Antiphospholipid antibodies (APLAs) are primarily directed toward phospholipid-binding proteins and are responsible for thrombotic events. APLAs include anti-β2Glycoprotein I (anti-β2GPI), anticardiolipin (anti-CL) antibodies, and lupus anticoagulant. These antibodies are typical markers of antiphospholipid syndrome (APS) and are a part of its diagnostic criteria. Many data underline the presence of APLAs in other rheumatic diseases (e.g., systemic lupus erythematosus, systemic sclerosis, Sjögren’s syndrome, rheumatoid arthritis and Behçet’s disease). However, they are also detected in patients with cancer, infection, and neurological disorders. Furthermore, healthy individuals may be carriers of APLAs. Chronic asymptomatic APLAs presence is most common in the elderly and subjects with chronic diseases (including malignancies). Specific kinds of APLAs are considered markers of oncological progression. These antibodies occur in 6% of pregnant women (without diagnosed APS) and are related to many pregnancy complications. Of worth, various types of APLAs are reported to have different prothrombotic properties. The risk of thrombotic events in APLA-positive but clinically naïve patients raises many questions in clinical practice. This manuscript analyses various clinical situations and consequences of the APLAs’ presence, particularly in patients without diagnosed APS. The prevalence, etiology, molecular background, and prothrombotic properties of numerous APLAs are broadly discussed. The new management approach in different clinical conditions and organ complications is present in the context of recent recommendations. Discussed data underlines that adequate and timely introduced thromboprophylaxis can decrease the risk of thrombus formation and prevent increased morbidity.

Sarcopenic obesity (SO) is a combination of obesity and sarcopenia, with diagnostic criteria defined as impaired skeletal muscle function and altered body composition (e.g., increased fat mass and reduced muscle mass). The mechanism of SO is not yet perfectly understood; however, the pathogenesis includes aging and its complications, chronic inflammation, insulin resistance (IR), and hormonal changes. Genetic background is apparent in the pathogenesis of isolated obesity, which is most often polygenic and is characterized by the additive effect of various genetic factors. The genetic etiology has not been strictly established in SO. Still, many data confirm the existence of pathogenic gene variants, e.g., Fat Mass and Obesity Associated Gene (FTO), beta-2-adrenergic receptor (ADRB2) gene, melanocortin-4 receptor (MC4R) and others with obesity. The literature on the role of these genes is scarce, and their role has not yet been thoroughly established. On the other hand, the involvement of systemic inflammation due to increased adipose tissue in SO plays a significant role in its pathophysiology through the synthesis of various cytokines such as monocyte chemoattractant protein-1 (MCP-1), IL-1Ra, IL-15, adiponectin or CRP. The lack of anti-inflammatory cytokine (e.g., IL-15) can increase SO risk, but further studies are needed to evaluate the exact mechanisms of implications of various cytokines in SO individuals. This manuscript analyses various immunogenetic and non-genetic factors and summarizes the recent findings on immunogenetics potentially impacting SO development.

Breast implant insertion for breast reconstruction or breast augmentation is a developing procedure, with high demand worldwide-being the second most common plastic surgery in the US as of 2022. Breast-implant-associated anaplastic large cell lymphoma (BIA-ALCL) is T-cell, non-Hodgkin lymphoma, typically CD30+, ALK-, presenting with fluid collection in the inner aspect of the peri-implant capsule in most patients, with the onset exceeding 1-year after implantation. The mean time between breast implant insertion and BIA-ALCL development is 7-10 years. The main risk factor is the use of textured implants because of their susceptibility to triggering local inflammation and immune stimulation finally leading to lymphoproliferation. Genetic predispositions to hereditary breast cancer increase the risk of disease development as well. BIA-ALCL seems to be underestimated in many countries and the initial symptom-seroma might be overlooked and misdiagnosed. Despite its rarity, the awareness of the disease should be improved among patients and medical professionals. This paper summarizes epidemiology, etiopathogenesis, differential diagnosis, and treatment-both surgical and hematological approaches.

Hemophilia A is a genetically conditioned disease leading to hemostatic disorders due to factor VIII (FVIII) deficiency. The treatment of hemophilia has evolved throughout the past years and has si...

Purpose: The admissions of nonagenarians to internal medicine wards are rising. The aim of this study was to analyse the causes of ward admission and blood and renal parameters as potential mortality predictors in this age group. Patients and Methods: Out of 1140 patients, 111 nonagenarians aged 90+ admitted to the Internal Medicine Ward in one general hospital in Poznan in 2019 were studied. Medical records of these patients were analysed to find factors attributable to the hospitalisation. Results: The leading causes of admission were infections and cardiovascular diseases, and the main causes of death were cardiovascular diseases. Elevated C-reactive protein (CRP) level was a statistically significant death predictor. Equally, decreased albumin level was found to be a mortality predictor. No such relationships were obtained for haematological or renal parameters. Conclusion: Our study uniquely analysed a relatively large group of hospitalised nonagenarians and identified those who need particular attention in the ward by identifying those with the highest risk of death. CRP and albumin levels may serve as useful indicators of in-hospital mortality in this age group.

Background: Susac syndrome is a rare, autoimmune, occlusive endotheliopathy that affects blood vessels in the central nervous system (CNS), retina, and inner ear. At initial medical evaluation, the classic triad of symptoms is present in less than one-third of patients, making diagnosis challenging. Methods: A brief review and retrospective analysis of the course, disease activity, exacerbations, and treatment of four patients with Susac syndrome. Results: The mean age of the patients was 25.8 years, and the average disease duration was 183.5 months +/- 90.65. The clinical triad was observed at the onset of the disease in only one patient. The first patient with predominant CNS symptoms was treated with prednisone, methotrexate, and sulfasalazine (IVIG and GCS i.v. were used during exacerbations). The next patient with exacerbation of ENT symptoms was treated with oral methylprednisolone (MP) and mycophenolate mofetil. The third patient had no clear predominance of any symptoms and responded well to azathioprine. The last patient presented mainly ophthalmological symptoms and was initially treated with cyclophosphamide (total dose 6200 mg) and IVIG. Later, azathioprine and mycophenolate mofetil were introduced. Conclusions: The described cases highlight differences in the course of the disease and response to immunosuppressive therapy. Patients initially responded very well to high doses of GCS and IVIG. However, in addition to long-term remissions, relapses also developed. Therefore, individual treatment based on the principles of personalized medicine is necessary.