Non-Hodgkin lymphoma (NHL) is a heterogeneous group of diseases encompassing all lymphoproliferative neoplasms other than Hodgkin lymphoma. It constitutes 85-90% of all lymphomas. Divided into B-cell (85%) and T-cell (15%) types. Low-grade (indolent: follicular, marginal zone, small lymphocytic) and high-grade (aggressive: diffuse large B-cell, Burkitt, mantle cell) types differ clinically and radiologically. Unlike Hodgkin lymphoma, NHL shows skip involvement pattern, frequent extranodal involvement (40%), tendency for necrosis, and conglomerate lymphadenopathy. Diagnosis at advanced stage (60-70%) is common.
Age Range
20-75
Peak Age
55
Gender
Male predominant
Prevalence
Uncommon
In non-Hodgkin lymphoma, neoplastic lymphocytes show clonal proliferation and completely disrupt normal lymph node architecture. In DLBCL, rapid cell division exceeds vascular supply leading to necrosis — this causes heterogeneous enhancement and central necrosis on CT. In follicular lymphoma, slow growth and low mitotic activity explain more homogeneous structure. Extranodal spread results from tumor cell migration via hematogenous and lymphatic channels to distant sites — creating skip pattern unlike HL's sequential spread. Conglomerate lymphadenopathy results from adjacent nodes breaching capsules and adhering. FDG uptake on PET-CT depends on tumor grade: aggressive NHL (DLBCL, Burkitt) shows intense uptake, while indolent types (follicular grade I-II) may show low-moderate uptake.
Appearance of mesenteric vessels (SMA and branches) sandwiched between lymphomatous masses. It is a highly specific finding for NHL mesenteric involvement and helps differentiate from other mesenteric pathologies (carcinomatosis, desmoid tumor).
Contrast-enhanced CT shows conglomerate lymphadenopathy in multiple stations. Nodes are adhering with indistinct borders. Heterogeneous enhancement and central necrosis areas may be seen (especially in DLBCL). Vascular encasement (SMA, aorta, IVC) may be present. Mesenteric, retroperitoneal, and pelvic stations are frequently involved. Sandwich sign (mesenteric vessels sandwiched between lymphomatous masses) is characteristic.
Report Sentence
Conglomerate lymphadenopathy in multiple stations with heterogeneous enhancement and central necrosis areas — consistent with non-Hodgkin lymphoma.
FDG uptake on PET-CT varies by tumor subtype. In aggressive NHL (DLBCL, Burkitt, mantle cell) SUVmax is usually >10-25. In indolent types (follicular grade I-II) SUVmax may be 3-8. Uptake shows skip pattern — non-contiguous stations. Extranodal involvement (spleen, bone marrow, GI tract, CNS) is best evaluated on PET-CT. During transformation (indolent→aggressive) SUVmax increases markedly.
Report Sentence
Intense FDG uptake (SUVmax: ...) in non-contiguous lymph node stations showing skip pattern — consistent with non-Hodgkin lymphoma.
Ultrasonography shows round, hypoechoic lymph nodes with lost hilum. Conglomerate structure — multiple nodes adhering, indistinct borders. Intranodal necrosis (cystic area) and heterogeneous echogenicity may be seen in aggressive types. Posterior acoustic enhancement (pseudocystic appearance) may be seen in very hypoechoic nodes.
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Multiple round, hypoechoic lymph nodes with lost hilum forming conglomerate structure — consistent with lymphoproliferative disease.
Color Doppler shows chaotic, irregular vascularity pattern. Hilar vascularity is lost, replaced by peripheral, subcapsular, and intranodal irregular vascular branching. Power Doppler shows rich vascularity but irregular distribution. Intranodal vascular resistive index may be elevated (RI >0.8). Avascular zones may be seen in necrotic areas.
Report Sentence
Lymph nodes show hilar vascularity loss with chaotic peripheral vascularity and intranodal avascular necrosis areas — consistent with malignant lymphadenopathy.
Marked diffusion restriction on DWI — ADC usually 0.4-0.8 × 10⁻³ mm²/s in aggressive types. ADC may be higher in indolent types (0.8-1.2). Heterogeneous ADC values in necrotic areas — necrosis shows high ADC, viable tumor shows low ADC. Diffusion restriction shows heterogeneous distribution in conglomerate masses.
Report Sentence
Marked and heterogeneous diffusion restriction on DWI in conglomerate lymph node mass with ADC increase in necrotic areas — consistent with aggressive lymphoma.
Contrast-enhanced CT shows mesenteric vessels (SMA branches) sandwiched between lymphomatous masses — sandwich sign. Large retroperitoneal soft tissue mass may encase aorta and IVC (vascular encasement). Splenic involvement may appear as focal hypodense lesions or diffuse splenomegaly. Bone marrow involvement may appear as diffuse sclerotic/lytic lesions.
Report Sentence
Mesenteric vessels are sandwiched between lymphomatous masses (sandwich sign) — consistent with non-Hodgkin lymphoma.
Criteria
Most common NHL subtype (30-35%). Aggressive, rapidly growing. Large, heterogeneous masses, necrosis common. SUVmax usually >10-15.
Distinct Features
Heterogeneous enhancement, necrosis, rapid growth. Extranodal involvement common (GI, CNS, bone). 60-70% cure rate with R-CHOP chemotherapy.
Criteria
Second most common NHL type (20-25%). Indolent, slow course. t(14;18) BCL2 translocation characteristic. Widespread LAP but symptoms may be mild.
Distinct Features
Homogeneously enhancing, small-medium sized multiple nodes. Necrosis rare. Low-moderate FDG uptake on PET (SUVmax 3-8). 3%/year risk of transformation to DLBCL.
Criteria
Very aggressive, one of fastest growing human tumors (doubling time 24-48 hours). MYC translocation. Common in children and young adults. Abdominal involvement predominant (ileocecal region).
Distinct Features
Large abdominal mass, prominent necrosis, tumor lysis syndrome risk. Very intense FDG uptake on PET (SUVmax >15-20). Requires urgent treatment — spontaneous tumor lysis may be life-threatening.
Distinguishing Feature
HL shows contiguous spread, anterior mediastinal predilection, homogeneous structure, and absence of necrosis — NHL shows skip pattern, conglomerate structure, necrosis, and extranodal involvement.
Distinguishing Feature
Metastatic adenocarcinoma shows primary tumor focus, peripherally enhancing centrally necrotic nodes, and limited involvement — NHL has no primary focus, widespread conglomerate LAP and sandwich sign are distinguishing.
Distinguishing Feature
TB shows rim enhancement, nodal matting, calcification, and perinodal infiltration — NHL shows homogeneous or heterogeneous enhancement, sandwich sign, and extranodal mass. TB is usually limited to one region.
Distinguishing Feature
Castleman disease (hyaline vascular type) shows single, markedly hypervascular mass with intense homogeneous enhancement — NHL shows multiple conglomerate nodes and heterogeneous enhancement.
Urgency
urgentManagement
medicalBiopsy
NeededFollow-up
specialist-referralTissue diagnosis by excisional or core biopsy is mandatory in suspected NHL — FNA is insufficient for subtype determination. Staging uses Ann Arbor/Lugano system. PET-CT is used for FDG-avid types (DLBCL, Burkitt, mantle cell), contrast-enhanced CT for FDG-nonavid types (marginal zone, SLL). Treatment varies by subtype: R-CHOP (DLBCL), R-CHOP/BR (follicular), hyper-CVAD/R (Burkitt). Urgent treatment initiation in aggressive types — due to tumor lysis syndrome risk. Watch-and-wait strategy may be applied in indolent types.
Non-Hodgkin lymphoma is a heterogeneous group of diseases. Prognosis and treatment differ greatly between indolent (low-grade — follicular) and aggressive (high-grade — diffuse large B-cell) types. Ann Arbor/Lugano staging system is used. PET-CT is standard for staging and treatment response. Aggressive NHL is treated with R-CHOP and has a 60-70% cure rate.