Effect of F11 Receptor/Junctional Adhesion Molecule-A-derived Peptide on Neointimal Hyperplasia in a Murine Model.

PURPOSE: To determine whether inhibition of the F11 receptor/JAM-A (F11R) using F11R-specific antagonist peptide 4D results in inhibition of smooth muscle cell (SMC) proliferation and migration in vivo, known as neointimal hyperplasia (NIH), using a mouse focal carotid artery stenosis model (FCASM). MATERIALS AND METHODS: The mouse FCASM was chosen to test the hypothesis because the dominant cell type at the site of stenosis is SMC, similar to that in vascular access stenosis. Fourteen C57BL/6 mice underwent left carotid artery (LCA) partial ligation to induce stenosis, followed by daily injection of peptide 4D in 7 mice and saline in the remaining 7 mice, and these mice were observed for 21 days and then euthanized. Bilateral carotid arteries were excised for histologic analysis of the intima and media areas. RESULTS: The mean intimal area was significantly larger in control mice compared with peptide 4D-treated mice (0.031 mm2 [SD ± 0.024] vs 0.0082 mm2 [SD ± 0.0103]; P = .011). The mean intima-to-intima + media area ratio was significantly larger in control mice compared with peptide 4D-treated mice (0.27 [SD ± 0.13] vs 0.089 [SD ± 0.081]; P = .0079). NIH was not observed in the right carotid arteries in both groups. CONCLUSIONS: Peptide 4D, an F11R antagonist, significantly inhibited NIH in C57BL/6 mice in a FCASM.

Triple negative breast cancer metastasis is hindered by a peptide antagonist of F11R/JAM­A protein.

BACKGROUND: The F11R/JAM-A cell adhesion protein was examined as the therapeutic target in triple negative breast cancer (TNBC) with the use of the peptide antagonist to F11R/JAM-A, that previously inhibited the early stages of breast cancer metastasis in vitro. METHODS: The online in silico analysis was performed by TNMPlot, UALCAN, and KM plotter. The in vitro experiments were performed to verify the effect of peptide 4D (P4D) on human endothelial cell lines EA.hy926 and HMEC-1 as well as on human TNBC cell line MDA-MB-231. The cell morphology upon P4D treatment was verified by light microscopy, while the cell functions were assessed by colony forming assay, MTT cell viability assay, BrdU cell proliferation assay, and Transepithelial/Endothelial Electrical Resistance measurements. The in vivo experiments on 4T1 murine breast cancer model were followed by histopathological analysis and a series of quantitative analyses of murine tissues. RESULTS: By in silico analysis we have found the elevated gene expression in breast cancer with particular emphasis on TNBC. The elevated F11R expression in TNBC was related with poorer survival prognosis. Peptide 4D has altered the morphology and increased the permeability of endothelial monolayers. The colony formation, viability, and proliferation of MDA-MB-231 cells were decreased. P4D inhibited the metastasis in 4T1 breast cancer murine model in a statistically significant manner that was demonstrated by the resampling bootstrap technique. CONCLUSIONS: The P4D peptide antagonist to F11R/JAM-A is able to hinder the metastasis in TNBC. This assumption needs to be confirmed by additional 4T1 mouse model study performed on larger group size, before making the decision on human clinical trials.

Review of Diagnostic Modalities for Adrenal Incidentaloma.

Adrenal incidentalomas are common findings in clinical practice, with a prevalence of up to 4.2% in radiological studies. Due to the large number of focal lesions in the adrenal glands, it can be challenging to make a definitive diagnosis and determine the appropriate management. The purpose of this review is to present current diagnostic modalities used to preoperatively distinguish between adrenocortical adenoma (ACA) and adrenocortical cancer (ACC). Proper management and diagnosis are crucial in avoiding unnecessary adrenalectomies, which occur in over 40% of cases. A literature analysis was conducted to compare ACA and ACC using imaging studies, hormonal evaluation, pathological workup, and liquid biopsy. Before deciding on surgical treatment, the nature of the tumor can be accurately determined using noncontrast CT imaging combined with tumor size and metabolomics. This approach helps to narrow down the group of patients with adrenal tumors who require surgical treatment due to the suspected malignant nature of the lesion.

Immunological and Metabolic Causes of Infertility in Polycystic Ovary Syndrome.

Infertility has been recognized as a civilizational disease. One of the most common causes of infertility is polycystic ovary syndrome (PCOS). Closely interrelated immunometabolic mechanisms underlie the development of this complex syndrome and lead to infertility. The direct cause of infertility in PCOS is ovulation and implantation disorders caused by low-grade inflammation of ovarian tissue and endometrium which, in turn, result from immune and metabolic system disorders. The systemic immune response, in particular the inflammatory response, in conjunction with metabolic disorders, insulin resistance (IR), hyperadrenalism, insufficient secretion of progesterone, and oxidative stress lead not only to cardiovascular diseases, cancer, autoimmunity, and lipid metabolism disorders but also to infertility. Depending on the genetic and environmental conditions as well as certain cultural factors, some diseases may occur immediately, while others may become apparent years after an infertility diagnosis. Each of them alone can be a significant factor contributing to the development of PCOS and infertility. Further research will allow clinical management protocols to be established for PCOS patients experiencing infertility so that a targeted therapy approach can be applied to the factor underlying and driving the "vicious circle" alongside symptomatic treatment and ovulation stimulation. Hence, therapy of fertility for PCOS should be conducted by interdisciplinary teams of specialists as an in-depth understanding of the molecular relationships and clinical implications between the immunological and metabolic factors that trigger reproductive system disorders is necessary to restore the physiology and homeostasis of the body and, thus, fertility, among PCOS patients.

The role of selected adipokines in tumorigenesis and metabolic disorders in patients with adrenal tumors.

Recently, more and more attention has been directed to the role of adipose tissue and adipocytokines in the pathogenesis of metabolic and inflammatory disorders in humans. Excess fat tissue has also been associated with a higher risk of malignancies. Advances in the research on the role of adipokines in adrenal tumors may elucidate the relationship between various types of adipose tissue (visceral, subcutaneous, and periadrenal) and metabolic disorders observed in hormonally active adrenal tumors, as well as associations with adrenal cortex cancer. In patients with active or cured Cushing syndrome, increased leptin and resistin concentrations as well as release of pro-inflammatory cytokines can be associated with cardiovascular risk. Also, the renin-angiotensin-aldosterone system in patients with primary hyperaldosteronism may affect the metabolic activity of the adipose tissue. Elevated resistin concentrations in this group of patients are associated with morphological changes of the myocardium independently of the effects of the metabolic syndrome. Further, it has been suggested that hypoadiponectinemia comprises an additional factor in the pathogenesis of carbohydrate metabolism disorders and the risk of cardiovascular complications in pheochromocytoma patients. Understanding the mechanisms of action of adipokines may be important in developing prophylactic and therapeutic strategies in hormonally active and malignant tumors of the adrenal glands.

The F11 Receptor (F11R)/Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A) in cancer progression.

The F11 Receptor (F11R), also called Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A), is a transmembrane glycoprotein of the immunoglobulin superfamily, which is mainly located in epithelial and endothelial cell tight junctions and also expressed on circulating platelets and leukocytes. It participates in the regulation of various biological processes, as diverse as paracellular permeability, tight junction formation and maintenance, leukocyte transendothelial migration, epithelial-to-mesenchymal transition, angiogenesis, reovirus binding, and platelet activation. Dysregulation of F11R/JAM-A may result in pathological consequences and disorders in normal cell function. A growing body of evidence points to its role in carcinogenesis and invasiveness, but its tissue-specific pro- or anti-tumorigenic role remains a debated issue. The following review focuses on the F11R/JAM-A tissue-dependent manner in tumorigenesis and metastasis and also discusses the correlation between poor patient clinical outcomes and its aberrant expression. In the future, it will be required to clarify the signaling pathways that are activated or suppressed via the F11R/JAM-A protein in various cancer types to understand its multiple roles in cancer progression and further use it as a novel direct target for cancer treatment.

Safe treatment with somatostatin analogues in a woman with acromegaly whilst pregnant and lactating.

CONTEXT: Pregnancy in acromegaly is rare, there have been few case reports and series published to date. Also breastfeeding under acromegaly treatment is extremely rare. The late diagnosis of pregnancy in acromegaly will sometimes dictate the treatment and management of the patient. MATERIAL AND METHOD: We present a 32-year-old woman with acromegaly, a late diagnosed pregnancy and a completed fetal organogenesis. Due to the gestation time and bothersome headaches accompanying a pituitary macroadenoma, we decided to continue long lasting somatostatin analogues treatment but with increased injection intervals of 6 weeks. We also continued this treatment during 12 months of breastfeeding. RESULTS: Our treatment did not cause any complication of premature birth or any health problems with the newborn baby. The child has since developed normally up to the age of 5. CONCLUSION: The course of acromegaly disease and the time of pregnancy diagnosis may prompt suitable drug and treatment regimes. We administered effective and safe somatostatin analogues treatment during gestation and breastfeeding which was safe for both mother and baby.

Sclerostin and bone remodeling biomarkers responses to whole-body cryotherapy (- 110 °C) in healthy young men with different physical fitness levels.

We investigated the effects of single and repeated exposures to whole-body cryotherapy on biomarkers of bone remodeling and osteo-immune crosstalk: sclerostin, osteocalcin (OC), C-terminal cross-linked telopeptide of type I collagen (CTx-I), osteoprotegerin (OPG) and free soluble receptor activator for nuclear factor κ B ligand (sRANKL). The study included 22 healthy males, grouped in high physical fitness level (HPhL) and low physical fitness level (LPhL), all undergone 10 consecutive sessions in a cryogenic chamber (- 110 °C). We observed a significant time-effect on sclerostin (p < 0.05), OC (p < 0.01), CTx-I (p < 0.001), OC/CTx-I (p < 0.05), and significant differences in sRANKL between the groups (p < 0.05) after the 1st cryostimulation; a significant time-effect on OC (p < 0.001) and OC/CTx-I (p < 0.001) after the 10th cryostimulation, and a significant time-effect on CTx-I (p < 0.001) and OC/CTx-I (p < 0.01) after 10 sessions of WBC. In conclusion, in young men, the first exposure to extreme cold induced significant changes in serum sclerostin. The changes in sRANKL, between groups, suggest that fitness level may modify the body's response to cold. The effects of the first stimulus and the whole session are not identical, probably due to the physiological development of habituation to cold.

Functional inhibition of F11 receptor (F11R/junctional adhesion molecule-A/JAM-A) activity by a F11R-derived peptide in breast cancer and its microenvironment.

PURPOSE: To examine the involvement of the F11R/JAM-A protein in breast cancer metastasis, we utilized the F11R/JAM-A antagonistic peptide 4D (P4D) in experiments of transendothelial migration (TEM) of breast cancer cells. METHODS: Experiments were conducted in the mouse 4T1 breast cancer model utilizing the human mammary epithelial cell and endothelial cell lines. The levels of soluble F11R/JAM-A (sJAM-A) in the murine plasmas were measured by ELISA. Levels of F11R/JAM-A mRNA and protein in cell lines were assessed by qRT-PCR and Western blot, respectively. Cell surface expression of F11R/JAM-A was demonstrated by flow cytometry. Functional tests included the TEM of breast cancer cells and adhesion of breast cancer cells to the endothelium. The endothelial permeability was studied by fluorescent tracer assay and by the Real-Time Cell Analysis (RTCA). RESULTS: The tumor inducers Tß4 and TGF-ß1 reduced the levels of sJAM-A in murine plasma, and reduced the F11R/JAM-A protein levels in the human microvascular endothelial cell line HMEC-1. The adhesion and TEM measured between breast cancer cells and inflamed or Tß4-treated endothelium were inhibited by P4D. The presence of P4D did not destabilize the pre-existing tight junctions in the endothelial monolayer. The barrier-protecting effect of P4D was stronger than that of forskolin, when a booster dose of P4D was applied to the inflamed endothelium. CONCLUSIONS: F11R/JAM-A protein can be considered as a novel target in the treatment of breast cancer metastasis. In vivo and clinical studies are needed to further investigate the effectiveness of F11R/JAM-A-derived peptide as a possible anti-metastatic drug.

Selected adipocytokines in patients with an incidentally discovered pheochromocytoma.

BACKGROUND: Adipose tissue secretes many adipokines and cytokines, which may be an additional risk factor of cardiovascular and metabolic diseases in patients with an incidentally discovered pheochromocytoma (PHEO). The aim of the study was to investigate levels of selected adipocytokines in these patients. METHODS: This prospective study included 12 patients with an incidentally discovered PHEO and 18 healthy participants. In all participants plasma/serum concentrations of triglycerides, HDL and LDL cholesterol, insulin, glucose, adipocytokines (adiponectin, leptin, resistin, TNFα, IL6, and MCP1) were determined, hormonal tests were performed in patients. RESULTS: Patients and controls did not differ significantly in terms of age, sex, and body mass index. Among incidentally discovered PHEO patients, adiponectin levels were lower, while TNFα concentrations higher than in controls. Concentrations of adiponectin correlated with 24-hour urinary excretion of normetanephrine in women. Significantly higher TNFα concentrations were found in hypertensive than in normotensive PHEO patients as well as in non-diabetic PHEO patients than controls. Further, resistin concentration was higher in PHEO patients with diabetes than in non-diabetic ones (P<0.001). Incidentally discovered PHEO tumor size correlated with leptin and IL6 levels. Adiponectin levels were higher, while TNFα and resistin lower among five patients re-examined after tumor resection. CONCLUSIONS: Among patients with an incidentally discovered pheochromocytoma, lower adiponectin, and higher resistin and TNFα levels may constitute additional factors for HT and DM. In our study, for the first time, correlations between incidentally discovered PHEO tumor size and concentrations of leptin as well as IL6 were found.

Expression of adiponectin receptors 1 and 2 and the leptin receptor in human adrenal tumors.

INTRODUCTION: The role of adipokines in neoplasms not related to obesity is unclear. The presence of adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) as well as the leptin receptor (Ob-R) has been recognized in human adrenal tumors. The authors of the present study were the first to compare the expression of these receptors in histopathologically distinct adrenal tumors. MATERIAL AND METHODS: The study encompassed tissue specimens of 128 patients with adrenal tumors (28 adrenal cortical adenomas (CA), 35 cortical nodular hyperplasia tumors (CNH), 20 cortical carcinomas (CC), 40 pheochromocytomas (PHEO), 5 malignant pheochromocytomas (PHEOM)) operated on at a single clinical center. The expression of the adiponectin receptors AdipoR1 and AdipoR2 as well as the leptin receptor Ob-R was assessed by immunohistochemistry. The results were correlated with body mass index (BMI) and gender of the patients. RESULTS: AdipoR1 expression was significantly higher in cortical cancers (p < 0.001) and pheochromocytomas (p < 0.001) as compared to benign cortical tumors. AdipoR2 expression was significantly higher in cortical carcinomas as compared to cortical adenomas and hyperplasia tumors (p = 0.01), and also significantly higher in pheochromocytomas in comparison to adrenocortical cancers (p = 0.004). Leptin receptor expression was absent or minimal in half of nodular hyperplasia tumors and adrenal cortex adenomas. This receptor's expression was significantly higher in adrenocortical cancers (p = 0.038). In pheochromocytomas this receptor was expressed more abundantly than in adrenocortical cancers (p = 0.004). CONCLUSIONS: These novel findings suggest that adiponectin and leptin receptors could play a regulatory role in human adrenal neoplasms.

A peptide antagonist of F11R/JAM-A reduces plaque formation and prolongs survival in an animal model of atherosclerosis.

BACKGROUND AND AIMS: The F11 Receptor (F11R), AKA Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A), is an adhesion protein constitutively expressed on the membrane surface of circulating platelets and the luminal surface of inflamed endothelial cells (EC). Platelet adhesion to an inflamed endothelium is one of the early steps of atherosclerotic plaque formation. Our previous studies, conducted with cultured EC in vitro, have demonstrated the expression of F11R/JAM-A on the luminal surface of inflamed EC, platelet adhesion to inflamed EC through F11R/JAM-A interactions, and inhibition of this interaction by the presence of F11R/JAM-A antagonistic peptide (F11Rpeptide 4D). In the present study, we examined in vivo the overall health-benefits and cardiovascular effects of long-term treatment of animals prone to atherosclerosis, ApoE-/- mice, with F11R-peptide 4D. METHODS: Twenty ApoE-/- mice were assigned to daily treatment with peptide 4D and compared to their counterparts control untreated mice. Mice were observed for wellness and survival. Plaque size in the aorta and heart was measured using histological analysis. Effects of peptide 4D (or scramble control) on platelet adhesion to inflamed endothelium were measured using intravital microscopy. RESULTS: Significant reductions in atherosclerotic plaques number and size, an overall robust health with longer survival were found in the peptide 4D treated group of ApoE-/- mice. Intravital microscopic studies conducted in exposed vessels of ApoE-/- mice demonstrated significant inhibition by peptide 4D of platelet adhesion to the cytokine-inflamed endothelium. CONCLUSIONS: Our results demonstrate that peptide 4D significantly reduces atherosclerotic plaque formation in ApoE-/- mice and inhibits platelet adhesion to the inflamed arterial endothelium.

Plasma Phospholipid Transfer Protein Promotes Platelet Aggregation.

It remains unclear whether plasma phospholipid transfer protein (PLTP) is involved in hyper-coagulation or hypo-coagulation. This study investigated the direct effect of PLTP on platelet aggregation and the underlying mechanism. Washed platelets from humans or mice and mouse platelet-rich plasma and human recombinant PLTP were isolated. PLTP is present in human platelets. We assessed adenosine diphosphate (ADP)-, collagen- and thrombin-induced platelet aggregation, phosphatidylserine externalization and photothrombosis-induced cerebral infarction in mice. PLTP over-expression increased platelet aggregation, while PLTP deficiency had the opposing reaction. Human recombinant PLTP increased both mouse and human platelet aggregation in a dose-dependent manner. Phosphatidylserine externalization provides a water/lipid surface for the interaction of coagulation factors, which accelerates thrombosis. Compared with wild-type controls, platelets from PLTP transgenic mice had significantly more phosphatidylserine on the exterior surface of the plasma membrane, whereas platelets from PLTP-deficient mice had significantly less phosphatidylserine on the surface, thus PLTP influences fibrinogen binding on the plasma membrane. Moreover, recombinant PLTP together with ADP significantly increased phosphatidylserine exposure on the plasma membrane of PLTP-deficient platelets, thereby increasing fibrinogen binding. PLTP over-expression significantly accelerated the incidence of photothrombosis-induced infarction in mice, whereas PLTP deficiency significantly reduced the frequency of infarction. We concluded that PLTP promotes phosphatidylserine externalization at the plasma membrane of platelets and accelerates ADP- or collagen-induced platelet aggregation. This effect plays an important role in the initiation of thrombin generation and platelet aggregation under sheer stress conditions. Thus, PLTP is involved in hyper-coagulation. Therefore, PLTP inhibition could be a novel approach for countering thrombosis.

Vitamin D Supplementation and Nordic Walking Training Decreases Serum Homocysteine and Ferritin in Elderly Women.

The aim of the study was to verify if coupling 12 weeks of vitamin D supplementation and Nordic walking training favoured lowering the homocysteine (Hcy) level. Ninety-four elderly women were divided into three groups: Nordic walking (NW), supplemented (SG) and control (CG). The NW and SG groups received a weekly dose of 28,000 IU of vitamin D3. A blood analysis was performed at baseline, 1h after the first training session and at the end of the experiment. The amino acid profile (methionine and cysteine) and homocysteine concentration were determined. Additionally, the concentration of myokine was assessed. The first session of NW training reduced serum homocysteine, particularly among women with baseline homocysteine above 10 µmol·L-1: 12.37 ± 2.75 vs. 10.95 ± 3.94 µmol·L-1 (p = 0.05). These changes were accompanied by shifts in the cysteine (p = 0.09) and methionine (p = 0.01) concentration, regardless of the Hcy concentration. Twelve weeks of training significantly decreased the homocysteine (9.91 ± 2.78, vs. 8.90 ± 3.14 µmol·L-1, p = 0.05) and ferritin (94.23 ± 62.49 vs. 73.15 ± 47.04 ng·mL-1, p = 0.05) concentrations in whole NW group. Also, in the NW group, ferritin correlated with the glucose level (r = 0.51, p = 0.00). No changes in the myokine levels were observed after the intervention. Only the brain-derived neurotrophic factor dropped in the NW (42.74 ± 19.92 vs. 31.93 ± 15.91 ng·mL-1, p = 0.01) and SG (37.75 ± 8.08 vs. 16.94 ± 12.78 ng·mL-1, p = 0.00) groups. This study presents a parallel decrease of homocysteine and ferritin in response to regular training supported by vitamin D supplementation.

Adipokine and cytokine levels in patients with adrenocortical cancer, subclinical Cushing's syndrome and healthy controls.

INTRODUCTION: In recent years researchers have focused at hormonal activity in Cushing's syndrome (CS) in connection with metabolic disorders and the role of adipokines and cytokines secreted by the adipose tissue. The aim of the study was to investigate levels of adipokines and cytokines in patients with: subclinical CS (SCS) - in relation to hormonal parameters of hypercortisolemia, and, adrenocortical cancer (ACC). MATERIALS AND METHODS: The study included 20 SCS as well as 7 ACC patients, and 18 healthy participants. Hormonal activity and serum concentrations of adiponectin, leptin, resistin, tumor necrosis factor alpha (TNFα), interleukin 6 (IL6), and monocyte chemoattractant protein 1 (MCP1), were analyzed. RESULTS: In SCS patients compared to healthy volunteers a trend toward higher concentrations of all pro-inflammatory cytokines was noted, however, statistically significant differences were only found for TNFα and IL6 (p = 0.047 and p = 0.028, respectively). Adiponectin concentrations were significantly lower in the SCS group (p = 0.006). Serum adipokine and cytokine levels were independent of the presence of diabetes mellitus (DM) and hypertension (HT) in the SCS group. A significant correlation was found between subclinical glucocorticoid secretion and IL6 concentration (Pearson's r = 0.517, p = 0.02). Acquired results were independent of BMI. In ACC patients compared to controls higher IL6, TNFα and MCP1 levels were recorded. CONCLUSION: It is possible that higher adipokine and pro-inflammatory cytokine concentrations as well as lower anti-inflammatory adiponectin concentrations comprise an additional risk factor of metabolic and cardiovascular diseases in SCS patients. It seems that at least among patients with SCS adipokine and cytokine secretion is independent of hormonal activity (except for IL6).

Adipokine and cytokine levels in non-functioning adrenal incidentalomas (NFAI).

Due to the fact that overweight or obesity is accompanied by hormonally active adrenal tumors: Cushing Syndrome-(CS) and Subclinical Cushing Syndrome (SCS), it is of high interest the correlation between different adipokines and cytokines secreted by adipose tissue, with metabolic disorders and hormonal activity in this group. Even in non-functioning adrenal incidentalomas (NFAI) elevated risk for cardiovascular disease and metabolic syndrome was demonstrated. The aim of the study was to investigate plasma adiponectin, leptin, resistin, tumor necrosis factor α (TNFα), interleukin 6 (IL6) and monocyte chemoattractant protein 1 (MCP1) levels in patients with NFAIs and healthy subjects. The study included 18 NFAI patients and 18 healthy subjects. The groups were homogeneous in terms of age, sex and body mass index (BMI). Patients with NFAI showed significantly higher circulating levels of pro-inflammatory cytokines compared to healthy controls (MCP 1: p < 0.001; TNFα p = 0.021; IL6 p = 0.012). On the other hand, adiponectin concentration was significantly lower in the NFAI group (p = 0.034). The serum leptin and resistin concentrations did not differ significantly between the two groups. Acquired results were not dependent on glucocorticoid and catecholamine secretion in NFAI patients. Also, there were no clear correlations between BMI and cytokine levels. It is possible that increased risk for cardiovascular and metabolic diseases reported in NFAI patients is at least partially dependent on adipose tissue activity.

Expression of adiponectin and leptin receptors in adrenal incidentaloma patients with subclinical hormone secretion.

BACKGROUND: The role of adopokines in adrenal tumors' hormonal activity remains unclear. Obesity may induce arterial hypertension, disorders of carbohydrate metabolism, and is a risk factor of cardiovascular disease. In patients with subclinical hormone secretion by the adrenal cortex or medulla the risk of metabolic disease is increased. OBJECTIVE: Authors of this retrospective study selected 78 patients with subclinical hormone secretion out of all adrenal incidentaloma patients hospitalized in the Department of Endocrinology and Internal Medicine between 1995 and 2014. METHODS: The analyzed group comprised of 38 subclinical Cushing's syndrome (SCS), 40 incidentally discovered pheochromocytoma (PHEO) and 42 patients operated due to an adrenal tumor without pathological hormonal activity. Expression of adiponectin (AdipoR1, AdipoR2) and leptin (Ob-R) receptors in adrenal tumors was assessed in relation to body mass index (BMI) and hormonal activity. RESULTS: We found statistically significant negative correlations between BMI and expression of all examined receptors in SCS patients (AdipoR1: p= 0.032; AdipoR2: p< 0.001; leptin Ob-R: p= 0.001). In PHEOs, BMI correlated negatively only with AdipoR2 (p= 0.014). CONCLUSIONS: Data obtained show that the most significant factor associated with the expression of AdipoR1, AdipoR2 and leptin Ob-R receptors in the adrenal tumor tissue is BMI, not their hormonal activity.

Bilateral Tolosa-Hunt syndrome mimicking pituitary adenoma.

The authors report a rare case of bilateral Tolosa-Hunt syndrome, which occurred in a 80-year-old female and remitted spontaneously. Inflammatory lesions were found not only in typical locations, i.e. superior orbital fissures and cavernous sinuses, but also in the pituitary; these imitated gland's macroadenoma in imaging studies.