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106 Future developments in diabetes care
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Figure 12.2 A portal venogram showing the
hepatic portal vein prior to administration of
isolated human islets. In the Edmonton protocol,
an adequate mass of freshly isolated islets is
infused through a catheter placed into the main
portal vein.
Since the initial Edmonton protocol, there have
been further renements in the immunosuppression protocols used for islet transplantation, with
more intensive T-cell depletion at the induction
of immunosuppression being widely favoured.
Overall, results from transplantation are good with
about 75% of patients achieving insulin independence in recent series, and with about half of recipients achieving long-term insulin independence.
Even among those who do not achieve insulin
independence, signicant improvements in glycaemic control were achieved and sustained, with
long-term freedom from severe hypoglycaemia
being achieved in the majority of patients, regardless of whether insulin independence is achieved.
e overall duration of insulin independence is
variable, with median rates of insulin independence of between 40% and 60% being reported at
3 to 5 years in dierent cohorts. In contrast, freedom from hypoglycaemia among recipients who
have had recurrent severe hypoglycaemia prior to
transplantation is sustained beyond 5 years in the
majority of recipients.
ere remain signicant limitations to islet
transplantation which mean that it has remained
a niche treatment for a small number of people
with T1DM. e need for lifelong immunosuppression is associated with signicant risks including an
increased risk of malignancy, particularly for skin
cancers and lymphoma. Furthermore, the available
supply of human islets remains small and is likely
to remain a limiting factor in the long term.
In view of this, the primary indication for
islet transplantation remains for patients with
intractable, recurrent severe hypoglycaemia that
persists despite optimised medical management
including use of insulin-pump and sensor technology. A secondary indication is in the management of patients with suboptimal glucose control
who have previously received a kidney transplant and are, thus, already on immunosuppression. Islet aer kidney (IAK) transplantation is
increasingly being used to optimise diabetes in
such patients and carries a more favourable risk–
benet ratio through not requiring additional
long-term immunosuppression and through the
potential to improve renal gra survival through
improved diabetes control.
Presently, the strongest evidence for the benets of islet transplantation is in the context of the
management of hypoglycaemia, with long-term
freedom from hypoglycaemia seen in recipients.
Ongoing research in this eld aims to improve
islet survival and duration of insulin independence. is is focused on a greater understanding of the immune response that ultimately leads
to islet loss and recurrence of T1DM and also on
understanding the impact of additional cellular
factors that help support islet cell survival and
function.
More widespread use of islet cell therapy will
require improvements in immunosuppression,
islet gra survival and alternative sources of
islets other than cadaveric human donor tissue.
While various studies have explored encapsulation of islets and use of humanised porcine islets,
the greatest interest, at present, is in the potential
for bioengineered human beta cells (β-cells) and
dierentiated islets derived from embryonic stemcells. Two companies ViaCell and Vertex have
recently performed rst-in-man studies and, of
particular note, Vertex presented data showing a
therapeutic eect in a single patient with a marked
reduction in insulin requirements, though not
complete insulin independence. Based on these
preliminary results, the United States Food and
Type 2 diabetes mellitus: surgical and endoscopic interventions 107
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Drug Administration (FDA) has granted investigational status for a novel device comprising
Vertex’ encapsulated embryonic stem-cell-derived
islets, which is now entering Phase 1/2 clinical trials as a potential treatment for T1DM.
T1DM PREVENTION
Greater understanding of the immune processes
underlying the onset of T1DM has now led to
the development of the rst proven treatment to
attenuate the immune response. e drug teplizumab, a humanised anti-CD3 monoclonal antibody, delays overt T1DM in at-risk individuals.
It received FDA approval in 2022 aer a 10-year
development programme and is now starting to
enter clinical practice. In clinical trials, teplizumab was associated with delay in the progression of diabetes by more than 2 years, with
preservation of some β-cell function as measured by C-peptide production. is gives the
potential for using immunotherapy to alter the
natural history of T1DM, as existing evidence
has shown that preservation of some β-cell function and C-peptide positivity is associated with
reduced risk of complications and better overall glycaemic stability with less hypoglycaemia.
A future challenge in immunotherapy will be
to determine screening strategies for the very
early detection of T1DM in the population, as
such treatment would be most eective when
the earliest changes in glucose metabolism occur
and while β-cell mass is well preserved. Another
challenge will be to bring down the extreme cost
of immunotherapy, which, at present, would
limit its uptake.
TYPE 2 DIABETES MELLITUS:
SURGICAL AND ENDOSCOPIC
INTERVENTIONS
A major area of advancement in type 2 diabetes
mellitus (T2DM) has been the recognition of the
importance of the gut and gut hormones in the
aetiology of insulin resistance and dysglycaemia.
Much has been learned from the eld of bariatric
surgery, which has been shown capable of reversing T2DM independent of its eect on weight.
Multiple studies have shown that for patients with
obesity, surgical intervention can be more eective than pharmacotherapy. ese observations
were initially made in patients with a BMI >35
and have now been extended to those with a BMI
in the range of 30–35, which, while still within the
diagnostic criteria for obesity, is below the level
at which surgical intervention would be considered. Data from observational studies, notably
the Swedish Obesity Study, have shown that surgical treatment, particularly in the early years
aer diabetes, is associated with improved glucose
control, reduction in requirement for pharmacotherapy and, in some cases, reversal of T2DM.
Furthermore, long-term follow up in the Swedish
cohort has shown that early surgery is associated
with a reduction in microvascular complications
and cardiovascular morbidity. Of note, improvements in blood glucose control and a reduction in
insulin requirements are observed very early aer
surgery and before major weight loss has occurred.
is has led to interest in the underlying mechanisms by which bariatric surgery improves glycaemia, and studies in animals and, in some cases in
man, have identied multiple changes that may
inuence glucose homeostasis. Given these extensive eects, it has been suggested that the term
‘metabolic’ rather than ‘bariatric’ surgery may be
more appropriate to describe surgical management aimed primarily at reversal or management
of diabetes (Figure 12.3).
The surgical procedures with the greatest
impact on metabolic parameters are those that
involve the duodenum and this has led to particular interest in the study of the duodenum’s
role in glucose metabolism and its identification as a potential target for diabetes interventions. Studies in rodent models showed that a
high fat and sucrose diet leads to a thickening of
the duodenal mucosa and that this is associated
with the development of insulin resistance and
associated metabolic derangement. Ablation of
the mucosa was shown to reverse these changes
and, based on these observations, a therapeutic
intervention has been developed. This intervention, Revita Duodenal Mucosal Resurfacing
(DMR) is an endoscopic technique by which a
balloon catheter is placed in the duodenum and
inflated with heated saline to produce a focal
thermal injury and ablate the mucosal surface.
In initial randomised controlled trials, DMR
108 Future developments in diabetes care
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Figure 12.3 Putative actions of bariatric surgery on metabolic regulation: A broad range of changes
have been described following Roux-en-Y gastric bypass, which may explain the impact of surgery to
improve diabetes control.
treatment was associated with improvements in
glucose control and insulin resistance. Of particular note, DMR was associated with a reduction in liver fat content and improvements in
liver transaminases in patients with elevated
baseline liver fat content, suggesting a potential benefit in the management of non-alcoholic
fatty liver disease, which is an increasing issue
in T2DM. DMR has now entered clinical practice in some regions. Other techniques involving ablation of the duodenal mucosa, including
radiofrequency ablation (repurposing a technique developed for treatment of oesophageal
dysplasia), are also in development. Another
approach to manipulation of the duodenum that
has entered clinical practice is the EndoBarrier
duodeno-jejunal bypass liner (GI Dynamics,
Boston, US), which was developed primarily to
support weight loss. The EndoBarrier is a 60 cmlong polymer tube that is placed endoscopically
into the duodenum and anchored at the duodenal bulb, allowing nutrients to pass directly
from the stomach into the jejunum. This is left
in place for up to 1 year and then removed at
a further endoscopy. The outcomes associated
with the use of the device were variable, with
a multicentre trial showing no improvement
in glycaemic control over standard treatments,
whereas significant improvements in weight
and glycemic control were observed and maintained for up to 3 years in a UK clinical practice
series of patients with longer-duration diabetes
that had proved refractory to standard treatment (Figures 12.4 and 12.5).
Type 2 diabetes mellitus: surgical and endoscopic interventions 109
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Figure 12.4 The RevitaTM Duodenal Mucosal resurfacing technique uses a balloon catheter linked to
a computerized operating console (top left) to deliver a thermal injury to the duodenal mucosa. The
catheter is placed endoscopically and under x-ray guidance into the duodenum (top right, 1). The
mucosa is separated from the underlying submucosa by a local injection of saline (2) and the catheter
balloon is inated with heated saline to produce a focal thermal injury, which leads to atrophy and
regrowth of the mucosa (3). The balloon catheter is then removed and the mucosa inspected before
withdrawal of the endoscope (4). The resultant ‘resurfacing’ of the mucosa is associated with changes
in multiple metabolic parameters including improved glycaemic control and reduced liver fat.
110 Future developments in diabetes care
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Figure 12.5 The EndoBarrierTM duodeno-jejunal
barrier liner is inserted endoscopically into the
duodenum, creating a barrier between nutrients passing from the stomach to duodenum
which are prevented from reaching the duodenal
mucosa.
BIBLIOGRAPHY
Bellin MD, Dunn TB. Transplant strategies for
type 1 diabetes: Whole pancreas, islet and
porcine beta cell therapies. Diabetologia.
2020; 63: 2049–56. doi: 10.1007/s00125-
020-05184-7
Butler PC, Gale EA. Reversing type 1 diabetes
with stem cell-derived islets: A step closer to
the dream? J Clin Invest. 2022 Feb 1; 132(3):
e158305. doi: 10.1172/J CI158305
Carlsson LMS, Sjöholm K, Karlsson C, et al.
Long-term incidence of microvascular
disease after bariatric surgery or usual care
in patients with obesity, stratied by baseline glycaemic status: A post-hoc analysis
of participants from the Swedish Obese
Subjects study. Lancet Diabetes Endocrinol.
2017 Apr; 5(4): 271–9. doi: 10.1016/S2213-
8587(17)30061-X
Cummings DE, Rubino F. Metabolic surgery for
the treatment of type 2 diabetes in obese
individuals. Diabetologia. 2018 Feb; 61(2):
257–64. doi: 10.1007/s00125-017-4513-y
Hering BJ, Ballou CM, Bellin MD, et al. Factors
associated with favourable 5-year outcomes
in Islet Transplant alone recipients with
type 1 diabetes complicated by severe
hypoglycaemia in the Collaborative
Islet Transplant Registry. Diabetologia.
2023 Jan;66(1):163–173. doi: 10.1007/
s00125-022-05804-4
Mingrone G, van Baar AC, Devière J, et al.
Safety and efcacy of hydrothermal duodenal mucosal resurfacing in patients with
type 2 diabetes: The randomised, doubleblind, sham-controlled, multicentre REVITA-2
feasibility trial. Gut. 2022 Feb; 71(2): 254–64.
doi: 10.1136/gutjnl-2020-323608
Ruban A, Miras A, Glaysher MA, et al. Duodenal-
jejunal bypass liner for the management
of type 2 diabetes mellitus and obesity:
A multicenter randomized controlled trial.
Annal Surg. 2022 March; 275(3): 440–47.
doi: 10.1097/SLA.0000000000004980
Ryder REJ, Yadagiri M, Burbridge W,
et al. Duodenal-jejunal bypass liner for the
treatment of type 2 diabetes and obesity:
3-year outcomes in the First National Health
Service (NHS) EndoBarrier Service. Diabet
Med. 2022 Jul; 39(7): e14827. doi: 10.1111/
dme.14827
Shapiro AMJ, Lakey JRT, Ryan EA, et al. Islet
transplantation in seven patients with type
1 diabetes mellitus using a glucocorticoidfree immunosuppressive regimen. N Engl
J Med. 2000; 343: 230–23. doi: 10.1056/
NEJM200007273430401
Tatovic D, Dayan CM. Replacing insulin with
immunotherapy: Time for a paradigm change
in type 1 diabetes. Diabet Med. 2021; 38:
e14696. doi:10 .1111/d m e.14696
van Baar ACG, Meiring S, Holleman F, et al.
Alternative treatments for type 2 diabetes
and associated metabolic diseases:
Medical therapy or endoscopic duodenal
mucosal remodelling? Gut. 2021 Nov;
70(11): 2196–204. doi: 10.1136/gutjnl-
2020-323931
Index
https://t.me/medicina_free
A
ABBOS, 8
Abbott Freestyle Libre, 35
ABCC8-NDM, 16
Acanthosis nigricans, 90, 91
Acromegaly, 4, 19
Action to Control Cardiovascular
Risk in Diabetes
(ACCORD) blood
pressure trial, 80
Acute complications of DM, 56–62
Addison’s disease, 20
Adenovirus, 17
Adhesive capsulitis, shoulder, 94
Aibercept, 67
Albumin-to-creatinine ratio (ACR),
69
Alcohol, 57, 61
α-glucosidase inhibitors, 44
Alprostadil (prostaglandin E1),
87–88, 89
American Diabetes Association
(ADA), 35, 72, 99
diagnostic criteria, 3, 26
etiologic classication, 5
GDM criteria, 102
Amitriptyline, 77
Amlodipine, 80
Amoxicillin-clavulanate, 85
Amputation, lower-limb, 77, 78
Amylin, 14
Anencephaly, 100
Angiotensin-converting enzyme
(ACE) inhibitor, 71–72, 80
Angiotensin receptor blockers
(ARBs), 71
Antibiotics, 85
Anticonvulsants, 77
Apomorphine, 87
Arthropathy
Charcot’s, 81, 82, 83
cheiroarthropathy, 94
Assessing the Eectiveness of
Communication erapy
in the North West
(ACTNOW) study, 26
Atheromatous lesions, 77
Atorvastatin, 98
Automated insulin-delivery
systems, 102
Ava nal, 87
Azathioprine, 25
Azilsartan, 80
B
Background diabetic retinopathy,
63
Bacterial infection, skin, 80, 95
Bacteroides spp., 81
Balanitis, 95
Banting, Frederick, 1
Bariatric surgery, 107–108
Basal bolus insulin regimes, 101
Becaplermin, 86
Best, Charles H., 1
β-cells, pancreatic
autoimmune destruction, 7, 8
dysfunction, 14–15
monogenetic defects, 2, 9
stem cell generated, 106
viral infection, 8–9
Bevacizumab, 67
Bicarbonate, 60
Biguanides (metformin), 43
Bioengineered skin substitutes,
85
Blood glucose, 34–35
monitoring systems, 34–35, 39
plasma prole
‘glucose excursions’, 37, 38
insulin injections, 32, 34
non-diabetic, 33
stable control, 44
self-monitoring technique, 35
subcutaneous continuous
glucose monitoring
system, 35
subcutaneously implanted
continuous monitoring
system, 35
Blood Pressure Control Study, 80
B lymphocytes, 9
Bovine serum albumin, 8
Brolucizumab, 67
Bullae, 92
Bullous lesions, 92
C
Calcium channel blockers, 80
Calorie restriction, 42
Canagliozin, 46, 61
Candesartan, 80
Candidiasis, 95
Captopril, 80
Carbohydrates, 33–34, 36, 42, 44
Cardiovascular disease (CVD), 53,
63, 73, 98
recurrent coronary heart disease
(CHD) events, 77
Carpal tunnel syndrome, 75, 76
CD4 T lymphocyte, 9
CD8 T lymphocyte, 9, 25
Centripetal obesity, 18
Cephalexin, 85
111
112 Index
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Cerebral oedema, 61
Charcot’s arthropathy, 81, 82, 83
Cheiroarthropathy, 94
Children and adolescents
childhood obesity, 19
childhood type 2 diabetes, 4
emotional problems, 51
hypoglycaemia, 51
insulin requirements, 51
macrosomic babies, 101
treatment, 51–52
Chlorthalidone, 80
Cholesterol, 98–99
Cholesterol Treatment Trialists, 98
Chronic complications of DM,
63–95
Chronic kidney disease (CKD), 70
Circinate exudative retinopathy, 65
Cirrhosis, 90
Classication of DM, 3–6
Clindamycin, 85
Closed-loop technology, 38
Collaborative Atorvastatin Diabetes
Study (CARDS), 98
Coma, 61
Coma, Hyperosmolar Nonketotic,
61
Continuous ambulatory peritoneal
dialysis (CAPD), 73
Continuous glucose monitoring
(CGM) systems, 38, 51, 101
Continuous glucose sensing
technology, 35
Continuous subcutaneous insulin
infusion (CSII), 35, 36
Coronary artery disease, 77
Counterpoint study, 27
Coxsackie B virus, 8, 9
C-peptide, 107
Creatinine level, 70, 71
Critical-care admission, 53
CTLA-4 gene, 8
Cushing’s syndrome, 4, 18, 19
Cyclosporine A, 25
Cystic brosis, 4, 22
Cytomegalovirus, 8, 17
D
Dapagliozin, 46, 61
Da Qing Study, China, 26
Denition of DM, 3
Dehydration, 59
Depression, 103
Dermopathy, 92
Dextrogel, 57
Diabetes burnout, 37
Diabetes Control and
Complications Trial
(DCCT), USA, 3, 29, 63,
72
Diabetes Distress Scale, 103
Diabetes Education and Self-
Management for
Ongoing and Newly
Diagnosed diabetes
(DESMOND)
programme, 42
Diabetes insipidus, diabetes
mellitus, optic
atrophy and deafness
(DIDMOAD) syndrome,
64
Diabetes mellitus (DM), denition,
3
Diabetes Mellitus Insulin Glucose
infusion in Acute
Myocardial Infarction
(DIGAMI) study, 79
Diabetes Prevention Program,
USA, 26
Diabetic autonomic neuropathy, 76
Diabetic cheiroarthropathy, 94
Diabetic dermopathy., 92
Diabetic foot
digital arterial calcication in,
78
osteomyelitis in, 83
Diabetic foot ulceration, risk factors
for, 80
Diabetic impotence, 89
Diabetic ketoacidosis (DKA), 59–61
Diabetic macular oedema, 67
Diabetic maculopathy, 66
Diabetic neuropathy, 73
Diabetic retinopathy, 69
Diabetic right-third cranial nerve
pa lsy, 75
Diagnostic criteria of DM, 3, 4
Dialysis, 73
Diazoxide, 4
Dietary advice, 33
DIGAMI study, 79
Digital arterial calcication in
diabetic foot, 78
Dipeptidyl peptidase-4 (DPP-IV)
inhibitor, 44, 45
DIRECT study, 42
Distal gangrene, 78
Dose Adjustment for Normal
Eating (DAFNE)
program, 34
Down’s syndrome, 4, 17
DQB1 gene, 8
DREAM (Diabetes Reduction
Assessment with
Ramipril and
Rosiglitazone
Medication) study, 26
Driver and Vehicle Licencing
Agency (DVLA), 103–104
Driving licence, UK, 103
Drug treatment, for type 2 diabetes,
42
Dulaglutide, 45
Duodenal mucosa, 108
Duodenal Mucosal Resurfacing
(DMR) technique,
107–109
Dupuytren’s contracture, 94
Dyslipidaemia, 98–99
E
Edmonton protocol, 105, 106
Empagliozin, 46, 61
EMPA-REG study, 47
Enalapril, 80
EndoBarrier duodeno-jejunal
bypass liner, 108, 110
Endocrine cells, 14
End-stage diabetic retinopathy, 67
End-stage renal disease (ESRD), 70
Entrapment syndrome, 73, 75
Environmental factors
for children and adolescents, 51
viral infection, 8–10
Epstein–Barr virus, 8
Equality Act 2010, 104
Erectile dysfunction (ED), 76,
86–89, 103
causes, 86
hypogonadism, 86
Index 113
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treatment, 86
vasoactive drug
injection, 88
transurethral application,
88, 89
Eruptive xanthomata, 91, 92, 93
Erythromycin, 77
Escherichia coli, 31, 81
Euglycaemic diabetic ketoacidosis
(EDKA), 61
Euglycaemic ketoacidosis, 46
European Association for the Study
of Diabetes (EASD), 72
Exercise, 35
and insulin sensitivity, 36
Exogenous insulin administration,
54
Eye disorders
DIDMOAD syndrome, 64
laser photocoagulation, 65, 66,
67, 68, 69
maculopathy, 63, 66
normal fundus, 63
retinal detachment, 65, 69
retinopathy, 63–69
thromboneovascular glaucoma,
67
triamcinolone therapy, 68
vitreous haemorrhage, 65, 66, 69
Ezetimibe, 99
F
Faricimab, 67
Fasting plasma glucose (FPG),
3, 14
Federal Aviation Administration,
104
Felodipine, 80
Fenobrate, 99
Fenobrate Intervention and Event
Lowering in Diabetes
(FIELD) trial, 99
Fibrates, 99
Fibrocalculous pancreatopathy, 4
15-15 Rule, 57, 58
Finerenone in Reducing Kidney
Failure and Disease
Progression in Diabetic
Kidney Disease
(FIDELIO-DKD) trial, 72
Finnish Diabetes Prevention Study,
26
Finnish study, 73
Fluid replacement, 60
Food and Drug Administration
(FDA), 72, 106–107
Foot disorders
burn injuries, 81
callus, 81
Charcot’s arthropathy, 81, 82, 83
deep infection, 82
digital arterial calcication, 78
gangrene, 78,
osteomyelitis, 82, 83, 84, 85
treatment, 85, 86
ulcer, 82, 85
weight-bearing reduction, 85
Fosinopril, 80
Free fatty acids (FFAs), 14, 15, 90
Freestyle Libre 2 ash glucose
Frozen shoulder, 94
Future developments
β-cells, stem cell generated, 106
insulin pumps, 106
islet cell transplantation, 105
pancreatic transplantation, 105
85
monitoring system, 36
G
Gabapentin, 77
Gastric inhibitory polypeptide
(GIP), 44, 90
Gastric Neurostimulator (GES)
system, 77
GCK-MODY, 16
Genes
DQB1, 8
glucokinase, 16
INS (insulin gene), 16
Genetic loci
IDDM2, 8
Genome-wide association studies
(GWA S), 8, 24
Geographic variation of DM, 1–2
Gestational diabetes mellitus
(GDM), 5, 26, 102
O’Sullivan–Mahan criteria
(USA), 5
WHO criteria, 5, see also
Pregnancy
Glitazones, 26, 44
Glomerulopathy, 70, 71
GLP-1 receptor agonists, 52
Glucagon, 58
Glucagon-like peptide-1 (GLP-1),
14, 44, 45, 54, 90
Glucocorticoids, 4
Glucogel, 57
Gluconeogenesis, 7, 58
Glucose
metabolism, brain, 57
tolerance, impaired, 3, 4, 22,
see also Blood glucose
Glucotoxicity, 14
Glutamic acid decarboxylase
(GAD) antibodies,
Gluten, 8
Glycaemic control, 34, 100
Glycogenolysis, 7, 58
Glycolysis, 59
Glycosuria, 59
Granuloma annulare, 93
GvokeHypoPen, 58
9
H
Haemochromatosis, 4, 20, 22, 23
Health-care costs, 3
Heart Outcomes Prevention
Evaluation (HOPE) study,
80
Heart Protection Study (HPS), 98
Hemoglobin (HbA
Hepatic gluconeogenesis, 59
Hepatic nuclear factors (HNFs), 5
Hepatic portal vein, isolated islet
administration, 106
Hereditary haemochromatosis, 20
Heterozygous mutations, 16
High-density lipoprotein (HDL),
98
HNF1A-MODY, 16
Human leukocyte antigen (HLA), 8
HLA antigens, 8
Human proinsulin, 30
Hyalin deposition, 71
Hydroxymethylglutaryl-coenzyme
A reductase inhibitor, 98
Hyperbaric oxygen, 86
Hyperglycaemia, 14, 49, 53, 59, 79
in pregnancy, 100
) targets, 33
1c
114 Index
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Hyperglycaemia-driven osmotic
diuresis, 61
Hyperglycaemic Hyperosmolar
Nonketotic Coma
(HONK), 61
Hyperinsulinaemia, 79
fetal, 101
Hyperlipidaemia, 49, 98–99
Hyperosmolar Hyperglycaemic
Nonketotic Syndrome
(HHNS), 61
Hyperosmolar Hyperglycaemic
State (HHS), 61–62
Hyperosmolarity, 59
Hyperosmolar Nonketotic Coma,
61
Hypertension, 71, 72–73, 79–80
Hypertriglyceridaemia, 98
Hypoglycaemia, 31, 56, 58, 103, 106
brain glucose metabolism, 57
causes of, 57
children and adolescents, 51
hypoglycaemia-induced cardiac
dysrhythmia, 57
neonatal, 100
self-treatment, 57
symptoms, 57
I
IDDM2, 8
Impaired fasting glucose (IFG), 2, 3
Impaired glucose tolerance (IGT),
2, 3, 14, 19, 22, 26
Incretin-based treatments, 44–45
Indapamide, 80
Inpatient management of diabetes,
53
Insulin, 30, 31, 47
biosynthesis, 31
biphasic response to glucose, 15
crystals, 30
deciency, biochemical
consequences, 10
discovery of, 1–3
impaired secretion, 14
injection technique, 32
lipid hypertrophy, 34
lipoatrophy, 33, 34
longer-acting, 47
pens, 32
plasma prole, non-diabetic, 33
proinsulin, protein sequence, 30
rapid-acting, 47
requirements, children and
adolescents, 51
resistance, 2–3, 14–16
Insulin analogs and formulations,
30
insulin aspart, 31
insulin detemir, 31
insulin glargine, 31, 33
insulin lispro, 31
isophane, 31
NPH (isophane), 31
porcine insulin, 31
Insulin autoantibodies (IAA), 9
Insulin crystals, 30
Insulin deciency, 10
Insulin degludec (Tresiba), 31
Insulin-dependent diabetes
mellitus (IDDM),
see Type 1 diabetes
Insulin detemir (Levemir), 31
Insulin independence, duration
of, 106
Insulin infusion rate, 60
Insulin injection technique, 32
Insulin-like growth factor (IGF)-1
receptors, 90
Insulin lipoatrophy, 33
Insulinoma, 12
Insulin pump, 102
Insulin-pump therapy, 51, 103
Insulin regimes
basal-bolus, 36
continuous subcutaneous
insulin infusion (CSII),
35
twice-daily, 31
Insulin requirements in children
with T1DM, 51
Insulin resistance, 79
Insulin resistance syndrome, 2–3,
6, 14–16
denition, 14
Insulin therapy, patients on, 54
Insulin-treated diabetes, 54
Insulitis, 9, 12
Insurance issues, 104
Interferon (IFN)γ, 9
Interleukin (IL)-2, 9
Intermediate-density lipoprotein
(IDL), 98
Intraretinal microvascular
abnormalities (IRMA), 64
Intravitreal triamcinolone, 67
Irbesartan, 80
Islet aer kidney (IAK)
transplantation, 106
Islet amyloid polypeptide (IAPP),
14
Islet cell antibodies (ICA), 9, 13
Islet cell transplantation, 105, 106
Islet of Langerhans, 9, 30
Coxsackie B viral infection
(LM), 9
cystic brosis, pancreas (LM),
22
glucagon immunostained, 11
insulin immunostained, 11
insulin storage granules, 11
insulitis hyperexpression, 14
normal pancreas, 11
somatostatin immunostained,
11
type 1 DM
β-cells, 11, 12
inltrate, 12
lymphocyte inltration, 12
type 2 DM
amyloid deposition, 15
Isradipine, 80
IV insulin, 55
K
KCN J11-NDM, 16
Ketoacidosis, 46, 53, 59–62
causes of death, 60
Ketoacids, 59
Ketones, 53, 59, 60
Ketosis, in surgery, 54
‘Ketosis-prone’ T2DM, 59
Klinefelter’s syndrome, 2, 4, 17, 21
L
Lactic acidosis, 43
Laser photocoagulation, 65, 66, 67,
68, 69
Latent Autoimmune Diabetes in
Adulthood (LADA), 4
Index 115
https://t.me/medicina_free
Late-onset diabetes mellitus, 2
immune-mediated type 1, 2
Levooxacin, 85
Lifestyle change, 25–26
Linezolid, 85
Lipid disorders, 98
Lipid hypertrophy, 34
Lipoatrophy, 33, 34
Lipohypertrophy, 32, 34
Lipolysis, 59
Lipoprotein abnormalities in
T2DM, 98
Lipoprotein A (Lp(a))
concentrations, 98
Liraglutide, 44
Liraglutide Eect and Action in
Diabetes: Evaluation of
Cardiovascular Outcome
Results (LEADER) study,
47
Lisinopril, 80
Liver
cirrhosis, 90
glucose output, 27
glucose production, 14, 15
hepatic nuclear factors (HNFs), 5
hepatic portal vein, isolated islet
administration, 106
Losartan, 80
Low-density lipoprotein (LDL),
98–99
M
Macrophages, 9
Macrosomia, 100
Macrosomic babies, 101
Maculopathy, 63, 66
Maggot debridement, ulcer, 86
Major histocompatibility complex
(MHC), 8
antigens, 9
Male excess, type 1, 6
Malignant otitis externa, 95
Massive eruptive xanthomata, 93
Maturity onset diabetes, 41
Maturity-onset diabetes of the
young (MODY), 4, 16
Mealtime insulin, 36, 102
Medicated Urethral System for
Erection (MUSE), 88
Medtronic 780 G, 37
Meglitinides, 44
Me proliferator-activated
receptorgamma (PPARγ),
44
Meropenem, 85
Metabolic syndrome, see Insulin
resistance syndrome
Metformin, 41, 43, 44, 47, 72, 90
Metoclopramide, 77
Microalbuminuria, 71
Migratory necrolytic erythema, 93
MiniMed continuous glucose
monitoring system, 35
Minocycline,
Mitochondrial diabetes, 16–17
Monitoring systems, blood glucose,
Monoclonal antibodies, 25
Monogenic diabetes
causes of, 17
subtypes, 16–18
Multiple Risk Factor Intervention
Mumps, 8, 9, 17
Myocardial infarction and
Myotonic dystrophy, 22
MySugarWatch glucose sensor
85
34–35, 37
Trial (MRFIT), 77
infection, 60
system, 37
N
National Diabetes Inpatient Audit
(NaDIA), 53
NAVIGATOR study, 26
Necrobiosis, 91
Necrobiosis lipoidica diabeticorum,
91–92
Neovascular glaucoma, 67
Nephropathy, 53, 69–73, 79, 80, 103
Neuropathic ulcer, 82
Neuropathy, 71, 81, 103
acute, 75
autonomic, 73, 76–77
chronic insidious sensory,
74–75
mononeuropathy, 75
pathogenesis, 74
prevalence, 74
proximal motor, 75–76
third cranial nerve palsy, 75
treatment, 81
ulnar, 75
Niacin, 99
Nitrosamines, 8
Non-alcoholic fatty liver disease
(NA FLD), 90
Non-alcoholic steatohepatitis
(NASH), 90
Non-insulin-dependent diabetes
mellitus (NIDDM),
see Type 2 diabetes
Non-insulin treatment, patients
on, 54
O
Obesity
body mass index (BMI), 18
childhood, 19
energy expenditure, 20–21
epidemic, 18–24
food consumption, 20
food intake, 19–20
genetics and, 21–24
sequelae of, 24
Obesity epidemic, 19
Obesity pandemic, 19
Olmesartan, 80
Omnipod, 37
Oral glucose tolerance test (OGTT),
3
Osmotic diuresis, 59
Osteomyelitis, 82,
foot, 85
Osteomyelitis in diabetic foot,
83
Osteoporosis, 83
O’Sullivan–Mahan criteria
(USA), 5
Outcome Reduction with Initial
Glargine (ORIGIN) study,
26
83, 84, 85
P
Pancreas, see also β-cells; Islet of
Langerhans
calcication, 23
ca ncer, 4, 24
pancreatic duct, normal, 23
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