Indian Journal of Pathology and Microbiology

: 2018  |  Volume : 61  |  Issue : 3  |  Page : 434--436

Coexisting prostate adenocarcinoma with multiple myeloma: A rare case report

Yelda Vyas1, Akanksha Salkar2, A Kalpana Bothale3,  
1 Consultant Pathologist, Dr. Lal Path Labs, Nagpur, Maharashtra, India
2 Consultant Pathologist, Care Hospital, Hyderabad, Telangana, India
3 Associate professor, Department of Pathology, NKP Salve Institute of Medical Sciences and Research Center, Nagpur, Maharashtra, India

Correspondence Address:
Yelda Vyas
Vyas Hospital, Opposite Police Station Sakkardara, Nagpur - 440 009, Maharashtra


We report a rare case of an 83-year-old male with synchronous occurrence of prostate adenocarcinoma and multiple myeloma. He presented with lower back pain and incontinence of urine for the past 6 months. Routine hematological and biochemical investigations were performed which pointed toward prostate adenocarcinoma. Transrectal ultrasonography and magnetic resonance imaging showed prostatomegaly along with osteolytic lesions in the skull and vertebrae. Prostate biopsy was performed and adenocarcinoma was confirmed. To rule out metastatic deposits in the bone and to rule out bone marrow infiltration, bone marrow aspiration and biopsy of the patient was done, and unexpectedly, it showed multiple myeloma. The association between these two disorders is poorly understood, but some studies show that bone marrow microenvironment plays an important role.

How to cite this article:
Vyas Y, Salkar A, Bothale A K. Coexisting prostate adenocarcinoma with multiple myeloma: A rare case report.Indian J Pathol Microbiol 2018;61:434-436

How to cite this URL:
Vyas Y, Salkar A, Bothale A K. Coexisting prostate adenocarcinoma with multiple myeloma: A rare case report. Indian J Pathol Microbiol [serial online] 2018 [cited 2021 Jul 25 ];61:434-436
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Full Text


Simultaneous occurrence of multiple myeloma and prostate adenocarcinoma is rare, with only a few cases reported in the literature.[1],[2],[3],[4] The association between both of these disorders is poorly understood, but it has been suggested by some of the studies that bone marrow microenvironment plays a crucial role in it.[5] Bone marrow microenvironment is composed of a cellular compartment and a noncellular compartment including the extracellular matrix, cytokines, growth factors, and chemokines.[6] Essential growth factors for myeloma cells such as interleukin 6 (IL-6) and insulin-like growth factor 1 (IGF-1) are responsible for prostate carcinoma. Both these factors suppress apoptosis.[7] Chemoattractants such as stromal-derived factor 1 (SDF-1) and vascular endothelial growth factor (VEGF) are released by the circulating myeloma cells leading to progression of prostate cancer.[5] Here, we report a rare case of simultaneous occurrence of multiple myeloma and prostate adenocarcinoma. This is the second case reported from India to the best of our knowledge since 2013.

 Case Report

An 83-year-old male presented with the complaints of lower back pain along with incontinence of urine. The patient was advised routine hematological investigations, transrectal ultrasonography, and magnetic resonance imaging (MRI). A complete hemogram showed hemoglobin of 8.6 g%, total leukocyte count of 11,200/mm 3, and platelet count of 73 × 109/l. Peripheral smear examination showed normocytic normochromic anemia with thrombocytopenia and erythrocyte sedimentation rate (ESR) was normal. Urine examination was normal. Blood chemistry showed alkaline phosphatase = 446 IU/l (35–105), LDH = 637 IU/l (225–450), and prostate-specific antigen (PSA) =140 ng/l. Liver function test and kidney function test were all within normal limits. Transrectal ultrasound was performed, in view of high prostate-specific antigen, which revealed a hypoechoic prostatic mass with irregular margins. Ultrasound-guided biopsy was performed, which on histopathology showed adenocarcinoma prostate with Gleason score of 4 + 4 [Figure 1]a and b]. MRI was done to rule out metastases in the bones as the patient complained of back pain. MRI revealed osteolytic lesions in the skull and vertebrae [Figure 2]a and [Figure 2]b along with the growth in the prostate.{Figure 1}{Figure 2}

Bone marrow aspiration and biopsy were done to rule out metastatic deposits in the patient and to know the cause of thrombocytopenia. It showed 65% plasma cells arranged in sheets and clusters with no evidence of secondary deposits of malignant epithelial cells and normal megakaryopoiesis [Figure 3]a. Trephine biopsy was performed to confirm the diagnosis, and it also showed sheets of plasma cells almost replacing all the normal myeloid and erythroid series cells [Figure 3]b. The clonality of plasma cells was demonstrated by performing Immunohistochemistry (IHC), and they were positive for CD 138. Immunoelectrophoresis of the patient was performed, which demonstrated IgG lambda monoclonal gammopathy with M-band positive. On immunofixation, free light chains kappa and lambda were positive with very high values. Hence, the final diagnosis of free light chain multiple myeloma with prostate adenocarcinoma was given.{Figure 3}


We reported a rare case of synchronous occurrence of prostate adenocarcinoma and multiple myeloma in an 83-year-old male patient. The incidence of simultaneous occurrence of prostate adenocarcinoma and hematolymphoid malignancy has been reported as 1.2%.[8] The updated criteria for the diagnosis of myeloma requires at least one of the following markers regardless of the presence or absence of symptoms of CRAB.[9]

60% or greater clonal plasma cells on bone marrow examinationSerum involved/uninvolved free light chain ratio of 100 or greater, provided the absolute level of the involved free light chain is at least 100 mg/L (a patient's “involved” free light chain – either kappa or lambda – is the one that is above the normal reference range; the uninvolved light chain is the one that typically is in, or below, the normal range)More than one focal lesion on MRI that is at least 5 mm or greater in size.

In our case, the findings in favor of multiple myeloma were – 60% or greater clonal plasma cells on bone marrow examination and the presence of >5-mm focal lesion in the skull and vertebrae. Immunofixation showed the presence of M band for kappa and lambda.

Liver function tests and kidney function tests of the patient were within normal limits. Sehgal et al. reported a similar case, in which bone marrow examination revealed infiltration by malignant epithelial cells, which were arranged in a glandular fashion along with 12% plasma cells on aspirate smear.[7] While in our study, there were 65% plasma cells arranged in clusters and sheets with no evidence of metastatic tumour deposits in bone marrow. Liver and kidney function tests were within normal limits in their study also.

Prostate adenocarcinoma and multiple myeloma occurred independently or whether one disease influenced the development of the other is still not known. Kao et al. suggested that immunosuppression from multiple myeloma and chemokines, including IGF-1, IL-6, SDF-1, and vascular endothelial growth factor (VEGF) are released by circulating myeloma cells leading to the progression of prostate cancer.[5] Data suggests that myeloma cells may stimulate the production of IL-6 from stromal and bone cells. IL-6 is an essential activating growth factor and antiapoptotic agent for myeloma cells, and it also plays a key role in signaling through the MAPK pathway in prostate cancer cells.[5] Both IL-6 and IGF-1 increase proliferation by activating the RAS-MAPK signal transduction pathway and suppressing apoptosis. VEGF, which is secreted by some myeloma cells lines, is an important mediator of angiogenesis. VEGF overexpression is present in the majority of prostate cancer patients, and it correlates with poor survival.[7] Kao et al. also stated that 45%–90% of advanced myeloma cells have c-myc dysregulation.[5] C-myc mutation correlates with a higher grade of malignancy along with worse prognosis in prostate cancer patients. Kyle and Lust also reported that repeated antigenic stimulation of the reticuloendothelial, genetic susceptibility for development of plasma cell dyscrasias in patients with positive family history, Epstein–Barr virus infection, lymphoid growth factors, and lack of suppression of B-cells by T-cells play a role in the development of gammopathy.[10]

In summary, we report this case because of its rarity, although further genetic studies are required to know the association between these two diseases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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