[Somatostatin receptor endoradiotherapy of neuroendocrine tumors: experience in Hungarian patients]. / Neuroendokrin daganatok szomatosztatinreceptor-endoradioterápiája: hazai betegeken szerzett tapasztalatok.

Beside conventional therapies for the treatment of neuroendocrine tumors, a new therapeutical approach, peptide receptor radionuclide therapy has been developed recently. There are two important features which make this therapy feasible: somatostatin receptors are strongly over-expressed in most neuroendocrine tumors resulting in a high tumor-to-background ratio and internalization of the somatostatin-receptor complex in neuroendocrine cells. Due to these features, neuroendocrine tumors can be treated with radiolabelled somatostatin analogues. For peptide receptor radionuclide therapy, somatostatin analogues are conjugated to a chelator that can bind a radionuclide. The most frequently used radionuclides for neuroendocrine tumor treatment are the ß-emitter Yttrium-90 (9°Y) and the ß+γ emitter Lutetium-177 (¹77Lu). Candidates for somatostatin receptor endoradiotherapy are patients with progressive, metastatic, somatostatin-receptor positive neuroendocrine tumors. Many patients have been successively treated with this approach: according to international results major remission can be achieved in 25% of the cases. Although this therapy is still unavailable in Hungary, Hungarian patients can be treated with somatostatin receptor endoradiotherapy with financial support from the National Health Fund in a co-operation with the University of Basel since 2005. During the past 5 years, 51 Hungarian patients have been treated with this therapy. This review briefly summarizes the theoretical background, indications, effectiveness and side effects of somatostatin receptor endoradiotherapy and the authors present the first data obtained from Hungarian patients.

[Intracranial propagation of invasive aspergilloma in an immuncompromised patient]. / Intracranialis terjedést mutató invazív aspergilloma immunszupprimált beteg esetében.

Aspergillus infection of the central nervous system is a rare disease, occasionally seen among immunocompromised patients. The most frequent pathway is hematogenic dissemination. Less known is the direct propagation from the paranasal sinuses, which is usually observed in immunocompetent patients. We report a patient who developed cavernous sinus syndrome due to an invasive intracranial aspergilloma after longlasting chemo- and steroid therapy for chronic lymphoid leukemia and immunhemolytic anemia. The characteristic features seen on radiological images--brain CT and MRI--suggested the possibility of invasive aspergilloma. Postoperative histology defined the diagnosis. Our case review highlights the importance of considering the possibility of an invasive opportunistic infection of the CNS in an immunocompromised patient presenting a new neurological sign.

In vitro effect of carboplatin, cytarabine, paclitaxel, vincristine, and low-power laser irradiation on murine mesenchymal stem cells.

BACKGROUND AND OBJECTIVES: Mesenchymal stem cells (MSCs) are promising for use in regenerative medicine. Cytostatics can decrease, but low-power laser irradiation (LPLI) can increase the growth of MSCs. The interaction of LPLI, MSCs and cytostatics is not known. This study investigated the effect of four cytostatics (carboplatin, cytarabine, paclitaxel, vincristine), LPLI, and combination of a cytostatic drug and LPLI on murine MSCs (mMSCs). STUDY DESIGN/MATERIALS AND METHODS: MMSCs were exposed to LPLI (660 nm diode laser; 60 mW output power; range of power density: 76-156 mW/cm(2); range of energy density: 1.9-11.7 J/cm(2)) and/or a cytostatic drug (carboplatin: 2, 10, 50; cytarabine: 0.4, 10, 50; paclitaxel: 0.4, 2, 10; vincristine: 0.02, 0.1, 0.5 microg/ml, respectively). Cell proliferation was measured after 24, 48, or 72 hours incubation. RESULTS: LPLI at 1.9 J/cm(2) dose increased the proliferation rate with 41% after 48 hours. However, 11.7 J/cm(2) LPLI caused 42% inhibition and cytostasis was still detectable after 72 hours. LPLI caused equivalent stimulation in single or in divided doses (3.8 vs. double 1.9 J/cm(2) in a 24-hour period). The cytotoxicity of 50 microg/ml carboplatin was eliminated, the inhibitory power of 0.1 microg/ml vincristine was attenuated by 1.9 J/cm(2) LPLI even 3 days post-treatment (attenuation >10%). The 11.7 J/cm(2) LPLI enhanced the cytotoxicity of 50 microg/ml cytarabine (from 48% to 73%) and 10 microg/ml paclitaxel (from 37% to 78%). Combination of the ineffective 0.4 microg/ml cytarabine or paclitaxel with the inhibitory 11.7 J/cm(2) LPLI exhibited stronger inhibition than the 11.7 J/cm(2) LPLI alone (69% and 69% vs. 42%). CONCLUSIONS: Low energy density of LPLI increases and high energy density of LPLI decreases the proliferation of mMSCs. Furthermore, LPLI can prevent or attenuate some drug's cytotoxicity and amplify others'. The result depends on the applied energy density, on the type and concentration of the cytostatics.

[Therapy in Hodgkin disease and non-Hodgkin lymphomas]. / A Hodgkin- és a non-Hodgkin-lymphomák kezelése.

The therapy of malignant lymphoproliferative diseases has changed many times in recent years. Treatment strategy of Hodgkin's disease is now based on risk adaptation, including not only the results of pretreatment diagnostic and prognostic factors but also the repeated PET/CT (restaging) made in the early treatment period. Possible reduction of irradiation therapy may contribute to lower the risk of secondary tumors, which are common late complications of radiochemotherapy. Autologous stem cell transplantation is the therapy of choice in chemosensitive relapsing patients. The complete remission rate today in Hodgkin's disease is around 85%. In the heterogenic group of Non-Hodgkin Lymphomas, progression of indolent lymphomas (CLL, multiple myeloma, hairy cell leukemia, cutaneous lymphomas, etc.) is slow in case of natural course. Their therapy is mostly palliative and complete remission with the latest treatment modalities is not possible. Aggressive lymphomas are characterized with rapid progression and early death without treatment.Most of them respond to chemotherapy and irradiation.With an adequate therapy, 60-70% of patients reach complete remission (CR) and 40-50% of them remain in remission. Using immune- and radioimmune therapy in indolent and aggressive NHL groups gives possibility to influence G0 tumor cells as well. Their use in combination with classic chemotherapy leads to more complete remissions and better therapy results. The introduction of routine PET/CT made the first and repeated staging of NHL more precise and contributed to more effective treatment. Using autologous stem cell transplantation in chemosensitive patients may improve outcome in selected patients.

[Systemic chemotherapy of liver cancer and patient follow-up]. / A májrák szisztémás kemoterápiája és a betegek gondozása.

We have many possibilities how to treat hepatocellular carcinoma. These therapeutic options depend on the stage of the disease, the condition of the patient and the available therapeutic modalities. At present, none of these treatments are fully successful and the results of systemic treatments are very poor. This paper introduces the role of systemic therapy concerning to prevention, curative and palliative treatments. As well, we emphasize the importance of early diagnosis and patient's follow up.

Multicentric Castleman's disease: a challenging diagnosis.

Multicentric Castleman's disease (MCD) is a sytemic disorder with flares of non-specific symptoms suggestive of a chronic inflammatory syndrome. It is typically accompanied by generalized lymphadenopathy and multiorgan involvement. Histologically, two main variants of Castleman's disease exist, the hyalin vascular type and the plasma cell variant. Upon localization unicentric (localized), and multicentric (diffuse, systemic) subtypes can be distinguished with more different disease outcomes. Patients often exhibit acute phase reactions and several autoimmune phenomena, and are at high risk for developing malignancies. Both the idiopathic and the HHV-8-driven infectious forms of MCD represent distinct disease entities with a less favorable prognosis. The induction of human IL-6 excess via yet unknown upstream mechanisms, and overexpression of viral IL-6 by HHV-8 can pivotally influence MCD biology. Based on the role of IL-6 in pathogenesis, MCD is also designated as IL-6 lymphadenopathy. To date there are no direct therapeutic evidences, but having been translated to daily practice the main regulatory factors may serve as promising therapeutic targets.

Successful tocilizumab treatment in a patient with human herpesvirus 8-positive and human immunodeficiency virus-negative multicentric Castleman's disease of plasma cell type nonresponsive to rituximab-CVP therapy.

We present and discuss the case of a HIV-negative female finally diagnosed upon histopathologic and molecular biologic evaluations with human herpesvirus 8 (HHV8)-positive multicentric Castleman's disease (MCD) of plasma cell type, but with no detectable HHV8-DNA in peripheral blood. She failed to respond to combination immunosuppressive therapeutic trials of corticosteroids and azathioprine, and neither an immunochemotherapy of rituximab-CVP (R-CVP) induced disease resolution. However, monoclonal anti-IL-6R antibody (tocilizumab) immunotherapy resulted in beneficial disease stabilization. A control lymph node biopsy indicated mild polyclonal plasmacytosis, and a negative HHV8 determination. The patient is still receiving tocilizumab. This case emphasizes the individual nature of MCD requiering more personalized disease management.