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Sarcoidosis is a systemic inflammatory disease of unknown aetiology. Given its complex clinical presentation, the disorder frequently causes diagnostic challenges. In most cases, the primary manifestation is in the lungs and mediastinum. Breast involvement as the primary manifestation of sarcoidosis is rare, accounting for less than 1% of cases. The authors present the case of a 44-year-old woman whose disease first manifested as multiple non-specific BIRADS 4 lesions in both breasts, accompanied by axillary lymphadenopathy, detected by ultrasound examination. The lesions were not visible on mammography. The course of the disease was clinically silent, with intermittent remissions, until the complete resolution of focal breast lesions on ultrasound after two years of follow-up. The paper presents an algorithm for the management of multifocal breast pathology with associated lymphadenopathy, which led to the prompt verification of sarcoidosis.

The incidence of ischemic heart disease (IHD) in patients with OSAS is estimated at around 20%. This greatly affect a common risk factors for both diseases: male gender, obesity, age and diabetes and hypertension. Attention is drawn to the possibility of genetic determinants of IHD. The aim of study was to answer the question whether the presence of polymorphisms of selected genes possibly related to IHD may be useful to isolate the group of patients with OSAS, especially vulnerable as a complication of IHD. Materials and methods. The study included 600 people with OSAS, which was isolated in patients with IHD (127 people). The remaining 473 individuals were observed as a control group. The polymorphism of three genes were evaluated to find possible influence on the occurrence of IHD or myocardial infarction as follows: SREBF1 (sterol regulatory element binding transcription factor 1), REBF2 (sterol regulatory element binding transcription factor 2) and HIF1 (hypoxia inducible factor 1, alpha subunit). Results. Analysis of relationship between polymorphisms of selected genes and the diagnosis of IHD in the whole group of patients with OSAS showed a relationship only for the gene SREBF1 finding the lowest frequency of its occurrence in AA homozygotes (at 13.6%) and twice with GG homozygotes (26.1%). Conclusions. Rating polymorphisms studied genes did not reveal their relationship to the occurrence of IHD in patients with OSAS, both in the whole group as well as separate subgroups.

Introduction: Results of earlier population and clinical studies confirmed relationship between stroke and obstructive sleep apnea. Our previous study on epidemiology of sleep-disordered breathing in Warsaw based on 676 subjects, mean age 56.6 +/- 8.2 years, confirmed OSA in 76 subjects (11.3%) mean apnea hypopnea index (AHI) - 25.3 +/- 16.1 revealed low incidence of stroke in OSA group (2 pts; 2.6%) and in subjects without OSA (20 pts; 3.4%). The aim of this study was to assess prevalence of stroke in newly diagnosed OSA subjects qualified to CPAP therapy., Material and Methods: We studied 342 consecutive pts (263 males and 79 females)--mean age--55.4 +/- 10.1 years with severe disease--AHI 39.7 +/- 22.5 and obesity--body mass index 35 +/- 6.6. History of stroke was confirmed in 16 pts before continuous positive airway pressure (CPAP) introduction (4.7%) - group 1. Group 2 (without history of stroke) comprised of 326 pts (95.3%)., Results: Multiple linear regression analysis revealed significant correlation between stroke and time spent in desaturation below 90% during polysomnography-- T90 (beta = -0.22, p = 0.009), diabetes (b = 0.16, p = 0.006), Epworth sleepiness score (beta = 0.14, p = 0.02) and coronary artery disease (b = 0.14, p = 0.03)., Conclusions: Stroke in OSA pts before CPAP treatment was related to overnight and daytime oxygenation, diabetes, daytime sleepiness and coronary artery disease. Incidence of stroke in our group was low (4.7%) and similar to previous data from population study.

Leptin is believed to play a significant role in the pathogenesis of obstructive sleep apnea syndrome (OSAS) as well as progression of OSAS-related obesity. It is also known that other factors such as gender and diurnal variations in serum strongly affect the measurement results making repeated blood sampling necessary for leptin precise monitoring. Since renal metabolism and urine secretion are the main elimination mechanism for leptin, in this study we evaluated urine relevance for leptin secretion monitoring. Serum and urine (collected during the day and overnight) sampled from 169 OSAS patients and 41 controls were assayed by immunoenzymatic method specific for human leptin. Only 5 (17%) controls and 10 (5.8%) OSAS patients had undetectable urine leptin. We observed significant relationships between serum and urinary leptin in both day-time (r=0.656, P<0.001) and night-time (r=0.518, P<0.001) samples and between day and night-time urine leptin (r=0.811, P<0.001). Significance values did not alter when urinary leptin levels were expressed as the ratio to urinary creatinine. Gender-related differences in leptin concentrations were present both in serum (P<0.001) and overnight urine (P<0.01) in the OSAS group. However, mean night-time urine leptin was lower in the OSAS patients (P<0.05) and their subgroups stratified according to disease severity (P<0.01), while serum leptin levels were comparable in both groups. We conclude that assaying leptin in urine by immunoenzymatic method is a reliable and useful non-invasive alternative for its serum measurement. However, night-time urine leptin levels better reflect differences in its turnover due to gender and OSAS severity.

It is increasingly recognized that obstructive sleep apnea (OSA) syndrome is a systematic rather than local disorder. There is also growing evidence that apart from the syndrome's major features: intermittent hypoxia and sleep fragmentation, functional activity of the immune system is altered in OSA patients, with several cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) taking active part in sleep regulation. Little is known about the effects exerted by chronic intermittent hypoxia combined with persistent pro-inflammatory activity of the immune system on the vascular micro milieu in OSA. In this study we attempted to confirm the hypothesized imbalance between pro- and anti-angiogenic factors by evaluating direct and indirect angiogenic activity of OSA patients' sera in the in vivo serum-induced angiogenesis (SIA) and leukocyte-induced (LIA) assays, respectively, in mice. Both tests revealed significantly inhibited angiogenic activity of OSA patients' sera compared with healthy controls (P<0.001). Moreover, differences related to the subject's weight regarding in the mean number of newly-formed vessels were observed with a significantly greater inhibition in the normal-weighing apneic subjects than in the overweight or obese ones (P<0.01). The angiogenesis inhibition index was positively related to the serum IL-6 level (r=0.35; P<0.05) in the OSA group, but not to TNF-alpha, fasting serum leptin, or OSA syndrome severity as assessed by the AHI index. Our results demonstrate that OSA is accompanied by disturbed serum angiogenic activity, apparently resulting from an imbalance between pro- and anti-angiogenic factors, some of them being produced by the adipose tissue. The disordered angiogenic activity might be related to the pathophysiology of OSA and should be considered an important causative factor for the increased prevalence of cardiovascular diseases in OSA patients.