Tubercular lymphadenitis and abdominal tuberculosis with autoimmune hemolytic anemia and severe intravascular hemolysis


Tuberculosis, a common disease in the developing world and a resurging problem in the developed world, is associated with numerous hematological manifestations. The most common manifestation is normochromic normocytic anemia of chronic disease. Hemolytic anemia is rare, and there are only a few previously reported cases. We report a case of autoimmune hemolytic anemia with severe intravascular hemolysis in a case of abdominal tuberculosis. To our knowledge, this is one of the few cases reported in the literature.

Keywords: Autoimmune hemolytic anemia, severe intravascular hemolysis, tuberculosis

How to cite this article:
Somalwar AM, Aher AA, Zanwar VG, Kolpakwar KS. Tubercular lymphadenitis and abdominal tuberculosis with autoimmune hemolytic anemia and severe intravascular hemolysis. Ann Trop Med Public Health 2013;6:123-4


How to cite this URL:
Somalwar AM, Aher AA, Zanwar VG, Kolpakwar KS. Tubercular lymphadenitis and abdominal tuberculosis with autoimmune hemolytic anemia and severe intravascular hemolysis. Ann Trop Med Public Health [serial online] 2013 [cited 2017 Nov 14];6:123-4. Available from:


Case Report

Twenty-two-year-old male patient presented with history of high-grade fever, generalized weakness, and easy fatigability since 15 days. There was history of pain and distension of abdomen since 7 days. There was no previous history of anemia, jaundice, or blood transfusions. On examination, he was febrile (101F), pulse 120/min, BP 120/80 mmHg, had pallor, mild jaundice, and palpable nontender left cervical lymph node of size 3×2 cm. He had ascites with diffuse abdominal tenderness and sluggish bowel sounds. Other systemic examination was unremarkable.

His laboratory investigations were as follows: hemoglobin – 35 g/L; total leukocyte count – 13.2×10 9 /L; platelet count – 180×10 9 /mm 3 ; MCV – 96 fl; MCH – 30 pg/cell; and MCHC – 300 g/L. Peripheral smear showe 2 anisopoikilocytosis, few target cells, and nucleated RBCs. Bone marrow was hyper cellular and showed erythroid hyperplasia. Reticulocyte count was 0.06 red cells, glucose-6-phosphate dehydrogenase activity was normal, hemoglobin electrophoresis was normal, serum LDH was 826 U/L, haptoglobin was 1 μmol/L, urine for hemoglobin was positive, and direct and indirect Coombs tests were positive. Total bilirubin was 64.98 μmol/L (indirect 51.3 μmol/L) with normal enzyme levels. Renal functions and blood sugar were normal. FNAC from cervical lymph node was suggestive of tubercular lymphadenitis. Chest X-ray was normal, CT abdomen showed moderate ascites, retroperitoneal and central mesenteric lymph nodes, and mild edematous thickened intestinal walls, which were suggestive of abdominal tuberculosis. Ascitic fluid was straw in color, with cobweb formation, protein 53.9 g/L, sugars 6.72 μmol/L, lymphocyte (100%) 1.2 × 10 9 /L, and adenosine deaminase level 97 U/L. Ascitic fluid polymerase chain reaction was positive for tuberculosis. Cytology for malignant cells was negative. ESR was 42 mm/hour, and Mantoux test was strongly positive. ANA, HIV-ELISA, and blood culture were negative.

Based on the clinical features and investigations, patient was diagnosed to have tubercular lymphadenitis and abdominal tuberculosis with autoimmune hemolytic anemia with severe intravascular hemolysis. He was started on four drugs (rifampin, 450 mg; isoniazid, 300 mg; ethambutol, 800 mg; and pyrazinamide, 1 g) daily, steroids, and received 5 units of blood transfusion for antitubercular treatment. In spite of the treatment, he continued to have severe intravascular hemolysis and hemoglobin levels did not improve. He finally died 18 days after admission.


A wide variety of hematological manifestations can be observed in patients with tuberculosis. The commonest are anemia and leukocytosis. [1] However, autoimmune hemolytic anemia is exceedingly a rare condition in tuberculosis. [1],[2]

Infection-associated hemolytic anemia is mostly related to virus and mycoplasmal infections. In humans, tubercle bacilli may occasionally provoke a marked proliferation of reticuloendothelial tissues, resulting in varied and severe hematological disorders through immune mechanisms. However, immune hemolytic anemia resulting in a hemoglobin level as low as 5 g/dl, as occurred in this case, is exceedingly rare.

Autoimmune hemolytic anemia is most often of a primary nature, but it can also be secondary. A secondary cause can be considered when autoimmune hemolytic anemia and the underlying disease occur together with greater frequency than can be accounted for by chance alone; or when it reverses simultaneously with the correction of the associated disease; or when AIHA and the associated disease are related by the evidence of immunological aberration. Our case falls under the second category.

A detailed search revealed only seven cases of AIHA in tuberculosis in the English literature; three of them responded to antituberculosis treatment alone without need for blood transfusion or steroids. [3],[4] Steroids are useful in addition to antitubercular therapy if there is severe hemolysis. However, as our patient had severe intravascular hemolysis, which was evident by low haptoglobin levels, hemoglobinuria, in spite of receiving multiple blood transfusions, AKT, and steroids, patient did not respond and expired.

In view of the known autoimmune associations of tuberculosis such as vasculitis, arteritis, and immune thrombocytopenia, and based on the available reports of autoimmune hemolytic anemia in tuberculosis, it is reasonable to suspect and rule out tuberculosis as a possible association in patients with autoimmune hemolytic anemia in patients in areas of high endemicity of tuberculosis. This is especially important, as autoimmune hemolytic anemia may require long-term steroid therapy that can aggravate tuberculosis. Physicians should immediately start antitubercular therapy once the diagnosis is made. Caution should also be exercised when selecting rifampin or para-aminosalicylic acid for these patients, as both drugs are known to induce hemolytic anemia. [5]



1. Siribaddana SH, Wijesundera A. Autoimmune haemolyticanaemia responding to anti-tuberculous treatment. Trop Doct 1997;27:243-4.
2. Kuo PH, Yang PC, Kuo SS, Luh KT. Severe immune hemolytic anemia in disseminated tuberculosis with response to antituberculosis therapy. Chest 2001;119:1961-3.
3. Turgut M, Usun O, Kelkytly E, Ozer O. Pulmonary tuberculosis associated with autoimmune hemolytic anemia: An unusual presentation. Turk J Haematol 2002;19:477-80.
4. Nandennavar M, Cyriac S, Krishnakumar, Sagar T. Immune hemolytic anemia in a patient with tuberculous lymphadenitis. J Glob Infect Dis 2011;3:89-91.
5. Bakhshi S, Rao IS, Jain V, Arya LS. Autoimmune hemolytic anemia complicating disseminated childhood tuberculosis. Indian J Pediatr 2004;71:549-51.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.115182

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