MACROCYTIC ANEMIA

Sahyuddin
Tutik Harjianti
A. Fachruddin B

Div. of Hematology & Medical Oncology

Dept. of Internal Medicine, Medical Faculty
Hasanuddin University
 Deficiency Cyanocobalamin

B12 : all of it made from diet

A food ingredients may from animal.
Absorbtion : 5 ug / days
Cofactor at 2 important reaction in a body

Division of Hematology & Medical Oncology – Dept. of Internal Medicine

 The role of Cyanocobalamin

Methyl-Cobalamin is a cofactor for methionine-

synthetase at rx change of homosystein 
metyonin.
Adenosyl-Cobalamin is a cofactor at rx change
of methyl-malonyl CoA  succinyl-CoA

Division of Hematology & Medical Oncology – Dept. of Internal Medicine

 Deficiency Cyanocobalamin

An important sign :
1. macrocytic Anemia

3. Level of Vit B12 <100 pg/ ml

sign

2. Peripheral blood smear:

macro-ovalocyte & hypersegmented neutrophil

Division of Hematology & Medical Oncology – Dept. of Internal Medicine

Macrocytic Normocytic
Division of Hematology & Medical Oncology – Dept. of Internal Medicine
 The Cause

1. Deficiency vit B12 (diet)

2. The decrease production of intrinsic factor
(Anemia perniciosa, post-gastrectomy)
2. The decrease absorbtion of vit B12 at the ileum
(Post-op, Crohn ds)
3. Helmynthyasis (tape-worm)
4. Deficiency Transcobalamin II

Division of Hematology & Medical Oncology – Dept. of Internal Medicine

 Physiology

Vit B12 come in from IT  binding with intrinsic

factor (made from parietal mucosa gaster cell)
 abs in ileum terminal by spesific receptor 
come in to the plasma  liver .
There are 3 protein transporter in the plasma :
Trans-cobalamin I, II & III (by leukocyte). Only
Trans-cobalamin II that can transport vit B12
into the cell.

Division of Hematology & Medical Oncology – Dept. of Internal Medicine

Division of Hematology & Medical Oncology – Dept. of Internal Medicine
 Phatogenesis

Hepar consist 2.000 – 5.000 ug vit B12

Need : 3 – 5 ug / hari

Defs vit B12 will be happen in 3 years after no

more absorpsi.

Defs caused by diet less vit B12 vary rare

( vegetarian )
 Example :

Gastrectomy  the area produce factor

intrinsik will decrease
Over-growth bactery in intestinal
Reseksi ileum  the area of absorpsi vit
B12 will decrease
Helmenthyasis
Crohn’s disease  ileum destruction
the area of absorpsi vit B12 will decrease
 Anemia Perniciosa

Often cause defs B12

Abnormality Auto-Imun herediter
Seldom show before 35 years old
Scandinavia / Eropa Utara
A black skin teenager, a hispanic woman
 Anemia Perniciosa

Clinic illustration :
Likely anemia caused byndefs vit B12,
- Gastritis atrophic
- Abnormal Auto-Imun ( rheumatoid arthritis
Grave’s disease, defs IgA )
- After several years some patient
Gastritis Atrophic => Carcinoma Gaster
 CLINIC ILLUSTRATION
DEFS. VIT B12
Megaloblastic anemia

 May a hard anemia ( hematokrit < 10 % )

A change mucosa cell : glossitis, anorexia,

diare.
Neurologic disturb:
1. Perifer  parestesi
2. Cerebral difunct
 Lab. Abnormal

1. Megaloblastic Anemia

2. MCV between 110 – 140 fl (increase)
at some patient : MCV normal
( thalassemia , defs Fe )

3. Blood Perifer : anisocitosis &

poikilocitosis. Specif : makro-ovalosit.
 Blood Perifer

4.Morfologi eritrosit very abnormal 

Likely Hemolytic Anemia

5. Hypersegmentasi netrofil

6. Reticulocit amount decrease

 Bone Marrow Asp

 Eritropoesis in-efektif ( ggn produksi RBC )

hiperplasi eritroid ( as respons )

 Cell megaloblast abnormal in SST diferent shape :

* big abnormal size,
* maturasi inti & sitoplasma tdk.sinkron.
Maturasi cytoplasm is normal,
DNA synthesis is bother

Seri mieloid : Giant sel meta-mielosit

 Other Lab. Abnormal :

In-efektif eritropoesis in SST  may happen

destruction eritroid cell that in the development
period  level LDH ( lactic-dehydrogenase )
very increase, and Bilirubin indireck increase
just for a little
 Diagnosis

1. Level vit B12 serum is less

( normal : 150 -350 pg / mL )
2. Schilling test ( for dx A Perniciosa /
the decrease absorpsi vit B12 oral )
1st step : the patient injection w/ Vit B12 i.m
Then give vit B12 that has di-label p.o
Retain urine 24 hours
 ( Normal : > 7 % )
 Test Schilling 2nd step

Give vit B12 that has ……, with the intrinsic

factor.
If the patient Anemia Perniciosa ( defs intrinsic
factor ), so absorpsi will fixed.
At a hard case ( epitel usus abnormal ) 
malabsorption  the result of test Schilling II
may still abnormal sp defek mukosa usus pulih.
 THERAPY
*At Anemia Pernisiosa ( oral absorpsi
disfun)
Intra-muscular Inj. Vit B12 ( IM )
Dosis : 200 ug
1st week : every day (replacement – tx)
2nd – 4th week : every week
Once a month
 Respons Therapy

Usually easy to show, GC better, the complain

decrease.
Retyculocitosys happen in 5 – 7 days.

Abnormalitas hermatologic will be dissappear

after 2 months.
SSP disorder will be dissappear if we give
therapy before 6 months sick.
Division of Hematology & Medical Oncology – Dept. of Internal Medicine
 Pathogenesis

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