Year : 2008 | Volume
: 51 | Issue : 4 | Page : 543--545
Multiple myeloma presenting with coexisting severe marrow hypoplasia
K Medhi, Dipti Kalita, Anita Chopra, Mona Anand, Vinod Raina, Rajive Kumar
Laboratory Oncology Unit, Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi 110 029, India
Laboratory Oncology, Institute Rotary Cancer Hospital, AIIMS, Ansari Nagar, New Delhi 110 029
A 68-year-old man was referred to us with clinical and bone marrow (BM) features compatible with aplastic anemia. The correct diagnosis, hypoplasia of the BM coexisting with multiple myeloma, became apparent after noting rouleaux in the peripheral blood (PB) and approximately 50% plasma cells in the touch imprint of one of the two BM biopsies done. As standard therapy was precluded, the patient was put on dexamethasone but died within 4 days. This first case of the coexistence of untreated myeloma with aplastic BM shows that even apparently straightforward hypoplasia seen on the BM biopsy should be interpreted in conjunction with the PB smear and the BM touch imprint findings. Among other things, the BM biopsy and imprint should be repeated if the PB has findings such as rouleaux that do not fit with straightforward aplastic anemia. The combination of myeloma and BM aplasia precludes standard therapy and is rapidly fatal.
|How to cite this article:|
Medhi K, Kalita D, Chopra A, Anand M, Raina V, Kumar R. Multiple myeloma presenting with coexisting severe marrow hypoplasia.Indian J Pathol Microbiol 2008;51:543-545
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Medhi K, Kalita D, Chopra A, Anand M, Raina V, Kumar R. Multiple myeloma presenting with coexisting severe marrow hypoplasia. Indian J Pathol Microbiol [serial online] 2008 [cited 2020 Apr 9 ];51:543-545
Available from: http://www.ijpmonline.org/text.asp?2008/51/4/543/43756
Multiple myeloma is one of the causes of bone marrow (BM) failure. Failure of hematopoiesis in myeloma may result from the replacement of normal hematopoietic tissue by plasma cells, it may be cytokine mediated, it may be due to fas ligand mediated apoptosis, or it may be the result of renal-failure-induced erythropoietin deficiency. ,, Bone marrow failure due to marrow hypoplasia, to the best of our knowledge, has not been described in untreated myeloma. In this article, we report the diagnostic and therapeutic issues pertaining to multiple myeloma presenting with coexisting severe marrow hypoplasia.
A 68-year-old man presented with progressive weakness and decreased appetite for 6 months and constipation for 1 month. There was no history of fever or bleeding from any site. There was no lymphadenopathy or organomegaly. In an earlier evaluation at another hospital, the patient had been diagnosed with aplastic anemia based on pancytopenia and a severely hypocellular BM ( 9 / L and his platelet count was 29 x 10 9 / L. The differential leukocyte count revealed neutrophils 30%, lymphocytes 68%, and monocytes 2%. A peripheral blood (PB) smear showed rouleaux formation and platelets were reduced. Blood chemistry revealed a random blood sugar of 134 mg/dl, uric acid of 6.1 mg/dl, total protein of 13.3g/dl, albumin of 2.1 g/dl, globulin of 11.2 g/dl, blood urea of 31 mg/dl, serum creatinine of 1.4 mg/dl, calcium of 8.7 mg/dl, phosphate of 1.4 mg/dl, sodium of 126 m Eq/L, potassium of 3.9 mEq/L, SGOT 17 U/L, SGPT 17/L, alkaline phosphatase 183 U/L, and LDH 212 U/L. The BM touch imprint was reviewed and found to be a cellular preparation of poor quality but showed increased plasma cells, approximately 50%, including several abnormal forms, compatible with multiple myeloma. Bone marrow biopsy, both the slides submitted by the referring hospital and another repeated in our hospital showed severely hypocellular marrow (cellularity , These considerations, however, did not apply to our case and the reason for the co-existence of untreated myeloma and marrow aplasia remained unclear. Such an association has, to the best of our knowledge, not been described before. Destruction of platelets due to autoimmune phenomena is known in myeloma.  It is possible that in this case the monoclonal protein had a suppressive effect on hematopoietic stem cells.
As with the diagnosis, management of our patient was difficult and needed considerations not relevant to most other patients of myeloma. There were problems with both the short- and long-term treatment plans owing to severe hypoplasia of the marrow. Use of alkylating agents in the first phase of treatment and high-dose chemotherapy with bone marrow autologous stem cell transplantation in the second were both precluded. Even the starting therapy with the standard simultaneous administration of thalidomide and dexamethasone had to be modified to begin with only dexamethasone with a plan to add thalidomide when the general condition improved. Unfortunately, since the patient died within 4 days of the start of treatment, response to therapy in such an uncommon setting could not be studied.
Our case shows that even an apparently straightforward hypoplastic BM should preferably be interpreted in conjunction with peripheral blood and touch imprint findings. Presence of unexplained features such as rouleaux on the peripheral blood smear should prompt a repeat BM biopsy and investigation for an underlying co-existing complicating factor. Also, the combination of BM aplasia and myeloma precludes standard therapy and would invariably be rapidly fatal.
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