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PL
Wstęp: Paranowotworowe zespoły endokrynne i metaboliczne w przebiegu nowotworów złośliwych są wynikiem ektopowego wytwarzania hormonów lub ich prekursorów w komórkach guza. O ile produkcja hormonów przez nowotwory pochodzenia neuroendokrynnego występuje stosunkowo często, o tyle ich wydzielanie przez komórki raka gruczołowego jest wyraźną rzadkością. W pracy przedstawiono przypadek potrójnie ujemnego raka inwazyjnego piersi, cechującego się ektopowym wydzielaniem ACTH, wywołującego poważne zaburzenia metaboliczne Materiał i metoda: Pacjentka została przyjęta do szpitala z objawami zespołu Cushinga. Badania diagnostyczne wykazały, że przyczyną zaburzeń metabolicznych był guz nowotworowy prawej piersi. Po wielodyscyplinarnym przygotowaniu pacjentka została zakwalifikowana do zabiegu operacyjnego. Wyniki: Po zabiegu mastektomii ustąpiły zaburzenia metaboliczne. Chora otrzymała uzupełniającą chemioterapię i radioterapię. W trakcie kontroli, 4 miesiące po zakończeniu leczenia systemowego stwierdzono progresję nowotworu. Kolejne modele chemioterapii okazały się nieskuteczne. Pacjentka zmarła 20 miesięcy po operacji i dwa miesiące po ostatnim cyklu chemioterapii Wnioski: Przypadek opisany w tym badaniu - potrójnie ujemny inwazyjny rak piersi, odpowiedzialny za ektopową produkcję ACTH i powodujący zespół Cushinga - jest rzadkim zjawiskiem. Leczenie pacjentów z rakiem piersi wykazujących aktywność hormonalną nie powinno różnić się od ogólnych zasad stosowanych w przypadku raka piersi. Jednak z powodu towarzyszących zaburzeń metabolicznych pacjenci potrzebują zindywidualizowanego podejścia onkologicznego, precyzyjnych testów diagnostycznych i wielodyscyplinarnego przygotowania przedoperacyjnego.
EN
Introduction: Endocrine and metabolic paraneoplastic syndromes in the course of malignant tumors result from ectopic production of hormones or hormone precursors in tumor cells. Production of hormones by endocrine tumors is relatively frequent, while such production by adenocarcinoma cells is definitely rare. The study presents a case of triple-negative invasive breast cancer, with the ectopic secretion of ACTH (adrenocorticotropic hormone), which provokes serious metabolic disorders. Materials and methods: The patient was admitted to hospital with symptoms of Cushing`s syndrome. Diagnostic tests revealed that the cause of metabolic disorders was breast cancer. After proper preparation, the patient was qualified for surgery. Results: After the mastectomy, the patient’s metabolism stabilized. The patient underwent adjuvant chemotherapy and radiotherapy. Four months after the last cycle of systemic treatment, cancer dissemination was found. The patient was treated with second-line chemotherapy, however, control CT revealed progression. The patient died 20 months after surgery and two months after the last cycle of chemotherapy. Conclusions: The case reported in this study – triple-negative invasive breast cancer, responsible for ectopic production of ACTH and causing Cushing’s syndrome – is a rare phenomenon. Treatment of patients with breast cancer showing hormonal activity should not differ from general rules applied for breast cancer. However, due to accompanying metabolic disturbances, the patients need individualized oncological approach, precise diagnostic tests, and adequate preoperative preparation.
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Non-opioid peptides for analgesia

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EN
Amongst the candidates believed to be involved in the mediation of analgesia, only somatostatin fulfills the criterium of a real analgesia substance. Spinal somatostatin specifically blocks the transmission of painful stimuli. Spinal calcitonin may lower the opioid dose requirement in patients with bone metastases but it fails to relieve acute pain. The usefulness of ACTH and CRF for treatment of pain remains to be established. The role of CCK-8, vasopressin and is unclear. The contradictory findings on antinociception using simple rodent withdrawl reflex tests (e.g. the tail test), or more complex behavioral tests in which supraspinal sensory processing is involved, (e.g. the hot plate test), indicate that these tests are inappropriate when neuropeptides are employed. Furthermore, due to their inability to predict analgesia in humans, they do not fulfill the guidelines proposed by the IASP that animal test procedured have to be for the benefit of humans.
EN
. Sustained exposure to glucocorticosteroids (GCs), adrenal hormones secreted during stress, can cause neural degeneration. This is particularly so in the hippocampus, a principal neural target site for GCs. The purpose of this research was an assessment of the neuroprotective effect of ACTH (4-9) in degenerative changes of hippocampal neurons induced by synthetic GC - dexamethasone. Experiments were conducted on male Albino-Swiss mice. We studied the morphology of neurons in the dorsal hippocampus in slides stained with cresyl violet. Immunocytochemical analysis was carried out with the use of monoclonal antibody anti-MAP2 in order to detect alterations in the the neuronal cytoskeleton. We also performed ultrastructural examinations of hippocampal neurons. Quantitative analysis of morphological changes was completed using a computer analyser of histological pictures. It was shown that dexamethasone administered in toxic doses evokes neuronal death in layer CA3 of the hippocampus. Results indicate that ACTH (4-9) shows protective effects in that model. Dexamethasone-induced damage to hippocampal pyramidal neurons (assessed by cell counts, immunocytochemical analysis of cytoskeletal alterations and ultrastructural studies) was significantly reduced in animals administered ACTH (4-9).
EN
The aim of the current investigation was to ascertain the role of ACTH and adrenal hormones on adrenomedullary and glycemic functions in soft-shelled turtles, Lissemys punctata punctata. All the experiments were carried out on sexually immature animals. Findings revealed that: (1) ACTH administration (0.5 IU/1.0 IU/2.0 IU per 100 g body wt. daily for 10 days) in all doses stimulated adrenomedullary function by increasing medullary cell nuclear diameter with elevations of norepinephrine, epinephrine and blood sugar levels. Only moderate and higher doses (50 mug/100 mug per 100 g body wt. daily for 10 days) of dexamethasone suppressed adrenomedullary activity and blood sugar level by reversing the changes to those of ACTH; the responses were dose-dependent. But these changes were no longer observed after ACTH treatment in dexamethasone (DMS) recipients (DMS: 100mug / 100 g body wt daily for the first 10 days and ACTH: 0.5 IU / 100 g body wt daily for the next 10 days); (2) Only moderate and higher doses (50 mug/100 mug per 100 g body wt daily for 10 days) of corticosterone increased adrenomedullary activity and blood sugar level and the responses were also dose-dependent. But aldosterone treatment in all doses (same as for corticosterone) had no significant effect on the adrenal medulla or blood sugar level; (3) Only moderate and higher doses of norepinephrine or epinephrine (same as for corticosterone) caused adrenomedullary atrophy with depletions of norepinephrine and epinephrine levels but elevated the glycemic level. The findings are briefly discussed.
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