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LETTER TO EDITOR
Year : 2013  |  Volume : 50  |  Issue : 4  |  Page : 301
 

Massive ascites as an presenting feature of plasma cell leukemia


1 Department of Medical Oncology, Dr. B. R.A. Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India
2 Department of Lab Oncology, Dr. B. R.A. Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication24-Dec-2013

Correspondence Address:
V Raina
Department of Medical Oncology, Dr. B. R.A. Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.123632

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How to cite this article:
Gogia A, Raina V, Gupta R. Massive ascites as an presenting feature of plasma cell leukemia. Indian J Cancer 2013;50:301

How to cite this URL:
Gogia A, Raina V, Gupta R. Massive ascites as an presenting feature of plasma cell leukemia. Indian J Cancer [serial online] 2013 [cited 2020 Oct 25];50:301. Available from: https://www.indianjcancer.com/text.asp?2013/50/4/301/123632


Sir,

Ascites is rarely seen in patients with plasma cell dyscrasias such as waldenstrom macroglobulenemia and myeloma. [1],[2] Ascites has never been reported as a presenting feature of primary plasma cell leukemia (PCL). Here, we present a 64-year-old lady with PCL with ascites.

A 64-years diabetic female presented with the history of fatigue, gradual is tension of abdomen for 2 months and fever and intermittent epistaxis is for 1 month. On examination, she had severe pallor and massive ascites. Investigations revealed hemoglobin 7.2 g/dL, white blood count 2.6 × 10 9 /L, platelet count 40 × 10 9 /L, peripheral smear showed 30% immature plasma cell, serum creatinine 1.2 mg/dL, uric acid 8.6 mg g/dL, calcium 10.2 mg/dL (8.4-10.2), total serum protein 9.4 g/dl, albumin 3.5 g/dL, bone marrow revealed 80% plasma cells including immature forms, skeletal survey normal, serum beta 2 microglobulin 11045 μg/L (670-1310), serum Mspike 2.5 g/dL: Immunoglobulin A lambda, urine Mspike: Negative, serum Immunoglobulin A 1822 mg/dL (85-450), Immunoglobulin M6.7 mg/dL (50-320), Immunoglobulin G 470 mg/dL (800-1000) and serum lactate dehydrogenase 815 IU/L (230-460). Abdominal paracentas is showed straw colored ascitic fluid with the serum/ascetic fluid albumin radient ratio of <1.1, consistent with exudative nature of fluid. Ascitic fluid showed Mspike (IgAlambda), cell count 300/mm 3 , polymorph 30, lymphocyte 60 andfewimmatureplasmacells. Gram stain, acid fast bacillus and polymerase chain reaction for tuberculosis were negative. Chest X-ray was normal and ultrasonogram of abdomen showed ascites. The final diagnosis of primary PCL was made. She was started on supportive care and anti-leukemia therapy with bortezomib scheduled day 1, 4, 8,11 and dexameth as one 40 mg for 4 days. After first cycle, patient showed symptomatic improvement. She received two more cycles of bortezomib with the dexameth as one; however, the disease progress and she died of bronchopneumonia and sepsis.

PCL is a plasma cell dyscrasia that presents either as a progression of previously diagnosed multiple myeloma (secondary PCL) or as the initial manifestation of disease (primary PCL). [3] The monoclonal protein in patients with PCL is IgG (60%), IgA (20%), Immunoglobulin D (14%) or Immunoglobulin E (6%). [4] Presenting signs and symptoms of PCL include those seen in multiple myeloma (e.g., renal dysfunction, hypercalcemia, lytic bone lesions, bone pain, and anemia) and in other leukemias (e.g., anemia, thrombocytopenia, infections, hepatomegaly and splenomegaly).

Ascites is a rare complication of PCL. There is one case of secondary PCL with as cites reported in Spanish literature. [5] The most common causes of ascitis in plasma cell dyscrasia are peritoneal in filtration by plasma cells, portal hypertension, infectious (tubercular peritonitis), congestive heart failure and nephrotic syndrome. The presence of Mspike and immature plasma cells in ascetic fluid suggest the infiltration of peritoneum by the plasma cells is the etiology of as cites in our case. This case is presented here due to its rarity.

 
  References Top

1.Morgan D, Cieplinski W. Myelomatous ascites. Am J Med Sci 1985;290:159-64.  Back to cited text no. 1
[PUBMED]    
2.Sekiguchi Y, Shirane S, Imai H, Sugimoto K, Wakabayashi M, Sawada T, et al. Response to low-dose bortezomibin plasma cell leukemia patients with malignant pleural effusion and as cites: A case report and a review of the literature. Intern Med 2012;51:1393-8.  Back to cited text no. 2
[PUBMED]    
3.Gertz MA. Managing plasma cell leukemia. Leuk Lymphoma 2007;48:5-6.  Back to cited text no. 3
[PUBMED]    
4.Pagano L, Valentini CG, DeStefano V, Venditti A, Visani G, Petrucci MT, et al. Primary plasma cell leukemia: A retrospective multicenter study of 73 patients. Ann Oncol 2011;22:1628-35.  Back to cited text no. 4
    
5.Young P, Finn BB, Pellegrini D, Bruetman JE, Shanley CM, Tolosa Vilell C, et al. Myelomatous ascites. An Med Intern 2008;25:85-9.  Back to cited text no. 5
    




 

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