Letters to Editor
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.
Institute of Medical Sciences, New Delhi, India Correspondence to: Dr. Vinod Raina, E‑mail: [email protected]
References 1. 2.
3. 4. 5.
Morgan D, Cieplinski W. Myelomatous ascites. Am J Med Sci 1985;290:159‑64. 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. Gertz MA. Managing plasma cell leukemia. Leuk Lymphoma 2007;48:5‑6. 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. Young P, Finn BB, Pellegrini D, Bruetman JE, Shanley CM, Tolosa Vilell C, et al. Myelomatous ascites. An Med Intern 2008;25:85‑9. Access this article online Quick Response Code:
DOI: 10.4103/0019-509X.123632
Gogia A, Raina V, Gupta R
1
PMID: *******
Departments of Medical Oncology, and 1Lab Oncology, Dr. B. R.A. Institute Rotary Cancer Hospital, All India
Cryptococcal meningitis in chronic lymphocytic leukemia
Website: www.indianjcancer.com
disease is in complete remission. We present a case of cryptococcal meningitis in a HIV negative patient with CLL.
Sir, Cryptococcal meningitis is caused by the encapsulated yeast Cryptococcus neoformans and often fatal without antifungal treatment. The most affected patients have a state of immunosuppression such as human immunodeficiency virus (HIV) infection, organ transplantation and glucocorticoid therapy. Chronic lymphocytic leukemia (CLL) patients are rarely associated with cryptococcal meningitis, especially when
In September 2004, a 45‑years‑old male referred to our hospital due to his asymptomatic lymphocytosis detected during the routine annual blood examination. Clinical examination was unremarkable. His hemogram showed hemoglobin‑12.5 g/dL, total leucocyte count ‑ 90 × 109/L and platelet counts ‑ 180 × 109/L. Peripheral blood smear examination showed 90% lymphoid cell, which were positive for CD5, CD23, and CD19. CD20, CD23, CD45 and negative for mouse monoclonal antibody (FMC 7) 7 and CD 3 on flow cytomery. Renal and liver functions were within the normal limit. Diagnosis of CLL Rai stage 0 was
Table 1: Base line feature and outcome in patients with CLL and cryptococcal meningitis Reference
Age Sex Symptoms
Previous treatment for CLL Antifungal treatment Outcome
Reisfeld‑Zadok et al.[2]
78
F
Altered behavior
Cyclophosphamide and prednisolone Fever and headache Leukeran
Reisfeld‑Zadok et al.[2]
82
M
Dizdar et al.[3]
54
M
Fever and headache Prednisolone for hemolytic anemia
Present case
45
M
Headache
Leukeran and prednisone
Amphotericin B and fluconazole Amphotericin B and fluconazole Amphotericin B
Patient responded
Patient died
Amphotericin B
Patient died
Patient responded
CLL=Chronic lymphocytic leukemia
372
Indian Journal of Cancer | October–December 2013 | Volume 50 | Issue 4
Letters to Editor
made and patient was kept under observation. After 5 years of follow‑up, he developed fatigue, generalized lymphadenopathy and hepatosplenomegaly. Further staging work‑up consisted with CLL Rai stage II. Blood sugar was normal and serology for HIV was negative. He was started on Leukeran (30 mg/m 2 divided in 4 days) and prednisolone (60 mg/m2 for 4 days), every month for eight cycle. Post eight cycle disease was in complete remission. After 4 months of his treatment, he presented with 15 days history of diffuse headache without any localizing sign. No abnormality detected in contrast enhanced computer tomogram of brain. Cerebrospinal fluid (CSF) examination showed low glucose level (12 mg/dL, corresponding blood sugar 107 mg/dL), high protein level (140 mg/dL) and total 100 cells/ml3 (90% lymphocyte). Gram stain and acid fast bacilli were negative. CSF smear showed Cryotococci using India ink preparation. CSF culture was positive for the same organism and blood cultures were sterile. He died of status epileptics after 3 days of antifungal (amphotericin B 1.5 mg/kg) treatment. CLL is associated with impaired humoral and cellular immunity, which results in susceptibility to infections. The main immune defect is humoral and carries an increased risk of bacterial infection Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae and impair cellular immunity due to decreased T helper activity, increased T suppressor activity, reversal of CD4/CD8 ratio and defects in natural killer cells and in complement function. [1] There are few case have been reported recently in CLL with cryptococcal meningitis [Table 1]. [2,3] The largest series consists of 41 patients with different malignancies who were diagnosed with cryptococcosis; five of them had CLL, who have been treated with high dose steroids.[4] The diagnosis of cryptococcal meningitis is based on CSF findings that are characterized by high opening pressure, low glucose and high protein levels, lymphocytosis,
positive India ink stain and growth in culture provides a definite diagnosis.[5] Imaging of the brain often normal as in our patient. Unfortunately, we could not document opening pressure during the lumbar puncture. Unlike many other publications of CLL and cryptococcal infection, our patient had no history of previous immunosuppressive treatment and the patient was in remission for CLL. Cryptococcal meningitis should be suspected in any CLL patient with headache and a lumbar puncture should be performed. Gogia A, Mehta P, Raina V Department of Medical Oncology, Dr. B. R. A. Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India Correspondence to: Dr. Vinod Raina, E‑mail: [email protected]
References 1. 2. 3. 4. 5.
Tsiodras S, Samonis G, Keating MJ, Kontoyiannis DP. Infection and immunity in chronic lymphocytic leukemia. Mayo Clin Proc 2000;75:1039‑54. Reisfeld‑Zadok S, Elis A, Szyper‑Kravitz M, Chowers M, Lishner M. Cryptococcal meningitis in chronic lymphocytic leukemia patients. Isr Med Assoc J 2009;11:437‑9. Dizdar OS, Karakeçili F, Coşkun BN, Ener B, Ali R, Mıstık R. Fatal cryptococcal meningitis in a patient with chronic lymphocytic leukemia. Mediterr J Hematol Infect Dis 2012;4:12 Kaplan MH, Rosen PP, Armstrong D. Cryptococcosis in a cancer hospital: Clinical and pathological correlates in forty‑six patients. Cancer 1977;39:2265‑74. Diamond RD, Bennett JE. Prognostic factors in cryptococcal meningitis. A study in 111 cases. Ann Intern Med 1974;80:176‑81. Access this article online Quick Response Code:
Website: www.indianjcancer.com DOI: 10.4103/0019-509X.123633 PMID: *******
Enlarging nonossifying fibroma mimicking aggressive bone tumour Sir, Nonossifying fibroma (NOF) (syn‑Nonosteogenic fibroma, fibroxanthoma, xanthogranuloma of bone) is one of the most common types of benign cortical defects that arise in the metaphysis of long bones, particularly the distal femur and tibia. On plain radiographs, NOFs are identified by a sclerotic Indian Journal of Cancer | October–December 2013 | Volume 50 | Issue 4
a
b
Figure 1(a and b): Initial radiographs of the left knee (AP View) taken six months apart in 2008 show a new well defined lytic lesion with a narrow zone of transition in the metaphyseal region of the proximal tibia. It measures 1 cm. The lesion shows typical features of a nonossifying fibroma
373
Copyright of Indian Journal of Cancer is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
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.
Institute of Medical Sciences, New Delhi, India Correspondence to: Dr. Vinod Raina, E‑mail: [email protected]
References 1. 2.
3. 4. 5.
Morgan D, Cieplinski W. Myelomatous ascites. Am J Med Sci 1985;290:159‑64. 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. Gertz MA. Managing plasma cell leukemia. Leuk Lymphoma 2007;48:5‑6. 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. Young P, Finn BB, Pellegrini D, Bruetman JE, Shanley CM, Tolosa Vilell C, et al. Myelomatous ascites. An Med Intern 2008;25:85‑9. Access this article online Quick Response Code:
DOI: 10.4103/0019-509X.123632
Gogia A, Raina V, Gupta R
1
PMID: *******
Departments of Medical Oncology, and 1Lab Oncology, Dr. B. R.A. Institute Rotary Cancer Hospital, All India
Cryptococcal meningitis in chronic lymphocytic leukemia
Website: www.indianjcancer.com
disease is in complete remission. We present a case of cryptococcal meningitis in a HIV negative patient with CLL.
Sir, Cryptococcal meningitis is caused by the encapsulated yeast Cryptococcus neoformans and often fatal without antifungal treatment. The most affected patients have a state of immunosuppression such as human immunodeficiency virus (HIV) infection, organ transplantation and glucocorticoid therapy. Chronic lymphocytic leukemia (CLL) patients are rarely associated with cryptococcal meningitis, especially when
In September 2004, a 45‑years‑old male referred to our hospital due to his asymptomatic lymphocytosis detected during the routine annual blood examination. Clinical examination was unremarkable. His hemogram showed hemoglobin‑12.5 g/dL, total leucocyte count ‑ 90 × 109/L and platelet counts ‑ 180 × 109/L. Peripheral blood smear examination showed 90% lymphoid cell, which were positive for CD5, CD23, and CD19. CD20, CD23, CD45 and negative for mouse monoclonal antibody (FMC 7) 7 and CD 3 on flow cytomery. Renal and liver functions were within the normal limit. Diagnosis of CLL Rai stage 0 was
Table 1: Base line feature and outcome in patients with CLL and cryptococcal meningitis Reference
Age Sex Symptoms
Previous treatment for CLL Antifungal treatment Outcome
Reisfeld‑Zadok et al.[2]
78
F
Altered behavior
Cyclophosphamide and prednisolone Fever and headache Leukeran
Reisfeld‑Zadok et al.[2]
82
M
Dizdar et al.[3]
54
M
Fever and headache Prednisolone for hemolytic anemia
Present case
45
M
Headache
Leukeran and prednisone
Amphotericin B and fluconazole Amphotericin B and fluconazole Amphotericin B
Patient responded
Patient died
Amphotericin B
Patient died
Patient responded
CLL=Chronic lymphocytic leukemia
372
Indian Journal of Cancer | October–December 2013 | Volume 50 | Issue 4
Letters to Editor
made and patient was kept under observation. After 5 years of follow‑up, he developed fatigue, generalized lymphadenopathy and hepatosplenomegaly. Further staging work‑up consisted with CLL Rai stage II. Blood sugar was normal and serology for HIV was negative. He was started on Leukeran (30 mg/m 2 divided in 4 days) and prednisolone (60 mg/m2 for 4 days), every month for eight cycle. Post eight cycle disease was in complete remission. After 4 months of his treatment, he presented with 15 days history of diffuse headache without any localizing sign. No abnormality detected in contrast enhanced computer tomogram of brain. Cerebrospinal fluid (CSF) examination showed low glucose level (12 mg/dL, corresponding blood sugar 107 mg/dL), high protein level (140 mg/dL) and total 100 cells/ml3 (90% lymphocyte). Gram stain and acid fast bacilli were negative. CSF smear showed Cryotococci using India ink preparation. CSF culture was positive for the same organism and blood cultures were sterile. He died of status epileptics after 3 days of antifungal (amphotericin B 1.5 mg/kg) treatment. CLL is associated with impaired humoral and cellular immunity, which results in susceptibility to infections. The main immune defect is humoral and carries an increased risk of bacterial infection Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae and impair cellular immunity due to decreased T helper activity, increased T suppressor activity, reversal of CD4/CD8 ratio and defects in natural killer cells and in complement function. [1] There are few case have been reported recently in CLL with cryptococcal meningitis [Table 1]. [2,3] The largest series consists of 41 patients with different malignancies who were diagnosed with cryptococcosis; five of them had CLL, who have been treated with high dose steroids.[4] The diagnosis of cryptococcal meningitis is based on CSF findings that are characterized by high opening pressure, low glucose and high protein levels, lymphocytosis,
positive India ink stain and growth in culture provides a definite diagnosis.[5] Imaging of the brain often normal as in our patient. Unfortunately, we could not document opening pressure during the lumbar puncture. Unlike many other publications of CLL and cryptococcal infection, our patient had no history of previous immunosuppressive treatment and the patient was in remission for CLL. Cryptococcal meningitis should be suspected in any CLL patient with headache and a lumbar puncture should be performed. Gogia A, Mehta P, Raina V Department of Medical Oncology, Dr. B. R. A. Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India Correspondence to: Dr. Vinod Raina, E‑mail: [email protected]
References 1. 2. 3. 4. 5.
Tsiodras S, Samonis G, Keating MJ, Kontoyiannis DP. Infection and immunity in chronic lymphocytic leukemia. Mayo Clin Proc 2000;75:1039‑54. Reisfeld‑Zadok S, Elis A, Szyper‑Kravitz M, Chowers M, Lishner M. Cryptococcal meningitis in chronic lymphocytic leukemia patients. Isr Med Assoc J 2009;11:437‑9. Dizdar OS, Karakeçili F, Coşkun BN, Ener B, Ali R, Mıstık R. Fatal cryptococcal meningitis in a patient with chronic lymphocytic leukemia. Mediterr J Hematol Infect Dis 2012;4:12 Kaplan MH, Rosen PP, Armstrong D. Cryptococcosis in a cancer hospital: Clinical and pathological correlates in forty‑six patients. Cancer 1977;39:2265‑74. Diamond RD, Bennett JE. Prognostic factors in cryptococcal meningitis. A study in 111 cases. Ann Intern Med 1974;80:176‑81. Access this article online Quick Response Code:
Website: www.indianjcancer.com DOI: 10.4103/0019-509X.123633 PMID: *******
Enlarging nonossifying fibroma mimicking aggressive bone tumour Sir, Nonossifying fibroma (NOF) (syn‑Nonosteogenic fibroma, fibroxanthoma, xanthogranuloma of bone) is one of the most common types of benign cortical defects that arise in the metaphysis of long bones, particularly the distal femur and tibia. On plain radiographs, NOFs are identified by a sclerotic Indian Journal of Cancer | October–December 2013 | Volume 50 | Issue 4
a
b
Figure 1(a and b): Initial radiographs of the left knee (AP View) taken six months apart in 2008 show a new well defined lytic lesion with a narrow zone of transition in the metaphyseal region of the proximal tibia. It measures 1 cm. The lesion shows typical features of a nonossifying fibroma
373
Copyright of Indian Journal of Cancer is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
