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Intravascular large B cell lymphoma

Intravascular large B cell lymphoma
Literature review current through: Jan 2024.
This topic last updated: Nov 29, 2023.

INTRODUCTION — Intravascular large B cell lymphoma (IVLBCL) is a rare subtype of B cell non-Hodgkin lymphoma characterized by proliferation of lymphoma cells within the lumina of small blood vessels, particularly capillaries and post-capillary venules. IVLBCL manifests no obvious lymphadenopathy, extravascular tumor mass, or readily observable circulating lymphoma cells in peripheral blood.

This type of lymphoma was previously described as intravascular lymphomatosis, angiotropic large cell lymphoma, and malignant angioendotheliomatosis. Criteria for diagnosis and classification of IVLBCL are the same in both the International Consensus Classification [1] and the World Health Organization 5th edition [2].

The clinical presentation of IVLBCL is highly variable and often includes symptoms related to organ dysfunction caused by occlusion of blood vessels. Particularly in the past, diagnosis of IVLBCL was usually only recognized at autopsy. Heightened awareness has resulted in more patients being diagnosed with IVLBCL during life, thereby allowing for treatment.

The clinical presentation, diagnosis, and treatment of IVLBCL are discussed in this topic.

Diagnosis and classification of other subtypes of large B cell lymphoma are presented separately.

(See "Epidemiology, clinical manifestations, pathologic features, and diagnosis of diffuse large B cell lymphoma".)

(See "Classification of hematopoietic neoplasms".)

EPIDEMIOLOGY — IVLBCL is a rare subtype of large cell lymphoma; the true incidence is unknown. The median age at diagnosis is in the sixth to seventh decades; there is no sex predilection [3-5].

CLINICAL PRESENTATION — Patients can present with a bewildering array of symptoms caused by the occlusion of small vessels. A peculiar aspect of IVLBCL is the lack of lymphadenopathy, which is a general characteristic of other types of malignant lymphomas.

Symptoms — Constitutional B symptoms (ie, fever, night sweats, and weight loss) are seen in the majority of patients (55 to 85 percent) [3-5]. The clinical presentation appears to differ by country of origin, although individual presentations vary tremendously and virtually any organ can be involved:

In Western countries, patients present most commonly with symptoms related to involvement of the central nervous system (39 to 76 percent) and skin (17 to 39 percent) [3,6]. Fever, skin lesions, and prominent, rapidly progressive neurologic signs (eg, dementia, progressive cerebral vascular accident, peripheral neuropathy) are frequent [3,6-8]. Less commonly involved tissues include the bone marrow (32 percent), spleen (26 percent), and liver (26 percent) [3].

In Asia, neurologic symptoms (27 percent) and cutaneous lesions (15 percent) are less common than in Western countries [9]. Patients frequently present with involvement of the bone marrow (75 percent), spleen (67 percent), and liver (55 percent) [4,10-12]. Hemophagocytic syndrome, a condition stemming from systemic macrophage activation that is associated with B symptoms and the hemophagocytosis of red cells, white blood cells, and/or platelets, can be seen [10]. (See "Treatment and prognosis of hemophagocytic lymphohistiocytosis".)

There is a cutaneous variant of IVLBCL that presents with symptoms limited to the skin [3]. This variant is seen more frequently in Western countries (24 percent) and is rare in Asia (3 percent) [13]. Patients are mostly younger females with good performance status [3]. Skin lesions are most commonly nodules, plaques, or macules of red to grayish-blue color on the leg (35 percent), thigh (41 percent), and trunk (31 percent) [14]. Telangiectasia, edema, and pain are often seen concomitantly, making it difficult to differentiate cutaneous IVLBCL from inflammatory skin diseases such as thrombophlebitis or erythema nodosum. To date, no criteria enable clinical distinction between IVLBCL restricted to the skin and skin lesions concurrent with IVLBCL in other organs.

Laboratory studies — Patients often present with the following laboratory abnormalities [3,6,13]:

Elevated serum lactate dehydrogenase (LDH), beta-2 microglobulin, elevated sedimentation rate, C-reactive protein

Anemia

Altered hepatic, renal, or thyroid function

Serum monoclonal protein

Patients from Western countries and Asian countries differ in their rates of thrombocytopenia (29 versus 76 percent) and hypoalbuminemia (18 versus 84 percent).

Anti-proteinase-3-anti-neutrophil cytoplasmic antibodies (ANCA) have been reported in patients with IVLBCL, which may be related to endothelial damage; this finding may delay the diagnosis [15-17].

PATHOLOGY — Involved tissues demonstrate neoplastic lymphoid cells lodged in the capillaries and post-capillary venules (picture 1). Malignant cells also may be found, albeit rarely, in cerebrospinal fluid or peripheral blood; bone marrow involvement varies with geographic location [18]. Like other subtypes of large cell lymphoma, the morphology varies; most often the lymphoid cells are large in size, have vesicular nuclei and prominent nucleoli (picture 2). Frequent mitotic figures are seen. Ki-67 staining demonstrates high proliferative activity. Immunophenotyping usually identifies the cells to be mature B cells; such cases can be considered an intravascular variant of diffuse large B cell lymphoma. Rare cases of IVLBCL are of T cell or NK cell origin [19,20]. A subset of the cases associated with hemophagocytic syndrome is positive for Epstein-Barr virus infection. An intravascular gamma-delta T cell lymphoma has been described [21]. (See "Epidemiology, clinical manifestations, pathologic features, and diagnosis of diffuse large B cell lymphoma", section on 'Pathology' and "Epidemiology, clinical manifestations, pathologic features, and diagnosis of diffuse large B cell lymphoma", section on 'Diagnosis'.)

In the skin, intravascular neoplastic lymphoid cells may be accompanied by reactive perivascular infiltrates of small lymphocytes and plasma cells (picture 3) [14]. Vessels containing lymphoma cells may be very few in number and can be located anywhere in the skin and subcutaneous tissue.

Relatively little is known about the genetics of IVLBCL. Case studies have identified diverse translocations involving oncogenes implicated in other B cell lymphomas, including BCL2, BCL6, and CCND1 (cyclin D1) [22-24]. A series of seven cases with abnormal karyotypes revealed complex chromosomal aberrations in all cases, including recurrent abnormalities involving chromosome 6q13, chromosome 8p11.2, and chromosome 19q13 [25]. Targeted exon sequencing of a series of 25 B cell tumors detected mutations in genes that encode B cell receptor signaling pathway components, particularly MYD88 (44 percent) and CD79B (26 percent) [26]; this finding is consistent with an origin from a non-germinal center B cell. Analysis of the genetics of 21 additional cases of IVLBCL based on sequencing of cell-free DNA from peripheral blood confirmed the presence of frequent mutations in MYD88 (57 percent) and CD79B (67 percent) and also identified 38 percent with mutations involving the genes encoding PD-L1 or PD-L2, suggesting that immune evasion may have a pathogenic role in IVLBCL [27].

DIAGNOSIS — IVLBCL should be suspected in patients with unexplained constitutional symptoms, rapidly progressive neurologic findings, and skin lesions that resemble inflammatory skin conditions.

The diagnosis is made by identifying large lymphoma cells within small to medium blood vessels [13].

When the diagnosis of IVLBCL is suspected, biopsies of involved skin, senile hemangiomata (if present), or random biopsies of apparently normal skin may be diagnostic [28-38]. Incisional biopsies are preferable to punch biopsies [39]. Deep skin biopsies must be performed because involved blood vessels are mostly in the subcutaneous fat [14]. The yield from random skin biopsies is controversial, but some experts advocate that random skin biopsies should include at least three specimens (eg, from both thighs and abdomen) [35,40-42]. In cases of suspected brain involvement of intravascular lymphoma, skin biopsies should be performed before brain biopsies [43].

Other sites may be biopsied if skin biopsies are non-diagnostic, especially if there is evidence of organ dysfunction. Case reports describe diagnostic specimens from liver, lung, and brain [13,28,32,44]. Although commonly involved in other subtypes of lymphoma, bone marrow, lymph nodes, peripheral blood, and cerebrospinal fluid are often uninvolved in IVLBCL [45]. Involvement of these sites can be subtle, and stains for lymphoid markers (eg, CD20) may detect rare tumor cells within small vessels that are missed by morphology alone. As discussed above, bone marrow involvement is more frequent in the so-called Asian variant of IVLBCL. (See 'Symptoms' above.)

Immunophenotyping of intravascular lymphoid cells is required to distinguish IVLBCL from T cell or NK cell IVLBCL. The rare NK/T cell phenotype (positive for CD2, cytoplasmic CD3, CD56 and cytotoxic proteins such as granzyme B, and negative for CD20, surface CD3, CD4, CD8, and CD5) reveals lymphoma cells that are positive for Epstein-Barr virus antigens; such cases usually follow an aggressive course [46,47]. Ki-67 proliferation index was reported to be an independent risk factor for duration of survival [48]. Double expressor status (ie, C-MYC plus BCL2) may also be a prognostic indicator, with higher mortality compared with non-double expressors [49].

DIFFERENTIAL DIAGNOSIS — IVLBCL must be distinguished from various inflammatory and immune reactions and from other lymphomas.

On occasion, clusters of activated lymphocytes may be observed within the post-capillary venules of tissues involved in inflammatory or immune reactions, particularly the lymph nodes. On purely morphologic grounds, these may be difficult to distinguish from focal involvement by IVLBCL. As noted above, however, most patients with IVLBCL have systemic constitutional symptoms, laboratory abnormalities, and evidence of organ dysfunction, all of which are typically associated with extensive intravascular disease in extranodal organs, allowing for the diagnosis to be established on clinicopathologic grounds.

Intralymphatic histiocytosis is a reactive condition of macrophages associated with rheumatoid arthritis that may present with clinical lesions like those of IVLBCL and with intravascular proliferations of large cells. Intralymphatic histiocytosis can be differentiated from IVLBCL by immunophenotyping, which will demonstrate expression of macrophage-specific markers (eg, CD68) and absence of lymphoid markers [50].

A benign atypical intravascular CD30+ T cell proliferation was described, in which CD30+ polyclonal T cells (Epstein-Barr virus negative) are found within lymphatics in close vicinity to ulceration or an inflammatory skin disease [51].

PRETREATMENT EVALUATION — The pretreatment evaluation both determines the extent of the disease and provides information about the individual's comorbidities that are likely to have impact on treatment options. In general, the pretreatment evaluation is the same as that performed for patients with diffuse large B cell lymphoma. This is presented in detail separately. Of note, patients with intravascular large B cell lymphoma have a high rate of central nervous system involvement. As such, we typically evaluate the central nervous system with a lumbar puncture and magnetic resonance imaging (MRI) of the brain. (See "Initial treatment of advanced stage diffuse large B cell lymphoma", section on 'Pretreatment evaluation'.)

TREATMENT — Treatment of IVLBCL includes both systemic therapy and treatments directed at the central nervous system.

Systemic therapy — Due to the presence of lymphoma cells within the blood vessels, all cases of IVLBCL are considered disseminated and are therefore treated as advanced disease. Only case reports and retrospective analyses have been reported on the treatment of IVLBCL. Most patients are treated with regimens used for the treatment of diffuse large B cell lymphoma. Specifically, a combination of cyclophosphamide, doxorubicin, vincristine, and prednisone with the recombinant anti-CD20 antibody rituximab (R-CHOP) is the most commonly employed treatment (table 1). (See "Initial treatment of advanced stage diffuse large B cell lymphoma".)

Anthracycline-based chemotherapy (eg, CHOP, CHOP-R) can achieve response rates in >60 percent and estimated three-year overall survival >30 percent; long-term survival appears to be possible [3,5,6,13,30,52-55].

Support for the use of rituximab plus anthracycline-based chemotherapy comes from case reports and retrospective studies [3,5,13,30,52-55]. The largest retrospective analysis of treatment included 106 patients with newly diagnosed IVLBCL treated either with chemotherapy alone (57 patients) or chemotherapy plus rituximab (49 patients) [5]. Approximately 83 percent of the patients received CHOP or CHOP-like chemotherapy with or without rituximab. There was no difference in the rate of treatment-related deaths. At a median follow-up of 18 months, patients treated with chemotherapy plus rituximab had significantly higher rates of:

Complete response (82 versus 51 percent)

Two-year progression-free survival (56 versus 27 percent)

Two-year overall survival (66 versus 46 percent)

CNS directed therapy — Central nervous system (CNS) involvement is seen in 30 to 40 percent of patients with IVLBCL at diagnosis and occurs in another 25 percent of patients during follow-up [9]. Systemic therapy with R-CHOP does not sufficiently penetrate the CNS, therefore patients with IVLBCL also require therapies directed towards the CNS, either as prophylaxis for or treatment of CNS involvement. As mentioned above, the pretreatment evaluation includes a lumbar puncture and MRI of the brain. CNS-directed therapy is determined based on the results of these tests:

For patients without tumor cells in the cerebrospinal fluid (CSF) and normal imaging by MRI, we administer CNS prophylaxis. (See "Secondary central nervous system lymphoma: Treatment and prognosis".)

For patients with secondary involvement of the brain or spinal cord at the time of diagnosis, we administer specific treatment targeting these areas. Such treatment varies based on the exact disease site, but can include intrathecal chemotherapy, systemic high dose methotrexate, and/or radiation to the sites of involvement. The treatment of CNS involvement is presented in detail separately. (See "Secondary central nervous system lymphoma: Clinical features and diagnosis".)

Patients with neurologic compromise from spinal cord compression require urgent therapy. The timing of chemotherapy and radiation therapy is controversial; however, many patients are treated with radiation therapy prior to receiving systemic therapy. The benefit of intrathecal therapy, particularly in the presence of a normal spinal fluid evaluation, is unclear. (See "Treatment and prognosis of neoplastic epidural spinal cord compression".)

EVALUATION OF RESPONSE — One month following the completion of planned therapy (or sooner if the outcome is unfavorable), the response to treatment should be documented by history, physical examination, and laboratory studies (complete blood count, lactate dehydrogenase, and biochemical profile). Positron emission tomography/computed tomography (PET/CT) should be obtained six to eight weeks after completion of chemotherapy and 12 weeks after the completion of radiation therapy [56-58]. PET/CT imaging obtained earlier than this is likely to demonstrate increased uptake due to an inflammatory reaction to treatment.

Given its unusual initial presentation and location of disease, the response criteria used for other types of non-Hodgkin lymphoma may not apply. Instead, prospective studies have used the following criteria for response [5]:

Complete response – Disappearance of all clinical symptoms and radiographic or laboratory abnormalities, including bone marrow involvement, observed at diagnosis and the absence of any new abnormalities.

Progressive disease – Appearance of new abnormalities associated with the disease or evident deterioration of the initial abnormalities associated with the disease.

Stable disease – Failure to achieve a complete response and lack of progressive disease.

Relapsed disease occurs when there is progression of the disease after an initial complete response.

PATIENT FOLLOW-UP — Although follow-up data are scarce, relapses may be more common in those with central nervous system involvement and less common in those with cutaneous involvement [13]. When the disease is restricted to the skin, the prognosis seems to be favorable [14].

Following the completion of therapy, restaging, and documentation of complete remission, patients are seen at periodic intervals to monitor for treatment complications and assess for possible relapse. The frequency and extent of these visits depends on the comfort of both the patient and physician. There have been no prospective, randomized trials comparing various schedules of follow-up. When planning the post-treatment surveillance strategy, care should be taken to limit the number of CT scans, particularly in younger individuals, given concerns about radiation exposure and the risk for second malignancies. (See "Radiation-related risks of imaging".)

Our approach to patient surveillance is to schedule patient visits every three months during the first year, every three to six months during the second year, and every six months starting two years after complete response. At these visits we perform a history and physical examination, complete blood count, chemistries, and lactate dehydrogenase. We do perform CT scans at months 6, 12, 18, 24, 30 or 36, and then yearly until five years after attainment of a complete remission. No more imaging is performed after five years unless an abnormality suggests the possibility relapse, or the patient requests it.

Relapsed disease can be suggested by changes on imaging studies but can only be confirmed by biopsy. As such, a biopsy should always be obtained to document relapsed disease before proceeding to salvage therapy. (See "Diffuse large B cell lymphoma (DLBCL): Suspected first relapse or refractory disease in patients who are medically fit".)

SUMMARY

Description – Intravascular large B cell lymphoma (IVLBCL) is a rare subtype of B cell non-Hodgkin lymphoma characterized by the proliferation of lymphoma cells within the lumina of small blood vessels, particularly capillaries and post-capillary venules, without an obvious extravascular tumor mass or detectable circulating tumor cells in the peripheral blood.

Clinical presentation – Patients present with a bewildering variety of symptoms caused by the occlusion of small vessels. Common presentations include constitutional symptoms (eg, fever, night sweats, weight loss), rapidly progressive neurologic signs (eg, dementia, progressive cerebral vascular accident, peripheral neuropathy), and skin lesions that resemble inflammatory skin conditions (eg, thrombophlebitis, erythema nodosum). (See 'Clinical presentation' above.)

Diagnosis – IVLBCL should be suspected in patients with unexplained constitutional symptoms, rapidly progressive neurologic findings, and/or skin lesions that resemble inflammatory skin conditions.

Diagnosis is based on identification of large B cell lymphoma cells in small to medium blood vessels from a biopsy of involved skin, senile hemangiomata (if present), or random biopsies of apparently normal skin. If this does not yield a diagnosis, biopsy of other sites of suspected involvement may be undertaken, as appropriate. (See 'Diagnosis' above.)

Differential diagnosis – Autoimmune/collagen diseases and infections can cause similar nonspecific symptoms (eg, fever, malaise, dyspnea) but no lymphadenopathy or tumor masses. (See 'Differential diagnosis' above.)

Pretreatment evaluation – All patients with IVLBCL require evaluation for central nervous system (CNS) involvement by lumbar puncture and magnetic resonance imaging, as discussed separately. (See "Initial treatment of advanced stage diffuse large B cell lymphoma", section on 'Central nervous system (CNS) evaluation'.)

Management – Treatment includes both systemic therapy and therapy directed at the CNS. (See 'Treatment' above.)

Systemic therapy – Systemic treatment of IVLBCL is like that for diffuse large B cell lymphoma, as discussed separately. (See "Initial treatment of advanced stage diffuse large B cell lymphoma".)

CNS – Management is guided by findings from the evaluation of the CNS:

-No documented CNS involvement – For patients with no documented CNS involvement, we provide CNS prophylaxis as discussed separately. (See "Initial treatment of advanced stage diffuse large B cell lymphoma", section on 'Central nervous system (CNS) evaluation'.)

-CNS involvement – Treatment of documented CNS involvement varies among institutions but generally involves intrathecal chemotherapy, with or without high-dose methotrexate, and/or radiation therapy. (See "Secondary central nervous system lymphoma: Treatment and prognosis".)

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References

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