A 14-year-old spayed female American Shorthair cat, weighing 2.8 kg, was presented at Azabu University Veterinary Teaching Hospital with a 6-month history of weight loss, vomiting, decreased activity and a palpable abdominal mass (day 0). Prior to the referral, the cat was treated with an elimination diet, metronidazole (15 mg/kg PO q12h [Flagyl; Shionogi]) and prednisolone (1–2 mg/kg SC [Prednisolone Injection KS; Kyoritsu Seiyaku]); however, the cat’s clinical signs did not improve. Physical examination showed a body condition score of 3/9, with dehydration, pale mucous membranes and a mid-cranial abdominal firm and irregular mass (4 cm in size). Informed consent for all procedures was provided by the owner. Haematological examination (XT-2000iv; Sysmex) showed neutrophilia (24,370 cells/µl; reference interval [RI] 2500–12,500 cells/µl) and mild regenerative anaemia (red blood cells 4.7 × 106/µl [RI 5.5–10.0 × 106/µl]; haematocrit [Hct] 20% [RI 24–25%]; reticulocytes 122 × 103/µl [RI <50 × 103/µl]). Feline leukaemia virus antigen and feline immunodeficiency virus antibody tests were both negative (SNAP FIV/FeLV Combo Kit; IDEXX). The serum biochemistry panel (cobas 6000; Roche) revealed mild hypoproteinaemia (5.3 g/dl; RI 5.4–7.8 g/dl), hypoalbuminaemia (2.1 g/dl; RI 2.5–3.9 g/dl) and increased serum amyloid A (SAA) (190.5 µg/ml [RI 0–2.5 µg/ml]; FUJIFILM VET Systems). No abnormalities were seen upon urine and faecal examination. Thoracic radiographs were unremarkable; however, abdominal radiographs revealed an irregularly rounded large soft tissue opaque mass (up to 6 cm in diameter) in the mid-ventral abdomen, slightly to the right of the midline, causing caudal and left caudolateral displacement of the small intestine (). The mass had a well-defined cranial margin and ill-defined caudal margin owing to decreased serosal margination. Abdominal ultrasonography (HI VISION Preirus; Hitachi) revealed a large irregularly rounded heterogeneously hypoechoic mass, measuring up to 4 cm in length, in the mid-ventral abdomen. The mass was connected to the intestinal loop with complete loss of layering and several hyperechoic foci with distal reverberation artefact within the centre of the mass. This mass was adjacent to the irregularly enlarged and hypoechoic jejunal lymph node and the portal vein without recognisable differentiation between the intestinal mass and the enlarged jejunal lymph nodes (). Peritoneal fat around the aforementioned mass was moderately hyperechoic. On cytology, Wright–Giemsa-stained slides of the mass were highly cellular and contained many atypical round cells, as well as some degenerative neutrophils, minimal macrophages, rare epithelioid macrophages and rare multinucleated giant cells (). Atypical round cells were round-to-oval in shape, 10–30 µm in diameter and contained an eccentrically located round-to-oval nucleus, reticular-to-coarse chromatin and sometimes a prominent nucleoli. The cytoplasm was moderate in amount, basophilic in colour, with perinuclear halos and sometimes with a small amount of light pink material at the cellular edge (,). A moderate number of atypical cells were multinucleated with prominent nucleoli, and large and small nuclei. A few neutrophils contained a moderate number of mixed bacteria in their cytoplasm (). CT (BrightSpeed Elite Pro; GE Healthcare) was performed the day after initial presentation (day 1) under general anaesthesia, and showed a duodenal mass with suspected intestinal perforation, in addition to an enlarged jejunal lymph node. There were no other abnormalities or other masses found during the CT examination. A transfusion of 38 ml whole blood was performed because the patient was expected to experience further progression of hypoproteinaemia and anaemia after correction of dehydration and surgical blood loss. The duodenal mass was surgically removed under general anaesthesia (day 2). The mass had adhered to the greater omentum and to a small portion of the right limb of the pancreas, and although the mass was perforated there was no free abdominal fluid because the site of perforation was covered by the omentum (). After resection of the mass and a small portion of pancreas, a duodenal–jejunal anastomosis was created. It was found, however, that the jejunal lymph node was markedly enlarged, adhering to the portal vein and causing an involution of the anterior mesenteric vessels. Therefore, resection of the jejunal lymph node was impossible. Moreover, there were already some suspected metastases on the serous surface of jejunum and on mesentery (). Six days after surgery, the enlarged jejunal lymph node was measured by abdominal ultrasonography as the baseline for future monitoring (measurements 3.5 × 2.9 cm). Histopathological examination of the surgical specimen revealed infiltration of round neoplastic cells with abundant extracellular acidophilic material that was positive for Congo red. The tumour cells were immunohistochemically positive for CD79 alpha (α), IgA and λ immunoglobulin light chain, and were negative for CD20, IgG, IgM and kappa (κ) immunoglobulin light chain. Amyloid deposits were immunohistochemically positive for λ immunoglobulin light chain. Based on these findings, a duodenal plasmacytoma with AL amyloidosis was diagnosed. Moreover, PCR for antigen receptor rearrangement of the tumour cells was performed as previously described, and showed a monoclonal rearrangement of the immunoglobulin heavy chain gene. Three days after surgery, SAA (2.9 µg/ml; RI 0–2.5 µg/ml) was almost normal. Upon suture removal on day 16, serum protein electrophoresis (FUJIFILM VET Systems) revealed a normal shape. Moreover, the albumin:globulin ratio (0.62; RI 0.6–1.32), cobalamin (>1000 ng/l [RI 290–1000 ng/l]; IDEXX) and folate (16.1 µg/l [RI 9.7–21.6 µg/l]; IDEXX) were all within normal ranges. Abdominal ultrasonography of the enlarged jejunal lymph node showed an increased size of 3.6 × 5.1 cm on day 16. Based on this finding, a chemotherapy regimen of cyclophosphamide (CPA [Endoxan; Shionogi]) at a dosage of 258 mg/m2 (50 mg tablet/cat) PO q3 weeks (86 mg/m2/week) with prednisolone (1 mg/kg PO q24h [Predonine; Shionogi]) was started. After 3 weeks, however, the lymph node further enlarged to 4.3 × 5.7 cm, at which point the dosage of CPA was increased to 300 mg/m2 IV q2 weeks (150 mg/m2/week). After 4 weeks of treatment with CPA (day 62), the lymph node had further enlarged (5.1 × 6.2 cm). CPA was then discontinued and a regimen of chlorambucil (CLB; [Leukeran; GlaxoSmithKline]) at a dosage of 20 mg/m2 PO q2 weeks and spironolactone (2 mg/kg PO q12h [Aldactone; Pfizer]) because of malignant ascites (3.3 g/dl protein, 5000 nucleated cells/µl with tumour cells, Hct 1.8%), was started. By day 72 the lymph node had further enlarged (5.5 × 6.7 cm) and 800 ml of free abdominal fluid was removed. CLB was discontinued and lomustine (CCNU; [CeeNU; Bristol Myers Squibb]) at a dosage of 50 mg/m2 PO q3 weeks was instituted with furosemide (0.5 mg/kg PO q12h [Lasix; Nichi-Iko]) added as a diuretic. As the CCNU was ineffective (jejunal lymph node 7.0 × 7.5 cm), L-asparaginase (400 U/kg SC [Leunase; Kyowa Kirin]) was used with continuous intravenous infusion at a rate of 3–5 ml/kg/h of saline (Terumo) because the cat was dehydrated owing to the diuretics. At that time, SAA (<0.1 µg/ml; RI 0–2.5 µg/ml) was within the expected range. Three days after the L-asparaginase injection, the cat was discharged from the hospital with a once-daily subcutaneous injection of saline at home by a visiting veterinarian, owing to concerns about the cat’s stress levels in the hospital. However, 3 days after discharge, on day 96, the cat died at home. A post-mortem examination was performed. Upon necropsy, ascites, an enlarged jejunal lymph node (6.0 × 7.0 cm) and some whitish nodules of 2–3 mm on the serous surfaces of the liver, and numerous whitish miliary nodules on serous surfaces of the small intestine and large, intestine were grossly observed. On histopathological examination, it was found that the tumour cells had infiltrated the stomach, small intestine, large intestine, liver, spleen, bladder, abdominal wall, diaphragm, mesentery, retroperitoneum, lymph nodes (cervical, thoracic, jejunal) and bone marrow. The tumour cells were large, round-shaped and with marked anisocytosis. The nuclei of the tumour cells showed marked anisokaryosis with dense and irregular nuclear membranes. Abundant extracellular acidophilic material, positive for Congo red, was also found in the all tumour tissues. The tumour cells were immunohistochemically positive for CD79α, IgA and λ immunoglobulin light chain, and negative for CD20, IgG, IgM and κ immunoglobulin light chain. Amyloid deposits were immunohistochemically positive for λ immunoglobulin light chain (). Based on these findings, systemic dissemination of plasmacytoma with AL amyloidosis was diagnosed.