10 research outputs found
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
Characteristics of T-cell large granular lymphocyte proliferations associated with neutropenia and inflammatory arthropathy
Coexistence of myeloma plasmocyticum and chronic myeloproliferative disease - report of two cases
Jednoczesne wyst臋powanie dw贸ch nowotwor贸w wywodz膮cych si臋 z uk艂adu ch艂onnego i krwiotw贸rczego
jest rzadko opisywane. Przedstawiono przypadki dw贸ch pacjentek, u kt贸rych w chwili rozpoznania szpiczaka
plazmocytowego obecne by艂y r贸wnie偶 cechy przewlek艂ej choroby mieloproliferacyjnej w obrazie
cytologicznym krwi obwodowej i szpiku kostnego. Objawy te rozpoznano pocz膮tkowo jako odczyn bia艂aczkowy
w przebiegu zasadniczej choroby nowotworowej i rozpocz臋to chemioterapi臋 specyficzn膮 dla
szpiczaka. Po leczeniu uzyskano cz臋艣ciow膮 remisj臋 szpiczaka, ale obserwowano stopniow膮 progresj臋
choroby mieloproliferacyjnej. Przeprowadzona ponowna diagnostyka doprowadzi艂a do rozpoznania u jednej
chorej wsp贸艂istnienia szpiczaka plazmocytowego i przewlek艂ej niesklasyfikowanej choroby mieloproliferacyjnej
oraz szpiczaka i przewlek艂ej bia艂aczki szpikowej u drugiej pacjentki. Opisane przypadki ilustruj膮
trudno艣ci diagnostyczne i terapeutyczne w przypadku bardzo rzadkiego wsp贸艂istnienia przewlek艂ych chor贸b
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 m臋偶czyzny rozpoznano jednocze艣nie nowotw贸r pod艣cieliska przewodu pokarmowego (GIST)
i szpiczaka plazmocytowego (MP). W badaniu immunofenotypowym wykazano ekspresj臋 c-kit (CD117)
zar贸wno na plazmocytach MP, jak i na kom贸rkach GIST. W wyniku leczenia MP z zastosowaniem schematu
VAD (winkrystyna, adriamycyna, deksametazon), a nast臋pnie 9-miesi臋cznej terapii talidomidem,
w po艂膮czeniu z podawanymi co miesi膮c melfalanem i deksametazonem, uzyskano i utrzymano trwaj膮c膮
14 miesi臋cy remisj臋 cz臋艣ciow膮 (PR). Leczenie GIST obejmowa艂o ca艂kowite usuni臋cie guza, a po pojawieniu
si臋 przerzut贸w w jamie brzusznej - systemow膮 terapi臋 przy u偶yciu inhibitor贸w kinaz tyrozynowych.
Zar贸wno 2-miesi臋czne leczenie imatynibem, jak i 2,5-miesi臋czne sunitynibem zako艅czy艂y si臋 niepowodzeniem.
Pacjent zmar艂 18 miesi臋cy od rozpoznania obu nowotwor贸w z powodu progresji GIST, znajduj膮c
si臋 w okresie PR MP. Stwierdzenie obecno艣ci ekspresji c-kit na kom贸rkach obu nowotwor贸w i ich
synchroniczne wyst膮pienie mo偶e sugerowa膰 wsp贸lne zdarzenie onkogenne (mutacji c-kit), a jednocze艣nie
wyklucza wyindukowanie GIST i/lub MP leczeniem przeciwnowotworowym. Podkre艣lenia wymaga
odmienna odpowied藕 obu nowotwor贸w na leczenie, kt贸ra sk艂ania do rozwa偶enia nieznanego efektu nowych
terapii celowanych i immunomoduluj膮cych synchronicznie i/lub metachronicznie wyst臋puj膮cych
nowotwor贸w na przebieg kliniczny ka偶dego 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, 脳100). Granzyme B highlights cytotoxic granules in these cells (EnVision stain, 脳200). Patient 10 with polyclonal T-LGL lymphocytosis. Staining for CD8 shows dispersed T cells (EnVision stain, 脳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, 脳100). Patient 9. The lymphoid nodule contains few CD20B cells (EnVision stain, 脳200). Patient 7 with RA and T-LGL leukemia. A decreased count of granulocytic precursors (myeloperoxydase) is shown (EnVision stain, 脳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鈥搉egative, 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