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247
3.5.2 Blood Test
Depending on the degree of renal failure, elevated
serumlevels of Cr, urea nitrogen (UN), and uric
acid (UA), decreased serum Na and Ca levels,
and elevated serum K and P levels are often
observed, and metabolic acidosis, renal anemia,
and hyperparathyroidism develop.
Serum Cr level is widely used to evaluate
renal function, but varies with gender and body
size, because its production is proportional to
muscle mass.
3.5.3 Diagnostic Imaging
With decreasein renal function, if the kidneys are
atrophic, it is chronic renal failure; if they are
enlarged, it may be acute renal failure.
3.5.4 Evaluation ofRenal Function
1. Estimated glomerular ltration rate (eGFR):
This test is widely used in recent years. eGFR
is calculated by a formula based on serum Cr
level, age, and gender, andis used to evaluate
glomerular function.
2. Creatinine clearance (Ccr): Endogenous Ccr
is measured using 24-h urine samples and is a
commonly used method in clinical practice to
evaluate glomerular function.
3.6 Treatment
Because the excretion of waste products, regulation of water and electrolytes, and erythropoietin
production are dysfunctional, treatment is
required for each condition. In particular, dietary
therapy that restricts salt, water, protein, K, and P,
and drug therapy for each condition are central of
treatment.
3.6.1 Lifestyle Guidance andDiet
Therapy
1. Salt and water: Excessive salt and water intake
and extreme restriction are harmful. In conservative renal failure, uid deciency is
likely to occur at the same time as uid excess
is easy to occur due to decreased accommodation ability. Basically, uid intake should be
equal to the volume of insensible perspiration
plus the daily urine output, and salt intake
should be 3–6g/day.
2. Protein and energy intake: The basic principle
of dietary therapy is to limit protein and salt
intake with adequate energy intake. The recommended energy intake is 25–35 kcal/kg/
day, depending on gender, age, and physical
activity level. If serum Crlevel is elevated and
dialysis therapy may be required in the future,
protein intake should be 0.6–0.8g/kg/day.
3. Tasty thing: Smoking cessation is necessary
to reduce the decline in renal function and to
prevent cardiovascular disease. Appropriate
alcohol consumption, in terms of ethanol,
should be 20–30mL/day or less for male and
10–20mL/day or less for female.
3.6.2 Blood Pressure Control
The goal of antihypertensive therapy is to prevent
the progression of chronic renal failure and to
reduce the risk of cardiovascular disease and
death, and the target of antihypertensive therapy
is below 140/90mmHg and, if possible, below
130/80mmHg.
The rst-line antihypertensive agents are
angiotensin receptor blockade (ARB) and angiotensin converting enzyme (ACE) inhibitors,
which inhibit the renin angiotensin system
(RAS). If the target level is not reached, a Ca
antagonist, an alpha blocker, a beta blocker, and a
diuretic should be used in combination.
3.6.3 Anemia Management
Patients with chronic renal failure develop renal
anemia due to decreased production of erythropoietin in the kidney. The erythrocyte stimulating
agent (ESA) is administered, which should be
started at a hemoglobin (Hb) concentration of
10 g/dL or less, and the therapeutic target Hb
level should be 10–13g/dL, not exceeding 13g/
dL.
3.6.4 Others
1. Dyslipidemia: The treatment of dyslipidemia
is expected to decrease proteinuria and suppress renal function decline. The goal is to
control low density lipoprotein (LDL) cholesterol below 120mg/dL.
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2. Mineral and bone disease (MBD): MBD
develops and progresses with the progression
of renal failure, and is collectively called
chronic kidney disease (CKD) associated
MBD (CKD–MBD). Because not only bone
changes but also systemic abnormalities such
as vascular calcication occur, CKD–MBD
has an impact on life prognosis. In the latest
studies, control of serum P is considered to be
the most important factor.
3. Hyperuricemia: Hyperuricemia is dened as a
serum uric acid level of 7mg/dL or higher. As
renal function declines, uric acid excretion
function also declines, and the frequency of
hyperuricemia increases. In order to lower the
serum uric acid level, it is necessary to improve
lifestyle and to administer appropriate drugs.
4. Avoidance of renal-impairing drugs: When
renal function is impaired, renal excretory
drugs may increase the frequency of side
effects due to increased blood concentrations
of the drugs. Since side effects can exacerbate
renal impairment, when renal excretory drugs
are used, renal function should be evaluated
by eGFR and Ccr, and the dose of the drug
should be reduced or the administration interval should be extended.
Antipyretic analgesic agents, contrast media,
anticancer agents such as cisplatin, and antimicrobial agents such as aminoglycoside
should be used with caution in patients with
chronic renal failure.
3.7 Prognosis
As chronic renal failure progresses and uremic
symptoms appear, patients are treated by hemodialysis (HD), peritoneal dialysis (PD), or renal
transplantation. Hemodialysis is often chosen in
Japan.
Renal transplantation is the only therapy that
can restore renal functions and presents a good
quality of life, more activatedactivities of daily
living, and bettervital prognosis. However, the
low number of donated kidney transplants has
become a social problemin Japan.
3.8 Notes fromDentistry
Perspective
AkiraSasaki
The most common causes of chronic renal failure are diabetic nephropathy, chronic glomerulonephritis, and hypertensive nephrosclerosis,
in that order. Especially, diabetic nephropathy is
increasing year by year, and nephrosclerosis is
also increasing. Therefore, when performing
dental treatment for patients with chronic renal
failure undergoing dialysis treatment (dialysis
patients)or not, it is necessary to consider not
only renal disease but also diabetes and hypertension, as well as associated anemia and bone
metabolism disorder. In 2002, the concept of
CKD was introduced, which broadly refers to
the decline in renal function regardless of the
causative disease, and prevention and treatment
of CKD should be started from an early stage.
The relationship between periodontal disease
and systemic diseases such as diabetes mellitus
has been pointed out, and it is necessary to
understand CKD also from the standpoint of
dentistry.
3.8.1 Oral Manifestations ofChronic
Renal Failure
It is generally associated with multiple caries
and parenchymal enamel defects due to the
reduction of oral self-cleaning action and poor
oral management. In particular, dialysis patients
often present with xerostomia. The incidence of
periodontal disease is also high. When bone
metabolism is abnormal, the lamina dura disappears and the trabeculae are obscured, resulting
in ground glass-like changes (Fig. 13.1). The
oral mucosa is characterized by pallor of the
gingival mucosa, stomatitis, and xerostomia due
to anemia and peripheral circulatory disturbance
caused by renal failure (Fig.13.2). These symptoms are inuenced not only by renal disease
but also by concomitant diseases and their
treatment.
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Fig. 13.1 Panoramic radiograph of a dialysis patient
Fig. 13.2 Oral photograph of a dialysis patient
3.8.2 Problems andDrug Metabolism
During Dental Treatment
It is important to assess the patient’s clinical
symptoms and renal function with a thorough
understanding of the patient’s history and current medical condition. It is also necessary to
understand the pathophysiology of concomitant
diseases such as diabetes, hypertension, and
bone metabolism disorders other than renal diseases, and the treatment status including medication. The severity of CKD is evaluated by the
CGA classication, which consists of cause (C),
renal function (GFR: G), and proteinuria (albuminuria: A). The correspondence to dental treatment depends on the severity of the CKD and
the degree of invasiveness of the dental treatment. If the renal function is mildly impaired
249
(G1A1, G2A1), usual dental treatment is possible, but it is important to consult with the attending physician to understand the condition of the
patient and to conrm the precautions to be
taken in dental treatment. In addition, oral
implant treatment is contraindicated in patients
with severe renal dysfunction or dialysis [11].
Becausepatients are often accompanied by cardiovascular disease, monitoring (blood pressure, pulse rate, and SpO2) is necessary during
dental treatment. The blood pressure manchette
should be worn on the opposite upper arm
toavoid the occlusion ofarterio- venous stula
in hemodialysis patients.
The number of dialysis patients in the world is
increasing, and the prevalence of oral diseases is
high, so there are many opportunities for dental
consultation. It is desirable to perform dental
treatment on the day after hemodialysis when the
patient is in good physical condition because of
the time and physical burden on the day of hemodialysis. In performing surgical procedures such
as tooth extraction, underlying diseases such as
diabetes mellitus and cardiovascular disease
should be noted, and bleeding tendency should
be considered if they are receiving antithrombotic therapy, heparin during dialysis is not
affected the day after dialysis. In general, surgical procedures should be performed under continuous antithrombotic therapy and local
hemostasis should be used. In patients with renal
disease, prophylactic administration of antibiotics is necessary because of decreased immunity
and delayed wound healing. In dentistry, antibiotics and analgesics are frequently used, but their
prescription should be based on (1) drug metabolism and excretion pathways and (2) renal function. The drugs, dosage, and administration
schedule should be adjusted based on Ccr orthe
estimated GFR (glomerular ltration rate) calculated from serum Cr levelbased on age and gender. In dialysis patients, the dialyzability of the
drug itself is also an important factor [12, 13]. In
the guidelines, NSAIDs are recommended to be
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M. Tokumoto et al.
avoided as much as possible in the elderlyand
CKD patients because of the risk of acute renal
failure due to renal ischemia caused by inhibition
of prostaglandin synthesis, and acetaminophen is
considered safer, but the safety of long-term
administration is uncertain [14].
References
1. Hishida A, etal., editors. Standard nephrology. Tokyo:
Igaku Shoin; 2002. (in Japanese).
2. Schrier RW, et al. Schrier’s diseases of the kidney.
8th ed. Philadelphia: Lippincott Williams & Wilkins;
2012.
3. Japanese Society of Nephrology, editor. Evidencebased clinical practice guideline for CKD 2018.
Tokyo: Tokyo Igaku-sha; 2018. (in Japanese).
4. Horino T, Terada N. Clinical practice guideline for acute kidney injury 2016. Med Frontline.
2018;73(12):1582–7. (in Japanese).
5. Khwaja A. KDIGO clinical practice guideline for
acute kidney injury. Kidney Int Suppl. 2012;2:1–138.
6. Yamamura Y, et al. Epidemiology and risk factors
of AKI. Jpn Soc Dial Ther. 2018;51(2):123–8. (in
Japanese).
7. Mori K, Mori N. Update and the prospect of prevention and treatment of AKI.J Jpn Soc Dial Ther.
2018;51(2):135–9. (in Japanese).
8. Uchiyama H, editor. Nephrology for specialists.
2nd ed. Tokyo: Igaku Shoin; 2009. p. 209–39. (in
Japanese).
9. Fukagawa M, Yasuda T, editors. Manual of kidney
diseases for residents. 3rd ed. Tokyo: Igaku Shoin;
2017. p.281–307. (in Japanese).
10. Fukai T, Kurokawa K, Supervised. Harrison’s principles of internal medicine. 5th ed. Tokyo: Medical
Science International; 2015. p. 1861–71. (in
Japanese).
11. Japanese Society of Oral Implantology, editor.
Guidelines for oral implant treatment 2020. Tokyo:
Ishiyaku Shuppan; 2020. (in Japanese).
12. KDIGO 2012 clinical practice guideline for
the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1–150.
https://kdigo.org/wp- content/uploads/2017/02/
KDIGO_2012_CKD_GL.pdf.
13. Usui J, et al. Clinical practice guideline for druginduced kidney injury in Japan 2016: digest version. Clin Exp Nephrol. 2016;20:827–31. https://doi.
org/10.1007/s10157- 016- 1334- 0.
14. Japanese Society of Nephrology, editor. Evidencebased CKD clinical practice guidelines 2018. Tokyo:
Japanese Society of Nephrology; 2018. (in Japanese).
https://cdn.jsn.or.jp/data/CKD2018.pdf.
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HirofumiSawai, MasaatsuYagi,
KimihiroMatsumoto, MasahiroIeko, SatoshiGoto,
ShigekiIto, andDaishiSaito
14
1 Anemia [1–3]
HirofumiSawai
Anemia is a condition in which the hemoglobin
concentration in the peripheral blood is decreased.
Anemia can be caused by bleeding (e.g., men-
strual bleeding, gastrointestinal bleeding), hemo-
H. Sawai
Kinki Health Care Center, Yodogawa-ku, Osaka, Japan
M. Yagi
Department of Dental and Oral Surgery, Iwate
Prefectural Central Hospital, Morioka, Iwate, Japan
K. Matsumoto
Department of Internal Medicine, Tokyo Dental
College, Ichikawa General Hospital, Ichikawa, Chiba,
Japan
M. Ieko
Department of Nursing, Faculty of Health and
Medical Sciences, Sapporo University of Health
Sciences, Sapporo, Hokkaido, Japan
S. Goto
Department of Oral and Maxillofacial Surgery,
National Hospital Organization Sendai Medical
Center, Sendai, Miyagi, Japan
S. Ito (*)
Division of Hematology & Oncology, Department of
Internal Medicine, Iwate Medical University School
of Medicine, Yahaba, Iwate, Japan
e-mail: shigei@iwate-med.ac.jp
D. Saito
School of Dentistry, Iwate Medical University,
Yahaba, Iwate, Japan
lysis (e.g., spherocytosis, autoimmune hemolytic
anemia), decreased red blood cell production in
the bone marrow (e.g., aplastic anemia, leukemia,
myelodysplastic syndrome), or abnormal blood
distribution (e.g., idiopathic portal hypertension).
Common symptoms of anemia include those
associated with decreased cerebral oxygenation
due to impaired oxygen supply (lightheadedness,
dizziness, headache, fainting, etc.) and those associated with cardiovascular overload due to compensatory increased blood ow (palpitations,
shortness of breath, fatigue, general malaise, etc.).
According to red blood cell indices (mean corpuscular volume: MCV; mean corpuscular hemoglobin: MCH; and mean corpuscular hemoglobin
concentration: MCHC) (Fig. 14.1), anemia is
classied into three groups: (1) microcytic hypochromic anemia (Table 14.1); (2) macrocytic
anemia (Table14.2); and (3) normocytic normochromic anemia (Table14.3).
1.1 Microcytic Hypochromic
Anemia (Table14.1)
Iron-deciency anemia is the most common
cause of microcytic hypochromic anemia.
1.1.1 Iron-Deciency Anemia
One hemoglobin molecule consists of four globin
subunits (alpha chain, beta chain, etc.), and one
heme is bound to each globin subunit. Heme is
© 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_14
251
252
2
1Mean Corpuscular Volume (MCV)
3
×100
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Fig. 14.1 Red blood
cell index
mean corpuscular volumefl=
Reference value80 100 fl
Mean Corpuscular Hemoglobin (MCH)
mean corpuscular hemoglobinpg=
(Reference value27 34 pg
Mean Corpuscular Hemoglobin Concentration (MCHC)
mean corpuscular hemoglobin concentrationg/dl=
Reference value3036 g/dL
Ht
RBC 10
Hbg/dl
RBC 10
4
/µl
×1000
4
/µl
×1000
Hbg/dl
H. Sawai et al.
Ht
Table 14.1
Classication by erythrocyte
index
Microcytic hypochromic
anemia
MCV <80 (fL)
MCHC <30 (g/dL)
Table 14.2
Classication by
erythrocyte index Classication by etiology
Macrocytic
anemia
MCV >100 (fL)
MCHC >30 (g/dL)
Table 14.3 Normocytic normochromic anemia
Classication by
erythrocyte index Classication by etiology
Normocytic
normochromic
anemia
MCV: 80–100 (fL)
MCHC: 30–36 (g/
dL)
Microcytic hypochromic anemia
Macrocytic anemia
synthesized in the mitochondria of erythroblasts,
and has an iron atom in its center that binds
reversibly to oxygen. When the body is decient
in iron, hemoglobin synthesis is reduced, leading
Classication by
etiology
1. Iron-deciency
anemia
2. Sideroblastic anemia
3. Thalassemia
4. Hemoglobinopathies
1. Megaloblastic anemia
(a) Vitamin B12 deciency:
Pernicious anemia, postgastrectomy, malabsorption
syndrome, etc.
(b) Folic acid deciency
2. Non-megaloblastic anemia
Secondary: Liver disease, etc.
1. Acute hemorrhage
2. Hemolytic anemia
3. Aplastic anemia
4. Leukemia, malignant
lymphoma, myeloma, bone
marrow metastasis of cancer
5. Secondary anemia
to anemia. Causes of iron deciency include
bleeding (menstrual bleeding, gastrointestinal
bleeding, etc.), inadequate iron intake, iron malabsorption, and increased iron requirements
(pregnancy, etc.). Iron-deciency anemia is the
most common cause of anemia.
In addition to the common symptoms of anemia
such as lightheadedness, palpitations, and shortness of breath, deformed nails (spoon nails), pica
(eating dirt, paper, etc.), and Plummer- Vinson syndrome (atrophic glossitis, dysphagia) are also seen.
As examination ndings, peripheral blood
tests show microcytic hypochromic anemia, with
no abnormalities in the leukocyte system, but an
increased platelet count is common. Biochemical
tests show a decrease in serum iron and ferritin
(storage iron) and increased unsaturated iron
binding capacity.
For treatment, iron is administered orally, but
if gastrointestinal disturbances are observed as an
adverse effect of iron or if the improvement of
anemia is urgent, iron is administered intravenously. If bleeding is suspected as the cause of
anemia, it is necessary to investigate and treat the
causal disease of bleeding.
1.1.2 Sideroblastic Anemia
Due to impaired mitochondrial heme synthesis,
erythroblasts accumulate iron in the absence of
hemoglobin synthesis and collapse. Sideroblastic
anemia includes hereditary sideroblastic anemia,
myelodysplastic syndromes, and secondary sideroblastic anemia due to vitamin B6 deciency or drugs.
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253
Examination ndings include microcytic
hypochromic anemia, increased serum iron and
ferritin, and decreased unsaturated iron-binding
capacity. In the bone marrow, iron staining shows
ringed sideroblasts.
Vitamin B6 may be effective as a treatment.
Drug-induced sideroblastic anemia can be improved
by the discontinuation of the causative drug.
1.1.3 Thalassemia
Thalassemia is an inherited disorder in which
globin synthesis is decreased due to abnormalities
in the globin genes, resulting in microcytic hypochromic anemia. Thalassemia includes alphathalassemia in which alpha-globin decreases and
beta-thalassemia in which beta- globin decreases.
1.2 Macrocytic Anemia
(Table14.2)
Macrocytic anemia is classied into two categories: megaloblastic and non-megaloblastic.
1.2.1 Megaloblastic Anemia
1. Pernicious anemia: Vitamin B12 is absorbed
in the ileum by binding to (gastric) intrinsic
factor produced by gastric parietal cells. Since
vitamin B12 acts as a cofactor for enzymes
involved in DNA synthesis, vitamin B12 deciency causes maturation disorders not only in
red blood cells (megaloblastic anemia) but
also in all blood cells.
Pernicious anemia is induced by impaired
absorption of vitamin B
secretion of intrinsic factor associated with
the loss of gastric parietal cells caused by
atrophic gastritis, or due to the production of
anti-intrinsic factor antibody (a type of
autoantibody).
In addition to the common symptoms of
anemia, Hunter glossitis (associated with redness and pain of the tongue) may be observed.
As neurological symptoms, subacute combined degeneration of spinal cord (numbness
of the limbs, loss of deep sensation, ataxia,
etc.) may occur.
As examination ndings, peripheral blood
tests show macrocytic anemia as well as leu-
due to decreased
12
kopenia, thrombocytopenia (pancytopenia),
and neutrophil hypersegmentation (ve or
more lobes). In the bone marrow, proliferation
of megaloblasts is observed. Anti-intrinsic
factor antibody can be detected in the serum
of about 60% of patients.
For treatment, vitamin B12 should be
administered by intramuscular injection
(because orally-administered vitamin B12 is
not absorbed).
In addition to pernicious anemia, postgastrectomy (due to lack of secretion of intrinsic
factor) and small intestinal lesions (e.g.,
Crohn’s disease) may reduce vitamin B12
absorption, resulting in macrocytic anemia.
2. Folic acid deciency anemia: Since folic
acid acts as a cofactor in various enzymatic
reactions, DNA synthesis is impaired by folic
acid deciency, resulting in megaloblastic
anemia. Folic acid deciency is mainly caused
by inadequate folic acid intake due to nutritional disorders or alcoholism. Folic acid deciency also occurs in folic acid metabolism
disorders caused by folic acid antagonists
(methotrexate).
The symptoms are similar to pernicious
anemia, but neurological symptoms are
absent.
Examination ndings include low levels of
serum folic acid.
For treatment, oral administration of folic
acid and improvement of dietary habits are
recommended.
1.2.2 Non-megaloblastic Macrocytic
Anemia
In secondary anemia associated with chronic
hepatitis and liver cirrhosis, macrocytic anemia
without megaloblasts in the bone marrow is
observed.
1.3 Normocytic Normochromic
Anemia (Table14.3)
The causes of normocytic normochromic anemia
include acute hemorrhage, hemolytic anemia,
aplastic anemia, leukemia, secondary anemia,
etc.
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1.3.1 Aplastic Anemia
A disorder of bone marrow hematopoietic stem
cells results in decreased production of all blood
cells. It may be idiopathic, hereditary, or secondary to the effects of drugs or radiation.
As symptoms, not only the common symptoms of anemia but also susceptibility to infection associated with leukopenia, and bleeding
tendency associated with thrombocytopenia are
observed.
Examination ndings include pancytopenia in
peripheral blood tests and decreased all hematopoietic cells without abnormal cells in bone marrow tests. An increase in serum iron and ferritin,
a decrease in unsaturated iron-binding capacity,
and a marked increase in erythropoietin are
observed.
For treatment, blood transfusions (red blood
cells, platelets) are administered as supportive
care. Drugs include anabolic hormones, erythropoietin, granulocyte colony-stimulating factor
(G-CSF), immunosuppressive agents, etc. Bone
marrow transplantation is performed as a radical
treatment.
1.3.2 Hemolytic Anemia
Hemolytic anemia is either hereditary (abnormalities in red blood cells) or non-hereditary (causes
other than red blood cells). Common symptoms
of hemolytic anemia include splenomegaly, jaundice, and gallstones, in addition to the symptoms
of anemia. Compensatory erythroblast hyperplasia in the bone marrow is associated with
increased reticulocytes (immature red blood
cells) in the peripheral blood. Biochemical ndings include an increase in indirect bilirubin and
a decrease in haptoglobin.
1. Hereditary spherocytosis: Hereditary sphe-
rocytosis is caused mainly by autosomal dominant inheritance, in which red blood cells are
spherical in shape and cannot pass through the
endothelial cell space in the spleen and are
phagocytosed by macrophages, resulting in
hemolytic anemia.
As examination ndings, peripheral blood
smears show spherocytes.
For treatment, splenectomy is performed,
which results in clinical cure, including
improvement of anemia and disappearance of
jaundice.
2. Sickle cell anemia: Mutations in the beta-
globin gene cause hemoglobin S, which lead
to sickle-shaped (crescent-shaped) red blood
cells, resulting in hemolysis in the spleen and
vascular occlusion. Sickle cell anemia is common in malaria-prone areas such as Central
Africa owing to its malaria resistance.
3. Hereditary hemolytic anemia due to
enzyme abnormalities: Genetic abnormalities of enzymes in red blood cells cause hemolytic anemia.
Glucose-6-phosphate dehydrogenase
(G6PD) deciency is inherited as an X-linked
recessive trait and occurs almost exclusively
in males. It is common in Africa and the
Mediterranean, and is rare in Japan. Acute
hemolytic attacks are induced by infections,
drugs, surgery, or ingestion of fava beans,
although anemia is usually absent.
Pyruvate kinase (PK) deciency is inherited as an autosomal recessive trait and causes
hemolysis in the spleen, resulting in splenomegaly, jaundice, and gallstones.
4. Paroxysmal nocturnal hemoglobinuria: A
deciency of GPI-anchored membrane protein due to an abnormality in the PIGA gene
causes increased complement sensitivity,
resulting in intravascular hemolysis during
nighttime sleep and reddish-brown hemoglobinuria in the early morning. Since abnormalities exist in hematopoietic stem cells,
pancytopenia occurs, and the disease may
progress to acute leukemia. Bone marrow
transplantation is performed as a radical
treatment.
5. Autoimmune hemolytic anemia: The production of anti-erythrocyte antibodies (autoantibodies against red blood cells) causes
hemolytic anemia. It is usually caused by
warm autoantibodies (autoantibodies that are
active at 37°C), but can be caused by cold
autoantibodies (autoantibodies that are active
at low temperatures).
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255
(a) Autoimmune hemolytic anemia caused
by warm autoantibodies (IgG): It may
be idiopathic (of unknown cause) or secondary (associated with systemic lupus
erythematosus, lymphocytic leukemia,
etc.). Hemolytic anemia is sometimes
complicated by thrombocytopenia and is
called Evans syndrome.
As examination ndings, the direct
Coombs test (detection of anti- erythrocyte
antibodies bound to the surface of red
blood cells) and the indirect Coombs test
(detection of anti-erythrocyte antibodies
in serum) are positive. Corticosteroids
and immunosuppressants are used for
treatment.
(b) Cold agglutinin disease: Cold agglutinin
(IgM), which is active at low temperatures, causes hemolytic anemia, resulting
in its aggravation in winter and relief in
summer. The acute form, secondary to
mycoplasma or viral infections, is more
common in the young, while the chronic
form, associated with idiopathic type or
malignant lymphoma, is more common in
the elderly. Raynaud’s phenomenon may
be observed in cold weather. To prevent
hemolysis, it is recommended to avoid
exposure to cold.
(c) Paroxysmal cold hemoglobinuria:
Donath- Landsteiner antibodies (IgG),
which bind to red blood cells at low temperatures and activate complement at 37°C,
causes hemolysis, resulting in chills, shivering, headache, abdominal pain, and hemoglobinuria after exposure to cold. It is often
secondary to syphilis or viral infections.
6. Drug-induced immune hemolytic anemia:
Hemolytic anemia may occur as adverse
effects of drugs (penicillin, quinidine, methyldopa, etc.). Recovery from anemia is observed
within 1–2weeks after discontinuation of the
drugs.
1.3.3 Secondary Anemia
Anemia caused by diseases other than hematologic disorders is called secondary anemia, and it
occurs not infrequently.
1. Anemia of chronic disease: Anemia caused
by chronic infections (e.g., tuberculosis), collagen diseases, malignant tumors, etc. usually
presents as normocytic normochromic anemia. As examination ndings, serum iron and
total iron-binding capacity are low, and ferritin is high (ferritin is low in iron-deciency
anemia). However, when iron deciency
(hemorrhage) is associated, microcytic hypochromic anemia is observed.
2. Renal anemia: In chronic renal failure, eryth-
ropoietin production in the kidney is
decreased, resulting in normocytic normochromic anemia. For the treatment of renal
anemia, erythropoietin preparation is
administered.
3. Anemia associated with liver disease: In
chronic hepatitis and liver cirrhosis, macrocytic anemia is observed.
1.4 Notes fromDentistry
Perspective
MasaatsuYagi
1.4.1 Types ofAnemia
There are several types of anemia, but irondeciency anemia, megaloblastic anemia, and
aplastic anemia, which are most frequently associated with oral manifestations, are reviewed.
Iron-Deciency Anemia
Iron-deciency anemia (IDA) is a common form
of hypochromic microcytic anemia that accounts
for more than 80% of all anemias. It is more
common in women than in men. It is caused by
iron deciency due to impaired heme synthesis
or inadequate iron absorption, and is common in
patients who have undergone gastrectomy.
Systemic symptoms include fatigue, tachycar-
dia, palpitations, and spoon nails.
Oral symptoms include a smooth tongue (red,
at tongue) due to atrophy of tongue papillae,
angular cheilitis, atrophy of the pharyngeal and
cervical esophageal mucosa, and dysphagia,
known as Plummer-Vinson syndrome (Figs.14.2
and 14.3).
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Fig. 14.2 Smoothing of the tongue is seen
Fig. 14.3 Atrophy of the pharyngeal mucosa is seen
H. Sawai et al.
tomy, megaloblastic anemia caused by decreased
secretion of intrinsic factor or anti-intrinsic antibodies is called pernicious anemia.
The oral manifestations include a smooth
tongue with atrophy of tongue papillae, dysgeusia, and dysphagia, which is called Hunter’s
glossitis.
As in iron-deciency anemia, there is no problem in dental treatment if Hb is 9.0 g/dL or
higher. Vitamin B12 or folic acid may be effective
in the treatment of tongue pain, but only injectable vitamin B12 is effective.
Aplastic Anemia
Aplastic anemia is normocytic normochromic
anemia caused by damage to hematopoietic stem
cells due to abnormal bone marrow function. It is
said to be caused by anticancer agents or radiation
exposure, but the cause is often unknown in Japan.
Because not only red blood cells but also white
blood cells and platelets are reduced, oral symptoms include worsening of inammatory symptoms such as periodontitis and gingival bleeding.
The problem in dental treatment is that platelets
should be kept above 50,000/mm3 when performing surgical procedures such as tooth
extraction. Because the white blood cell count
is also low, antimicrobial agents (in normal
doses) should be administered from the day
before tooth extraction. In any case, when performing surgical procedures, it is necessary to
consult with the attending hematologist and to
make adequate preparations.
As for dental treatment, if Hb is 9.0g/dL or
higher, there is no problem with surgical procedures such as tooth extraction. For tongue pain
caused by atrophic glossitis, the treatment of the
primary disease should be prioritized, and iron
supplements should be administered.
Megaloblastic Anemia
Macrocytic megaloblastic anemia is caused by
deciency of vitamin B12 or folic acid, and vitamin B12 deciency is more common. Vitamin B12
is often found in patients who have undergone
gastrectomy because it is not absorbed into the
body when the intrinsic factor secreted by the
gastric mucosa is decient. Even without gastrec-
2 Leukemia
KimihiroMatsumoto
2.1 Disease Overview,
Pathogenesis, andSymptoms
In the bone marrow, the site of hematopoiesis in
adults, normal hematopoiesis is impaired by the
space-occupying proliferation of leukemic cells
derived from mutated hematopoietic stem cells
and progenitor cells. Leukemia is a lifethreatening disease that progresses into blood
ow (peripheral blood) due to an increase in leu-
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