Introduction and purpose: Acromegaly is a rare disease which occurs with the frequency of 0.2-1.1 cases per 100 000 patients per year. The main cause is the excess level of growth hormone (GH) which stimulates the liver to the insulin-like growth factor type 1 (IGF-1) secretion. IGF-1 leads to the tissues overgrowth. In addition, acromegalic patients suffer from many comorbidities, such as: cardiovascular, endocrinological, neoplastic and musculoskeletal complications. The main aim of this review is the update of the latest information concerning cardiovascular comorbidities in patients with acromegaly.State of knowledge: Studies revealed that 80% of acromegalic patients will develop cardiovascular comorbidities. Complications such as: hypertension, cardiomyopathy, arrhythmia, heart valve disease, atherosclerosis and coronary heart disease as well as myocardial infarction were the most widely described. They are responsible for 44% of deaths in the first decade of the acromegaly and 23% in the second one.Conclusions: Because of the delayed diagnosis of acromegaly in most patients, most comorbidities are discovered in advanced stages leading to the decrease in patients’ life span. Adequate knowledge about potential complications is necessary to increase patients’ quality of lives.

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Myelodysplastic syndromes (MDS) constitute a heterogeneous group of diseases characterised by ineffective haematopoiesis, dysplasia and cytopenias. The treatment for high-risk MDS (HR-MDS) depends on individual factors such as the stage of the disease, age, comorbidities, and infections.Allogeneic haematopoietic stem cell transplantation (allo-HSCT) with reduced intensity conditioning has allowed more HR-MDS patients to be transplant-eligible, regardless of age. Hypomethylating agents, including azacitidine and decitabine, remain the standard of care for HR-MDS patients who are not qualified for curative allo-HSCT. Combination therapy of azacitidine with some new drugs resulted in higher response rates than azacitidine in monotherapy. Other targeted therapies are under investigation. They include HMA with different antibodies targeting immune checkpoints -programmed cell death (ligand) 1, cytotoxic T lymphocyte antigen 4, T-cell immunoglobulin mucin-3 or cluster of differentiation 47. Larger studies are necessary to confirm their efficacy in the treatment of HR-MDS.

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Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology. An important role in the pathogenesis of SLE has been attributed to interferon alpha (IFN-α), which stimulates the expression of numerous genes, resulting in an increased autoinflammatory response. Recent studies have demonstrated  increased levels of this cytokine in patients with SLE, as well as in relatives, indicating that IFN- α is an inherited risk factor for lupus. Cases of induction of SLE/lupus-like syndrome after IFN- α therapy also point to the involvement of interferon in the pathogenesis of the disease. Interferon being a probable initiator of the disease, as well as a marker to examine its exacerbations, is a potential research target to better understand the etiology and pathogenesis of lupus. More research is needed to determine the feasibility of using INF-blocking agents for new therapies in SLE.