Superficial lymph nodes involved by lymphoma in modern gray-scale ultrasound imaging

Background: Clinical evaluation by palpation of superficial lymph nodes involved by lymphoproliferative process is not sufficient. Ultrasound is a useful method of the initial differential diagnosis of lymph nodes. The aim was to assess the spectrum of ultrasound features of superficial lymphomatous nodes and possible diagnostic pitfalls. Material/Methods: Fifty five lymph nodes in 55 patients were prospectively examined in ultrasound with application of blood flow imaging modes and modern imaging techniques. Only forty lymph nodes with histopathologically proven lymphoma were selected for this analysis (3 Hodgkin, 37 non-Hodgkin). Results: 27.5% of the examined lymph nodes were longitudinal; 42.5% had an oval or round shape; 30% were oval-lobulated or lobulated. 32.5% of the nodes did not show an echogenic hilum, 20% had a normal hilum, and 25% - evidently abnormal. 12.5% of the nodes were anechoic. The general ultrasound impression of a reactive lymph node was presented by 37.5% of the lymphomatous nodes; 45% were suspicious. Among 26 patients with non-Hodgkin lymphoma with multiple lymph nodes involved, in 15 (58%) lymph nodes were modeling on each other. Conclusions: Lymphomatous nodes reveal diverse ultrasound presentations: from appearances indistinguishable from benign reactive lymph nodes to features typical of metastases. Ultrasound internal structure of lymphomatous nodes may be anechoic, causing the possibility of confusion with a cyst, especially in case of a single lymphomatous node. Multiple lymphomatous nodes with non-Hodgkin lymphoma often model on each other assuming geometrical shapes

Coexistence of myeloma plasmocyticum and chronic myeloproliferative disease - report of two cases

Jednoczesne występowanie dwóch nowotworów wywodzących się z układu chłonnego i krwiotwórczego jest rzadko opisywane. Przedstawiono przypadki dwóch pacjentek, u których w chwili rozpoznania szpiczaka plazmocytowego obecne były również cechy przewlekłej choroby mieloproliferacyjnej w obrazie cytologicznym krwi obwodowej i szpiku kostnego. Objawy te rozpoznano początkowo jako odczyn białaczkowy w przebiegu zasadniczej choroby nowotworowej i rozpoczęto chemioterapię specyficzną dla szpiczaka. Po leczeniu uzyskano częściową remisję szpiczaka, ale obserwowano stopniową progresję choroby mieloproliferacyjnej. Przeprowadzona ponowna diagnostyka doprowadziła do rozpoznania u jednej chorej współistnienia szpiczaka plazmocytowego i przewlekłej niesklasyfikowanej choroby mieloproliferacyjnej oraz szpiczaka i przewlekłej białaczki szpikowej u drugiej pacjentki. Opisane przypadki ilustrują trudności diagnostyczne i terapeutyczne w przypadku bardzo rzadkiego współistnienia przewlekłych chorób limfo- i mieloproliferacyjnych.Coexistence of two neoplastic disorders derived from lymphoid and hematopoietic lineage is rarely described. We present two patients with initial presentation of myeloma plasmocyticum and symptoms of chronic myeloid disease in peripheral blood and bone marrow cytology. At first, the myeloid abnormalities were diagnosed as reactive due to underlying malignancy and patients were initially treated with cytotoxic drugs specific for myeloma. After completion of therapy, partial remission of myeloma was achieved but simultaneous progression of myeloid abnormalities was observed. Additional diagnostic tests were performed which allowed to establish the final diagnosis of coexistence of myeloma plasmocyticum with unclassified chronic myeloproliferative disease in the first patient and myeloma plasmocyticum with chronic myeloid leukemia in the second one. These cases illustrate diagnostic and therapeutic quandaries in course of the very rare coexistence of chronic lympho- and myeloproliferative disorders

Synchronous appearance of gastrointenstinal stromal tumor and myeloma plasmocyticum with c-kit expression - a case report

U 60-letniego mężczyzny rozpoznano jednocześnie nowotwór podścieliska przewodu pokarmowego (GIST) i szpiczaka plazmocytowego (MP). W badaniu immunofenotypowym wykazano ekspresję c-kit (CD117) zarówno na plazmocytach MP, jak i na komórkach GIST. W wyniku leczenia MP z zastosowaniem schematu VAD (winkrystyna, adriamycyna, deksametazon), a następnie 9-miesięcznej terapii talidomidem, w połączeniu z podawanymi co miesiąc melfalanem i deksametazonem, uzyskano i utrzymano trwającą 14 miesięcy remisję częściową (PR). Leczenie GIST obejmowało całkowite usunięcie guza, a po pojawieniu się przerzutów w jamie brzusznej - systemową terapię przy użyciu inhibitorów kinaz tyrozynowych. Zarówno 2-miesięczne leczenie imatynibem, jak i 2,5-miesięczne sunitynibem zakończyły się niepowodzeniem. Pacjent zmarł 18 miesięcy od rozpoznania obu nowotworów z powodu progresji GIST, znajdując się w okresie PR MP. Stwierdzenie obecności ekspresji c-kit na komórkach obu nowotworów i ich synchroniczne wystąpienie może sugerować wspólne zdarzenie onkogenne (mutacji c-kit), a jednocześnie wyklucza wyindukowanie GIST i/lub MP leczeniem przeciwnowotworowym. Podkreślenia wymaga odmienna odpowiedź obu nowotworów na leczenie, która skłania do rozważenia nieznanego efektu nowych terapii celowanych i immunomodulujących synchronicznie i/lub metachronicznie występujących nowotworów na przebieg kliniczny każdego z nich z osobna.We report a case of a 60-year-old man in whom synchronous appearance of gastrointenstinal stromal tumor (GIST) and myeloma plasmocyticum (MP) with c-kit expression on both tumors. The treatment of MP with VAD (vincristine, adriamycin, dexamethasone), followed by a 9-month administration of thalidomide, combined with melphalan and dexamethasone given once a month, resulted in achieving and maintaining partial remission (PR) for 14 months. The therapy of GIST included a total resection of the tumor and, after tumor metastasizing within abdominal cavity, systemic treatment with c-kit kinase inhibitors. Both 2-month imatinib administration and 2.5-month sunitinib therapy were unsuccessful. The patient died 18 months since diagnosis of both tumors due to progression of GIST, in PR of myeloma. A simultaneous occurrence meof both tumors excludes carcinogenic effect of therapy. Expression of c-kit by cells of both malignancies may suggest one oncogenic event, namely c-kit mutation, in pathogenesis of both tumors. It is also worthy to stress different response of MM and GIST to treatment. This case raises also the question of potential cross-effect of targeted and immunomodulatory therapies on synchronous and/or metachronous neoplasms'clinical course

Histopathological features of bone marrow in patients with arthritis and T-cell large granular lymphocyte (T-LGL) lymphocytosis

Patient 1 with rheumatoid arthritis (RA) and T-LGL leukemia. Staining for CD57 demonstrates intrasinusoidal linear arrays and interstitial clusters of T cells (EnVision stain, ×100). Granzyme B highlights cytotoxic granules in these cells (EnVision stain, ×200). Patient 10 with polyclonal T-LGL lymphocytosis. Staining for CD8 shows dispersed T cells (EnVision stain, ×200). Patient 9 with unclassified arthritis, T-LGL leukemia, and and gene rearrangements. CD3 staining shows interstitial and nodular infiltration of T cells (EnVision stain, ×100). Patient 9. The lymphoid nodule contains few CD20B cells (EnVision stain, ×200). Patient 7 with RA and T-LGL leukemia. A decreased count of granulocytic precursors (myeloperoxydase) is shown (EnVision stain, ×200). IGKV, immunoglobulin kappa variable; IGLV, immunoglobulin lambda variable<p><b>Copyright information:</b></p><p>Taken from "Characteristics of T-cell large granular lymphocyte proliferations associated with neutropenia and inflammatory arthropathy"</p><p>http://arthritis-research.com/content/10/3/R55</p><p>Arthritis Research & Therapy 2008;10(3):R55-R55.</p><p>Published online 12 May 2008</p><p>PMCID:PMC2483444.</p><p></p

Ethidium bromide-stained polyacrylamide gel showing polymerase chain reaction products derived from gene rearrangements in patients with rheumatoid arthritis and T-cell large granular lymphocyte (T-LGL) proliferations

Polyclonal expansion of T-LGLs in patient 10. Lane 1: gene rearrangement–negative, polyclonal smear (tube A); lane 2: gene rearrangement-negative, polyclonal smear (tube B); lane 3: gene rearrangement-negative, polyclonal smear (tube C); lane 4: standard 50 base pairs (bp); lane 5: gene rearrangement-negative, polyclonal smear (tube A); lane 6: gene rearrangement-negative, polyclonal smear (tube B); and lane 7: gene rearrangement-negative, polyclonal smear. Monoclonal expansion in polyclonal background in patient 7. Lane 1: gene rearrangement: monoclonal product 180 bp (i) in tube A; lane 2: gene rearrangement: monoclonal product 210 bp (ii) in polyclonal background (tube B); lane 3: gene rearrangement: monoclonal product 160 bp (iii); lane 4: (tube A) gene rearrangement-negative, polyclonal smear; lane 5: standard 50 bp; lane 6: (tube B) gene rearrangement-negative, polyclonal smear; and lane 7: (tube C) gene rearrangement-negative, polyclonal smear. Monoclonal gene rearrangements in patient 1 with T-LGL leukemia. Lane 1: gene rearrangement-negative (tube A); lane 2: gene rearrangement-positive, monoclonal product 250 bp (iv) in tube B; lane 3: (tube C): gene rearrangement-negative, polyclonal smear; lane 4: standard 50 bp; lane 5: gene rearrangement-positive, monoclonal product 230 bp (v) in tube A; lane 6: gene rearrangement-positive, monoclonal product 180 bp (vi) in tube B; and lane 7: gene rearrangement-negative, polyclonal smear. TCR, T-cell receptor.<p><b>Copyright information:</b></p><p>Taken from "Characteristics of T-cell large granular lymphocyte proliferations associated with neutropenia and inflammatory arthropathy"</p><p>http://arthritis-research.com/content/10/3/R55</p><p>Arthritis Research & Therapy 2008;10(3):R55-R55.</p><p>Published online 12 May 2008</p><p>PMCID:PMC2483444.</p><p></p