Diabetes & ramadan (2)

ALAA WAFA. MDAssociate Professor of Internal Medicine

PGDIP DM Cardiff University UKDiabetes and Endocrine unit

Mansoura university

Diabetes Dilemma

Blood glucose

Insulin and Glucagon Regulate Normal Glucose Homeostasis

Glucose output Glucose uptake

Glucagon (α cell)

Insulin(β cell)

Pancreas

Liver

Muscle

Adipose tissue

Fasting state Fed state

Porte D Jr, Kahn SE. Clin Invest Med. 1995;18:247–254.Adapted with permission from Kahn CR, Saltiel AR. In: Kahn CR et al, eds. Joslin’s Diabetes Mellitus. 14th ed. Lippincott Williams & Wilkins; 2005:145–168. 4

Islet dysfunction

Adapted from Buse JB et al. In Williams Textbook of Endocrinology. 10th ed. Philadelphia, Saunders, 2003:1427–1483; Buchanan TA Clin Ther 2003;25(suppl B):B32–B46; Powers AC. In: Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw-Hill, 2005:2152–2180; Rhodes CJ Science 2005;307:380–384.

The Pathophysiology of Type 2 Diabetes Includes Multiple Defects

Pancreas

Insulin deficiency

LiverMuscle & Fat

Excess glucagon Diminished

insulin

Diminished

insulin

Beta cellproduces less insulin

Alpha cellproduces excess glucagon

Insulin resistance (decreased glucose

uptake)Excess Glucose

Output

HYPERGLYCEMIA

Time

Pancreatic Islet Cells in Type 2 Diabetes

B cells

α cells

B cells

α cells

The Core Defects in type 2 diabetes:

Insulin resistance in

peripheral tissues

Excess Hepatic Glucose Production due to

1)increased glucagon2)insulin insufficiency3)insulin resistance

Insulin deficiency due to insufficient pancreatic insulin

release

Reprinted from Primary Care, 26, Ramlo-Halsted BA, Edelman SV, The natural history of type 2 diabetes. Implications for clinical practice, 771–789, © 1999, with permission from Elsevier.

Development and Progression of Type 2 Diabetes and Related Complications*

*Conceptual representation.

Insulin level

Insulin resistance

Hepatic glucose production

Postprandial glucose

Fasting plasma glucose

Beta-cell function

Progression of Type 2 Diabetes Mellitus

Impaired Glucose Tolerance

Diabetes Diagnosis

Frank Diabetes

4–7 years

Development of Macrovascular ComplicationsDevelopment of Microvascular Complications

Type 2 diabetes is a progressive disease8

Conceptual representation adapted from Ramlo-Halsted BA, Edelman SV. Prim Care 1999;26(4):771–789. © 1999 Elsevier

Insulin level

Insulin resistance

Hepatic glucose production

Postprandial glucose

Fasting plasma glucose

Beta-cell function

Progression of Type 2 Diabetes

Impaired Glucose Tolerance

Diabetes Diagnosis

Diabetes

4–7 years

Development of Macrovascular ComplicationsDevelopment of Microvascular Complications

New era of treatment of T2DM

peripheralglucose uptake hepatic

glucose production

pancreatic insulinsecretion

pancreatic glucagonsecretion

gutcarbohydratedelivery &absorption

incretineffect

HYPERGLYCEMIA?

Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011

Multiple, Complex Pathophysiological Abnormalities in T2DM

_

_

+renal glucose excretion

peripheralglucose uptake hepatic

glucose production

pancreatic insulinsecretion

pancreatic glucagonsecretion

gutcarbohydratedelivery &absorption

incretineffect

HYPERGLYCEMIA?

Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011

Multiple, Complex Pathophysiological Abnormalities in T2DM

_

_

+renal glucose excretion

DA agonists

T Z D sMetformin

S U sGlinides

DPP-4 inhibitors

GLP-1Ragonists

A G I s

Amylinmimetics

Insulin

Bile acidsequestrants

Lifestyle Changes

Adapted from Riddle MC. Endocrinol Metab Clin North Am. 2005;34:77–98.

Diet and Exercise

Oral Monotherapy

Standard Approach to the Management of T2DM: Treatment Intensification

Oral Combination +

+Oral + InjectableIncretin Mimetics

Oral + Insulin + +

Insulin

Management of Hyperglycemia in Type 2 Diabetes, 2015:

A Patient-Centered ApproachUpdate to a Position Statement of the American Diabetes Association (ADA)

and the European Association for the Study of Diabetes (EASD)

Diabetes Care 2015;38:140–149Diabetologia 2015;58:429–442

Glycemic targets

- HbA1c < 7.0% (mean PG 150-160 mg/dl [8.3-8.9 mmol/l])

- Pre-prandial PG <130 mg/dl (7.2 mmol/l)

- Post-prandial PG <180 mg/dl (10.0 mmol/l)

- Individualization is key: Tighter targets (6.0 - 6.5%) - younger, healthier Looser targets (7.5 - 8.0%+) - older, comorbidities,

hypoglycemia prone, etc.

- Avoidance of hypoglycemia

PG = plasma glucose

ADA-EASD Position Statement Update: Management of Hyperglycemia in T2DM, 2015

Diabetes Care 2012;35:1364–1379; Diabetologia 2012;55:1577–1596Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442

Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442

Figure 1. Modulation of the intensiveness of glucose lowering therapy in T2DM

Oral Class Mechanism Advantages Disadvantages CostBiguanides • Activates AMP-

kinase (?other)• Hepatic glucose production

• Extensive experience• No hypoglycemia• Weight neutral• ? CVD

• Gastrointestinal• Lactic acidosis (rare)• B-12 deficiency• Contraindications

Low

Sulfonylureas • Closes KATP channels• Insulin secretion

• Extensive experience• Microvascular risk

• Hypoglycemia• Weight • Low durability• ? Blunts ischemic preconditioning

Low

Meglitinides • Closes KATP channels• Insulin secretion

• Postprandial glucose• Dosing flexibility

• Hypoglycemia• Weight • ? Blunts ischemic preconditioning• Dosing frequency

Mod.

TZDs • PPAR-g activator• Insulin sensitivity

• No hypoglycemia• Durability• TGs (pio)• HDL-C • ? CVD events (pio)

• Weight • Edema/heart failure• Bone fractures• LDL-C (rosi)• ? MI (rosi)

Low

Table 1. Properties of anti-hyperglycemic agents Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0

Oral Class Mechanism Advantages Disadvantages Costa-Glucosidase inhibitors

• Inhibits a-glucosidase• Slows carbohydrate digestion / absorption

• No hypoglycemia• Nonsystemic• Postprandial glucose• ? CVD events

• Gastrointestinal• Dosing frequency• Modest A1c

Mod.

DPP-4inhibitors

• Inhibits DPP-4• Increases incretin (GLP-1, GIP) levels

• No hypoglycemia• Well tolerated

• Angioedema / urticaria• ? Pancreatitis• ? Heart failure

High

Bile acid sequestrants

• Bind bile acids• ? Hepatic glucose production

• No hypoglycemia• LDL-C

• Gastrointestinal• Modest A1c• Dosing frequency

High

Dopamine-2agonists

• Activates DA receptor• Alters hypothalamic control of metabolism• insulin sensitivity

• No hypoglyemia• ? CVD events

• Modest A1c• Dizziness, fatigue• Nausea• Rhinitis

High

SGLT2 inhibitors

• Inhibits SGLT2 in proximal nephron• Increases glucosuria

• Weight• No hypoglycemia• BP• Effective at all stages

• GU infections• Polyuria• Volume depletion• LDL-C• Cr (transient)

High


Injectable

Class

Mechanism Advantages Disadvantages Cost

Amylin mimetics

• Activates amylin receptor• glucagon• gastric emptying• satiety

• Weight• Postprandial glucose

• Gastrointestinal• Modest A1c • Injectable• Hypo if insulin dose not reduced• Dosing frequency• Training requirements

High

GLP-1 receptor agonists

• Activates GLP-1 R• Insulin, glucagon• gastric emptying• satiety

• Weight• No hypoglycemia• Postprandial glucose• Some CV risk factors

• Gastrointestinal• ? Pancreatitis• Heart rate• Medullary ca (rodents)• Injectable• Training requirements

High

Insulin • Activates insulin receptor• Myriad

• Universally effective• Unlimited efficacy• Microvascular risk

• Hypoglycemia• Weight gain• ? Mitogenicity• Injectable• Patient reluctance• Training requirements

Variable


Figure 2. Anti-hyperglycemic therapy in T2DM: General recommendations Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442


HbA1c ≥9%

Metformin intolerance or

contraindication

Uncontrolled hyperglycemia

(catabolic features, BG ≥300-350 mg/dl,

HbA1c ≥10-12%)

Figure 3. Approach to starting & adjusting insulin in T2DM


DOSINGSEE REVERSE FOR TIPS

CHOOSE AN INSULIN CATEGORY

CHOOSE A BRAND

ADA-EASD Position Statement Update: Management of Hyperglycemia in T2DM, 2015

Long (Detemir)

Rapid (Lispro, Aspart, Glulisine)

Hours

Long (Glargine)

0 2 4 6 8 10 12 14 16 18 20 22 24

Short (Regular)

Hours after injection

Insu

lin le

vel

(Degludec)

3. ANTI-HYPERGLYCEMIC THERAPY

•Therapeutic options: Insulins

Lifestyle changes plus metformin (± other agents)

BasalAdd basal insulin

Basal PlusAdd prandial insulin at main meal

Basal BolusAdd prandial insulin before each meal

Progressive deterioration of -cell function

Basal Plus: once-daily basal insulin plus once-daily* rapid-acting insulin

Matching treatment to disease progression using a stepwise approach

*As the disease progresses, a second daily injection of glulisine may be addedAdapted from Raccah D, et al. Diabetes Metab Res Rev 2007;23:257–64

Proper Basal titrationTitrate insulin

Clinical challenge:Selecting the appropriate treatment for your patient

Adapted from Nathan DM. N Engl J Med. 2007;356:437-40and Nathan et al. Diabetes Care. 2009;32:193-203

0.5-1.01.5 1.5 1.0-1.5 0.5-1.0 0.8-1.0

≥2.5

Sulfonylureas Biguanides(metformin) Glinides DPP-IV

inhibitors TZDs Insulin

0.0

0.5

1.0

1.5

2.0

2.5

3.0

HbA

1c r

educ

tion

(%

)

Efficacy as mono therapy

Anti diabetic agents

GLP-1agonists

Insulin is the most effectiveglucose-lowering agent

Management of

T2DM in Ramadan.

45

يام ( 183) يا أيها الذين آمنوا كتب عليكم الصكما كتب على الذين من قبلكم لعلكم تتقون

ريضا 184( عدودات فمن كان منكم م ) أياما م

ن أيام أخر وعلى الذين أو على سفر فعدة مع يطيقونه فدية طعام مسكين فمن تطوخيرا فهو خير له وأن تصوموا خير لكم إن

كنتم تعلمون

) شهر رمضان الذي أنزل فيه القرآن 185(ن الهدى والفرقان هدى للناس وبينات مهر فليصمه ومن كان فمن شهد منكم الش

ن أيام أخر يريد مريضا أو على سفر فعدة مالله بكم اليسر وال يريد بكم العسر ولتكملوا العدة ولتكبروا الله على ما هداكم ولعلكم

تشكرون

46

The Current decade…

Over the current decade, the number of fasting hours will progressively

increase in the northern hemisphere as Ramadan falls in the

summer months. This will have important implications

for Muslims with diabetes who wish to fast.

Raised Questions ……?

Ramadan Between Diabetes and Fasting

· Although the Koran exempts sick people from the duty of fasting, many Muslims with diabetes may not perceive themselves as sick and are keen to fast.

· 43% of patients with type 1 and 86% of those with type 2 diabetes fasted during Ramadan.

1-IBRAHIM SALTI, et al . Diabetes Care 27:2306–2311, 20042-E Hui et al , BMJ, 26 june 2010 , Volume 340

49

During Ramadan about 60% of patients change their antidiabetic drug intake:

35% stop treatment 8% change the dosage schedule 25% decrease the drug dose. Importantly, this is done at the

patients’ own initiative without medical supervision.

Salti I, Benard E, Detournay B et al. A population-based study of diabetes and its characteristics during the fasting month of Ramadan in 13 countries. Diabetes Care 2004; 27: 2306–11.Aslam M, Healey MA. Compliance and drug therapy in Moslem patients. J Clin Hosp Pharm 1986; 11: 321–5.Aslam M, Assad A. Drug regimens and fasting during Ramadan: a survey in Kuwait. Public Health 1986; 100: 49–53.

The Risks of Fasting Include:

Hypoglycemia

Hyperglycemia

Diabetic ketoacidosis

Dehydration and thrombosis

M. al-Arouj et al, “Recommendations for management of diabetes during Ramadan,” Diabetes Care, 28(2005), 2305-2311.

12,243 subjects, in 13 countries including Egypt 1

Almost 90% was T2DM The important finding was: · 5 folds Increase in severe hyperglycemia with Ketoacidosis that required hospital

admission · 7.5 folds increase in the risk of severe hypoglycemia during Ramadan · 2% Of fasting patients experienced at least one episode of sever hypoglycemia

requiring hospitalization

1-IBRAHIM SALTI, et al . Diabetes Care 27:2306–2311, 20042- E Hui et al , BMJ 2010;340:c3053;

Classification of hypoglycemia according to severity: American Diabetes Association

1- Documented symptomatic hypoglycemia.

An event during which typical symptoms of hypoglycemia are accompanied by a measured plasma glucose concentration ≤ 70 mg/dl (3.9 mmol/l).

2- Asymptomatic hypoglycemia.

An event not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose concentration ≤ 70 mg/dl (3.9 mmol/l).

3- Probable symptomatic hypoglycemia.

An event during which symptoms of hypoglycemia are not accompanied by a plasma glucose determination.

4- Relative hypoglycemia.

An event during which the person with diabetes reports any of the typical symptoms of hypoglycemia, and interprets those as indicative of hypoglycemia, but with a measured plasma glucose concentration >70 mg/dl (3.9 mmol/l).

5- Severe An event requiring assistance of another person to actively administer carbohydrate, glucagons, or other resuscitative actions.

52 American Diabetes Association Workgroup on Hypoglycemia. Defining and Reporting Hypoglycemia in Diabetes. Diabetes Care . 2005;28 (5):1245–1249.This material can only be shown reactively to answer specific questions from physicians.

Hypoglycemic Events Increased by 84% During Ramadan

Significant increasing in hypoglycemic events during Ramadan mainly with patients ＞ 60 years old

Fatima J et al , Indian J Endocrinol Metab. 2012 Mar;16(2):323-4.

164

Num

ber o

f Hyp

ogly

cem

ic ev

ents

302

147

N= 179 84%

Pathophysiological cardiovascular consequences of hypoglycaemia

CRP=C-reactive protein; IL-6=interleukin 6; VEGF=vascular endothelial growth factor.Desouza CV, et al. Diabetes Care. 2010; 33: 1389–1394.

VEGF IL-6 CRP

Neutrophilactivation

Plateletactivation

Factor VII

Blood coagulationabnormalities

Sympathoadrenal response

Inflammation

Endothelialdysfunction

Vasodilation

Heart rate variability

Rhythm abnormalities Haemodynamic changes Adrenaline Contractility Oxygen consumption Heart workload

HYPOGLYCAEMIA

54

Health and economical consequences of hypoglycemia

55This material can only be shown reactively to answer specific questions from physicians.

Hypoglycemia

CV complications2

Weight gain by defensive eating3

Coma2

Car accident4

Hospitalization costs1

Dizzy turn unconsciousness2

Seizures2

Death6

Increased risk of dementia5

Quality of Life7

1. Jönsson L, et al. Cost of Hypoglycemia in Patients with Type 2 Diabetes in Sweden. Value In Health. 2006;9:193–198 2. Barnett AH. CMRO. 2010;26:1333–13423. Foley J & Jordan. J. Vasc Health Risk Manag. 2010;6:541–5484. Canadian Diabetes Association’s Clinical Practice Guidelines for Diabetes and Private and Commercial Driving. CanJ Diabetes. 2003;27(2):128 –140.5. Whitmer RA, et al. JAMA. 2009;301:15655–15726. Zammitt NN, et al. Diabetes Care. 2005;28:2948–29617. McEwan P, et al. Diabetes Obes Metab. 2010;12:431–436

Hypoglycemia and Treatment Adherence

· Patients’ reports of hypoglycemic symptoms are associated with significantly lower treatment satisfaction and with barriers to adherence.

Alvarez Guisasola F, et al. Diabetes Obes Metab. 2008 Jun;10 Suppl 1:25-32.

Diabetic Ketoacidosis

Patients with type 1 diabetes and severe insulin deficiency may have excessive glycogenolysis, gluconeogenesis and ketogenesis. All of this may lead to hyperglycemia and ketoacidosis that may be life-threatening.

Karamat et al, J R Soc Med 2010: 103: 139–147.

DKA:Pathophysiology

beta-cell

alpha-cell

Loss of beta cell function is gradual over time

B L O O D

MUSCLE

DKA:Pathophysiology

Normal – glucose in blood

B L O O D

MUSCLEInsulin

Diabetic Ketoacidosis:Pathophysiology

Normal Mechanism

B L O O D

MUSCLE

1. Insulin deficiency*lack of glucose in muscle

2. glucagon excess*increase in gluconeogenesis


Insulin

Liver Glucagon

B L O O D

MUSCLEketones


3. Rapid lipolysis into free fatty acids and ketone bodies

release of Beta-hydroxybutyrate

ketones resoposible for all s&sketonesketones

ketones

B L O O D

MUSCLE


4. Hypovolaemia – vomitting + osmotic diuresis

Increases concentration of ketones + glucose

ketones

ketones

Dehydration and Thrombosis

Limitation of fluid intake

Hot and humid climates

Hard physical labor

Excessive perspiration.

Hyperglycemia• Osmotic

diuresis&

• Volume and electrolyte depletion.

Adapted from : M. al-Arouj et al, “Recommendations for management of diabetes during Ramadan,” Diabetes Care, 28(2005), 2305-2311.

Dehydration and Thrombosis

• Patients with diabetes exhibit a hypercoagulable state due to an increase in clotting factors, a decrease in endogenous anticoagulants, and impaired fibrinolysis.

• Increased blood viscosity secondary to dehydration may enhance the risk of thrombosis.

• A report from Saudi Arabia suggested an increased incidence of retinal vein occlusion in patients who fasted during Ramadan

M. al-Arouj et al, “Recommendations for management of diabetes during Ramadan,” Diabetes Care, 28(2005), 2305-2311.

Patients who insist on fasting need to be aware of the associated risks and be ready to adhere to the recommendations of their health care providers to achieve a safer fasting experience.

Al-Arouj M, et al. Diabetes Care. 2005;28(9):2305-11.

For Safer Fasting

Pre-Ramadan Medical Assessment

Management of Diabetic Patients During Ramadan

Safer Fasting

High

Moderate

Low risk of adverse events

Categories of risks for patients fasting Ramadan

E Hui et al , BMJ 2010;340:c3053; Al-Arouj M. et al, Recommendations for management of diabetes during Ramadan. Diabetes Care. 2010;33: 1895-1902.

High

Moderate

Low risk of adverse events

• Poor glycemic control, Severe and recurrent episodes of hypoglycemia.

• Experience ketoacidosis three months before Ramadan.

• Elderly and Pregnant women• Advanced complications

• Well controlled patients treated with short acting insulin secretogogue, sulphonylurea, insulin, or taking combination oral or oral plus insulin

• Well controlled patients treated with Metformin, Dipeptidyl peptidase-4 inhibitors, or thiazolidinediones who are otherwise healthy


Patients classed as high risk are advised not to fast Before Ramadan they must make necessary changes to their diabetes treatment

Those at low risk can fast without healthcare advice.

Cate

gorie

s of

risk

s fo

r

patie

nts

fast

ing

Ram

adan

Categories of risks for patients fasting Ramadan

Diabetic patients at risks during fasting:

Acute Peptic Ulcer Pulmonary Tuberculosis Bronchial Asthma Cancer Diabetes –Type 1 and 2

who have poor glycemic control (HbA1c >12%), non compliant with diet or drug/oral regimes, four OR more episodes of hypoglycemia AND/OR hyperglycemia during preceding month, on 2 and MORE insulin injection/day.

ESRD Cardiovascular disease Psychiatry Liver disorder, hepatic dysfunction where the liver enzyme is >> 2 x Upper

Normal Limit. Intercurrent infections

Pre-Ramadan Medical Assessment


Safer Fasting


Patients Education

T2DM Pharmaceutical Management in Ramadan

Four key areas in Ramadan focused education

1-

Meal

pl

anni

ng

and

di

et

ar

y

advic

e

2-Exercise

3-

Bl

ood

gl

ucose

monit

ori

ng

4-

Recogni

zi

ng

and

managi

ng

compli

cati

ons

E Hui et al , BMJ 2010;340:c3053;

Breaking the Fast

All patients must always and immediately end their fast if:

1. Hypoglycaemia (blood glucose of <60mg/dl).

2. Blood glucose reaches <70 mg in the first few hours after the start of the fast, especially if insulin, sulfonylurea drugs, or neglitinide are taken at predawn.

3. Blood glucose exceeds 300 mg with symptoms of hyperglycaemia.

Recommendations for Diabetic Individuals during Ramadan, Diabetes Care , vol 33, num. 8, August2010

Oral hypoglycaemic agents

Short acting insulin Sus

Take twice daily at suhur and iftar

TZDsNo treatment adjustment required 2–4 weeks to exert substantial antihyperglycemic effectsDPP4 inhibitors

The best tolerated drugs, Consider DPP4i if the risk of hypoglycemia is high.

SUs. Consider dose adjustment.

Metformin

Modify timing of doses:• Two thirds of dose at iftar• One third at suhur.

T2DM Pharmaceutical Management in Ramadan


77

Fasting during Ramadan in patients

on insulin therapy

78

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00

Breakfast Lunch Dinner

Time8:00

Physiological Serum Insulin Secretion Profile

79

Human Insulins and AnaloguesTypical Times of Action

Insulin Preparations

Onset of Action Peak Duration of Action

Aspart, glulisine, lispro

~15 minutes 1–2 hours 4–6 hours

Human regular 30–60 minutes 2–4 hours 6–8 hours

Human NPH, lente

2–4 hours 4–10 hours 12–20 hours

Premixed insulin

½ -1 hour 6-8hours 10-12 hours

GlargineDetemir

2–4 hours Flat ~24 hours12-20 hs (0.2-0.4 U/kg/d)

80

Action Profiles of Insulin Analogues

0 1 2 53 4 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24

Plasmainsulinlevels

Regular 6–8 hours

NPH 12–20 hours

Hours

Glargine or detemir 24 hours

Aspart, glulisine, lispro 4–6 hours

81

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00 8:00 12:00 16:00 20:00 24:00 4:00


Time8:00

Basal/ Oral regimen

Bedtime NPH

50

Oral agents25

82

Time of day

20

40

60

80

100 B L D

Split-Mixed RegimenHuman Insulins

B=breakfast; L=lunch; D=dinner

0600 0600 0800 18001200 2400

NPHRegular

NPHRegular

Normal pattern

U/mL

83

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00


Time8:00

Twice daily premixed

84

Time of day

20

40

60

80

100 B L D

Multiple Daily Injections MDIHuman Insulins


0600 06000800 18001200 2400

Regular NPHNPHRegular

Normal pattern

U/mLRegular

85

0600 0800 18001200 2400 0600

Time of day

20

40

60

80

100 B L D

Basal-Bolus Insulin TreatmentWith Insulin Analogues


Glargine/ detemir

Lispro, glulisine, or aspart

Normal pattern

U/mL

86

Recommendations for Management of Diabetes During Ramadan for Patients on Insulin

The major objective of insulin therapy during Ramadan is to

provide adequate insulin to prevent the post meal hyperglycemia and also prevent hypoglycemia during the period of fasting

The choice of insulin therapy is decided by the previous therapy that the patient is taking and also the blood glucose profiles.

Ensure adequate fluid intake

87Aly A. Abdel-Rahim.

Bed time insulin

88

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00 8:00 12:00 16:00 20:00 24:00 4:00


Time8:00

Basal/ Oral regimen

Bedtime NPH

50

Oral agents25

89

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Oral agents

Can NPH be used in Ramadan•Peak at a time which is not needed. NPH at breakfast•Will not cover breakfast.•Poor coverage of day time

90

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Oral agents

Can NPH be used in Ramadan

•Dangerous time of peakNPH after sohour

91

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00 8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Can peakless insulin replace NPH in Ramadan ??

•No peak, no hypoglycaemia.•Control meals with oral•Free time of injection

50

Oral agents25

basalinsulin

92

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Peakless insulin+ once daily oral secretagogue

basal insulin8-12 pm

Oral agent once

93

4:00

25

50

75

8:00 12:00 16:00 18:00 22:00 4:00

Plas

ma

Insu

lin µ

U/m

l)

Time8:00

One peakless Insulin + One Oral

OAD e.g DPP-4inhibitors Glargine Detemir

8-12PM

• No Peak• No Hypoglycemia• Control Iftar meal with OAD

94

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

50

25

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Peakless insulin+ premeal short acting oralsecretagogue

•Glinides offers ideal combination•Similar to intensive insulin therapywhen there is beta cell reserve•Adjust the dose according to the timeand size of meal

Short acting secretagogues basal insulin8-12 pm

95

Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Short actingOral agents

Once daily premixed in Ramadan:once daily+ oral

•50/50 is better to control breakgast.•Short acting secretagogues additionalcontrol on sohour•Not suitable for exhausted beta cells


Premixed insulin

97

4:00

25

50

75

8:00 12:00 16:00 18:00 22:00 4:00

Plas

ma

Insu

lin µ

U/m

l)

Time8:00

Twice Premix in Ramadan

98

Plas

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insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Twice daily premixed in Ramadan

•Fear of daytime hypoglycaemia•Overlap between sohour short acting andiftar intermediate acting

99

Plas

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insu

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U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Twice daily premixed in Ramadan

Dangerous even if dose size changed

100100

Ensure adequate fluid intake. 70/30 premixed insulin twice daily, e.g., 30 units

in morning and 20 units in evening……

In Ramadan,,,,,Use the usual morning dose at the sunset meal (Iftar) and half the usual evening dose at predawn (Suhur), e.g., 70/30 premixed insulin, 30 units at Iftar and 10 units at suhur.

Diabetes CareSeptember 2005 , pages 2305-11

Premixed insulin :

101

Premixed insulins Mix insulin 50/50 at iftar instead of Mix30

reduced postprandial glucose excursions and reduced hypoglycemia

Consider changing premixed insulin preparations to glargine or detemir plus lispro or aspart .

Mattoo V, Diabetes Res Clin Pract 2003;59:137-43

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Time of day

20

40

60

80

100 B L D

Multiple Daily Injections MDIHuman Insulins


0600 06000800 18001200 2400

Regular NPHNPHRegular

Normal pattern

U/mLRegular

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Plas

ma

insu

lin (µ

U/m

l)

Aly A. Abdel-Rahim.

4:00

25

50

8:00 12:00 16:00 20:00 24:00 4:00Time

8:00

Peakless insulin+ premeal rapid acting insulin

basal insulin8-12 pm

Rapid acting insulin

104104

MOST patients will require short-acting insulin administered in combination with the intermediate, or long-acting insulin at the sunset meal to cover the large caloric load of Iftar & an

additional dose of short-acting insulin at predawn.

1. ADA. Diabetes Care 2006;29(suppl 1):S4–S42.

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Patients on Basal insulin analogueglargine or detemir

It is advised that patients who take long

acting basal insulin, such as glargine, to reduce the dose by 20% to avoid hypoglycemia.

Continue taking the same doses of repaglinide or short acting insulin


Advantages of rapid acting insulins

• Given at meal time not pre meal.• Can be modified according to the meal size.• Better post prandial profile.

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PLEASE REMEMBER


Remember

Patient education regarding fasting during theholy month of Ramadan is badly needed.

Diabetic patients with established renal diseaseare high-risk category.

Fasting for prolonged periods, especially in hotclimates, may impose negative impacts on renalfunction from hypovolemia and dehydration.

The mainstay of management of those patients istargeted toward arresting the progression of theirunderlying renal disease, and fasting duringRamadan should not be recommended.


Remember

Patients with history of cerebrovascularaccidents or severe cardiovascular diseases aswell as those with critical limb ischamiashould be recommended not to fast.

Avoid long acting SU at sohour.

Metformin, TZDS, DPP4 inhibitors and glinidesare safe.

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Remember

Careful use of intermediate- or long-acting insulin preparations plus a short-acting insulin administered before meals would be an effective strategy.

Adjustment to treatment necessary: e.g.· Reduce the dose of Basal insulin by 20%· Use Mix 50 in the evening instead of Mix 30

to avoid post prandial hyperglycemiaDiabetes Care 28.9 (Sept 2005): p2305(7).


Treatment should be tailored and

adjusted

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Some Parting Thoughts

“Fasting is for Me and I (Allah) only will reward it” (Hadith Qudsi)

“While fasting , if one does not give up falsehood in words and actions ,

then Allah has no need of him giving up food and drink (saying of Prophet

Muhammad-pbuh)”

HAVE A BLESSED RAMADAN

How to Help Patients Fast Safely ??

Patient Education Program.Individualization of anti diabetic drugsSelect more safe drugs.Adjust dose if neededEnsure good non – sugar fluid intake.Avoid heavy physical exercise at

afternoon.Ensure good calorie distribution.

Summary

Thank you

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Diabetes & ramadan (2)

Health & Medicine

Transcript of Diabetes & ramadan (2)