Diagnosis and differential diagnosis of Cushing's syndrome remains a challenge in clinical endocrinology. The aim of this study was to establish the value of assessing adrenocorticotropic hormone (ACTH) levels in differential diagnosis of hypercorticism using receiver operating characteristic (ROC) curve. We have evaluated 114 patients with Cushing's syndrome testing the value of pathohistological examination and postoperative testing. The control group consisted of 53 obese healthy persons. ACTH level was determined using a commercial RIA (CIS, France). ACTH secreting pituitary adenoma was found in 56.14% examinees, ectopic secretion in 6.14%, cortisol secreting adrenal adenoma in 37.57%, and adrenal carcinoma in 6.14% of all patients with Cushing's syndrome. Basal ACTH level for pituitary adenoma was 107.29 +/- 75.69 pg/mL; for ectopic secretion 181.63 +/- 149.84 pg/mL; for adrenal adenoma 4.22 +/- 2.32 pg/mL; for adrenal carcinoma 5.50 +/- 7.72 pg/mL; and 34.76 = 10.07 pg/mL in control group. Testing the value of assessing ACTH the area under ROC curve was 0.9965 +/- 0.0071. Test sensitivity was 99.89% and test specificity was 97%. For ACTH cut-off level of 8 pg/mL, test sensitivity was 88.50%, with specificity of 99%. For ACTH cut-off level of 22 pg/mL, test sensitivity was 99.30%, with specificity of 98%. Our intermediate zone from 8 to 22 pg/mL confirms that assessment of ACTH level is a reliable tool in differential diagnosis of Cushing's syndrome.

Chronic fatigue syndrome (CFS) is defined as constellation of the prolonged fatigue and several somatic symptoms, in the absence of organic or severe psychiatric disease. However, this is an operational definition and conclusive biomedical explanation remains elusive. Similarities between the signs and symptoms of CFS and adrenal insufficiency prompted the research of the hypothalamo-pituitary-adrenal axis (HPA) derangement in the pathogenesis of the CFS. Early studies showed mild glucocorticoid deficiency, probably of central origin that was compensated by enhanced adrenal sensitivity to ACTH. Further studies showed reduced ACTH response to vasopressin infusion. The response to CRH was either blunted or unchanged. Cortisol response to insulin induced hypoglycaemia was same as in the control subjects while ACTH response was reported to be same or enhanced. However, results of direct stimulation of the adrenal cortex using ACTH were conflicting. Cortisol and DHEA responses were found to be the same or reduced compared to control subjects. Scott et al found that maximal cortisol increment from baseline is significantly lower in CFS subjects. The same group also found small adrenal glands in some CFS subjects. These varied and inconsistent results could be explained by the heterogeneous study population due to multifactorial causes of the disease and by methodological differences. The aim of our study was to assess cortisol response to low dose (1 microgram) ACTH using previously validated methodology. We compared cortisol response in the CFS subjects with the response in control and in subjects with suppressed HPA axis due to prolonged corticosteroid use. Cortisol responses were analysed in three subject groups: control (C), secondary adrenal insufficiency (AI), and in CFS. The C group consisted of 39 subjects, AI group of 22, and CFS group of nine subjects. Subject data are presented in table 1. Low dose ACTH test was started at 0800 h with the i.v. injection of 1 microgram ACTH (Galenika, Belgrade, Serbia). Blood samples for cortisol determination were taken from the i.v. cannula at 0, 15, 30, and 60 min. Data are presented as mean +/- standard error (SE). Statistical analysis was done using ANOVA with the Games-Howell post-hoc test to determine group differences. ACTH dose per kg or per square meter of body surface was not different between the groups. Baseline cortisol was not different between the groups. However, cortisol concentrations after 15 and 30 minutes were significantly higher in the C group than in the AI group. Cortisol concentration in the CFS group was not significantly different from any other group (Graph 1). Cortisol increment at 15 and 30 minutes from basal value was significantly higher in C group than in other two groups. However, there was no significant difference in cortisol increment between the AI and CFS groups at any time of the test. On the contrary, maximal cortisol increment was not different between CFS and other two groups, although it was significantly higher in C group than in...

Sažetak: Uvod: Karcinom pankreasa je najčešće lokalizovan u glavi pankreasa. Ima visok mortalitet, najčešće zbog kasne kliničke manifestacije bolesti i odsustva ranih simptoma, kao i visokog procenta recidiva posle hiruške terapije i rezistencije na konvencionalnu onkološku terpaiju. Faktori rizika za nastanak karcinoma pankreasa su pušenje, prekomerno unošenje masti i mesa, gojaznost, dijabetes mellitus, hronični pankreatitis. Neke studije ukazuju na povezanost hronične infekcije hepatitisom B sa pojavom karcinoma pankreasa. Cilj rada je ukazivanje na značaj primarne prevencije i izmene stila života s obzirom da ne postoji skrining program za rano otkrivanje bolesti. Prikaz slučaja: Pacijent muškog pola, star 51 godinu žali se na nelagodnost u epigastrijumu koja traje nekih desetak dana, ređe stolice, gubitak na telesnoj težini 10 kilograma za godinu dana i žutu prebojenost beonjača. Boluje od hroničnog hepatitisa B, šećerne bolesti i od hipertenzije. U porodičnoj anamnezi majka boluje od DM tip 2 i HTA, otac bolovao od sarkoma. Zaposlen, oženjen, troje dece; pušio je 20 godina po 10-15 cigareta, ne puši unazad 5 godina; Alkoholna pića konzumira povremeno u umerenim količinama. Negira alergije na hranu i lekove. Inspekcijom se uočava ikterična koža i sklere. Abdomen je u ravni grudnog koša, palpatorno mek, lako bolno osetljiv u epigastrijumu. Jetra se palpira 3 centimetra ispod desnog rebarnog luka. Ostali nalaz je uredan. Laboratorijske analize: povišene transaminaze, GGT, alkalna fosfataza. Vrednost tumorskog markera CA19.9 je 550. Na kompjuterizovanoj tomografiji (CT) abdomena je nadjeno uvećanje glave pankreasa sa tumorskom promenom 25mm. Pacijent je podvrgnut hirurškoj intervenciji u dva navrata, histopatološki nalaz (HP) je bio: adenocarcinoma ductale invasivum capitis pancreatis. Nakon toga je sprovedena hemioterapija po protokolu 5-FU/LV. Nakon IV ciklusa savetovana je hemioiradijacija. Nakon sprovedene terapije redovno se kontroliše skoro 3 godine i nema znakova recidiva bolesti. Zaključak: I pored primenjene terapije karcinom pankreasa i dalje ima visok mortalitet. Treba raditi na modifikaciji faktora rizika i izmeni stila života, kao i sprovođenje mera zaštite radi sprečavanja nastanka hepatitisa B uključujući i vakcinaciju protiv B hepatitisa kod osoba koje su u riziku.