Problem Solving in Diabetes

241 Pages·2006·2.86 MB·English

by  Lee Kennedy

Problem Solving in
Diabetes
LEE KENNEDY
James Cook University, Queensland, Australia
ISKANDAR IDRIS
Sherwood Forest Hospitals, Sutton-in-Ashfield, UK
ANASTASIOS GAZIS
Queen’s Medical Centre University Hospital, Nottingham, UK
C L I N I C A L P U B L I S H I N G
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© Atlas Medical Publishing Ltd 2006
First published 2006
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Electronic ISBN 978 1 84692 565 8
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Contents
Abbreviations vii
SECTION 01 Prevention and Diagnosis 1
1 Preventing type 1 diabetes 1
2 Preventing type 2 diabetes 5
3 Diabetes risk after the menopause 9
4 Genetic diabetes syndromes (MODY) 13
5 Screening and impaired glucose tolerance 17
6 Type A/B diabetes and insulin resistance 21
SECTION 02 Acute Diabetes 25
7 Diabetic ketoacidosis 25
8 Hyperosmolar hyperglycaemic state 30
9 Recurrent hypoglycaemia 34
10 Diabetes and acute myocardial infarction 40
11 Diabetes and acute stroke 43
12 Diabetes and critical limb ischaemia 47
13 Perioperative management of diabetes 51
14 The hot foot 55
SECTION 03 Managing Diabetes 61
15 Insulin pumps 61
16 Type 1 diabetes and exercise 65
17 Adolescent diabetes 69
18 Low-carbohydrate diets 72
19 Treatments that stimulate insulin production 77
20 Treatments that improve insulin resistance 81
21 Diabetes and enteral feeding 85
22 Obesity and diabetes 89
23 Diabetes in the elderly 93
SECTION 04 Reproductive Complications 99
24 Polycystic ovarian syndrome 99
25 Gestational diabetes 103
26 Type 1 diabetes and pregnancy 107
vi Contents
27 Erectile dysfunction 111
28 Pre-eclampsia 115
SECTION 05 Cardiovascular Risk Factors in Diabetes 121
29 Smoking cessation 121
30 Hypertriglyceridaemia 125
31 Hyperlipidaemia in type 1 diabetes 129
32 Hyperlipidaemia in type 2 diabetes 133
33 Aspirin use in diabetes 137
34 Hypertension—uncomplicated 140
35 Hypertension—hard to control 143
SECTION 06 Microvascular Complications 149
36 Painful neuropathy 149
37 Microalbuminuria 154
38 ACE inhibitor treatment 159
39 Advancing renal failure 163
40 Background retinopathy 167
41 Proliferative and pre-proliferative retinopathy 171
42 Macular disease 175
43 Autonomic neuropathy 178
44 The Charcot foot 182
SECTION 07 Macrovascular and Other Complications 187
45 Angina in patients with type 2 diabetes 187
46 Advances in management of peripheral arterial disease 191
47 Renal artery stenosis 195
48 Foot ulceration 199
49 Transient ischaemic attack 203
SECTION 08 Diabetes in Special Groups of Patients 207
50 Diabetes and respiratory disease 207
51 Diabetes and cystic fibrosis 212
52 Diabetes and dialysis 216
53 Diabetes and coeliac disease 220
General index 225
Abbreviations
4S Scandinavian Simvastatin Survival Study CHD Coronary heart disease
ABCD trial Appropriate Blood Pressure Control in CHHIPS Controlling Hypertension and
Diabetes Trial Hypotension Immediately Post-Stroke trial
ABPI Ankle–brachial pressure index CI Confidence interval
ABPM Ambulatory blood pressure monitoring CK Creatine kinase
ACAS Asymptomatic Carotid Atherosclerosis CPAP Continuous positive airway pressure
Study CSII Continuous subcutaneous infusion ofinsulin
ACE Angiotensin-converting enzyme CSMO Clinically significant macular oedema
ACR Albumin–creatinine ratio CT Computed tomography
ACHOIS trial Australian Carbohydrate Intolerance CWS Cotton-wool spot
Study in Pregnant Women DAN Diabetic autonomic neuropathy
AER Albumin excretion rate DCCT Diabetes Control and Complications Trial
AHI Apnoea–Hypopnea Index DIGAMI Diabetes and Insulin-Glucose Infusion in
ALLHAT Antihypertensive and Lipid-Lowering Acute Myocardial Infarction study
Treatment to Prevent Heart Attack Trial DIRECT DIabetic Retinopathy Candesartan Trial
AMD Age-related macular degeneration DKA Diabetic ketoacidosis
ANG-1 and ANG-2 Angiopoetin DMa Diabetic maculopathy
APT Anti-Platelet Trialists DME study Diabetic Macular Edema study
ARB Angiotensin receptor blocker DPN Distal sensory peripheral neuropathy
ASTRAL trial Angioplasty and Stent for Renal DPP Diabetes Prevention Program
Artery Lesions trial
DPP-IV Dipeptidyl peptidase IV
BARI trial Bypass Angioplasty Revascularization
DPS Diabetes Prevention Study
Investigation
DRS Diabetic Retinopathy Study
BMI Body mass index
ECG Electrocardiogram
BP Blood pressure
ECST European Carotid Surgery Trial
CABG Coronary artery bypass grafting
EDIC Epidemiology ofDiabetes Interventions and
CALM study Candesartan And Lisinopril
Complications
Microalbuminuria study
ELISA Enzyme-linked immunosorbent assay
CAPD Continuous ambulatory peritoneal dialysis
ENDIT European Nicotinamide Diabetes
CAPRIE study Clopidogrel versus Aspirin in Intervention Trial
Patients at Risk ofIschaemic Events study
ETDRS Early Treatment Diabetic Retinopathy
CARDS Collaborative Atorvastatin Diabetes Study Study
CARE study Cholesterol and Recurrent Events ETF Enteral tube feeding
study
EUCLID study EURODIAB Controlled Trial of
CAS Carotid artery stenosis Lisinopril in Insulin-Dependent Diabetes
CETP Cholesteryl ester transfer protein Mellitus
CF Cystic fibrosis FEV(1) Forced expiratory volume in one second
CFRD Cystic fibrosis-related diabetes FOOD Feed or ordinary diet trial
viii Abbreviations
FSH Follicle-stimulating hormone LIFE study Losartan Intervention For Endpoint
GABA Gamma-aminobutyric acid reduction in hypertension
G-CSF Granulocyte–colony stimulating factor LIPID study Long-term Intervention with
Pravastatin in Ischaemic Disease study
GDM Gestational diabetes mellitus
LH Leuteinizing hormone
GFD Gluten-free diet
MA Microaneurysm
GFR Glomerular filtration rate
MDI Multiple daily injections
GI Glycaemic index
MDRD study Modification ofDiet in Renal Disease
GIK Glucose insulin potassium
Study
GIST Glucose Insulin in Stroke Trial
MIDD Maternally inherited diabetes and deafness
GLP-1 Glucagon-like peptide-1
MO Macular oedema
HAAF Hypoglycaemia associated autonomic
MODY Maturity-onset diabetes ofyouth
failure
MRA Magnetic resonance angiography
HAIR-AN syndrome HyperAndrogenism,Insulin
MRFIT Multiple Risk Factor Intervention Trial
Resistance and Acanthosis Nigricans
MRI Magnetic resonance imaging
HbA1c Glycosylated haemoglobin
MRSA Methicillin-resistant Staphylococcus aureus
HDL High-density lipoprotein
NAOIN Non-arteritic optic ischaemic neuropathy
HELLP syndrome Haemolysis,Elevated Liver
NASCET North American Symptomatic Carotid
enzymes,Low Platelets
Endarterectomy Trial
HERS Hormone Estrogen-Progestin Replacement
NGF Nerve growth factor
Study
NHANES National Health and Nutrition
HHS Hyperosmolar hyperglycaemic state
Evaluation Study
HLA Human leucocyte antigen
NMR Nuclear magnetic resonance
HOPE Heart Outcomes Protection Evaluation
NO Nitric oxide
study
NTD Neural tube defects
HOT study Hypertension Optimal Treatment
NRT Nicotine replacement therapy
study
OAD Oral antidiabetic agent
HPS Heart Protection Study
oGTT Oral glucose tolerance test
HRT Hormone replacement therapy
OSA Obstructive sleep apnoea
ICU Intensive care unit
PAD Peripheral arterial disease
IFG Impaired fasting glucose
PARP Poly-ADP-ribose polymerase
IGF Insulin-like growth factor
PCI Percutaneous coronary intervention
IgG Immunoglobulin G
PCOS Polycystic ovarian syndrome
IGT Impaired glucose tolerance
PDE Phosphodiesterase
IHD Ischaemic heart disease
PDGF Platelet-derived growth factor
IMT Intima–media thickness
PEDF Pigment Epithelial-Derived Factor
INR International normalized ratio
PEG Percutaneous endoscopic gastrostomy
IRS Insulin resistance state
PKC Protein kinase C
IRMA Intraretinal microvascular abnormality
PPAR Peroxisome proliferator-activated receptor
ISDN Isosorbide dinitrate
PPP Primary Prevention Project
IV Intravenous
PROGRESS Perindopril PROtection aGainst
IVF in vitro fertilization Recurrent Stroke Study
LAD Left anterior descending RAS Renin–angiotensin system
LDH Lactate dehydrogenase RANKL Receptor Activator ofNuclear factor
LDL Low-density lipoprotein Kappa B Ligand
01
S E C T I O N O N E
Prevention and Diagnosis
1 Preventing type 1 diabetes
2 Preventing type 2 diabetes
3 Diabetes risk after the menopause
4 Genetic diabetes syndromes (MODY)
5 Screening and impaired glucose tolerance
6 Type A/B diabetes and insulin resistance
P R O B L E M
1 Preventing Type 1 Diabetes
Case History
The parent of a 4-year-old boy with type 1 diabetes consults you wanting to know if there
is anything he can do to prevent a future child developing the condition. He already has an
8-year-old daughter with diabetes and there is a strong family history of autoimmune
thyroid disease on both his and his wife’s side of the family. They are contemplating
having a third child.
Is there any evidence that type 1 diabetes is preventable?
Is there any general advice the parents can usefully follow?
Can we predict the onset of type 1 diabetes?
Background
Preventing or curing type 1 diabetes is one of the holy grails for those who research
autoimmune disease or treat patients with diabetes. The disease typically presents in
childhood,currently necessitates lifelong use of insulin injections and exposes the indi-
©Atlas Medical Publishing Ltd, 2006
2 §01 Prevention and Diagnosis
vidual to increased risk ofvascular complications.The risk oftype 1 diabetes in the gen-
eral population is about 1 in 300,and this is increased up to 20-fold in first-degree rela-
tives.Genetic markers do not provide an accurate prediction ofdiabetes,with only 5% of
those with susceptibility markers actually developing the disease.However,the fact that
the disease has a long latent period and that the pre-diabetic phase can be identified by
measuring islet cell antibodies or by assessing beta cell function yields an opportunity for
preventative therapy.The results of trials using non-specific immunosuppression in the
1980s were disappointing with only temporary improvements in insulin production
demonstrated.
Type 1 diabetes in children became much more common in the course of the 20th
century.1 In fact, available evidence suggests that the disease was quite uncommon,
although generally fatal,in children during the 19th century.This,along with the geo-
graphical variation in the prevalence of childhood diabetes that is not accounted for by
variations in the prevalence ofsusceptible genotypes,strongly suggests that environmen-
tal factors are important.2 The wide variation in incidence rates applies much more to
childhood than to adult type 1 diabetes.3It is not surprising that there has been intensive
research into environmental triggers for diabetes that might be modified,or into safe and
effective nutritional or immunological manipulations that might decrease risk ofdevel-
oping the disease (Figure 1.1).Recent evidence suggests that most parents ofchildren at
risk oftype 1 diabetes will attempt preventative measures,4and it is increasingly impor-
tant for health professionals to be able to enter into a balanced discussion with parents
and would-be parents.
Both macronutrient and micronutrient components of the diet have received atten-
tion.5A protective effect of breast-feeding has been proposed,but not confirmed in all
Factors Predisposing To Type 1 Diabetes Level of Evidence
Genetic (including HLA) ***
Non-breast-fed *
Early exposure to cows’ milk *
Low vitamin D status **
Viral infection *
Rapid weight gain in childhood *
The Following Do Not Appear To Modify Risk
Childhood vaccination
Treatment with nicotinamide
Oral insulin therapy
*** Strong evidence supported by multiple well-conducted and randomized clinical studies
** Reasonable evidence supported by clinical studies (not randomized)
* Some evidence supported by observational studies and expert opinion
Fig.1.1 Factors predisposing to type 1 diabetes. HLA = human leucocyte antigen.
1 Preventing type 1 diabetes 3
studies.Breast-feeding may afford protection through early oral exposure to human milk
(inducing tolerance to insulin;see below),through protection against infectious agents,
and by decreasing the risk ofexcessive weight gain in infancy.The latter is also probably a
trigger for diabetes during adolescence.On the other hand,early exposure to cows’milk
may increase risk through exposure to bovine insulin or (cid:1)-casein, the latter being a
known immunomodulatory protein contained in cows’milk.Bottle-feeding can also be
associated with excessive weight gain.Amongst micronutrient components of the diet,
nitroso compounds (related to streptozotocin),nitrates and nitrites,all used as preserva-
tives in meat products, have been considered. Variations in vitamin D status may be
another reason for the geographical variation in the incidence oftype 1 diabetes.Vitamin
D has important regulatory effects on the immune system.A protective effect ofcod liver
oil (a source ofboth vitamin D and long-chain n-3 fatty acids,which are also anti-inflam-
matory) was shown against childhood diabetes in the recent study reported by the
Norwegian Childhood Diabetes Study Group.6
Certain infectious agents,including enteroviruses,have been associated with develop-
ment of diabetes in animal models and in rare cases of human diabetes.This has led to
worries that childhood vaccination,particularly with live attenuated vaccines,may be a
risk factor for type 1 diabetes.A Danish study,along with other recent evidence,has gone
a long way to dispel worries on this score;Hviid and colleagues7studied a cohort includ-
ing all Danish children born between 1990 and 2000,and found no evidence ofany asso-
ciation between childhood vaccinations and diabetes.On the contrary,the vaccines may
be protective by limiting the effect of potentially diabetogenic infections, particularly
rubella.
Recent Developments
1 Vitamin B (niacin) consists ofnicotinic acid and nicotinamide.The latter is tolerated
3
in high doses,and has been shown to decrease the incidence ofdiabetes in streptozo-
tocin-treated animals,and in non-obese diabetic mice.Some early preclinical studies
showed promise for the agent. The vitamin inhibits poly-ADP-ribose polymerase
(PARP),an enzyme involved in DNA repair.Activation ofPARP leads to depletion of
intracellular nicotinamide adenine dinucleotide. This depletion of cellular energy
stores may predispose to cell damage, including in the pancreatic beta cell. The
European Nicotinamide Diabetes Intervention Trial (ENDIT)8 was a randomized,
double-blind,placebo-controlled trial in which 552 islet cell antibody-positive first-
degree relatives ofpatients with diabetes took either nicotinamide or placebo.There
was no difference in the incidence ofdiabetes during the five years ofthe trial (82 vs 77
cases,respectively).
2 Autoimmunity directed at insulin epitopes is one ofthe critical driving forces in the
pathogenesis of type 1 diabetes. In animal models, exposure to mucosal insulin
induces tolerance and thus decreases risk ofdiabetes.This mechanism is ofparticular
interest because ofthe recent developments ofinsulin formulations which are active
after oral or nasal administration. The Diabetes Prevention Trial-Type 1 reported
recently.9In this trial,a large number offirst- and second-degree relatives ofpatients
with diabetes were screened for pre-diabetes.Those found to be positive were ran-