Hepatosplenic T cell lymphoma

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Epidemiology and Demographics

Risk Factors

Screening

Differentiating Hepatosplenic T cell lymphoma from other Diseases

Natural History, Complications and Prognosis

Diagnosis

Staging

History and Symptoms

Physical Examination

Laboratory Findings

Biopsy

CT

MRI

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Other Imaging Findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [3]

Synonyms and Keywords: Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL

Overview

Hepatosplenic T cell lymphoma is a rare type of non Hodgkins lymphoma that occurs in states of immunosupression such as post organ transplant and treatment of inflammatory bowel disease. Hepatosplenic T cell lymphoma was discovered by Farcet et al in 1990. It is also known as "gamma-delta" hepatosplenic T-cell lymphoma. The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow. The incidence of hepatosplenic T cell lymphoma is 0.3 per 100000 individuals per year. If left untreated, patients can develop liver failure, pancytopenia or spleen rupture. Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic T-cell lymphoma. Chemotherapy including CHOP is the mainstay of the treatment along with bone marrow transplant and radiation therapy.

Historical Perspective

Hepatosplenic T cell lymphoma was discovered by Farcet et al in 1990.

Classification

There is no established system for the classification of hepatosplenic T cell lymphoma.

Pathophysiology

  • Hepatosplenic T-cell lymphoma is a peripheral T-cell lymphoma, a type of non Hodgkin's lymphoma.[1]
  • It is also known as "gamma-delta hepatosplenic T-cell lymphoma".[2]
  • It usually occurs in young men with history of immunosuppression including solid organ transplantation.[3]
  • Patients with inflammatory bowel disease receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing hepatosplenic T-cell lymphoma.
  • The T-cell receptor consists of either a gamma delta or alpha-beta entity on their cell surface which are a part of the innate immune system.[4][5]
  • Gamma delta T cells represent the first line of defense against bacterial peptides, such as heat-shock proteins.
  • Gamma delta T cells are CD4 and CD8 negative, but CD56 positive which is NK cell marker.
  • Gamma delta cells respond to a stimulus and are responsible for lymphokine production and proliferation.
  • Gamma delta cells are predominantly located in the spleen, liver sinusoids and intestinal epithelium.
  • 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.
  • Chronic antigen stimulation in states of immunosuppression is responsible for the development of the lymphoma.
  • Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic T cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.
  • Mutations in SETD2, INO80, TET3 and STAT5B occur exclusively in hepatosplenic T cell lymphoma as compared to other T and B cell lymphoma types.
  • The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.
  • Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes.
  • The atypical lymphocytes are present within the cords and sinuses of the red pulp.
  • There occurs a complete loss of the white pulp.
  • The liver also shows sinusoidal infiltration by neoplastic lymphoid cells.
  • The bone marrow is characterized by neoplastic cells in the sinusoids.
  • Bone marrow infiltration results in pancytopenia.
  • The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.
  • It manifests as hepatosplenomegaly without peripheral lymphadenopathy.
  • Pancytopenia and abnormal liver functions are the laboratory findings.
  • Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.

Causes

Common causes of hepatosplenic T cell lymphoma are: [6][7]

Differentiating hepatosplenic T cell lymphoma from Other Diseases

Differential diagnosis for the lymphoma is based on the below table:

Differentiating diagnosis of Lymphoma Symptoms Signs Diagnosis Additional Findings
Fever Rash Diarrhea Abdominal pain Weight loss Painful lymphadenopathy Hepatosplenomegaly Arthritis Lab Findings
Lymphoma + + + + Increase ESR, increased LDH Night sweats, constant fatigue
Brucellosis + + + + + + + Relative lymphocytosis Night sweats, often with characteristic smell, likened to wet hay
Typhoid fever + + + + + Decreased hemoglobin Incremental increase in temperature initially and than sustained fever as high as 40°C (104°F)
Malaria + + + + + Microcytosis,

elevated LDH

"Tertian" fever: paroxysms occur every second day
Tuberculosis + + + + + + Mild normocytic anemiahyponatremia, and

hypercalcemia

Night sweats, constant fatigue
Mumps + + Relative lymphocytosis, serum amylaseelevated Parotidswelling/tenderness
Rheumatoid arthritis + + ESR and CRP elevated, positive rheumatoid factor Morning stiffness
SLE + + + + ESR and CRP elevated, positive ANA Fatigue
HIV + + + + Leukopenia Constant fatigue

Differentiating different types of T-cell Non-Hodgkin lymphoma. The gold standard for differentiation different types of Non-Hodgkin lymphoma is biopsy.

Disease Etiology Clinical manifestations Paraclinical findings Associated findings
Lab findings
Symptoms Signs Immunochemistry Histopathology
Constitutional symptoms Rash Abdominal

pain

Diarrhea Mass Other
Hodgkin's Lymphoma
[8][9][10][11][12]
  • Activation of (NF-kB)
  • Mutations in JAK-STAT pathway
  • NF-kB leads to activation of many genes like:
- ± -
  • Painless lymphadenopathy with a rubbery consistency.
  • Mostly above the diaphram
Nodular lymphocyte predominant
  • Effacement of the lymph node architecture by Reed-Sternberg cells .
  • Reed-Sternberg cell is a large often bi-nucleated cells with prominent nucleoli and an unusual immuno phenotype.
Non-Hodgkin's Lymphoma (B Cell Lymphoma)
Diffuse large B cell lymphoma
[13][14][15][16][17][18]
  • Mature B-cell Lymphoma
  • 8q24/MYC translocations
  • Hypermutated immunoglobulin genes
  • Mutation of BCL6, MYC, PAX5, PIM1, RhoH /TTFn, TP53 genes
  • Translocations involving c-MYC, BCL6, and IgH gene.
- + +
  • CD20
  • CD3
  • CD5
  • CD45
  • CD10
  • BCL-2
  • BCl-6
  • MYC
  • IRF-4/ MUM-1
  • Ki-67

Centroblastic

Immunoblastic

  • > 90% immunoblasts
  • Trapezoid shaped large lymphoid cells with significant basophilic cytoplasm

Anaplastic

  • Very large cells with a round, oval, or polygonal shape that may resemble Reed-Sternberg cells
_
Mantle cell lymphoma
[19][20][21][22][23]
+ +
  • CD5+
  • B-cell antigen positive
  • Overexpression of Cyclin D1
  • Germinal centers filled by small-to-medium atypical lymphocytes
  • Nodular appearance
Abdominal distention
B-lymphoblastic leukemia/lymphoma
[24][25][26]
  • Precursor B-cell lymphoma
  • Unknown
  • Inherited mutations of PAX5, ETV6, and TP53
+
  • CD20+
  • CD10+
  • Consists of small to medium-sized lymphoid cells with blastic nuclear chromatin and a high mitotic rate.
Follicular lymphoma
[27][28][29][30][31]
  • Mature B-cell lymphoma
  • Reciprocal translocation t(14;18)
  • Overexpression of BCL2
20% of patients present with: + + ±
  • CD21
  • CD23
  • Nodular growth pattern
  • Most common clinically indolent NHL
  • Peripheral nerve compression
Burkitt's lymphoma
[32][33][34][35][36][37][38][39]
  • Mature B-cell lymphoma
  • Translocation of chromosome 8 myc locus such as:
    • t(8;14)
    • t(2;8)
    • t(8;22)
+
  • Round and small nucleoli
  • basophilic cytoplasm
  • "Starry-sky pattern"
B cell chronic lymphocytic leukemia/small lymphocytic lymphoma
[40]
  • Mature B-cell Lymphoma
  • Ch 13 abnormalties

33% of patients present with:

  • CD5
  • CD38
  • Monoclonal small well differentiated B cells.
  • Significant number of smudge cells or basket cells.
Marginal zone lymphoma Extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type
[41][42][43][44][45][46][47][48][49][50]
  • Mature B-cell lymphoma
  • Recurrent translocation of such as:
    • t(1;14)(p22;q32)
    • t(11;18)(q21;q21)
    • t(14;18)(q32;q21)
    • t(3;14)(p14.1;q32)
  • B symptoms may or may not be present
± + + B-cell associated antigens that co-express

Negative for:

  • Presence of dense diffuse lymphoid infiltrate of marginal‐zone cells in lamina propria
  • Prominent lymphoepithelial lesions and consisting of small atypical cells with monocytoid features.
Splenic marginal zone lymphoma
[51][52][53][54][55][56][57]
  • Mature B-cell lymphoma
  • Clonal rearrangements of the immunoglobulin genes (heavy and light chains)
    • Deletion 7q21-32
    • Translocations of the CDK6 gene located on 7q21
+ +
  • Small lymphocytes
  • Transformed blasts
  • Epithelial histocytes
  • Plasmacytic differentiation of neoplastic cells
Nodal marginal zone B-cell lymphoma
[58][59]
  • Mature B-cell Lymphoma
  • Stimulation of antigen receptor by autoantigen and co-stimulatory molecule CD40
  • Mutations in KMT2D, PTTPRD, NOTCH2, KLF2
+
  • Follicular cells in reactive zone
  • Centrocyte like cells in marginal zone lymphoma
Lymphoplasmacytic lymphoma (Waldenstrom’s macroglobulinemia)
[60][61][62][63][64]
+ Express pan B-cell antigens

Variable expression of

Majority express:

  • IgM surface immunoglobulin

Fewer express

  • Russell bodies (intracytoplasmic inclusions) and Dutcher bodies (intranuclear inclusions)
  • Prominent epithelioid histiocytes
Hairy cell leukemia
[65][66][67][68][69]
  • Production of cytokines, such as TNF alpha and IL-2R, provide important stimuli for malignant B cells proliferation in hairy cell leukemia.
    • The p38-MAPK-JNK cascade
    • The MEK-ERK cascade
    • The Phosphatidylinositol 3 kinase (PI3K)-AKT cascade
+
  • N/A
  • Small cells with "fried egg"-like appearance
  • Well-demarcated thread-like cytoplasmic extensions
  • Clear cytoplasm
  • Central round nucleus
  • Peri-nuclear clearing ("water-clear rim" appearance)
Disease Etiology Constitutional symptoms Rash Abdominal pain Diarrhea Mass/Lesion Other Immunochemistry Histopathology Associated findings
Non-Hodgkin's Lymphoma (T Cell Lymphoma)
Precursor T-cell lymphoblastic leukemia/lymphoma
[70][71]
  • Precursor T-cell lymphomas
+ - -
T-cell granular lymphocytic
[72][73][74]
- - - May be associated with the following conditions:
T-cell prolymphocytic leukemia
[75]
  • Abnormal proliferation of mature T cells (post thymic)
+ - -
  • Lymphocytes with abundant basophilic, nongranular cytoplasm, atypical nucleus
  • Cytoplasmic protrusions (blebs)
Adult T cell leukemia/lymphoma
[76][77][78]
+ - -
  • Charecterstic leukemia cells with sharp nuclear indentations and a prominent nucleoli
  • "Cloverleaf" or "flower" cells
Anaplastic large cell lymphoma
[79][80][81][82]
  • Mature T-cell lymphoma
+ + -

Painless swelling in :

Strongly immunoreactive for :
  • Nucleoli tend to be more prominent
  • The cytoplasm may be either basophilic or eosinophilic and the cell might have many nuclei with dispersed or clumped chromatin
  • May be caused by textured breast implants
Cutaneous T-cell lymphoma Mycosis fungoides / Sézary syndrome
[83][84][85]
+ + -
  • Cutaneous manifestations
  • Polymorphous inflammatory infiltrate in the dermis that contains small numbers of frankly atypical lymphoid cells
  • These cells may line up individually along the epidermal basal layer
  • The presence of spongiosis is highly suggestive of mycosis fungoides
Peripheral T-cell lymphoma Subcutaneous panniculitis-like T-cell lymphoma
[86][87][88]
  • Mature T-cell lymphoma
- - - Painless swellings on:
  • Extremities
  • Trunks
Positive for:
Hepatosplenic T-cell lymphoma
[89][90][91]
+ + - Painless swelling in :
  • Intermediate sized tumor cells with clear cytoplasm, oval nuclei, slightly dispersed condensed chromatin, inconspicuous nucleoli
  • Patients with inflammatory bowel diseases taking immunosuppressant and anti-tumor necrosis factor-α agent are also have a higher risk for developing hepatosplenic T-cell lymphoma
Enteropathy-type intestinal T-cell lymphoma
[92][93][94]
  • Mature T-cell lymphoma
+ + + Painless swelling in the :
  • Lymphomatous infiltrate with neoplastic large cells
  • May have pleomorphic, multinucleated cells
  • Adjacent mucosa shows villous atrophy, crypt hyperplasia, increased inflammatory cells
  • Lymphocytosis
  • Mostly diagnosed in the small intestine
Extranodal T-cell lymphoma, nasal type
[95][96][97]
  • Mature T-cell lymphoma
+ - - Painless swelling in :
  • Medium sized tumor cells and polymorphic infiltrate of non-neoplastic inflammatory cells
  • Lymphoma cells may be admixed with a polymorphic infiltrate of non-neoplastic inflammatory cells
Angioimmunoblastic T-cell lymphoma
[98][99][100]
  • Mature T-cell lymphoma
+ + -
Peripheral T-cell lymphoma, unspecified
[101][102]
  • Mature T-cell lymphoma
- + -
  • Clear cytoplasm, resemble Reed-Sternberg cells, with irregular, pleomorphic, hyperchromatic or nuclei
  • A lot of mitotic figures; very broad cytologic spectrum

Epidemiology and Demographics

  • The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.
  • It occurs in younger group of patients, most cases falling in 20-40 years of age group.
  • Men are more affected than the females.

Risk Factors

Common risk factors include:

Screening

There is insufficient evidence to recommend routine screening for hepatosplenic T cell lymphoma.

Natural History, Complications, and Prognosis

Natural history

  • Patients have a history of immunosupression such as inflammatory bowel disease under treatment or organ transplant.[103]
  • The mean age group is 35 years and most of the patients are males.
  • Initial symptoms are fever, weight loss, night sweats and then progress to more severe symptoms depending on the organ involvement but there is no lymphadenopathy.
  • Patients also present with symptoms of liver, spleen and bone marrow dysfunction.
  • If left untreated, patients can develop liver failure, pancytopenia, or spleen rupture.

Complications

Prognosis

  • The prognosis is very poor, with patients dying within 2-3 years of diagnosis even after recieving treatment[104].

Diagnosis

Diagnostic Study of Choice

  • Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic T cell lymphoma[105].
  • CT scan and PET scan are used to assess the spread of the lymphoma.

Symptoms

The most common symtoms are[106]:

  • Fever
  • Weight loss
  • Night sweats
  • Pain abdomen
  • Jaundice
  • Fatigue
  • Recurrent infections
  • Bleeding

Physical Examination

Temperature

Skin

Thorax

Abdomen

Extremities

Laboratory Findings

  • Biopsy of the tumor:
    • Histology - small-to intermediate sized T lymphocytes infiltrate the sinusoids of the liver and the splenic red pulp.
    • Flow cytometry and immunophenotyping - The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression[107].
    • Karyotyping - Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome[108].
  • Bone marrow biopsy; The bone marrow is characterized by neoplastic cells in the sinusoids.
  • Complete blood count; Pancytopenia
  • Liver function tests: Deranged LFT

Electrocardiogram

There are no ECG findings associated with hepatosplenic T cell lymphoma.

X-ray

There are no x-ray findings associated with hepatosplenic T cell lymphoma but pleural effusion might be present.

Echocardiography or Ultrasound

  • There are no echocardiography findings associated with hepatosplenic T cell lymphoma.
  • On ultrasound of abdomen:

CT scan

Tumor mass can be seen in liver or spleen or both.

MRI

Tumor mass can be seen in liver or spleen or both.

Other Imaging Findings

PET scan: On PET scan, tumor mass can be seen in liver or spleen or if it has metastasized to any other organ.

Treatment

Medical Therapy

Surgery

Surgical intervention is not recommended for the management of hepaosplenic T cell lymphoma.

Primary Prevention

There are no established measures for the primary prevention of hepatosplenic T cell lymphoma.

Secondary Prevention

There are no established measures for the secondary prevention of hepatosplenic T cell lymphoma.

References

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