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INTRODUCTION: Bone marrow examination (BME) is performed in Human Immunodeficiency Virus-infected (HIV+) children with haematologic abnormalities to exclude specific disease (SD). AIMS: To describe the: (1) indications for BME , (2) utility of BME to diagnose SD, (3) patient characteristics associated with SD or non-specific disease (NSD). METHODS: Design: Retrospective review. Definitions: SD: BME positive for opportunistic infection (OI) or HIV-related malignancy. NSD: HIV-related changes only. RESULTS: Eighty six BME’s were done. Suspected SD in 56/86(65.1%) was the most common clinical indication. Bicytopaenia(n=32) and isolated cytopaenia(n=31) were the most common haematologic indications. NSD 48/86 (55.8%) was a more common finding than SD 32/86 (37.2%). Granulomas, pure red cell aplasia and malignancy were the SD identified. Pre- highly active antiretroviral therapy (HAART), advanced stage, and not being virally suppressed were significantly associated with NSD. CONCLUSION: The yield of SD (37.2%) on BME is comparable to adult studies. HAART should be instituted before BME as NSD will be the most likely finding.

The case is presented of a female patient with history of anaemia (haemoglobin 9 g/dL) of 4 years onset, who was referred to the Internal Medicine department complaining of fatigue, dyspnoea, and syncope. She also had a burning pain in the costal region radiating to dorsal and lumbar spine, and lower limbs, which persisted for more than 6 months. The laboratory results reported a haemoglobin value of 8.4 g / dL. There were also high levels of immunoglobulin A (2087). The serum protein electrophoresis revealed the presence of a monoclonal peak, with immunofixation showing the presence of Kappa type IgA. The histopathological examination of the bone marrow biopsy showed the presence of osteosclerosis and few plasma cells. Multiple myeloma was confirmed by CD 138 immunohistochemical staining. A review is presented on multiple myeloma, its clinical presentation, and differential diagnosis. / Revisión por pares

Plasma cells, the effector stage of the B cell compartment, secrete large amounts of antibody. These cells arise in two waves during T-­‐dependent immune responses; an early wave (extrafollicular plasma cells) generate low-­‐affinity antibodies that provide a first line of defence against invading pathogens. Later, plasma cells emerge from the germinal centre reaction and secrete high-­‐affinity antibodies. These plasma cells have the capacity to migrate to the bone marrow, where they become established as long-­‐lived, non-­‐dividing plasma cells. Here, I show that plasma cells found in the bone marrow of young (5-­‐week-­‐old) mice had a turnover comparable to that seen in the spleen. Long-­‐lived plasma cells accumulated over the ensuing weeks until they came to dominate the bone marrow plasma cell compartment by 30-­‐weeks of age. This accumulation required MHC II, CD40 and a normal B cell receptor repertoire, implying that these cells are generated during T-­‐dependent immune responses. Secondly, I determine the signalling pathways required to generate splenic extrafollicular plasma cell responses in the T-­‐dependent response to sheep red blood cells (SRBC) and in bacterial infection with Salmonella. While T cell help, antigen recognition through the B cell receptor (BCR) and TLR signalling were required for maximal plasma cell responses to SRBC, in Salmonella infection TLR signalling was required for day 4 IgM plasma cell responses, whereas class-­‐ switched responses at day 8 required T cell help. The extrafollicular responses generated in Salmonella persisted for around 35 days, far greater than the 2-­‐3 days seen following SRBC immunisation. This was likely due to both antigen persistence causing the generation of new plasma cells, and the induction of cellular populations that produced the plasma cell survival factor APRIL. Thirdly, I document the failure of chronic immune responses to generate long-­‐ lived bone marrow plasma cells. This was accomplished by measuring the generation and survival of bone marrow plasma cells in models of rheumatoid arthritis (K/BxN mice), long-­‐term infection with Salmonella, and a direct comparison between acute and chronic delivery of the T-­‐dependent protein antigen NP-­‐KLH. In all cases, chronic immune responses generated few bone marrow plasma cells, ostensibly due to a failure to migrate to the organ. Finally, I show the depletion of bone marrow plasma cell populations caused by inflammatory episodes. This was observed in Salmonella infection, Schistosoma mansoni infection and immunisation with protein antigen plus adjuvants. This depletion mediated a reduction of antigen-­‐specific bone marrow plasma cell populations and serum antibody previously established by the secondary response to NP-­‐KLH.