix 70/30 (combination of fast and Analog** Aspart - Novolog (Novo Nordisk) Analog** intermediate acting insulin with action similar to that Lispro - Humalog (Lilly) Analog** of Humalog 75/25 mix) Glulisine – Apidra (Aventis) Insulin for Special Use Short Acting (Onset 0.5-1 hr, duration hrs 5-7)* Buffered Insulin (for pumps) Human Insulin Humulin BR Novolin R (Rugular) (Novo Nordisk) Human** Refills for Novolin Pen Humulin R (Regular) (Lilly) Human** Novolin R PenFill Human** Purified Insulin Novolin N PenFill Human** Regular Iletin II (Lilly) Pork Novolin 70/30 PenFill Human** Novolog Mix 70/30 PenFill Analog** Intermediate Acting (Onset 1-4 hrs, duration hrs 18-24)* Prefilled Pens Human Insulin Novolin R Human** Novolin N (NPH) (Lilly) Human** Novolin N Human** Humulin N (NPH) (Lilly) Human** Novolin 70/30 Human** Humulin L (Lente) (Lilly) Human** Novolog Analog** Novolog Mix 70/30 Analog** Purified Insulin NPH Iletin III (Lilly) Pork Humalog Analog** Long Acting (Onset 4-6 hrs, duration hrs 24-34)* Humalog Mix 75/25 Analog** Humalog Mix 50/50 Analog** Human Insulin Humulin N Human** Humulin Ultralente (Lilly) Human** Apidra Analog** Basal Peakless Insulin Glargine-Lantus (Aventis) Analog** Detemir – Levemir (Novo Nordisk) Analog** * Onset and duration are rough estimates. They can vary greatly within the Mixed Insulins range listed and from person to person 70/30 Insulin ** Human insulin is made by recombinant DNA technology Novolin 70/30 (Novo Nordisk) Human** Humulin 70/30 (Lilly) Human** Humulin 50/50 (Lilly) Human** Humalog 50/50 Analog**
- 10. COMO INICIAR EL TRATAMIENTO CON INSULINA • USO DE INSULINA BASAL (NPH, Glargina, Detemir) • Uso de mezclas de insulinas, uso de insulina pre-prandial, basal • Tratamiento intensivo Bolo-Basal • Hipoglicemia
- 11. UKPDS: Adición de Insulina a Orales en Diabetes Tipo 2 Pacientes (%) alcanzaron un A1c <7% a los Seis Años 60 p=0.011 50 P>0.05 40 % pacientes 30 20 10 0 Control de Sólo Insulina Clorpropamida Glipizida Glucosa (± Insulina) (± Insulina) Convencional (dieta) Control de Glucosa Intensiva Wright, et al. Diabetes Care. 2002;25:330-336
- 12. Estudio “Treat to Target” Insulina Glargine vs NPH Añadida a Terapia Oral • Ensayo de 24 sem, multicéntrico, randomizado, paralelo • Compara insulina glargina vs NPH dada a la hora dormir en DM tipo 2 mal controlados 1 ó 2 ADO • Dosis de insulina fue ajustada semanalmente por un esquema de titulación ajustada semanalmente a una meta de GA≤100 mg/dL • La meta de la Hb A1C ≤7% sin hipoglicemia nocturna clínicamente singnificativa • 756 paciente nuevos con Glargine =367,con NPH = 389, edad media: 55yr, duración of diabetes de 8-9 años, A1c basal = 8.6%, IMC = 32 kg/m2. Riddle M, Rosenstock J, HOE901/4002 Study Group. Diabetes. 2002;51(suppl 2):A113. Abstract 457-P
- 13. Insulin Glargine vs Insulina Añadida a Tratmiento Oral Método Fórmula de Titulación Iniciar con 10 IU/d a las 10 pm y ajustar semanalmente la dosis Control Glucosa Ayunas (mg/dl)* ↑ Dosis Insulina (IU/day) ≥180 mg/dL 8 ≥140 but <180 mg/dL 6 ≥120 but <140 mg/dL 4 >100 but <120 mg/dL 2 Llegar a la meta FPG ≤100 mg/dL * Si en 2 días consecutivos de hipoglicemia severa o GA 0dL, ↓ (2–4 IU/día ) se debe reajustar la dosis cuando la GA<56 mg/dL o cuando ha ocurrido hipoglicemia. Riddle M, Rosenstock J, HOE901/4002 Study Group. Diabetes. 2002;51(suppl 2):A113. Abstract 457-P severe hypoglycemic episode occurs
- 14. Insulin Glargine vs NPH Insulin Added to Oral Therapy Resultados ANALISIS ITT Insulina Glargine NPH FPG, mg/dL 117 120 mM 6.5 6.68 A1C, % 6.96 6.97 Final A1C ≤7% (% patients) 57 57 Hipoglicemia nocturna Patients,* % 40 49 Severe hypoglycemia Patients, % 2.5 2.3 *P<0.01; †P<0.002 Riddle M, Rosenstock J, HOE901/4002 Study Group. Diabetes. 2002;51(suppl 2):A113. Abstract 457-P
- 15. Meta-análisis de Insulina Glargina vs. NPH: Menos Hipoglicemia Severa con Insulina Glargina Porcentaje de pacientes con episodios severos de hipoglicemia 5 Insulina Glargina P=0.0237 NPH 4 P=0.0159 Pacientes, % 3 2.8 2 1.8 1.4 1 0.7 0 Hipoglicemia Severa Hipoglicemia Severa Nocturna Dailey G et al. American Diabetes Association 63rd Scientific Sessions; June 13-17,2003; New Orleans, La. Abstract 1925-PO
- 16. Type 2 Titulación de Una Dosis Diaria con Levemir®: 3-0-3 • Para pacientes usando Levemir® una vez al día, la dosis puede ser ajustada para llegar GA 80 mg/dL - 110 mg/dL • Ajuste de la dosis puedern ser realizada cada tercer dia basados en el promedio de 3 días consecutivos de GA Mean 3-day Titration at a FPG (mg/dL) once-daily dose 3 Units increase dose FPG (mg/dL) >110 mg/dL Target range 80-110 mg/dL 0 Maintain dose <80 mg/dL decrease dose 3 Units 1. Meneghini L et al. Diabetes Obes Metab. 2007;9:902-913. 2. Data on file. Princeton, NJ: Novo Nordisk Inc.; 2007.
- 17. COMO INICIAR EL TRATAMIENTO CON INSULINA • Uso de insulina basal (NPH, Glargina, Detemir) • Mezclas de insulinas, uso de insulina prandial (lispro, aspartica, glulisine) y basal • Tratamiento intensivo Bolo-Basal • HIPOGLICEMIA
- 18. One-year Results 43rd EASD Meeting, Amsterdam, 2007
- 19. Inyecciones de Insulina y Control 758 pacientes, 50 centros UK, randomizados en diferentes régimenes de análogos insulina. G ayunas y pre-prandial: 70-99 mg/dl Dos horas post-prandial: 90-126 mg/dl 12 6 12 18 24 6 Biphasic * * Prandial * * * * * * * Basal < > * * Injection * Self-measured glucose N Engl J Med 2007; 357: 1716-30
- 20. Primary and Secondary Outcomes at 1 Year Holman RR et al. N Engl J Med 2007;357:1716-1730
- 21. Cambios Promedio al Año Hb A1c, GA, GPP, Peso, hipoglicemia Holman RR et al. N Engl J Med 2007;357:1716-1730
- 22. CONCLUSIONES 4T • Adicionar un análogo de insulina a metformina y SU puede bajar la HbA1c entre 0.8-1.4% con valores sostenidos sobre un año • Los régimenes usando insulina bifásica o prandial reducen al Hb A1c a más cerca de lo normal pero se asocian con mayor riesgo de hipoglicemia y ganancia de peso • Ensayo 4T sugiere que muchos pacientes van a necesitar más de un tipo de insulina a largo plazo N Engl J Med 2007; 357: 1716-30
- 23. COMO INICIAR EL TRATAMIENTO CON INSULINA • Insulina Basal (Ultralenta, NPH, glargina) • Mezclas de insulinas y uso prandial • Tratamiento intensivo Bolo-Basal • HIPOGLICEMIA
- 25. Ventajas de los Análogos de Insulinas • Permite predictabilidad/menos variabilidad • Incidencia baja de hipoglicemia • Menos ganancia de peso (Levemir, Lantus) • Inicio de acción más rápido • Limita picos de hiperglicemia post-prandial * Specific to rapid acting insulin analogs
- 26. The Basal-Bolus Principle: Adding Mealtime Control Rapid-acting insulin analog Long-acting insulin analog Insulin level 0:00 06:00 08:00 10:00 12:00 14:00 16:00 18:00 20:00 22:00 0:00 Time of day Theoretical representation of insulin profiles
- 27. The Kumamoto Trial: Effects of Conventional vs. Intensive Insulin Therapy 50 44% Conventional Intensive Cumulative Development or 40 32% 32% 28% Progression (%) 30 19.2% 20 11.5% 7.7% 7.7% 10 0 Primary Secondary Primary Secondary Prevention Prevention Prevention Prevention Retinopathy Nephropathy Ohkubo Y, et al. Diabetes Res Clin Pract. 1995;28:103-117.
- 28. Control Glicémico en Diabetes Tipo 2: CSII vs. MDI en 127 Pacientes 8.4 Basal 8.2 Final del estudio 8 (24 semanas) A1c (%) 7.8 7.6 7.4 7.2 7 CSII MDI Raskin P, Diabetes 2001;50(S2):A106
- 29. Terapia Intensificada • DM tipo 2: utiliza más 30 U/d, bajo estrés, DMG. Caso clínico: – DM tipo2 lesión en base del 3er y 4to dedo, fiebre > 39ºC, secreción purulenta, leucocitos 19,000, VS de 40, glucosa: 350 – Dosis 72 kg x 0.3 = 22 U/d Se fraciona la dosis 2/3 antes desayuno (15U) y 1/3 (7 U) a 10 pm – Insulina R: 3U > 200, 4U >250, 5U > 300 y 6U > 350 mg/dl Cobertura agresiva con Vancomicina + Cipro. – 5to día persiste fiebre, aumento de volumen, dolor, glicemia > 450 mg y Velocidad Sedimetación 70, se inicia terapia intensificada: basal de NPH 60% del total de la insulina y el resto se le indica R en escala móvil
- 30. TERAPIA INTENSIFICADA-II Total dosis 72 x 0.5 U = 36 U NPH --- 65% Rápida--- 35% RP: 16U de NPH 30’ antes desayuno + insulina Rápida a escala móvil 08 de NPH a las 10 pm + adicional (Resta 12U) Desayuno Almuerzo Comida 10 pm < 70 1 3 2 71-110 2 4 3 0 111-150 3 5 4 0 151-200 4 6 5 1 200-250 5 7 6 2 251-300 6 8 7 3 > 350 7 9 8 4 Reajuste de dosis según resultados de glicemias antes D,A, C 10 pm
- 31. COMO INICIAR EL TRATAMIENTO CON INSULINA • Uso de insulina basal (NPH, Glargina, Detemir) • Uso de mezclas de insulinas, uso de insulina pre-prandial, basal • Tratamiento intensivo Bolo-Basal • Hipoglicemia
- 32. Causas y Riesgo de Factores para Hipoglicemia • Causas generales de of hipoglicemia1,2 - Inadecuada, falta o pérdida de una comida – Ejercicio – Demasiada insulina o medicación oral de la diabetes – Consumo de drogas/alcohol – Increamento de la sensibilidad de la insulina – Depuración reducida de la insuoina • Factores de riesgo para hypoglycaemia severa3,4 – Edad/duración del tratamiento con insulina – Contros estricto de la glucosa – Compromiso de hipoglicemia no reconocida – Sueño – Historia de previa severa hipoglicemia – Falla renal 1.Briscoe and Davis. Clin Diabetes 2006;24(3):115–21; 2. Workgroup on Hypoglycemia, American Diabetes Association. Diabetes Care 2005;28(5):1245–9; 3. Frier. Diabetes Metab Res Rev 2008;24(2):87–92; 4. Cryer. Diabetes 2008;57(12):3169–76
- 33. Hipoglicemia in the Manejo de la Diabetes • Prevención de hipoglicemia es esencial en éxito • Incrementa la morbilidad y mortalidad • Añade costos significativos • Disminuye el cumplimiento y el éxito en general • Cómo prevenir la hipoglicemia • Estar conciente de los momentos de mayor riesgo (Ejm: hipoglicemia nocturna) • Individualizar la terapia con insulina • Tomar ventajas de las nuevas preparaciones de insulina asociadas con menos hipoglicemia
- 34. Cuanto Intensivo el Tratamiento Tenga en cuenta – HbA1c < 7% para más jóvenes, saludables, pacientes recién diagnosticados con un compatible estilo vida. Sin contraindicaciones y sin St de hipoglicemia. Considerar más baja(< 6.5%) sí es fácil y seguro – Existen guías apropiadas si se aplican flexiblemente y en circunstancias individualizadas: Guia Nice – La DM tipo 2 es heterogenea y progresiva, con rutas patogénicas multivariables (tratar un blanco móvil)
- 35. Cuanto de Tto Intensivo • Precoz y Durable – Para evitar una herencia vascular de “memoria hiperglicémica” • Suficientemente intensivo pero seguro – Minimizar complicaciones sin causar eventos hipoglicémicos – Debe ser práctico sin imposición inducida • Integral – Con un programa que incluya metas PA y lípidos para reducir riesgo cardiovascular
- 36. CONCLUSIONES • Insulina es la terapia más poderosa para el tratamiento de la DM • La insulinización debería ser iniciado lo más pronto, cuando los pacientes fallan a llegar a la meta con uno ó dos agentes orales. • Análogos de insulinas proveen de un control glicémico fisiológico y son de elección • El régimen con insulina requiere ser individualizado para cada paciente Slide No 36
- 37. Impacto de la diabetes IDF 1 persona muere por DM cada 8 segundos 1 caso nuevo es diagnosticado cada 40 segundos 1 millon de amputaciones Más muertes que el SIDA y el cáncer de mama en conjunto Expectativa de vida 15 años menos que la población general
Notes de l'éditeur
- DCCT-EDIC: Long-term Risk of Macrovascular Complications At the end of the randomized treatment phase in the Diabetes Control and Complications Trial, the research group found a difference in the concentration of hemoglobin A 1c between the patients with type 1 diabetes in the intensive treatment group and those in the conventional treatment group. At the end of the trial, there was a nonsignificant reduction in cardiovascular outcome in the intensively treated group. The trial ended at approximately 9 years; afterward, there was convergence of treatments and similar levels of glycemic control were achieved. There was persistent benefit, however, among the intensively treated group such that there was a statistically significant reduction in cardiovascular disease when compared to the conventionally treated group in the follow-up phase (up to 20 years) of the study. These data would indicate that 10 years of intensive treatment yielded a cardiovascular benefit during the first 10 years that was sustained and became greater in the follow-up phase. During the DCCT/EDIC follow-up period, intensive treatment reduced the risk of nonfatal myocardial infarction, stroke, or death from cardiovascular disease by 42 percent (95 percent confidence interval, 9 to 63 percent; P=0.02). References: Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. JAMA . 2002;287:2563-2569. Nathan DM, Cleary PA, Backlund JY, et al, for the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study Research Group. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med . 2005;353:2643-2653.
- The natural history of type 2 diabetes is progressive and complex. Increasing insulin resistance characterizes the prediabetic state. When β - cells function well, insulin resistance results in compensatory hyperinsulinemia, which maintains relatively normal glucose metabolism. In this compensated, insulin-resistant state, individuals may have either normal glucose tolerance or IGT but not diabetes. Eventually, the β -cells begin to fail, and insulin secretion falls, resulting in postprandial hyperglycemia and further loss of insulin secretion. Fasting hyperglycemia and hepatic overproduction of glucose then occur, resulting in overt diabetes, which may or may not be diagnosed in a timely manner. This process typically begins 4 to 7 years prior to diabetes diagnosis.1 Importantly, although early type 2 diabetes may be asymptomatic, evidence suggests that the degree of associated hyperglycemia may be severe enough for microvascular complications of diabetes to begin to develop.1 • β -cell function declines progressively in type 2 diabetes • The deterioration of β -cell function can precede the diagnosis of diabetes Analyses of the United Kingdom Prospective Diabetes Study (UKPDS), a randomized, controlled trial conducted with 5102 patients, demonstrated that type 2 diabetes is a progressive disease marked by declining β -cell function. Moreover, the rate of decline does not differ regardless of the therapy used to control hyperglycemia. An extrapolation of the observed rate of decline in β -cell function, as evaluated by homeostasis model assessment (HOMA), suggests that patients ’ loss of function began approximately 10 to 12 years before type 2 diabetes was diagnosed. As the graph indicates, by the time of diagnosis, β -cell function was impaired to the point of <50% of normal functioning.1,2
- Slide 6 Insulin Glargine vs NPH Insulin Added to Oral Therapy The purpose of this study was to evaluate basal insulin glargine vs the currently used basal insulin, NPH insulin, in combination with oral therapy to determine if an insulin with smoother basal characteristics (no pronounced peak of activity) would provide better glycemic control and less frequency of nocturnal hypoglycemia The role of insulin glargine was also evaluated in restoring glycemic control in patients inadequately controlled on OHA Riddle MC, Rosenstock J, HOE901/4002 Study Group. Diabetes. 2002;51(suppl 2):A113. Abstract 457-P OBJECTIVE: To compare the abilities and associated hypoglycemia risks of insulin glargine and human NPH insulin added to oral therapy of type 2 diabetes to achieve 7% HbA(1c). RESEARCH DESIGN AND METHODS: In a randomized, open-label, parallel, 24-week multicenter trial, 756 overweight men and women with inadequate glycemic control (HbA(1c) >7.5%) on one or two oral agents continued prestudy oral agents and received bedtime glargine or NPH once daily, titrated using a simple algorithm seeking a target fasting plasma glucose (FPG) <or=100 mg/dl (5.5 mmol/l). Outcome measures were FPG, HbA(1c), hypoglycemia, and percentage of patients reaching HbA(1c) <or=7% without documented nocturnal hypoglycemia. RESULTS: Mean FPG at end point was similar with glargine and NPH (117 vs. 120 mg/dl [6.5 vs. 6.7 mmol/l]), as was HbA(1c) (6.96 vs. 6.97%). A majority of patients ( approximately 60%) attained HbA(1c) <or=7% with each insulin type. However, nearly 25% more patients attained this without documented nocturnal hypoglycemia (<or=72 mg/dl [4.0 mmol/l]) with glargine (33.2 vs. 26.7%, P < 0.05). Moreover, rates of other categories of symptomatic hypoglycemia were 21-48% lower with glargine. CONCLUSIONS: Systematically titrating bedtime basal insulin added to oral therapy can safely achieve 7% HbA(1c) in a majority of overweight patients with type 2 diabetes with HbA(1c) between 7.5 and 10.0% on oral agents alone. In doing this, glargine causes significantly less nocturnal hypoglycemia than NPH, thus reducing a leading barrier to initiating insulin. This simple regimen may facilitate earlier and effective insulin use in routine medical practice, improving achievement of recommended standards of diabetes care.
- Slide 8 Insulin Glargine vs NPH Insulin Added to Oral Therapy The forced-titration schedule with basal insulin (either NPH or glargine) is described here. Patients self-monitored their FPG for 2 consecutive days in which they suffered no episodes of hypoglycemia. Based on these results, insulin levels were titrated until patients reached a target FPG of 100 mg/dL Hypoglycemia was considered severe if measured by the patient to be 72 mg/dL. Patients with self-monitored glucose levels <56 mg/dL were allowed small decreases (2 – 4 IU/day) of insulin to adjust their FPG levels Riddle MC, Rosenstock J, HOE901/4002 Study Group. Diabetes. 2002;51(suppl 2):A113. Abstract 457-P
- Slide 12 Insulin Glargine vs NPH Insulin Added to Oral Therapy This study provided evidence that both insulin treatments improved glycemic control, reducing FPG and A1C 57% of patients in each group reached target A1C 7% Insulin glargine – treated patients showed a significantly lower risk for nocturnal hypoglycemia (fewer patients and fewer events) Severe hypoglycemia was uncommon in both study groups ( P =NS), as measured by PG <56 mg/dL Riddle MC, Rosenstock J, HOE901/4002 Study Group. Diabetes. 2002;51(suppl 2):A113. Abstract 457-P
- Titration at a Once-Daily Dose With Levemir ® : 3-0-3 If taking Levemir ® once daily, the dose can be adjusted to reach a goal FPG level between 80 mg/dL and 110 mg/dL by using the average of 3 consecutive FPG values and titrating as noted in the figure above: <80 mg/dL: decrease dose by 3 units 80-110 mg/dL: no change >110 mg/dL: increase dose by 3 units Reference Meneghini L, Koenen C, Weng W, Selam JL. The usage of a simplified self-titration dosing guideline (303 Algorithm) for insulin detemir in patients with type 2 diabetes – results of the randomized, controlled PREDICTIVE ® study. Diabetes Obes Metab . 2007;9:902-913.
- Figure 2. Primary and Secondary Outcomes at 1 Year. Panel A shows mean levels of glycated hemoglobin in the three study groups. Panel B shows the proportion of patients in each group whose glycated hemoglobin values were below various levels, as compared with the distribution of values for all patients at baseline. Panel C shows mean body weight. Panel D shows eight-point self-measured capillary glucose values, with box-and-whisker plots representing medians and interquartile ranges and the 10th and 90th percentiles. Horizontal lines represent titration targets for fasting plasma glucose (99 mg per deciliter) and 2-hour postprandial levels (126 mg per deciliter). Panel E shows median insulin doses. Panel F shows the proportion of patients who reported grade 2 or grade 3 hypoglycemic events. I bars denote 90% confidence intervals.
- Figure 3. Mean (±SE) Percentage Change from Baseline to 1 Year in Glycated Hemoglobin, Fasting Plasma Glucose, Postprandial Glucose, and Body Weight (Panel A) and Mean (+SD) Hypoglycemic-Event Rate (Panel B). For all measures, P<0.001, with values adjusted for baseline values (except hypoglycemia), center, baseline glycated hemoglobin level, and oral antidiabetic therapy where appropriate. Missing data were imputed with the use of a multiple-imputation technique.14 To convert the values for glucose to millimoles per liter, multiply by 0.05551.
- The advantages of rapid-acting analogs include: Convenient administration immediately before meals Limitation of post-prandial hyperglycemic peaks Predictable with less variability than human insulin. However, when using a rapid-acting insulin, basal insulin replacement is required for most patients.
- The Basal-Bolus Principle: Adding Mealtime Control The basal-bolus principle is the concept of using a long-acting insulin for basal (FPG) control, as well as a rapid-acting insulin to cover mealtime (PPG) control
- Risk factors for hypoglycaemia Key message: Multiple risk factors can lead to hypoglycaemia in patients with diabetes. Review as stated References 1. Briscoe VJ, Davis SN. Hypoglycemia in type 1 and type 2 diabetes: physiology, pathophysiology, and management. Clin Diabetes 2006;24(3):115–121. 2. Workgroup on Hypoglycemia, American Diabetes Association. Defining and reporting hypoglycemia in diabetes: a report from the American Diabetes Association Workgroup on Hypoglycemia. Diabetes Care 2005;28(5):1245–9. 3. Frier BM. How hypoglycaemia can affect the life of a person with diabetes. Diabetes Metab Res Rev 2008;24(2):87–92. 4. Cryer PE. The barrier of hypoglycemia in diabetes. Diabetes 2008;57(12):3169–76.