Deciphering the enigmatic symptoms of Pancoast tumors: Navigating the complex landscape of pain management-A case report.

Pancoast tumors, also known as superior sulcus tumors, encompass a diverse spectrum of neoplasms that infiltrate the apex of the chest wall, yielding distinctive clinical presentations. One of the earliest signs of tumor growth is pain radiating to the upper limb, stemming from peripheral nerve involvement, which can mimic joint pain or spinal radicular irritation. In this case report, we present the clinical history of a 64-year-old female smoker who had previously been recommended for orthopedic elbow surgery due to epicondylitis. Subsequent to the development of additional symptoms and rigorous investigation, a Pancoast tumor was diagnosed. Furthermore, we discuss the characteristic treatment modalities available for Pancoast tumors, including pharmacological pain management and interventional strategies such as spinal cordotomy and spinal alcoholysis. This case underscores the significance of recognizing atypical presentations and emphasizes the importance of comprehensive evaluation in the diagnosis and management of Pancoast tumors.

Changes in Cross-Sectional Area of the Median Nerve and Body Composition Parameters after Treatment of Acromegaly: 1 year Follow-Up.

Objective: Median neuropathy is a common manifestation of acromegaly, although its pathology is uncertain. Changes in levels of growth hormone (GH) and insulin-like growth factor I (IGF-I) and body composition are potential parameters in pathology of median neuropathy in acromegaly. We aimed to assess changes in the cross-sectional area (CSA) of the median nerve and body composition in newly diagnosed acromegalic patients 1 year after treatment and to determine their mutual relationships. Design: This prospective study included 30 patients with newly diagnosed acromegaly and 30 healthy controls matched for age, gender, and body mass index. Physical and laboratory examinations, dual-energy X-ray absorptiometry (DXA), and ultrasound evaluations were performed at baseline and 1 year after initial treatment. Results: The CSA of the median nerve was increased in acromegalic patients compared with controls (13.1 mm2 [12.2-14.9] vs 7.5 mm2 [6.4-8.4], P < 0.001). One year after treatment of acromegaly, GH and IGF-I levels decreased significantly. The median nerve CSA was significantly reduced after treatment (11.6 mm2 [10.2-13.1], P < 0.001). Reduction of IGF-I levels correlated with a decrease in lean mass and increase in fat mass. The median nerve CSA positively correlated with IGF-I levels (R = 0.492, P=0.006) and lean mass (R = 0.419, P=0.021) in acromegalic patients before treatment. Conclusion: This study demonstrates a reduction in the median nerve CSA 1 year after treatment of acromegaly. These changes are closely associated with a reduction in IGF- I levels and in lean body mass. The enlargement of the median nerve in acromegaly can be reversed with adequate treatment.

Two rare endocrinological diagnoses in one patient.

Not required for Clinical Vignette.

Heart failure as a manifestation of acromegaly.

Acromegaly is a rare disease with incidence of 3-4 patients per 1 000000 per year, which is mainly caused by benign tumour of the pituitary gland. Long-term presence of elevated growth hormone (GH) and insulin like growth factor 1 (IGF-1) levels accompanying this disease is associated with rheumatologic, cardiovascular, pulmonary and metabolic complications. Cardiovascular complications of acromegaly include a cardiomyopathy, arterial hypertension, arrhytmias, valvulopathy as well as endothelial dysfunction. Cardiovascular diseases are the leading cause of mortality in patients with acromegaly. An early diagnosis of acromegaly significantly influences both morbidity and mortality of patients suffering from this disease. We describe a 39-year-old patient with undiagnosed acromegaly presented with acute heart failure caused by acromegalic cardiomyopathy.

Cushings syndrome and acromegaly based on picoadenoma of the pituitary gland.

Cushings syndrome (CS) is a relatively rare disease characterized by autonomous hypersecretion of cortisol. The incidence of CS is estimated to be equal to 2-3 cases per million inhabitants per year. The incidence of acromegaly is 3-4 patients per 1 000 000 per year. The disease is caused by hypersecretion of growth hormone which is mainly caused by benign tumour of the pituitary gland. In our case report we present a 41- year old woman suffering from both Cushings syndrome and acromegaly. The patient was examined in National Institute of Endocrinology and Diabetology Ľubochňa for a centripetal type of obesity and hirsutism. Laboratory tests revealed high plasma cortisol levels without circulating variation, hypercortisoluria and elevated plasmatic levels of ACTH. A 2 mg dexamethasone blockade was performed without adequate cortisol suppression in serum and urine up to 8 mg blockade resulted in suppression of 24 hour urine free cortisol. A magnetic resonance imaging (MR) scan revealed suspect pikoadenoma of the pituitary gland (size 2mm). Subsequently trans-sphenoidal resection was performed. Histopathological and immunohistochemical examinations did not reveal the ACTH-producing pituitary adenoma. After surgery hypercortisolism persisted with newly revealed hypersomatotropism. Treatment with Ketoconazole at dose 200mg 1/ 2-0-1 and somatostatin analogues (Lanreotide) at dose 120mg every 42 days were initiated. Control magnetic resonance imaging of the sella demonstrated small tumour of pituary gland of size 3×5mm. Later 3 years after first surgery another trans-sphenoidal resection of residue was performed. Histological and immunohistochemical examinations did not confirm adenoma with ACTH and RH secretion. After second surgery, IGF-1 plasma levels were not normalized with persistence of hypercortisolism. The treatment with Lanreotide at the initial dose as well as Ketoconazole was reinitiated (with increased dose of Ketoconazole to 1-1-1 tbl per 200mg).

The combination of acromegaly and Klinefelter syndrome in one patient.

Acromegaly is a rare disorder usually caused by a benign tumour of the pituitary gland. Long-term presence of elevated growth hormone (GH) and insulin like growth factor 1 (IGF1) levels accompanying this disease is associated with complications such as cardiomyopathy, diabetes mellitus, sleep apnoea and arthropathy. Incidence of acromegaly is 3-4 patients per million per year. Klinefelter syndrome (KS) is the most common sex chromosome disorder occuring in about 1/500 live male births. Common physical features include particularly small testes, among other symptoms are tall stature, reduced muscle tone, delayed pubertal development, lack of secondary male sex characteristics and gynecomastia. We present a 32-year-old man suffering from both acromegaly and 47, XXY Klinefelter syndrome. The patient with typical acromegalic features. Laboratory tests revealed high level of GH which was not suppressed after glucose administration, high level of IGF1, low testosterone concentration with high concentation of luteinizing hormone and follicle stimulating hormone. A magnetic resonance imaging scan revealed a 25 × 18 × 18 mm macroadenoma involving the pituitary gland. A diagnosis of acromegaly was established. After this examination trans-sphenoidal resection was performed. Histopathologic and immunohistochemical findings revealed growth hormoneproducing pituitary adenoma. The presence of infertility with clinical features such as small testes, lack of secondary male sex characteristics and laboratory findings revealed hypergonadotropic hypogonadism that could not be explained by the diagnosis of acromegaly. A chromosomal karyotyping revealed a 47, XXY, confirming the diagnosis of KS. Testosterone replacement therapy wasn´t begun because of patient disagreement Postoperatively elevated plasma concentration of GH and IGF1 levels persist. Treatment by somatostatin analogues (lanreotid) was initiated at dose 120 mg every 28 days. Control magnetic resonance imaging of the sella demonstrated a residue of pituary adenoma size 14 × 14 × 7 mm. The patient is currently undergoing endoscopic revision of the residue. acromegaly - growth hormone - IGF1 - Klinefelter syndrome - testosterone.

Leptin - A new marker for development of post-transplant diabetes mellitus?

INTRODUCTION: Obese patients have increased leptin production and selective resistance to its central anti-adipogenic effects, yet its pro-inflammatory immunostimulating effects persist. MATERIAL AND METHODS: In a group of 70 patients who underwent primary kidney transplantation (KT) we examined adiponectin and leptin levels at the time of KT and 6 months post-transplantation. Patients with diabetes mellitus type 1 or type 2 at the time of KT were excluded from the study. RESULTS: We found that leptin levels significantly increased during the post-transplant period (P = 0.0065). Overall, leptin levels were positively correlated with the level of triacylglycerols, post-transplant diabetes mellitus (PTDM) development and acute rejection (AR). We discovered that, in particular, high leptin levels were associated with AR [OR 2.1273; 95% CI 1.0130-4.4671 (P = 0.0461)] and PTDM development [OR 7.200; 95% CI 1.0310-50.2836 (P = 0.0465)], whereas, low adiponectin levels represent a risk factor for the development of insulin resistance [HR 38.6135; 95% CI 13.3844-67.7699 (P < 0.0001)] and obesity [HR 3.0821; 95% CI 0.8700-10.9192 (P = 0.0053)]. CONCLUSION: We found that a high serum concentration of leptin before KT is associated with both PTDM development and AR and merits further investigation in relation to KT.

[Rare combination of Turner syndrome and congenital adrenal hyperplasia with 21-hydroxylase deficiency: case report]. / Raritná kombinácia Turnerovho syndrómu a kongenitálnej adrenálnej hyperplázie s deficitom 21-hydroxylázy: kazuistika.

Combination of Turner syndrome (TS) and classic congenital adrenal hyperplasia (CAH) is rare. Globally, the incidence of CAH, autosomal recessive disorder caused by enzyme defect of steroidogenic pathway, is very low (1 : 10 000-16 000). 90 % of CAH cases are caused by 21-hydroxylase gene mutation (CYP21A2). Globally, the incidencie of Turner syndrome reaches 1 : 2 500. Phenotypically, females with TS may render wide spectrum of clinical features. Dominant symptoms are lowered terminal height and gonadal dysgenesia, ultimately leading to absence of puberty and infertility. Virilisation may be evident among TS women with chromosome Y 45, X/46, XY. We present a 57 year old woman suffering from both TS 45, X/46, XX and 21-hydroxylase deficiency. Based on the intersex, she was misdiagnosed as a male after the birth. Dominant signs were intrauterine growth retardation and Prader 5 virilisation of the external genitalia. Testes were not palpable. Laparoscopy at the age of 6 showed uterus and ovaries. After this examination, clitoroplasty and vaginoplasty was performed. Karyotyping revealed a 45, X/46, XX pattern. The presence of virilising features at the time of puberty however could not be explained with the diagnosis of Turner syndrome. Laboratory tests revealed elevated level of 17-hydroxyprogesterone, dehydroepiandrosterone with low cortisol concentration and elevated ACTH. With the genomic analysis CYP21A2 gene, namely IN2G (IVS 2-13 A/C>G), large deletion/conversion was detected. Glucocorticoid treatment was initiated. Due to increased plasma renin concentration, fludrocortisone therapy was also initiated. Within this therapy, patient´s state improved significantly.Key words: congenital adrenal hyperplasia - CYP21A2 - Turner syndrome - 21-hydroxylase deficiency.

[Parathyroid cancer]. / Karcinóm pristítneho telieska.

Parathyroid cancer is a rare endocrine malignancy, representing less than 1 % of all cases of primary hyperparathyroidism. The exact etiology of the disease remains unknown. Known risk factors include neck irradiation, end stage renal failure, genetic factors, particularly the the HPRT2/CDCT73 gene mutation. The clinical picture is often indolent, yet progressive with a trend of local invasion and metastasis formation in advanced disease. The clinical picture includes symptoms of severe and resistant hypercalcemia, requiring intensive therapy often with the need of dialysis. Radical surgery is the mainstay of the parathyroid cancer treatment. Chemotherapy and radiotherapy are generally ineffective. An early and correct diagnosis of parathyroid carcinoma significantly influences both morbidity and mortality.Key words: diagnosis - hyperparathyroidism - parathyroid cancer - treatment.

[Diabetic Kidney Disease 3rd stage - laboratory markers of mineral bone disorder]. / Diabetické ochorenie obliciek 3. stádia - laboratórne markery minerálovej a kostnej poruchy.

BACKGROUND: Diabetes mellitus is the most common cause of end stage kidney disease in the developed countries. Chronic kidney disease-mineral and bone disorder (CKD-MBD) develops with deteriorating of the renal functions. Diabetic patients on hemodialysis are characterized by low bone turnover, higher prevalence of severe and progressive vascular calcification with increased cardiovascular morbidity and mortality. The main factor which causes vascular calcification in patients with diabetic kidney disease (DKD) is poor glycemic control. The recent trial findings describe an inverse correlation between intact parathyroid hormone (iPTH) serum levels and glycemic control in a group of diabetic patients on hemodialysis. AIM: The objective of the proposed project is to access the difference of the laboratory markers MBD in the group of patients with 3rd stage DKD depending on glycemic control. We focused on the relationship between the glycemic compensation of diabetes (HbA1c) and iPTH serum level. PATIENTS AND METHOD: Ninety one patients with 3rd stage DKD were investigated. There were 46 women (50.5 %) and 45 men (49.5 %), average age of patients was 71.2 ± 7.0 years, with creatinine level 128 ± 30 µmol/l and estimated glomerular filtration (eGF, MDRD) 0.82 ± 0.16 ml/s. There were 60 patients with better glycemic control of diabetes (HbA1c < 7 %) vs 29 patients with poorly controlled diabetes (HbA1c > 7 %). MBD markers were compared in both groups. Patients were further stratified into subgroups based on the serum level of iPTH (iPTH < 35 pg/ml vs iPTH > 35 pg/ml) and MBD markers compared. Statistical analysis was performed using and Mann-Whitney test. RESULTS: We have found the statistical significance in the serum phosphate and proteinuria levels in between groups with HbA1c < 7 % vs patients with HbA1c > 7 %. Diabetics with better glycemic control had significant reduction in serum phosphate level (1.14 ± 0.20 vs 1.23 ± 0.18 mmol/l, p = 0.038) and in 24 hrs proteinuria level (0.56 ± 1.35 vs 1.30 ± 1.61 g/day, p = 0.007). In the group of presumed low bone turnover (iPTH < 35 pg/ml) we have found the trend towards increased serum calcium level (2.49 ± 0.12 vs 2.43 ± 0.10 mmol/l, p = 0.063) and increased HbA1c value (7.5 ± 1.8 vs 6.4 ± 1.6 %, p = 0.023). CONCLUSION: Our results suggest the closer relationship between glycemic control of diabetes and mineral-bone disorder in earlier stages of DKD. KEY WORDS: diabetes mellitus type 2 (DM2T) - chronic kidney disease (CKD) - mineral and bone disorder (MBD).

[The role of epicardial fat and obesity parameters in the prediction of coronary heart disease]. / Význam epikardiálneho tuku a obezitných parametrov pri predikcii koronárnej choroby srdca.

BACKGROUND: To assess the relationship of parameters of obesity in relationship to coronary angiography findings with correlation of epicardial fat (EF) thickness in uppermentioned context. METHODS: There were 80 patients examined (43 males, 37 postmenopausal females) undergoing elective coronary angiography. We examined the regular obesity parameters - BMI, waist circumference (WC), neck circumference (NC), total body fat (TBF), and visceral fat (VF) using bioimpedance. We assessed the echocardiographically measured EF thickness. We added examination of lipidogram, glycaemia, HOMA-IR (insulin resistance index) and AIP (aterogenic index of plasma). The set was divided into group with coronarographically proved stenosis or stenoses (withCS), and a group without finding of quantifiable stenosis or stenoses (withoutCS). RESULTS: The average thickness of EF in withCS group was 6.3 vs 5.6 mm in group withoutCS (p < 0.025). The differences in the thickness of EF in mentioned groups were 6.5 vs 5.2 mm in males (p < 0.025, = 20 %) and 6.1 vs 6.0 mm in females (p < 0.025, = 1.64 %). In males in withCS group, there was a dominant fat increase in epicardial region and TBF, and in females in withCS group, the fat deposits were increased in general. BMI was not a dominant parameter of adiposity in neither group (males in withCS group 31.11 vs withoutCS 30.41 kg/m(2); females in withCS group 31.40 vs withoutCS 31.20 kg/m(2)). EF was correlated the most by WC in males (r = 0.488; p < 0.005), and in females too (r = 0.564, p < 0.005). The patients in withCS group had increased HOMA-IR 4.75 vs 3.56 in withoutCS group, and AIP 0.22 vs 0.17. CONCLUSION: Thickness of EF in males and VT in females could be considered obesity parameters in assessment of pre-clinical stages of coronary atherosclerosis and prediction of risk of coronary heart disease. In adipose parameters, EF thickness was correlated the most by WC. Risk stratification of coronary artery disease is supplemented by increased HOMA-IR and AIP.

The association of HLA-DRB1 and HLA-DQB1 alleles with genetic susceptibility to multiple sclerosis in the Slovak population.

OBJECTIVE: The aim of the present study was to assess the association between HLA-DRB1 and -DQB1 allele groups with the genetic predisposition to multiple sclerosis (MS) in the Caucasian Central European Slovak population. METHODS: A total of 282 unrelated patients with sporadic MS were enrolled in this case-control study. HLA-DRB1 and HLA-DQB1 allele groups were genotyped using a polymerase chain reaction with sequence-specific primers. The DRB1 and DQB1 allele carrier frequencies, genotypes and haplotype frequencies were compared between MS cases and healthy controls. RESULTS: Positive association with MS was found for alleles HLA-DRB1*15 (OR = 3.64; Pcor = 6.9x10-11), DRB1*03 (after elimination of carriers of DRB1*15, OR = 2.8; Pcor = 0.0029), DQB1*06 (OR = 1.99; Pcor = 7.0x10-4), genotypes HLA-DRB1*15/*15 (OR = 7.6; Pcor = 0.001) and DQB1*06/*06 (OR = 3.81; Pcor = 4.0x10-4) and for haplotype DRB1*15-DQB1*06 (OR = 3.03; Pcor = 0.001). Carriage of alleles DRB1*07 (OR = 0.53; Pcor = 0.04), DRB1*13 (OR = 0.39; Pcor = 4.0x10-4), DQB1*03 (OR = 0.46; Pcor = 1.0x10-4), genotypes HLA-DRB1*13/*11 (OR = 0.12; Pcor = 0.004), DQB1*05/*03 (OR = 0.39; Pcor = 0.035), DQB1*03/*03 (OR = 0.38; Pcor = 0.029) and haplotypes DRB1*13-DQB1*06 (OR = 0.47; Pcor = 0.0128) and DRB1*11-DQB1*03 (OR = 0.58; Pcor = 0.0352) was found to be protective against MS development. DISCUSSION: This is the first study performed to analyse the association of HLA-DRB1/DQB1 with susceptibility to MS in Slovakia. The results of our study confirm that HLA class II alleles, genotypes and haplotypes are associated with MS risk.

Triggering receptor expressed on myeloid cells-1 and 2 in bronchoalveolar lavage fluid in pulmonary sarcoidosis.

BACKGROUND AND OBJECTIVE: Pulmonary sarcoidosis (PS) is characterized by the formation of granulomas in the lungs and has been associated with infection by microorganisms. Triggering receptor expressed on the surface of myeloid cells (TREM)-1 is overexpressed in response to infection while TREM-2 is involved in granuloma formation. We hypothesized that these receptors are overexpressed in PS and might be useful for diagnostic testing. METHODS: Cell surface TREM-1 and TREM-2 expression in cells obtained at bronchoalveolar lavage (BAL) was measured in individuals with sarcoidosis (n = 26) and compared with that seen in individuals with other interstitial lung diseases (ILD) (n = 27). RESULTS: TREM-1 and TREM-2 expression was significantly increased in sarcoidosis compared with other ILD: total number of TREM-1, P = 0.0039 (23.81 vs 13.50 cells/µl), TREM-2, P < 0.0001 (32.81 vs 7.76 cells/µl); percentage of TREM-1: P = 0.0002 (41.30% vs 15.70%), TREM-2: P < 0.0001 (34% vs 9.60%); and mean fluorescence of TREM-1: P = 0.0005 (5.43 vs 1.96), TREM-2: P = 0.0011 (6.85 vs 2.77). Increase in both of these receptors seems to be typical for PS. In discriminating sarcoidosis from other ILD, the specificity (96%) and sensitivity (72%) of the combination of TREM-1 and TREM-2 was high. CONCLUSIONS: Increased TREM-1 and TREM-2 cell surface expression is observed in sarcoidosis. Evaluation of BAL cell expression of both of these receptors may serve as a diagnostic marker for sarcoidosis.