High grade abdominal lymphoma with secondary pancreatic involvement mimicking tuberculosis

A 55-year-old female came with the complaints of abdominal pain radiating to back. On abdominal examination, there is a hard non-tender epigastric mass. Complete blood count reveals elevated lymphocytes - 84.6% (reference range 45-75%). Rest of the clinical examination was unremarkable.

A triple-phase Multidetector Computed Tomography (MDCT) shows multiple enlarged predominantly conglomerate lymph nodes in periportal, peri-pancreatic, infra-pancreatic, pre-aortic, bilateral para-aortic, peri-renal, peri-mesenteric, retrocrural, aorto-caval, retrocaval and right iliac fossa region. Many of them shows non-enhancing central necrotic area within. The largest lymph node is in infra-pancreatic region measuring 8.8 x 3.1 cm . Peripancreatic lymphnodes causes compression of ampulla and duodenum leading to mild intrahepatic biliary radical dilatation (IHBRD). The lymph node around the peri-pancreatic region is in close proximity with the head and uncinate process of pancreas with loss of fat plane between the lymph nodal mass and pancreas( arrows in figure 3b). No significant pancreatic duct dilatation seen. Patient was planned for diagnostic laparoscopy with laparotomy which shows multiple conglomeratemesenteric nodes and were taken for biopsy.

Lymphomatous proliferation is defined as clonal malignant proliferation of a mature lymphocyte from a secondary lymphoid structure- a lymph node or an extranodal structure i.e. the spleen and also the structures attached to the mucosa like Peyer’s patches [1]. The cause remains unknown but certain lymphomatogenic factors have been identified [2]. Extranodal can involve any organ, while secondary involvement from a disseminated form is most frequent. Isolated pancreatic lymphoma arising from lymphoid elements are extremely rare, and is defined by certain clinical criteria like normal leukocyte count, absence of palpable superficial lymphadenopathy, no enlargement of mediastinal nodes, predominance of pancreatic mass with peripancreatic lymphnodes and absent hepatic or splenic involvement [3]. Alimentary canal involvement occurs in 10-30% of cases of Non- Hodgkin’s lymphoma. The stomach is the most frequent site of extranodal lymphomas [4]. Pancreatic lymphoma are rare, representing less than 1% of NHL. [5, 6].

Tuberculous lymphadenopathy appears to show various pattern from an increased number (> 3) of normal-sized nodes to large nodal masses. The most commonly involved groups are upper para-aortic, peripancreatic, mesenteric and omental lymph nodes. Four types of contrast patterns perceived in tuberculous lymphadenitis are (a)peripheral rim enhancement with hypodense centres (b) inhomogeneous enhancement (c) non enhancing nodes and (d) homogenous enhancement. Other patterns include calcified lymphnode and conglomerate lymphnode masses with areas of necrosis secondary to perinodal inflammation. Like in our case these nodes shows peripherally enhancing lymph nodes with low density centres in contrast enhanced CT. This appearance is highly suggestive but not pathagnomic of tuberculosis. Similar pattern can also seen in case of high-grade lymphoma[7,8].However, when faced with a pancreatic mass, certain signs should draw attention which includes a discordant large mass with no jaundice, moderate dilatation of pancreatic duct,a raised serum lactic acid dehydrogenase concentration or lymphadenopathy presenting below the level of renal veins and suggest the possibility of lymphoma [9,10]. Although conglomerate necrotic lymph nodes are specific to tuberculosis, but not sensitive since high grade lymphoma can mimic tuberculosis in this aspect. Treatment is based on a variable combination of chemotherapy, radiotherapy and immunotherapy, according to type. In addition to the classic staging of disease, knowledge of varied extranodal presentations is important so as to avoid any inappropriate corticosteroid therapy or unnecessary tuberculosis treatment before confirmation.