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made and patient was kept under observation. After

5years of followup, he developed fatigue, generalized
lymphadenopathy and hepatosplenomegaly. Further
staging workup consisted with CLL Rai stage II. Blood
sugar was normal and serology for HIV was negative.
He was started on Leukeran(30mg/m 2 divided in
4days) and prednisolone(60mg/m2 for 4days), every
month for eight cycle. Post eight cycle disease was in
complete remission. After 4months of his treatment,
he presented with 15days 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(12mg/dL, corresponding blood sugar
107mg/dL), high protein level(140mg/dL) and
total 100cells/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 3days of
antifungal(amphotericin B 1.5mg/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[Table1]. [2,3] The largest series consists
of 41patients 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,
NewDelhi, India
Correspondence to:
Dr.Vinod Raina, Email:vinodraina@hotmail.com

References
1.
2.
3.
4.
5.

TsiodrasS, SamonisG, KeatingMJ, KontoyiannisDP. Infection

and immunity in chronic lymphocytic leukemia. Mayo Clin Proc
2000;75:103954.
ReisfeldZadokS, ElisA, SzyperKravitzM, ChowersM, LishnerM.
Cryptococcal meningitis in chronic lymphocytic leukemia patients.
Isr Med Assoc J 2009;11:4379.
DizdarOS, Karakeili F, Cokun BN, EnerB, AliR, Mstk R. Fatal
cryptococcal meningitis in a patient with chronic lymphocytic
leukemia. Mediterr J Hematol Infect Dis 2012;4:12
KaplanMH, RosenPP, ArmstrongD. Cryptococcosis in a cancer
hospital: Clinical and pathological correlates in fortysix patients.
Cancer 1977;39:226574.
DiamondRD, BennettJE. Prognostic factors in cryptococcal
meningitis. Astudy in 111cases. Ann Intern Med 1974;80:17681.
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Enlarging nonossifying
fibroma mimicking
aggressive bone tumour
Sir,
Nonossifying fibroma(NOF)(synNonosteogenic
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 | OctoberDecember 2013 | Volume 50 | Issue 4

Figure1(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 1cm. The lesion shows typical features of a
nonossifying fibroma

373

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Figure2: (ac) Serial radiographs of the left knee(AP views) obtained 6, 11 and 13months later show similar lesion morphology. The lesion has
progressively increased in size to 1.25, 1.75 and 2.75cm, respectively. The patient was on growth hormone therapy during this time

Figure 3: Plain radiograph of the left knee (AP view) following

withdrawal of the growth hormone shows that the lesion has started
healing with progressive sclerosis with no further increase in size

border that is usually scalloped and slightly expansile.

Since the tumor is benign, it usually doesnt enlarge
substantially and is asymptomatic in the majority of
cases. Serial enlargement of the lesion mimicking an
aggressive lesion has not been reported before.
A 15yearold girl with growth hormone deficiency
was imaged with knee radiographs to monitor her
growth, while on replacement therapy. She was
incidentally found to have a new left proximal
posteromedial tibia lesion with features suggesting a
NOF [Figure1a and b]. On examination, she had no
local tenderness or weakness. Followup imaging at
6, 11 and 13 months showed gradual increase (up to
three times) in the size of the lesion [Figure2ac].
Therefore, she was referred to the orthopedic
oncologist for further management. Since the lesion
appearance still suggested a nonaggressive lesion,
it was simply followed while the growth hormone
replacement was withheld. Radiograph5months
later confirmed healing of the lesion and progressive
sclerosis without further enlargement[Figure3].
NOF belongs to tumorlike lesions according to
the World Health Organization classification.[1] It is
common in children with 30 to 40% cases harboring
374

multiple lesions. The etiology is unknown and the

lesion is believed to be caused by developmental
defect. [2] Due to the asymptomatic nature, these
lesions are incidentally discovered on imaging. [3]
Given the characteristic radiographic appearance of
a well circumscribed subcortical lytic lesion with
narrow zone of transition, peripheral sclerosis and
scalloped margins, these lesions are classified as
do not touch lesions, implying that biopsy is
considered to be excessively invasive. In our case, the
lesion was new, however, characteristic appearance
warranted only followup imaging. These lesions
usually spontaneously regress(sclerose). Curettage
and bone grafting may be performed for large lesions
that may cause pathologic fracture and symptomatic
lesions.[4]
Expansion while on a growth replacement therapy has
not been reported before. It may raise a false alarm
of the lesion being aggressive however; characteristic
imaging features should deter the radiologist from
being overly aggressive to avoid unnecessary biopsy.
Withholding the hormonal treatment halts its spurious
growth and subsequent healing of the lesion confirms
its otherwise benign nature as observed in this case.
To conclude, NOF can enlarge on growth hormone
treatment and may masquerade aggressive bone
tumor. Withholding hormonal treatment results in
healing of the lesion.
Wadhwa V, Thakkar RS, Carrino JA, Chhabra A
The Russell H. Morgan Department of Radiology and
Radiological Science, Johns Hopkins University School of
Medicine,
Baltimore, MD, USA
Correspondence to:
Dr. Avneesh Chhabra, Email: achhabr6@jhmi.edu

References
1.
2.

SchajowiczF. International histological classification of tumors.

Histological typing of bone tumors. Geneva: World Health
Organization; 1993. p.368.
BetsyM, KupersmithLM, SpringfieldDS. Metaphyseal fibrous

Indian Journal of Cancer | OctoberDecember 2013 | Volume 50 | Issue 4

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Letters to Editor

3.
4.

defects. JAm Acad Orthop Surg 2004;12:8995.

HettsSW, HilcheySD, WilsonR, FrancB. Case 110: Nonossifying
fibroma. Radiology 2007;243:28892.
HatcherCH. The Pathogenesis of localized fibrous lesions in the
metaphyses of long bones. Ann Surg 1945;122:101630.

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Disseminated tuberculosis
mimicking relapse in hairy
cell leukemia
Sir,
Unusual presentations of hairy cell leukemia(HCL)
include, marked leucocytosis, spontaneous splenicrupture,
bulky lymphadenopathy, bone lesions, neuropathy,
meningitis and ascites.[1,2] We report 52yearsold male
presented with pancytopenia and ascites.
A 52yearsold male presented with 6months
history of fever, fatigue, weight loss, pancytopenia,
splenomegaly and ascites. On evaluation he had
40% hairy cell in bone marrow aspirate, which
were positive for CD19, CD20, CD11c, CD25 and
CD103 and kappa light chain restriction consistent
with HCL. Hairy cells was also found in ascetic
fluid and serum/ascetic fluid albumin radient ratio
of<1.1. Rest of staging workup including contrast
enhancement computer tomogram(CECT) of chest
and abdomen was normal except 13cm spleen
and ascitis. There was no history of tuberculosis
in past. The patient was treated with cladribine
0.14mg/kg/day as 2h infusion for 5days. He
achieved complete remission after cladribine and
kept under followup. After 6months, he again
presented with pancytopenia, splenomegaly(12cm)
and reappearance of ascites. Clinical features were
suggestive of relapse of disease. Investigation
revealed hemoglobin 9.3g/dL, white blood cell
count 2.110 9 /L, and platelets 6410 9 /L.
Bonemarrowexaminationwasnormal. Bone marrow
biopsy revealed 4550% cellularity with hematopoitic
elements of all series was identified. Serology for
HIV was negative. CECT scan chest showed mild
pleurapericardial effusion and CECT abdomen
revealed multiple small hypodense lesions in both
the lobes of liver, splenomegaly with multiple
deposits[Figure1]. Mantoux test was negative.
Abdominal paracentas is showed straw colored
fluid with serum/ascetic fluid albumin radient
ratio of<1.1, cell count 460/mm 3 P40 L60,
Indian Journal of Cancer | OctoberDecember 2013 | Volume 50 | Issue 4

Figure1: CECT scan chest: Pleropericardial effusion (a), CECT scan

abdomen: Multiple small hypodense lesions in both the lobes of liver,
splenomegaly with multiple deposits (b)

Gram staining negative, acid fast bacillus negative,

adenosinedaminase(ADA) level 90U/L, polymerase
chain reaction(PCR) for tuberculosis was positive.
The final diagnosis of disseminated tuberculosis was
made was made and he was put on ant tubercular
treatment(ATT) containing rifampicin, isoniazide,
pyrazinamide and ethombutol. Clinical sign(normal
size of spleen on ultrasonogram and no evidence
of ascitis), symptoms and hematological parameters
improved after 2months of ATT. He completed
9months of ATT and remains off treatment for
6months without any illness.
Disseminated tuberculosis in one of the complications
of chronic lymphoproliferative disorders. It occurs
by either reactivation of acid fast bacilli by due to
disease chemotherapy(fludarabine and cladribine)
induced immune suppresion, in Indian patients
where the prevalence of subclinical tuberculosis is
high. Diagnostic criteria of disseminated tuberculosis
are as follows:(a) Clinical feature compatible with
tuberculosis,(b) concurrent involvement of atleast
two nonadjacent organs or sites of the body, or
detection of mycobacterium tuberculosis in the blood
or bone marrow,(c) microbiologic and/or histologic
evidences of tuberculosis,(d) significant improvement
with antitubercular treatment. [3,4] Disseminated
tuberculosis may mimic the features of pancyopenia and
hypersplenism.[35] In our case ascetic fluid PCR, ADA
level were raised, sign and symptoms was completely
improved with antitubercular treatment.
This report highlight reappearance of baseline features
not always relapse of disease, the risk of immune
375