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lla+Is Small type 2 colorectal cancer
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3.6 Clinical Examinations
3.6.2 Colonoscopy
An endoscope is inserted through the anus and
3.6.1 Fecal Occult Blood Test
It is a screening test for the detection of colorectal cancer and is performed by collecting a small
amount of stool during defecation. Early detection and treatment of colorectal cancer, as well as
detection and resection of adenomas, is expected
to reduce the incidence of colorectal cancer and
has been demonstrated to reduce the risk of death.
observed from the inside. Although pretreatment
with an intestinal cleaning is required, pathological diagnosis can be made not only by diagnosing
the presence of the lesion but also by biopsy
under direct vision. It is also excellent for qualitative diagnosis, such as the depth of the lesion, and
the possibility of endoscopic treatment can be
examined (Fig.11.8).
Type 2 colorectal cancer
occupying 1/3 of the septa cavity
Fig. 11.8 Endoscopic observation of colorectal cancer
Type 2 colorectal cancer with stenosis
of the duct cavity (lsp is also seen in the
lower right)
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T. Terashima et al.
3.6.3 Enterography
Contrast medium and air are injected through the
anus, and the deformation of the colon is radiographed. With the development of endoscopy, the
number of procedures is decreasing. The entire
image and position of the colon can be conrmed
(Fig.11.9).
3.6.4 CT, MRI, PET Scan
Localized diagnosis, distant metastasis to other
organs such as liver, and lymph node metastasis
can be searched.
3.6.5 Capsule Endoscopy, CT
Colonography
Capsule endoscopy and computed tomographic
colonography have been developed as new examination methods.
In capsule endoscopy, a swallowed capsule is
advanced to the anus by peristalsis, and the gastrointestinal tract is observed under physiological
conditions during transit. The advantage of capsule endoscopy is that it is painless.
In addition, CT colonography, which is a virtual endoscope reconstructed from CT images, is
said to have almost the same diagnostic ability as
colonoscopy.
not high and increases in proportion to the stage
of the disease. It is recommended as an adjunct to
postoperative monitoring.
3.7 Treatment
The treatment includes endoscopic therapy, surgical treatment, chemotherapy, and radiotherapy.
Based on the results of various examinations, the
degree of progression (stage classication) is rst
determined, and then the treatment method is
selected.
Endoscopic treatment is indicated for intramucosal carcinoma or mildly invasive carcinoma of
the submucosa, which has little possibility of
lymph node metastasis (Fig.11.10). Technological
advances have made it possible to remove lesions
larger than 2cm by endoscopic submucosal dissection (ESD).
aa
3.6.6 Blood Test
Carcinoembryonic antigen (CEA) is measured as
a tumor marker. However, the positivity rate is
Fig. 11.9 Stenosis due to colorectal cancer (apple core
sign) at the transition of rectosigmoid colon
bb
Fig. 11.10 (a) 0-Ip, cancer in adenoma. (b) Resection
with endoscopic ligation. The photograph shows the
indwelling snare after resection
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Surgical treatment consists of intestinal resection and lymph node dissection of those lymph
nodes where the cancer may have spread. In principle, resection of the cancer lesion is performed,
and even in stage IV patients with distant metastases, if resection of the primary lesion is possible, resection of the primary lesion and metastases
should be considered.
Chemotherapy consists of postoperative adjuvant therapy to prevent recurrence in patients
with resectable disease and systemic chemotherapy to prolong life and alleviate symptoms in
patients with unresectable disease. In stage III,
oral anticancer agents are administered for about
6months as adjuvant therapy. In stage IV, molecular targeted agents are used according to the
presence or absence of RAS mutation, and the
patients are treated with other agents.
3.8 Prognosis
Colorectal cancer has a high curative ratio, and
more than 90% of patients can be cured if
detected early. The treatment of colorectal cancer
in advanced, unresectable patients has been
greatly improved by the development of various
drugs and therapies. The survival time has been
remarkably extended.
3.9 Recent Findings
Chemotherapy, in particular, has evolved in complexity with the development of novel anticancer
agents, molecularly targeted therapies, and
immune checkpoint inhibitors. Genetic testing
has become inevitable not only for risk assessment of hereditary tumors but also for treatment
decisions in chemotherapy using molecularly targeted agents and immune checkpoint inhibitors
corresponding to the genetic mutations.
4 Perioperative Period
HiroyukiHarada
4.1 Check theStage oftheCancer
Malignant tumors are broadly classied into carcinomas (epithelial tumors), sarcomas (nonepithelial tumors), and others (hematologic
neoplasm, myeloid tumors, malignant melanoma,
etc). Staging is based on (T) the size of the local
tumor, (N) the status of the involved lymph
nodes, and (M) the presence or absence of distant
metastases. Table 11.2 and Fig. 11.11 show the
TNM classication (Union for International
Cancer Control: UICC 8th edition, 2017) [10]
and stage classication of lip and oral cancer. The
TNM classication and the stage classication of
Table 11.2 TNM classication of oral cancer and oral
cavity cancer
T: Primary tumor
TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
Tis: Epithelial carcinoma
T1: Tumor with a maximum diameter of 2cm or less
and a depth of 5mm or less
T2: Tumors with a maximum diameter of 2cm or less
and a depth of more than 5mm, or tumors with a
maximum diameter of more than 2cm but less than
4cm and a depth of less than 10mm
T3: Tumor with a maximum diameter greater than 2cm
but less than 4cm and a depth greater than 10mm, or a
tumor with a maximum diameter greater than 4cm and
a depth less than 10mm
T4a (lip): Tumor penetrating the cortical bone of the
mandible, inferior alveolar nerve, oor of mouth, or
skin (of the muzzle or external nose)
T4a (oral cavity): Tumors with a maximum diameter
greater than 4cm and a depth greater than 10mm, or
tumors that penetrate the bony cortex of the mandible
or maxilla or invade the maxillary sinus, or tumors that
invade the facial skin
T4b (lip and oral cavity): Tumor invading the
masticatory muscle gap, pterygium, or skull base, or
tumor encircling the internal carotid artery
circumferentially
a
a
(continued)
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T. Terashima et al.
Table 11.2 (continued)
N: regional lymph node
NX: Unable to assess regional lymph node metastasis
N0: No regional lymph node metastasis
N1: Ipsilateral solitary lymph node metastasis with a
maximum diameter of less than 3cm and no extranodal
invasion
N2: Transition described below:
N2a: Single ipsilateral lymph node metastasis with a
maximum diameter greater than 3cm but less than
6cm and no extranodal invasion
N2b: Multiple ipsilateral lymph node metastases with a
maximum diameter of 6cm or less and no extranodal
invasion
N2c: Bilateral or contralateral lymph node metastases
with a maximum diameter of 6cm or less and no
extranodal invasion
N3a: Lymph node metastasis with a maximum diameter
greater than 6cm and no extranodal invasion
N3b: Single or multiple lymph node metastases with
clinical extranodal involvement
M: Distant metastasis
M0: No distant metastasis
M1: With distant metastasis
(Reproduced with permission from [10])
a
Cases in which the primary lesion is gingival and there is
supercial erosion of bone and alveolus only are not considered T4a
b
It is classied as a clinical extranodal invasion if there is
skin involvement or soft tissue involvement with strong
adherence or union to underlying muscle or adjacent structures, or if there are clinical signs of nerve involvement.
The median lymph node is the ipsilateral lymph node
b
oral cancer are used to determine the treatment
strategy and to predict the prognosis.
4.2 Conrmation
ofTreatmentPlan
The treatment of malignant tumors can be broadly
divided into surgical therapy, radiation therapy,
and drug therapy. In advanced cases, multidisciplinary treatment is often performed by combining these methods.
4.3 Oral Environment
It is very important to maintain the oral environment during the perioperative period, not only for
the performance of surgery but also for the prevention of postoperative complications.
During intubation for general anesthesia, preoperative oral treatment is necessary because
severe carious teeth and periodontitis can cause
tooth prolapse and fracture fragments to enter the
airway. Postoperative periodontal cleaning and
extraction of carious teeth and severe periodontitis are important because the patient often suffers
from pneumonia and infection.
4.4 Radiation Therapy
Radiotherapy is classied into two types: interstitial irradiation, in which a small radiation source
is inserted into the primary lesion (brachytherapy), and external irradiation. External irradiation includes electron beams, X-rays, gamma
rays, proton beams, and heavy particle beams,
and is used depending on the primary site, the
condition of the patient, and the presence or
absence of concomitant chemotherapy.
Because mucositis and dermatitis occur frequently as adverse events, management of these
conditions is necessary (Figs. 11.12 and 11.13).
For severe mucositis, patients should be advised to
limit intake of irritants and avoid mechanical cleaning with toothpaste or a hard toothbrush. Relatively
nonirritating gargles such as sodium azulene sulfonate hydrate are recommended. Ointments containing antibacterial or anti- inammatory agents are
effective against dermatitis. Other complications
include osteonecrosis, xerostomia due to salivary
gland damage, and radiation-induced cancer.
4.5 Drug Therapy
Drug therapy for cancer often includes cellkilling anticancer agents, molecularly targeted
agents, and immunotherapy. The National Cancer
Institute (NCI)-Common Terminology Criteria
for Adverse Events (CTCAE) [11] is the standard
method for evaluating adverse events, which are
classied from grades 1 to 5, ranging from mild
to fatal. The most common adverse events are
gastrointestinal disorders, myelosuppression,
pulmonary toxicity, nephrotoxicity, hepatotoxicity, cardiotoxicity, and mucositis. It is necessary
to evaluate and control these adverse events.
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Fig. 11.11 Chart for a disease stage
Fig. 11.12 A patient underwent 50Gy of radiotherapy
after tongue cancer surgery. Mucositis with hemorrhage
was observed on the left cheek mucosa and tongue
4.6 Susceptibility to Infection
Patients with underlying diseases such as diabetes mellitus, liver cirrhosis, renal failure,
malnutrition, malignancy, and hypogammaglobulinemia, and patients taking steroids, anticancer
drugs, and immunosuppressive drugs are at high
risk of infection, and care should be taken to
avoid postoperative infection. Systemic ndings
Fig. 11.13 A patient underwent external beam radiation
therapy of 50 Gy to the neck (with cetuximab). Severe
erythema and hemorrhage were observed in the right side
of the neck
include fever, leukocyte count and fraction, CRP,
procalcitonin, and other results of blood test.
Local ndings include inammatory symptoms
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Fig. 11.14 Neck dissection. A continuous suction drain
should be placed before the wound is closed
such as redness and swelling, and drainage
volume and characteristics. (Fig.11.14).
References
1. Katanoda K, Sobue T, Tanaka H, Miyashiro I, editors. JACR monograph supplement no. 2. Tokyo:
Japanese Association of Cancer Registries 2016. (in
T. Terashima et al.
Japanese). http://www.jacr.info/publicication/Pub/m_
supp_02/m_supp2_all.pdf. Accessed 9 Feb 2022.
2. Japanese Gastric Cancer Association. Japanese classication of gastric carcinoma: 3rd English edition.
Gastric Cancer. 2011;14:101–12.
3. Japanese Society of Medical Oncology, editor.
Clinical oncology. (Shin Rinsho Shuyougaku). 5th ed.
Tokyo: Nankodo; 2018 (in Japanese).
4. National Cancer Center Institute for Cancer Control.
Guidelines for the screening for gastric cancer
based on efcacy evaluation. (Yukousei Hyoukani
Motozuku Igan Kenshin guideline). 2014 ed. Tokyo:
National Cancer Center Institute for Cancer Control;
2015. (in Japanese). http://canscreen.ncc.go.jp/guide-
line/iganguide2014_150421.pdf.
5. Ono H, Yao K, Fujishiro M, etal. Guidelines for endoscopic submucosal dissection and endoscopic mucosal resection for early gastric cancer (second edition).
Dig Endosc. 2021;33:4–20. https://doi.org/10.1111/
den.13883.
6. Colorectal Cancer Research Society, editor.
Guidelines for the treatment of colorectal cancer
2022. (Kanjyasanno Tameno Daichougan Chiryo
guideline). Tokyo: Kanehara Shuppan; 2022. (in
Japanese).
7. Committee of Accuracy Control for Colorectal Cancer
Screening, Japanese Society of Gastrointestinal
Cancer Screening. Manual of colorectal cancer
screening (Daichogan Kenshin manual). Tokyo:
Igakushoin; 2013. (in Japanese).
8. Quintero E.Colonoscopy versus fecal immunochemical testing in colorectal-cancer screening. N Engl J
Med. 2012;366:697–706.
9. Japanese Society for Cancer of the Colon and Rectum,
editor. Guidelines for the treatment of hereditary
colorectal cancer 2022. (Idensei Daichougan Shinryo
Guideline). Tokyo: Kanehara Shuppan; 2022. (in
Japanese).
10. Brierley JD, et al., editors. TNM classication of
malignant tumours. 8th ed. NewYork: Wiley; 2017.
11. National Cancer Institute. Cancer Therapy Evaluation
Program, editor. Common terminology criteria for
adverse events (CTCAE) version 5.0. https://ctep.
cancer.gov/protocoldevelopment/electronic_applications/ctc.htm. Accessed 10 Feb 2022.
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KazutakaAoki, KoichiroUeki, KunioYoshizawa,
TadashiToyama, YasushiIshigaki, TakayoshiSakai,
MasashiWatanabe, IkuyaMiyamoto,
FumikoMiyanaga, andHiroyukiYamada
12
1 Diabetes Mellitus
KazutakaAoki
1.1 An Overview ofDiabetes
Mellitus
Diabetes mellitus is a metabolic disease characterized by chronic hyperglycemia secondary to
insufcient insulin action [1]. Complications of
diabetes are associated with persistent chronic
hyperglycemia.
K. Aoki
Department of Diabetes and Endocrinology, Kanagawa
Dental University, Yokosuka, Kanagawa, Japan
K. Ueki · K. Yoshizawa
Department of Oral and Maxillofacial Surgery,
Division of Medicine, Interdisciplinary Graduate
School, University of Yamanashi, Chuo, Yamanashi,
Japan
T. Toyama
Department of Nephrology and Rheumatology,
Graduate School of Medical Sciences, Kanazawa
University, Kanazawa, Ishikawa, Japan
Y. Ishigaki (*)
Division of Diabetes, Metabolism and Endocrinology,
Department of Internal Medicine, Iwate Medical
University, Yahaba, Iwate, Japan
e-mail: ishigaki@iwate-med.ac.jp
1.2 Hormones Associated
withRegulation ofBlood
Glucose Levels
1.2.1 Insulin
Insulin, an important hormone secreted by the
β-cells of the pancreatic islets of Langerhans
lowers blood glucose levels. Hormones include
basic secretion and additional secretion that is
stimulated following food intake.
1.2.2 Glucagon
Glucagon secreted by the α-cells of the pancreatic islets of Langerhans increases blood glucose
levels.
T. Sakai
Department of Rehabilitation for Orofacial Disorders,
Division of Growth and Development Dentistry,
Osaka University Graduate School of Dentistry,
Suita, Osaka, Japan
M. Watanabe
School of Life Dentistry at Tokyo,
The Nippon Dental University,
Chiyoda-ku, Tokyo, Japan
I. Miyamoto · H. Yamada
Division of Oral and Maxillofacial Surgery,
Department of Oral and Maxillofacial Reconstructive
Surgery, School of Dentistry, Iwate Medical
University, Morioka, Iwate, Japan
e-mail: yamadah@iwate-med.ac.jp
F. Miyanaga
Osaka Dental University, Hirakata, Osaka, Japan
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
T. Chiba, H. Yamada (eds.), Internal Medicine for Dental Treatments,
https://doi.org/10.1007/978-981-99-3296-2_12
213
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K. Aoki et al.
1.2.3 Incretins
Glucagon-like peptide-1 (GLP-1) is secreted by
the L cells in the lower part of the small intestine, and glucose-dependent insulinotropic polypeptide (GIP) by K cells in the upper part of the
small intestine. GLP-1 promotes insulin secretion in a glucose-dependent manner and inhibits
glucagon secretion, whereas GIP promotes insulin secretion in a glucose-dependent manner.
1.3 Epidemiology
According to the National Health and Nutrition
Survey performed by the Ministry of Health,
Labour and Welfare in 2016, the number of
individuals with “strongly suspected diabetes
mellitus” and those in whom “the possibility of
diabetes mellitus cannot be denied” is estimated
to be approximately tenmillion each; therefore,
this disease is known to affect a signicantly
large number of patients.
1.4 Classication
1.4.1 Etiological Classication
(Table12.1) [2, 3]
1. Type 1 diabetes mellitus: Type 1 diabetes mel-
litus is common in young individuals and is
characterized by an absolute insulin deciency, which necessitates insulin injections.
This condition is classied into an autoimmune type, in which patients show positive
islet-cell autoantibodies (the anti-glutamic
acid decarboxylase [GAD] antibody and antiinsulinoma- associated protein-2 [IA-2] antibody, among others) and an idiopathic type.
Based on the mode of onset, it may be classied into acute onset, fulminant, and slowly
progressive disease.
2. Type 2 diabetes mellitus: Type 2 diabetes mel-
litus, the most common type of diabetes, is
characterized by decreased insulin secretion
or insulin resistance, with a consequent
decrease in insulin action. It is more commonly observed in patients aged >40 years,
although the incidence of type 2 diabetes mellitus is increasing in young patients in recent
times. Patients with obesity or a family history of diabetes mellitus are predisposed to
this metabolic disorder.
3. Diabetes associated with other specic mechanisms or diseases is categorized into the following groups:
(a) Diabetes mellitus with identied genetic
abnormalities: For example, maturityonset diabetes of the young (MODY) and
mitochondrial genetic abnormalities.
(b) Certain types of diabetes are associated
with other disorders and conditions: for
example, blood glucose levels tend to
increase with administration of glucocorticoids. Endocrine disorders such as
Cushing’s syndrome and acromegaly are
known to cause diabetes.
4. Gestational diabetes: This condition refers to
abnormalities in glucose metabolism that are
rst detected or develop during pregnancy and
do not lead to well-established diabetes mel-
Table 12.1 Etiological classication of diabetes mellitus
and glucose metabolism disorders [2]
I. Type 1 (Destruction of pancreatic β-cells, usually
leading to absolute insulin deciency)
A.Autoimmune
B.Idiopathic
II. Type 2 (Ranging from predominantly insulin
secretory defect, to predominantly insulin resistance
with varying degrees of insulin secretory defect)
III.Due to other specic mechanisms or diseases
A. Those in which specic mutations have been
identied as a cause of genetic susceptibility
(1) Genetic abnormalities of pancreatic β-cell
function
(2) Genetic abnormalities in the mechanism of
transfer of insulin action
B. Those associated with other diseases and
conditions
(1) Diseases of exocrine pancreas
(2) Endocrine diseases
(3) Liver disease
(4) Drug- or chemical-induced
(5) Infection
(6) Rare forms of immune-mediated diabetes
(7) Various genetic syndromes often associated
with diabetes
IV.Gestational diabetes mellitus
The occurrence of diabetes-specic complications has not
been conrmed in some of these conditions. Those that
cannot at present be classied as any of the above called
unclassiable
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215
litus. The diagnostic criteria for gestational
diabetes differ from those applicable for diabetes in non-pregnant women.
1.4.2 Pathophysiological
Classication
1. Insulin-dependent state: this refers to a state
of absolute insulin deciency in which insulin
injections are essential.
2. Insulin-independent state: this refers to a state
of relative insulin deciency.
1.5 Symptoms
Mild elevation in blood glucose levels is
accompanied by few subjective symptoms;
however, signicant hyperglycemia manifests
with thirst, polyuria, polyphagia, fatigue, and
weight loss.
1.6 Blood Tests
1. Plasma glucose levels: The normal fasting
blood glucose concentration is <110mg/dL.
2. Hemoglobin A1c (HbA1c): HbA1c is an
important indicator of blood glucose control
over 1–2months prior to blood sampling. The
Guidebook for Diabetes Treatment published
by the Japan Diabetes Society recommends a
normal value of 4.6–6.2%; however, HbA1c
around 6.2% may be associated with mixed
normal, borderline, and diabetic types of glucose tolerance [4].
3. Glycoalbumin represents the mean blood glucose level measured over 2 weeks prior to
blood sampling; normal values range between
11% and 16% [4].
4. 1,5-anhydroglucitol reects rapid changes in
glucose metabolism and is correlated with urinary glucose excretion. The normal value is
>14.0μg/mL [4].
5. The 75 g oral glucose tolerance test (75 g
OGTT): Patients visit the hospital in a fasting
state in the morning and are administered a
drink containing 75 g glucose (TRAILAN
G®), after which blood samples are drawn
continuously. Figure 12.1 shows the classication and criteria [2, 5].
1.7 Diagnosis
“Diabetic type” is diagnosed based on fulllment
of one or two of the following criteria:
1. Fasting plasma glucose level of ≥126mg/dL, a
2-h level of ≥200mg/dL on the 75g OGTT, or
a random plasma glucose level of ≥200mg/dL.
2. HbA1c≥6.5%.
Denitive diagnosis of diabetes mellitus is
established after the diabetic type is reconrmed
by tests performed on different days; however, at
least one of the tests must meet the diagnosis of
blood glucose levels. The patient is diagnosed
with diabetes mellitus if both the blood glucose
and HbA1c levels measured on the same day
indicate diabetic type.
Fig. 12.1 Categories of state of glycemia as indicated by fasting blood glucose levels and 75g OGTT with reference
value. (Excerpted with slight modication from [2, 5])
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K. Aoki et al.
1.8 Complications
Complications of diabetes include acute complications secondary to severe deciency of insulin
action and chronic complications associated with
persistent hyperglycemia.
1.8.1 Acute Complications
1. Hyperosmolar hyperglycemic state: This
complication is commonly caused by extreme
dehydration in elderly patients with type 2
diabetes.
2. Diabetic ketoacidosis: This is a serious metabolic disorder associated with severe deciency of insulin action, which results in the
accumulation of ketone bodies and metabolic
acidosis, which often occur in patients with
type 1 diabetes.
1.8.2 Chronic Complications
1. Microangiopathy: Microangiopathy, a specic complication of diabetes mellitus, represents the following three complications:
(a) Diabetic retinopathy: This condition
causes retinal hemorrhages, retinal white
spots, and edema. Progressive retinopathy results in maculopathy, vitreous hemorrhage, and retinal detachment, which
may lead to blindness. This condition is
classied into the following three stages:
(a) simple retinopathy; (b) preproliferative retinopathy; (c) proliferative
retinopathy. Laser photocoagulation or
surgery of the vitreous body is used to
treat advanced retinopathy.
(b) Diabetic nephropathy: Based on the 2014
classication, diabetic nephropathy is
categorized into the following ve stages.
Stage 1 (pre-nephropathy); stage 2 (incipient nephropathy) with microalbuminuria; stage 3 (overt nephropathy) with
persistent proteinuria; stage 4 (kidney
failure); and stage 5 (dialysis therapy) [6].
(c) Diabetic neuropathy: This complication is
classied as polyneuropathy and mononeuropathy. Polyneuropathy is the most
common type characterized by sensory
nerve impairment in bilateral feet, which
commonly manifests with numbness, pain,
and dysesthesia in both lower extremities.
Progression of hyposensitivity may lead to
ulceration or gangrene of the feet.
Autonomic nervous system impairment is
associated with orthostatic hypotension,
gastrointestinal motility disorders, such as
diarrhea and constipation, neurogenic
bladder, and erectile dysfunction.
2. Macroangiopathy: Macroangiopathy represents the following three complications:
(a) Coronary artery disease: Patients with
diabetes are at a high risk for angina pectoris and myocardial infarction. Some
patients are asymptomatic.
(b) Cerebrovascular disease: Patients with
diabetes are also at a high risk of atherothrombotic cerebral infarction and show a
high incidence of lacunar infarction secondary to concomitant hypertension [7].
(c) Peripheral arterial disease (PAD): PAD is
dened as arteriosclerosis of the peripheral arteries of the lower extremities;
patients typically initially experience
coldness of the affected extremity, and
with intermittent claudication and lower
extremity ulcers in advanced stages.
Smoking, hypertension, and dyslipidemia
are known to predispose patients to PAD.
3. Diabetic foot lesions such as ulcers and gangrene are likely to occur in patients with
neuropathy- induced hypoesthesia concomitant
with PAD, trauma, and infection. Appropriate
foot care can prevent diabetic foot and should
be recommended for high-risk patients.
4. Periodontal disease: Periodontal pathogens such
as Porphyromonas gingivalis cause periodontal
infection and subsequent chronic inammation
of periodontal tissues. Poor blood glucose control results in progressive periodontal disease;
conversely, progressive periodontal disease
worsens blood glucose control. Therefore, a
bidirectional association is observed between
periodontal disease and blood glucose control.
5. Dementia: Compared with patients without
diabetes, those with diabetes show a higher
risk of Alzheimer’s disease and vascular
dementia; onset of dementia in patients with
diabetes is associated with worsening of glycemic control [8].
6. Cancer: Diabetes mellitus increases the risk of
colonic, liver, pancreatic, breast, endometrial,
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