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Year : 2015  |  Volume : 58  |  Issue : 1  |  Page : 48-54
A young leukemic patient with unusual catastrophic intestinal complication

1 Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, Punjab, India
2 Department of Pediatrics, Post Graduate Institute of Medical Education and Research, Chandigarh, Punjab, India
3 Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Punjab, India
4 Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, Punjab, India

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Date of Web Publication11-Feb-2015


A 14-year-old child with acute lymphoblastic leukemia who had completed induction chemotherapy presented with fever and diffuse musculoskeletal pains which was thought to be a constellation of myositis, arthralgias and arthritis. Investigations revealed initially showed normal peripheral blood counts but had pancytopenia and pre-terminally blasts were seen in the peripheral blood smear. He had bone marrow necrosis. Disseminated intravascular coagulation was suspected with a positive fungal serology. At autopsy, he had evidence of disease relapsed in lymph nodes, liver, spleen, testes and kidneys. There was extensive pseudomembranous colitis and appendicitis with changes of toxic megacolon.

Keywords: Acute leukemia, Clostridium difficile, pseudomembranous appendicitis,pseudomembranous colitis, toxic megacolon

How to cite this article:
Vaiphei K, Trehan A, Singh Sachdeva MU, Malhotra P. A young leukemic patient with unusual catastrophic intestinal complication. Indian J Pathol Microbiol 2015;58:48-54

How to cite this URL:
Vaiphei K, Trehan A, Singh Sachdeva MU, Malhotra P. A young leukemic patient with unusual catastrophic intestinal complication. Indian J Pathol Microbiol [serial online] 2015 [cited 2021 Mar 4];58:48-54. Available from: https://www.ijpmonline.org/text.asp?2015/58/1/48/151187

   Clinical Protocol Top

A 14-year-old male was admitted on 10 th June and died in the hospital on 26 th June. The boy had been admitted on 11 th April and was diagnosed to have acute lymphoblastic leukemia (ALL). Following which, he was started on induction therapy as per the modified BFM protocol (Vincristine, Daunorubicin, and Prednisolone) on 27 th April. He completed 4 cycles of induction uneventfully and underwent a bone marrow examination on 4 th June, which had shown the remission of the disease. ([Figure 1]) He complained on 4 th June of pain in his hands and feet which were treated with analgesics and oral antibiotics. By 10 th June, the pain had worsened involving both feet, hands, and elbows associated fever necessitating the hospital admission.
Figure 1: Two sets of microphotographs to show the findings before (upper half) and after (lower half) treatment

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   Examination at Admission and Investigation Top

Hematology and [Table 1], [Table 3], and [Table 4] Biochemical [Table 2]
Table 1: Hematological profiles

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Table 2: Biochemical profiles

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Table 3: Coagulogram

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Table 4: Bone marrow examination

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He was poorly nourished weighing 30 kg, afebrile, heart rate of 100/min, blood pressure of 130/80 mm Hg. He also had pallor. Local examination revealed tenderness and swelling over the ankles and wrist joints bilaterally, no redness or increase temperature. He had restricted movement due to pain, and the calf muscles were also tender. There was no associated muscle weakness (power 5/5, grip 60%) with normal reflexes. Examinations of the respiratory, central nervous, and cardiovascular systems were within normal limits. However, examination of the abdomen revealed palpable liver of 3 cm below right costal margin with a span of 12 cm. Soft but mildly tender abdomen on palpation with no localization. Bowel sounds were heard but fickle.


  • 10/6: Left calf and right arm-bulky muscles suggestive of myositis.

    • Compression USG of lower limbs: No evidence of deep vein thrombosis.
  • 15/6: Both feet muscles are edematous with fluid between muscle layers.
  • 18/6: Right forearm-edema of subcutaneous tissue; muscle-increased echogenicity with echogenic strands in the lateral compartment of leg joint effusion seen in bilateral ankle joints.
  • 23/6: Both feet-minimal fluid collection on the ventral aspect of the ankle joint with few internal echoes.

Chest X-rays: Within normal limits.

X-ray of the bones: Evolving osteolytic lesion in metatarsals.

Bone Scan: Extensive skeletal infiltration.

Blood C/S (10/6 and 24/6): Sterile

Fungal serology: Candida agglutinin titer 1: 256; positive for A. fumigates and niger

Widal test (10/6): Negative

   Course in Hospital Top

Patient was considered to have either a tropical pyomyositis or myositis and started on Klox and Amikacin. There was no improvement in the symptoms.

Clindamycin was added after 5 days. He became afebrile on the 19 th June, but pain and tenderness in feet and hands persisted. He underwent a repeat bone marrow aspiration on 24.6.08 in view of blasts in the peripheral smear. On 26 th June morning, he was noted to have tachypnea, tachycardia, and abdominal distension with absent bowel sounds. He soon went into shock and expired at 1.15 p.m. on the same day.

   Unit's Final Diagnosis Top

  1. ALL (relapse).
  2. Diffuse bony infiltration.
  3. Myositis? Leukemic infiltration? Infective.
  4. Sepsis, Septic shock? Disseminated intravascular coagulation (DIC).

Cause of death: Septic shock

   Discussion on Clinical Protocol (Amita Trehan) Top

Data base

This was a 14-year-old child with ALL. He was high risk by age criteria, age and counts being universal prognostic criteria. Adolescents with ALL have a poor prognosis with an EFS of 65% compared to 80% in children. This is because their immunophenotype and cytogenetics are worse. This patient achieved remission after induction with three drugs (Vincristine, Daunorubicin, and Prednisolone) after 4 cycles of induction therapy. He was readmitted on 04/06/04. His problems were fever and musculoskeletal pains which were probably a constellation of myositis, arthralgias, and arthritis. We have a bone scan showing infiltration.([Figure 1]) He had normal counts initially which went on to pancytopenia, and preterminally blasts were seen in the peripheral blood smear. He had a bone marrow necrosis (BMN). DIC was suspected. His fungal serology was positive. He had sudden deterioration and expired.

There are certain questions which need to be answered. The 1 st would be did he have arthritis? He had mild swelling over ankles and wrists with tenderness which indicated to be arthritis. Or was this pyomyositis/myositis? There was no evidence or redness to suggest a collection/cellulites. His power and reflexes were normal. However, the generalized tenderness definitely points towards a myositis. The nonlocalized mild abdominal tenderness was considered to be a part of myositis. The question that needs to be answered is that could the patient had deep vein thrombosis terminally? But he had a normal study of the compression ultrasound. There was no other sign to suggest DVT. His muscle pain was present in both the calves and a bilateral DVT is extremely a rare situation and unlikely to be underlying the cause in this patient.

There is a host of organisms which can lead to infectious myositis. These include bacteria, parasites, fungi, and viruses. There are no clinical features to suggest a bacterial, parasitic or fungal infection in this patient. However, a viral infection like influenza, coxsackie or alpha virus cannot be ruled out. If we think of septic arthritis, it is extremely unlikely as >2 joints are involved in just 4.4% cases, and arthritis involving small joints is rare. [1] Reactive arthritis could be considered where the infectious agent is not recoverable and usually follows an infection in the gastrointestinal, genito-urinary or sino-pulmonary areas. Again there are no clinical features to suggest a bacterial or parasitic infection. A viral arthritis following Togavirus, alpha, parvo, adeno always remains a distinct possibility.

Commenting on the imaging in this child, the ultrasound has shown increased echogenicity in the muscles indicating myositis. Collections are well made out by ultrasound. There was minimal fluid in the ankle joints suggesting the arthritis. There was no deep vein thrombosis for which a compression ultrasound has a high sensitivity. However, one must remember that MRI is the gold standard for musculoskeletal imaging. The bone scan showed extensive infiltration of the long bones which is an expected finding as this child was diagnosed as leukemia just 2 months ago.

The interesting feature in this patient was the presence of BMN. BMN was first reported in 1942 in association with sickle cell disease. If we do a literature search, one finds plenty of case reports of BMN being associated with a malignancy and a few scattered reports of septicemia and drug-induced necrosis. A meta-analysis of 240 cases diagnosed ante-mortem over a period of 20 years has shown malignancy to be the cause in 91% cases of which 40% are leukemia. [2] This is followed by lymphomas and solid tumors. Infections account for just 9.5% and include tuberculosis, parvovirus, fungal (cryptococcal and mucormycosis). In another study of 20 cases of BMN in 1083 bone marrow performed 80% were associated with malignancies (Hodgkin's and non-Hodgkin's lymphoma (NHL), ALL and chronic myelogenous leukemia). The rest were seen with tuberculosis, drug ingestion, and anti-phospholipid Antibody syndrome anti-phospho lipid antibody (APLA). [2],[3] In our institute, 17 cases of BMN were identified in 3740 biopsies done. Malignancies (NHL, ALL and Hodgkin's disease) were seen in 65% cases whereas infections, myelofibrosis, hyperoxalosis, and deficiency anemia constituted the rest. [4] Looking at the clinical features of BMN, bone pain, which is debilitating as compared to leukemia, is seen in 80% cases, fever in 70%, anemia in 90%, and thrombocytopenia in 80%. The white cell count may be elevated, normal or decreased. The alkaline phosphatase is increased in 40% and the lactate dehydrogenase in 50%. The clinical features of our index case can all fit well into BMN. [5],[6]

After about 10 days of admission, this patient was seen to have blasts in the peripheral blood film (PBF). Was this a relapse? His first PBF had a few atypical cells and subsequently 18% blasts were demonstrated on 2 occasions. His clinical features of musculoskeletal pains and the blood film indicate a relapse. 35-40% children have musculoskeletal pains at presentation, and joint effusion is seen in about 6%. [1] How early can a relapse occur? Looking up literature in patients <18 years most relapses have occurred after about 2 years of therapy. In a report of 233 relapses, the time range for relapse has been reported to be 1-64 months. In another study of 347 relapsed patients, the range has been seen to be 0-6 months to 87 months the mean being 32 months. In the adult, Leukemia Clinic at PGI the mean time to relapse in 47 patients was 16.5 months, the range being 1-58 months. [4] In the Pediatric Oncology Clinic at our institute, 125 patients relapsed at a mean time of 24 months with a range of 3-54 months.

The index patient had musculoskeletal symptoms, fever and pancytopenia which fit into the clinical features both of a relapsed disease and BMN. This patient was considered to have DIC. He had a normal coagulogram, increased fibrinogen, low platelets, and increased d-dimers. However, there were no features of acute DIC, and he does not fulfill criteria to be called a DIC. It is possible that this was chronic compensated DIC related to malignancy. Leukemia has a 2-fold increased risk of thrombosis. He also had a positive fungal serology. Candida agglutinin titer was borderline which is frequently seen in patients on antibiotics. His antibodies to aspergillosis were positive which are usually seen in allergic bronchopulmonary aspergillosis or a fungal ball. There were no clinical or radiological features of an invasive disease. He had not been neutropenic for long and did not fulfill criteria for invasive fungal disease.

He had an acute deterioration and died within hours. He was noted to have tachycardia, tachypnea, and sudden onset abdominal distension with absent bowel sounds. This could be a rapid onset nosocomial sepsis going on to septic shock. He was not on any drugs to result in illness. His potassium levels were normal. He had no features of intra-abdominal inflammation, peritonitis or neutropenic colitis. Fat and necrotic tissue embolism from the marrow in patients with BMN to the pulmonary arteries may result in pulmonary thromboembolism (PTE). A PTE can explain his rapid deterioration but cannot explain the abdominal symptoms.

   Final Clinical Diagnosis (Amita Trehan) Top

  1. ALL,
  2. With an early relapse after induction therapy,
  3. BMN and,
  4. Possible septicemia.

The cause of death is possibly PTE or septic shock.

   Pathology Protocol (PM 20053) (Kim Vaiphei) Top

At autopsy, there excess of straw colored pleural fluid bilaterally measuring about 500 ml on either side.

Lymph nodes

Generalized enlargement of the deep groups-mesenteric, mediastinal, peripancreatic, para-aortic, and hilar. Larger mesenteric nodes measured 1-2.5 cm in diameter [[Figure 2]a and b]. Cut sections were fleshy in appearances, and some were hemorrhagic. On microscopy, there was partial to complete effacement of nodal architecture with heavy capsular and pericapsular infiltration by monomorphic population of round to oval cells [[Figure 2]c]. The monomorphic tumor cells showed large areas of drop out necrosis. The monomorphic cells were composed of immature lymphoid cells with scanty to moderate amount of pale cytoplasm. Most of the cells had round to oval nuclei, some with nuclear convolution and occasional prominent nucleoli. These immature lymphoid cells showed positivity for leucocyte common antigen on immunohistochemistry. In between these immature cells and also separate foci showed collections of hematopoietic cells of both myeloid and erythroid series with many megakaryocytes [[Figure 2]d]. The sinus histiocytes showed features of hemophagocytosis.
Figure 2: Panel of photographs showing the lymph nodes pathology. The upper two photographs (a and b) show the enlarged multiple lymph nodes in mesentery and mediastinum. (c) representative microphotograph of one of the lympho nodes showing effacement of nodal architecture by diffuse sheets of the monomorphic population of immature lymphoid cells (H and E, ×40). (d) photomicrograph of lymph node where there was a loss of cells, and the sinuses are filled with various types of hematopoietic cells, the large easily visible multilobated cells the megakaryocytes (H and E, ×40)

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Liver (weight-1540 g)

moderately enlarged and golden brown in color [[Figure 3]a]. Microscopy: Normal architecture was maintained. Hepatocytes in zone 2 and 3, and the kupffer cells showed many golden brown finely granular pigments which were positive for hemosiderin pigment on Perl's staining [[Figure 3]b]. There was nodular portal tract infiltration by the immature lymphoid cells [[Figure 3]c]. Hepatocytes otherwise were well-preserved. Sinusoids were dilated and showed immature lymphoid cells and scattered extramedullary hematopoietic cells [[Figure 3]d]. Kupffer cells were hyperplastic and occasionally showed of erythrophagocytosis.
Figure 3: (a) Gross photograph of a slice of liver showing golden brown discolouration. (b) medium power photomicrograph of liver to show the granular blue colored pigments within zone 1 and 2, and within Kupffer cells (Perl's stain, ×20). (c) Medium power photomicrograph to show nodular portal tract infiltration by the leukemic cells (H and E, ×20). (d) High power photomicrograph showing dilated sinusoids with many immature nucleated hematopoietic cells (H and E, ×40)

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Spleen (weight-240 g)

Size was mildly enlarged for the young patient. Cut slices showed multiple millet size diffuse paler looking micronodules dominantly located in the sub-capsular region [[Figure 4]a]. Microscopy showed diffuse infiltration of the white pulp by monomorphic immature lymphoid cells replacing the native lymphoid follicles [[Figure 4]b]. Red pulp area including the sinusoids was packed with hematopoietic cells [[Figure 4]c]. There was prominence of the macrophages containing golden brown hemosiderin pigments, which were highlighted better in Perl's stain [[Figure 4]d].
Figure 4: (a) Gross photographs showing both capsular as well as the cut surface of the spleen. To be note is the fine nodular deposits along the subcapsular area. (b) Medium power photomicrograph of the spleen to show diffuse effacement of the normal splenic lymphoid tissue by sheets of monomorphic population of immature lymphoid cells (H and E, ×20). (c) Medium power photomicrograph of the deeper splenic tissue to show dilated sinusoids containing many primitive hematopoietic cells including megakaryocytes (H and E, ×40). (d) Medium power photomicrograph of the spleen to show blue color hemosiderin pigments within sinusoidal macrophages (Perl's stain, ×20)

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Kidneys (weight 276 g together)

grossly normal appearance [[Figure 5]a]. Microscopy: Normal glomeruli with multiple foci of interstitial infiltration by the immature lymphoid cells [[Figure 5]b] and occasional intra tubular calcification [[Figure 5]c].
Figure 5: (a) Gross photograph of kidney and part of the abdominal aorta with enlarged and congested matted para-aortic lymph nodes. The kidneys were grossly looked normal. (b) Medium power photomicrograph to show normal glomeruli and leukemic cell infiltration of the interstitium (H and E, ×20). (c) Medium power photomicrograph to show renal tubules, some with intra-tubular calcification (H and E, ×20). (d) Medium power photomicrograph to show leukemic cells infiltrating the interstitium (H and E, ×20)

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grossly normal. Microscopy: Interstitial infiltration by immature cells [[Figure 5]d].


The colonic mucosa in its entirety showed diffuse involvement by raised plaques and nodules [[Figure 6]a]. These nodules had an average size of 10 mms or more with central umbilication covered by necrotic pale yellow colored exudates. Many of the discrete nodules showed blackish discoloration. These nodules were becoming confluent at places forming larger nodules [[Figure 6]b]. Pseudomembrane formation was much more mark at proximal portion of the colon. Also involving the appendix [[Figure 7]a]. There were dilatation and blackish discoloration of the cecum and the proximal portion of the ascending colon measuring >10 cm, which was more almost, double the dimension of the remaining colonic segment. This dilated segment showed blackish discoloration seen better on the serosal aspect [[Figure 7]b]. Distal portion of sigmoid colon and rectum was relatively lesser involved. Ileum and jejunum including the ileal aspect of the ileocecal valve were within normal limit. Microscopy: multiple sections were studied from different segment of the colon, rectum, and appendix. Discolored areas showed hemorrhages involving the mucosa and submucosa with heavy inflammation covered on the surface by thick membrane composed of fibrin, mucous, neutrophils and degenerating epithelial cells. Underlying the membranous exudates, the crypts showed degenerative changes and filled with abundant mucin and the exudates giving a volcano like appearance [Figure 8], [[Figure 9]a and b]. Submucosa showed marked edema and hemorrhages. The lamina propria and submucosal blood vessels showed marked dilatation and congestion. In most of the colonic segment, the changes were restricted to mucosa and submucosa, in the areas where there was dilatation and marked hemorrhagic serosa, the muscualris propria also showed myonecrosis and marked vascular dilatation and congestion. No evidence of vascular fibrin thrombosis. Section from the appendix also showed similar kind of exudative lesion involving the mucosa, extending and involving the inner layer of muscularis propria. Grossly uninvolved segment of the colon [[Figure 9]c] and rest of the gastrointestinal tract did not show any significant pathology.
Figure 6: (a) Gross photograph of colon to show diffuse mucosal discolouration by plaque lesions of varying size and shapes, sparing the terminal ileum. (b) Close up photograph of the colon to show the umbilications, and pale yellowish exudates covering many of the lesions, which have become confluent alternating with areas of hemorrhages

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Figure 7: (a) A close up gross picture showing the cecum with the ileocecal valve which are covered with the pale yellow colored membranous exudate. Also seen is the cut open appendix to show the complete luminal occlusion by the exudates and the normal mucosa of the terminal ileum. (b) Gross photograph to show grossly hemorrhagic serosa and dilated portion of cecum and ascending colon. Also to be noted are the grossly discolored paracolic lymph nodes

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Figure 8: Low power photomicrograph of the colon covered by the pseudomembrane composed of fibrin, inflammatory exudates, and abundant mucin and degenerated and shedded off epithelial cells. The sub-mocusa is grossly edematous and hemorrhagic with inflammation (H and E, ×1)

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Figure 9: (a and b) Higher power photomicrographs to bring out the character of the membranous exudates better (H and E, ×40). (c) Medium power photomicrograph to show the normal rectal mucosa (H and E, ×40)

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Lungs (weight 330 g)

Normal weight, sub crepitant. Microscopy showed patchy interstitial thickening.

Bone marrow section of the post mortem sample showed grossly fibrotic marrow spaces. There were few scattered cells composed of proliferating fibroblast and occasional scattered immature cells, which were not possible to categorize exactly, but likely to be a part of the normal hematopoietic cells [[Figure 10]a and b]. However, there was no overt evidence of residual disease.
Figure 10: (a) Low power photomicrograph of bone marrow section to show the hypoplasia (H and E, ×20). (b) High power photomicrograph of marrow to show the proliferating fibroblasts and few scattered normal marrow cells (H and E, ×40)

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Rest of the other organs including biopsies from bilateral calf muscles were essentially within normal limit.

   Final Autopsy Diagnosis Top

In a partially treated case of ALL L1 with clinical relapsed with:

  1. Evidence of disease relapsed in lymph nodes, liver, spleen, testes and kidneys,
  2. Extensive pseudomembranous colitis (PMC) and appendicitis with toxic megacolon.
  3. Extramedullary hematopoiesis, and hemophagocytosis in lymph nodes, liver, and spleen,

   Brief Comment on Pseudomembranous Colitis in Children Top

Pseudomembranous colitis is commonly associated with hospitalization and prior antibiotic exposure. PMC is currently believed to be caused almost exclusively by toxins produced by Clostridium difficile (CD). The clinical spectrum of this disease may range from mild nonspecific diarrhea to severe colitis with toxic megacolon, perforation, and death. [7] Discontinuation of antibiotics and supportive therapy usually lead to resolution of this disorder. [8] PMC may affect all age groups although a lower incidence has been noted in children. [9] CD infection leads to a spectrum of diseases including the asymptomatic carrier, simple antibiotic-associated diarrhea, PMCs and fulminant colitis. Here, we present a patient who developed unexpected fatal colitis due to CD infection during the most popular chemotherapy for leukemia serving a warning to the daily clinical care. Other species of Clostridium (Clostridium innocuum, Clostridium oroticum, and Clostrid-ium ramosum) have also been implicated in rare cases in PMC along with Candida species and aerobic Gram-negative bacilli. [7] Some reports have also described infants and adults with severe PMC associated with CD toxin in the stools without previous antibiotic exposure. [10],[11],[12]

Over the last decade, the incidence of CD colitis has increased markedly as has the severity of the disease. It has been well-documented, however that patients with CD colitis do not always present with a history of these typical characteristics. The presentation can be atypical, particularly in elderly or immune suppressed patients. When CD colitis is not diagnosed and treated in a timely fashion, it can progress with catastrophic consequences. Toxic megacolon is an unusual but well-recognized presentation of the CD colitis. [12],[13],[14]

Fulminant colitis occurs in only 3% of patients with CD infection. Patients may exhibit severe abdominal pain and diarrhea, high fever, and marked peripheral leukocytosis. Diarrhea may be absent if ileus develops, and these patients are at the greatest risk to develop toxic megacolon. [14]

   References Top

Sinigaglia R, Gigante C, Bisinella G, Varotto S, Zanesco L, Turra S. Musculoskeletal manifestations in pediatric acute leukemia. J Pediatr Orthop 2008;28:20-8.  Back to cited text no. 1
Janssens AM, Offner FC, Van Hove WZ. Bone marrow necrosis. Cancer 2000;88:1769-80.  Back to cited text no. 2
Paydas S, Ergin M, Baslamisli F, Yavuz S, Zorludemir S, Sahin B, et al. Bone marrow necrosis: Clinicopathologic analysis of 20 cases and review of the literature. Am J Hematol 2002;70:300-5.  Back to cited text no. 3
Gupta N, Kumar V, Varma N, Garewal G, Das R, Ahluwalia J, et al. Myxomatous stromal changes and necrosis of bone marrow - a retrospective study of 3 years. Indian J Pathol Microbiol 2004;47:351-3.  Back to cited text no. 4
Reiter A, Schrappe M, Ludwig WD, Hiddemann W, Sauter S, Henze G, et al. Chemotherapy in 998 unselected childhood acute lymphoblastic leukemia patients. Results and conclusions of the multicenter trial ALL-BFM 86. Blood 1994;84:3122-33.  Back to cited text no. 5
Bermejo A, González FA, Villegas A, Alarcón C. Bone marrow necrosis. Am J Hematol 1995;50:65-6.  Back to cited text no. 6
Cleary RK. Clostridium difficile-associated diarrhea and colitis: Clinical manifestations, diagnosis, and treatment. Dis Colon Rectum 1998;41:1435-49.  Back to cited text no. 7
McFarland LV, Surawicz CM, Stamm WE. Risk factors for Clostridium difficile carriage and C. difficile-associated diarrhea in a cohort of hospitalized patients. J Infect Dis 1990;162:678-84.  Back to cited text no. 8
Samore MH. Epidemiology of nosocomial Clostridium difficile diarrhoea. J Hosp Infect 1999;43 Suppl:S183-90.  Back to cited text no. 9
Zwiener RJ, Belknap WM, Quan R. Severe pseudomembranous enterocolitis in a child: Case report and literature review. Pediatr Infect Dis J 1989;8:876-82.  Back to cited text no. 10
Morris AM, Jobe BA, Stoney M, Sheppard BC, Deveney CW, Deveney KE. Clostridium difficile colitis: An increasingly aggressive iatrogenic disease? Arch Surg 2002;137:1096-100.  Back to cited text no. 11
Klipfel AA, Schein M, Fahoum B, Wise L. Acute abdomen and Clostridium difficile colitis: Still a lethal combination. Dig Surg 2000;17:160-3.  Back to cited text no. 12
Trudel JL, Deschênes M, Mayrand S, Barkun AN. Toxic megacolon complicating pseudomembranous enterocolitis. Dis Colon Rectum 1995;38:1033-8.  Back to cited text no. 13
Velanovich V, LaPorta AJ, Garrett WL, Richards TB, Cornett PA. Pseudomembranous colitis leading to toxic megacolon associated with antineoplastic chemotherapy. Report of a case and review of the literature. Dis Colon Rectum 1992;35:369-72.  Back to cited text no. 14

Correspondence Address:
Kim Vaiphei
Department of Histopathology, Room No 505, 5th Floor, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
Pankaj Malhotra
Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, Punjab
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.151187

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]

  [Table 1], [Table 2], [Table 3], [Table 4]

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