AIHA

Pulmonary Tuberculosis Associated
with Autoimmune Hemolytic Anemia:

An Unusual Presentation
Mehmet TURGUT*, Ouz UZUN**, Engin KELKTL*, Okay ZER*
* Department of Hematology, Medical School, Ondokuz Mays University,

** Department of Chest Medicine, Medical School, Ondokuz Mays University, Samsun, TURKEY
ABSTRACT
Coombs positive hemolytic anemia is exceedingly rare in tuberculosis. We herein report a patient with tuberculosis associated with Coombs positive hemolytic anemia that was responded to antituberculosis therapy. She was
admitted to the hospital because of recent-onset fatigue, weakness, nonproductive cough, pallor and scleral jaundice. Coombs positive hemolytic anemia and pulmoner tuberculosis was diagnosed. Following antituberculosis therapy, laboratory and clinical finding related to autoimmune hemolytic anemia disappeared.
Key Words: Tuberculosis, Autoimmune hemolytic anemia, Coombs positivity.
Turk J Haematol 2002;19(4): 477-480
Received: 29.04.2002
Acceppted: 13.08.2002
INTRODUCTION
Tuberculosis is a multi-systemic specific infection,
which can lead protean manifestations in any organsystem. Therefore, the clinical presentation of the disease is quite diverse. Hematological finding in tuberculosis is not uncommon and usually due to non-immunological mechanisms. Normochrom normocythic anemia is the most frequent hematological finding at presentation and during the long clinical course of tuberculosis. Anemia is usually due to bone marrow granuloma, nutritional insufficiency, malabsorption and im-
paired iron utilization. Coombs positive hemolytic

anemia is exceedingly rare in tuberculosis. We herein
report a patient with tuberculosis associated with Coombs positive hemolytic anemia that was responded
to antituberculosis therapy.
A CASE REPORT
A 30-year-old previously healthy woman was admitted to the hospital because of recent-onset fatigue,
weakness, nonproductive cough, pallor and scleral jaundice. Physical examination revealed a blood pressure of 80/55 mmHg, pulse 92/min, respiration 35/min
477
Turgut M, Uzun O, Kelkitli E, zer O.
and body temperature 39.5C orally. In the examination of the respiratory system, there were fine rales heard in the left apical zone during inspiration and expiration together with a harsh bronchial noise. There was
a systolic cardiac murmur of grade I-II heard all over
the precordium. The laboratory findings on admission
revealed a WBC 6600/mm3 (75% neutrophils, 13%
lymphocytes, 11% monocytes and 0.5% eosinophiles),
hemoglobin 4.6 g/dL, MCV 98.7 and MCH of 22.7 fL,
platelet count 175.000/mm3 and reticulocyte 19.7%.
Direct and indirect Coombs test was positive without
any transfusion. Erythrocyte morphology was polychromacytic together with macrocytosis, spherocytosis,
anisopoikilocytosis and 6% normoblasts. Bone marrow
examination disclosed significant erythroid hyperplasia and hypercellularity. Biochemical tests on admission were: Total bilirubin 4 g/dL, direct bilirubin 1.9
g/dL, AST 295 IU/L, ALT 81 IU/L, LDH 1902 U/L,
ferritin 7685 ng/dL and haptoglobin 31 mg/dL. In the
chest X-ray there was bilateral reticulonodular infiltration in the upper zones and in the high resolution computerized tomography bilateral apical reticulonodular
infiltration and a cavitary lesion 2 cm in diameter seen
in the right upper lobe posterior segment (Figures 1,2).
Tests for ANA, anti-DNA, HIV and blood cultures were all negative. In the bronchoalveolar lavage obtained
from the right upper pole there were acid-fast bacilli
and Mycobacterium tuberculosis was cultivated in the
Lwenstein-Jensen agar.
The drug regimen including INH 300 mg PO, rifampicine 450 mg PO, pyrazinamide 1500 mg PO and
streptomycine 750 mg IM was initiated in April 2001.
After one week time fever was subsided. Since the liver enzymes were elevated (ALT 540 IU/L and AST
560 IU/L), all of the drugs except streptomycin were
holded and ethambutol 1500 mg PO was added to the
treatment schema. When the enzymes (ALT and
AST) were 39 IU/L and 100 IU/L respectively INH,
pyrazinamide and rifampicine were added to the drug
regimen with 5 days of intervals. There were no increments in the enzymes following the reinitiation of the
treatment. The control laboratory tests of the patient
are depicted in Table 1.
No blood or blood product was given to the patient
and the clinical symptoms were gradually improved.
Patient is discharged because of her will to continue the
treatment at home in June 2001. The sputum examina-
478
Pulmonary Tuberculosis Associated with Autoimmune Hemolytic

Anemia: An Unusual Presentation
Figure 1. Anteroposterior X-ray of the chest on admission showing bilateral reticulonodular infiltration in
upper zones.
Figure 2. HRCT of the patient on admission showing

bilateral apical reticulonodular infiltrations and cavitary lesions.
tion made at July 2001 revealed no acid-fast bacilli and
there were no M. tuberculosis in the control cultures.
The control Chest X-ray obtained in December 2001
showed no abnormalities except the bilateral apical fibrotic opacities.
DISCUSSION
A wide variety of hematological manifestations
can be observed in patients with tuberculosis, which
Turk J Haematol 2002;19(4):477-480

Table 1. Essential laboratory findings and follow-up of the patient with tuberculosis and hemolytic anemia
Parameters
On admission
Eight months later
4.6
12.2
Reticulocyte (%)
19.7
0.98
LDH (IU/L)
1902
270
4.6/1.9
0.32/0.05
88
20
37
18
31 (N above 50)
80
Hemoglobin (g/dL)
Bilirubin-total/direct (mg/dL)
AST (IU/L)
ALT (IU/L)
Haptoglobin (mg/dL)
has a chronic inflammatory nature. The commonest of

those are anemia and leukocytosis, which are reported
as 60% and 40% respectively[1]. Anemia is present in
63% of miliary tuberculosis patients[2]. Anemia of tuberculosis is usually due to nutritional deficiency, failure of iron utilization, malabsorption syndrome and
bone marrow suppression. However, autoimmune hemolytic anemia is exceedingly rare condition in tuberculosis.
Infection-associated hemolytic anemia is mostly
related to virus and mycoplasmal infections. Four hemolytic anemia cases due to tuberculosis were previously reported in the English literature[3-6]. Only two
of those cases responded to antituberculous chemotherapy alone successfully[3,4]. In the third patient, prednisolone 60 mg three weeks and splenectomy due to subcapsular hemotoma preceded antituberculosis therapy[5]. The fourth patient required prolonged steroid
therapy to prevent the recurrence of hemolysis[6].
Another complicated issue while treating the patients is hemolytic effects of antituberculosis drugs, rifampisin, streptomycin and para-aminosalicylic acid
induced hemolytic anemia reported in the literature[79]. Our patient received both rifampisin and streptomycin, but we did not observe any hemolytic adverse effect of these drugs.
evidences of immune mediated hemolytic anemia due

to tuberculosis.
In summary, pulmonary tuberculosis can cause autoimmune hemolytic anemia, although the exact mechanism of the association is not clear. Fiberoptic bronhoscopic procedure should be instituted in any suspected tuberculosis patient who do not produce sputum.
Because any delay in the diagnosis of tuberculosis in
anemic patients could be life-threatening.
REFERENCES
1.
2.
3.
4.
5.
6.
MacGregor RR. A years experience with tuberculosis in

a private urban teaching hospital in the postsanatorium
era. Am J Med 1975;58:221-8.
Glasser RM, Walker RI, Hewrion JC. The significance
of hematologic abnormalities in patients with tuberculosis. Arch Intern Med 1970;125:691-5.
Siribaddane SH, Wijesundera A. Autoimmune haemolytic anemia responding to antituberculous treatment. Trop
Doc 1997;27:243-4.
Kuo PH, Yang PC, Kuo SS, et al. Severe immune hemolytic anemia in disseminated tuberculosis with response to antituberculosis therapy. Chest 2001;119:19613.
Blance P, Rigolet A, Massault PP, et al. Autoimmune hemolytic anemia revealing miliary tuberculosis. J Infect
2000;40:292.
Cameron SJ. Tuberculosis and the blood: A special relationship? Tubercle 1974;55:55-72.
Disappearance of hematological abnormalities via

antituberculosis therapy alone is an important proof
that tuberculosis is the underlying cause of hemolytic
anemia in our patient. Recovery of hemoglobin, reticulocyte, haptoglobulin, biluribin, levels and Coombs
negativity after antituberculous therapy were all strong
Turk J Haematol 2002;19(4):477-480
479
7.
8.
9.

Ouz A, Kanra T, Gkalp A, et al. Acute hemolytic anemia caused by irregular rifampicin therapy. Turk J Pediatr 1989;31:83-8.
Letona JM, Barbolla L, Frieyro E, et al. Immune hemolytic anemia and renal failure induced by streptomycin. Br J Haematol 1977;35:561-71.
Mueller-Eckhardt C, Kretschmer V, Coburg KH. Allergic, immunohemolytic anemia due to para-aminosalicylic acid (PAS). Immunohematologic studies of three cases. Dtsch Med Wochenschr 1972;97:234-8.
Address for Correspondence:

Mehmet TURGUT, MD
Denizevler Mahallesi
Erzurum Apartman No: 349/8
TR-55200, Atakum, Samsun, TURKEY
e-mail: mturgut@omu.edu.tr
480
Turk J Haematol 2002;19(4):477-480

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Pulmonary Tuberculosis Associated

with Autoimmune Hemolytic Anemia:

* Department of Hematology, Medical School, Ondokuz Mays University,

paired iron utilization. Coombs positive hemolytic

Turgut M, Uzun O, Kelkitli E, zer O.

Pulmonary Tuberculosis Associated with Autoimmune Hemolytic

Figure 2. HRCT of the patient on admission showing

Turk J Haematol 2002;19(4):477-480

Pulmonary Tuberculosis Associated with Autoimmune Hemolytic

Turgut M, Uzun O, Kelkitli E, zer O.

Eight months later

has a chronic inflammatory nature. The commonest of

evidences of immune mediated hemolytic anemia due

MacGregor RR. A years experience with tuberculosis in

Disappearance of hematological abnormalities via

Turk J Haematol 2002;19(4):477-480

Turgut M, Uzun O, Kelkitli E, zer O.

Pulmonary Tuberculosis Associated with Autoimmune Hemolytic

Address for Correspondence:

Turk J Haematol 2002;19(4):477-480

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