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EN
The aim of this study: is to demonstrate epidemiological and clinical parameters of the group of patients with sinonasal malignancies and to analyze its impact on development of recurrences after primary surgical treatment conducted in Head and Neck Surgery Department of Holly Cross Cancer Center Kielce during 7-years period 2001-2007. The retrospective analysis of the group of 42 patients with sinonasal malignancies was made, based on medical record and outpatient follow-up, considering: age, sex, primary focus, histological outcome, local and clinical stage and methods of the therapy. In the group of patients with at least 3-years period of follow-up (n=42) the dependence the rate of oncological failures such as local recurrence, nodal metastases, distant metastases or the second primary focus on clinical and epidemiological factors was analyzed. The probability of survival rate was also estimated. The studied group consists of 42 patients (27M, 15K, M:K =1.8:1). Age ranged from 28 to 87. The most common localization was maxillary sinus – 59.5%. Patients with high local (T3, T4) and clinical (III, IV) stage constitute 77,5% of the studied group. In 66.7% cases the radiation therapy had to follow the surgery. In the group of 42 patients with at least 3-years period of follow-up the oncological failure appeared in 17 cases (40.5%): local recurrence (8), nodal metastases (7), distant metastases (1) and all of them in 1 case. The treatment was performed through: local recurrence (surgery in 2 cases, CHTH – 3, symptomatic treatment – 3), nodal metastases (RND – 3, SND – 4, supplementary radiotherapy –7), distant metastases – CHTH – 2 cases. Thanks to these procedures the 5-year survival rate is 23.1% and the 3-year survival rate is 29.4%. Conclusions: 1. The oncological failure after primary surgical treatment in the group of patients with sinonasal malignancies developed in 40.5% cases, mainly as local recurrence or nodal metastases. 2. Primary localization and sex have no impact on the rate of the recurrence. 3. The oncological failures signifi cantly more often relate to young patients with high local, clinical stage and low grade of malignancies. 4. The recurrence after primary surgical treatment in the group of patients with sinonasal malignancies substantially reduces 3- and 5-year survival rate (29.4%; 23.1%) compared with the entire studied group – 54.8%; 40.0%.
EN
Use of allogeneic hematopoietic stem cell transplantation is increasing continuously as a consequence of continuing progress of medical techniques, allowing implementation of this procedure even in patients where previously it was considered contraindicated. It is successfully used in the treatment of both several hematologic malignancies and other conditions. Still, a major concern remains the development of graft-versus-host disease (GvHD) as a complication of this kind of therapy. Treatment of choice in acute forms of stage II-IV GvHD are steroids (prednisolone, 1-2 mg/kg/d) combined with calcineurin inhibitors (cyclosporine A or tacrolimus). Steroid-resistant patients constitute a considerable therapeutic challenge, as they require enhanced immunosuppression. Standard management of these patients depends on experiences of particular center and usually an individual therapeutic strategy is warranted. No controlled clinical trials are available, documenting a favorable effect on survival of a particular salvage procedure in the setting of a steroid-resistant GvHD. In this situation, the following agents may be used: mycophenolate mofetil, methotrexate, pentostatin, mTOR inhibitors, anti-TNF-α and anti-IL-2 antibodies as well as mono- and polyclonal anti-T-lymphocyte antibodies. Non-pharmacological options include the use of extracorporeal photopheresis and infusion of allogeneic mesenchymal stem cells. In order to improve its effectiveness, salvage therapy should be instituted as quickly as possible, at best during the first 2 weeks after diagnosis of GvHD. Nevertheless, overall effectiveness and toxicity of most therapeutic modalities are far from satisfactory. Current research focuses on regulatory T-lymphocytes and small molecules affecting signal transmission between antigen-presenting cells and effector cells.
PL
Zastosowanie przeszczepiania alogenicznych komórek macierzystych krwiotworzenia stale wzrasta z uwagi na stały postęp technik medycznych, pozwalających na kwalifikację do wykonania tej procedury u chorych, którzy uprzednio mieli do niej przeciwwskazania. Jest ona z powodzeniem stosowana w leczeniu wielu nowotworów hematologicznych oraz innych schorzeń. Nadal poważnym problemem pozostaje rozwój choroby przeszczep przeciwko gospodarzowi (GvHD) jako powikłanie użycia tej formy terapii. Leczeniem z wyboru ostrej postaci GvHD w stopniu II-IV są glikokortykoidy (prednizolon) w dawce 1-2 mg/kg/dziennie, w połączeniu z inhibitorami kalcyneuryny (cyklosporyna A lub takrolimus). Chorzy stery-dooporni stanowią bardzo poważny problem terapeutyczny, wymagają bowiem nasilenia immunosupresji. Standard postępowania u tych pacjentów zależy od doświadczeń ośrodka leczącego i zazwyczaj obowiązuje indywidualne podejście do chorego. Brakuje kontrolowanych badań klinicznych udowadniających wpływ na przeżycie konkretnego postępowania ratunkowego w leczeniu sterydoopornej ostrej GvHD. Można zastosować w tej sytuacji: kwas mykofenolowy, metotreksat, cyklofosfamid, pentostatynę, inhibitory mTOR, przeciwciała przeciwko TNF-a czy IL-2 oraz mono- i poliklonalne przeciwciała skierowane przeciwko limfocytom T. Opcje niefarmakologiczne obejmują użycie zewnątrzustrojowej fotote-rapii czy alogenicznych mezenchymalnych komórek macierzystych. W celu poprawy jego skuteczności leczenie ratunkowe w przypadku stwierdzenia sterydooporności powinno być zastosowane jak najszybciej, najlepiej w ciągu 2 tygodni od rozpoznania GvHD. Niemniej jednak ogólna skuteczność i toksyczność większości podejść terapeutycznych są niezadowalające. Przyszłość to zastosowanie regulatorowych limfocytów T czy użycie małych cząsteczek wpływających na przekazywanie sygnału pomiędzy komórkami prezentującymi antygen a komórkami efektorowymi.
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