A 45 year old male patient presented to me with hepatosplenomegaly, thrombocytopenia, neutropenia and microcytosis. He has recurrent lung abscees. He was treated as pulmonary tuberculosis initially 3 years back and HIV also was ruled out. His bone marrow examination is normal. Again he was started on anti TB drugs recently for lung abscess considering a relapse of TB. We have stopped ATT as he developed alteration in liver profile.Tuberculosis and anti TB drugs also can cause bicytopenia. But microcytosis cannot be explained.Is it an immunodeficiciency syndrome?
An hypersplenism might explain the pancytopenia while the microcytosis need to check inflammation, hyposideremia and beta thalassemia
Anaemia of Chronic Disease usually starts off as normocytic normochromic, but it may eventually become microcytic and hypochromic. You obviously have to exclude haemoglobinopathies and absent iron stores.
Does he have any evident risk factors for HIV and was his test a recent one? If so his HIV test (Ab/Ag) needs to be repeated using a reliable kit. As you know some immunodeficiency states may delay window period.TB itself may result in microcytic anemia.
When we do a bone marrow aspiration in anemic patients, it's a good practice to performe a Perls stain. This allow to evaluate easily the iron stores situation (iron in reticular tissue): increased = Anaemia of Chronic Disease; decreased= iron deficency. Iron stores in bone marrow has a good correlation with plasma ferritin
Pancytopenia could be secondary due to hypersplenism, otherwise surely have to rule out infectious causes including HIV.
In addition to those provided by dr Thirunavukarasu, to study a case of anaemia we need more information: number of RBC and reticulocytes as well as the other Wintrobe's; parameters (Haemoglobin content and concentration in the RBC); a microscopic review of PB smears. These results should be used to address subsequent investigations in accordance with a first step decision making: (i) regenerative anaemia vs. non-regenerative; (ii) microcytic vs macrocytic vs normocytic; (iii) normochromic vs hypochromic. Without this logical path in which every diagnostic outcome leads the successive stages, we play the target shooting or the treasure hunt as evidenced by the different diagnostic hypotheses so far formulated that are the easiest way to waste time and resources. Can Dr Thirunavukarasu give us all the available parameters?