Vnitrni lekarstvi最新文献

Treatment of HIV infection has modified the initially fatal infection into a typically chronic disease requiring lifelong treatment. However, there is no complete normalization of immune activation, signs of inflammation and prothrombotic state in treated patients. This condition is the result of many factors, but the main cause is thought to be the residual production of HIV-1 RNA and viral proteins by infected cells in cellular reservoirs. Persistence of immune activation/inflammation/prothrombotic state leads to the pathophysiology of "sterile inflammation" and so-called non-AIDS diseases, which manifest one to two decades earlier in those infected. Despite all the pitfalls and unwanted secondary manifestations of antiretroviral drugs, the treatment of HIV infection has managed to reverse the trajectory of a fatal pandemic and has made it possible to approach therapeutic modalities that were absolutely unimaginable just a few years ago. Solid organ transplantation is now a completely legitimate therapeutic method for patients living with HIV, and highly suppressive treatment even allows transplantation from an HIV-infected donor. The text below presents a brief overview of the basic pitfalls, but also of the successes, of the current highly suppressive treatment of HIV infection.

The most common immune-mediated inflammatory rheumatic diseases, rheumatoid arthritis, psoriatic arthritis and axial spondyloarthritis and have reached significant advances in recent years with the introduction of biological therapies against cytokines and immune cells, but also against intracellular enzymes, specifically Janus kinases (JAKs). Intracellular JAK signalling is activated by binding of various cytokines or growth factors to the respective cellular receptors, allowing the activation of STAT (Signal Transducers and Activators of Transcription) transcription factors and ultimately the transcription of genes with important roles during the innate and adaptive immune response. Four Janus kinases have been described: JAK1, JAK2, JAK3 and tyrosine kinase-2 (TYK2). Four JAK inhibitors (tofacitinib, baricitinib, upadacitinib and filgotinib) are currently approved for the treatment of rheumatoid arthritis, and some for the treatment of psoriatic arthritis and axial spondyloarthritis. JAK inhibitors have varying selectivity against individual kinases. Some JAK inhibitors are being tested in other rarer systemic connective tissue diseases. The general advantages of JAK inhibitors are oral administration, rapid onset of action, and efficacy in monotherapy. The safety profile of JAK inhibitors compared with biologic therapy appears to be comparable, with a higher incidence of herpes zoster, and an increased incidence of major cardiovascular disease, thromboembolic complications, and cancer in at-risk patients is discussed. The aim of this paper will be to summarize the latest findings on JAK inhibitors in approved indications for the most common rheumatic diseases.

The article summarizes new advances in cardiology published in 2022, which have an impact to everyday practice of not only internists and cardiologists. The administration of polypill to patients after myocardial infarction (SECURE study), early pharmacotherapy of hypertension in pregnant women with blood pressure exceeding 140/90 mmHg (CHAP study), or the administration of dapagliflozin to patients with heart failure with preserved or mildly reduced ejection fraction (DELIVER study) have been shown to be effective. Patients with heart failure do not have to limit their sodium intake (SODIUM-HF study), on the contrary, they benefit from up-titration of guideline-recommended drugs to the maximum tolerated doses as quickly as possible (STRONG-HF study). For antihypertensives, it does not matter whether they are taken in the morning or in the evening (TIME study), nor has there been found any difference in the incidence of cardiovascular events with hydrochlorothiazide and chlortalidone (DCP study). In patients with increased cardiovascular risk, highly sensitive troponin should be measured before non-cardiac surgery as well as 24 and 48 hours after surgery to detect perioperative myocardial infarction. Different blood pressure and oxygenation targets in patients after resuscitation for out-of-hospital cardiac arrest do not affect the outcomes of their treatment.

Barakat syndrome, also known as HDR syndrome, is a clinically heterogenous, autosomal dominant rare genetic disease, which frequency is unknown. It is primarily caused by deletion of chromosome 10p14 or mutation of GATA3 gene, located on chromosome 10. Although this syndrome is phenotypically defined by its triad of HDR: hypoparathyroidism (H), deafness (D), renal disease (R), the literature identifies cases with different components, consisting of HD, DR, HR (1). The syndrome was first described by Amin J. Barakat et al. in 1977 in siblings with hypocalcemia and proteinuria (2). So far, about 180 cases have been reported in the worldwide medical literature (3). In this report we present our own case report of patient with Barakat syndrome with hypoparathyrodism, unilateral deafness and renal impairment.

Diabetic foot (DF) is one of the most serious complications of diabetes, leading to high morbidity and mortality in patients with diabetes, significantly affecting their quality of life and placing a huge burden on the healthcare system. Diabetic foot infection (DFI) is a major factor in the non-healing of diabetic ulcerations of the lower limbs, increases the number of hospital admissions, prolongs their duration and is a frequent cause of increased number of amputations. The most serious form of foot infection is osteomyelitis. Management of infection in SDN includes proper diagnosis, including obtaining appropriate specimens for culture, indication of rational antimicrobial therapy or early surgical intervention, and provision of all other necessary wound care and overall patient care to prevent recurrence of DFI.

Dentists commonly encounter patients taking oral antithrombotic agents who require invasive dental procedures. Although antithrombotics can cause an increase in bleeding, there is consensus that treatment regimens with antiplatelet agents, older anticoagulants (warfarin) and direct oral anticoagulants should not be altered before routine dental procedures when the risk of bleeding is low. Thromboembolic risk of their discontinuing likely outweighs potential bleeding complications associated with surgery. Therefore, the risks of stopping or reducing these medications must be weighed against the potential consequences of prolonged bleeding, which can be controlled with local measures such as mechanical pressure, suturing, haemostatic agents or antifibrinolytics. Some patients who are taking antithrombotic medications may have additional comorbid conditions or receive other therapy that can increase the risk of prolonged bleeding after dental treatment. Where a patient is believed to be at high bleeding risk, the dentist should consider a consultation with the patient's physician to discuss temporarily discontinuing the antithrombotic therapy.

A review article discussing the reliability of Point-of-Care ultrasound and education in this method in various fields of medicine.

The article summarize the most important changes regarding the management of valvular heart disease, which have been made in the ESC Guidelines 2021. Based on the randomized clinical study data, which were recently published, the most frequent changes were done in terms of the choice of mode of intervention in the aortic and mitral valves as well as in the management of the antithrombotic therapy.

Levothyroxine therapy in management of diferentiated thyroid carcinoma (DTC) has been common practice for decades. Levothyroxine is being administered to patiens with DTC after total thyreoidectomy (with or without postopreative radioiodine treatment) not only to restore euthyroidism but to suppress the production of thyroid-stimulating hormone (TSH) as well because TSH is considered as a growth factor for thyroid follicular cells. However there has been a downside to this threatment recently. The main concerns are the known risks related to iatrogenic subclinical or even mild but clinicaly overt iatrogenic hyperthyroidism. Therefore individualized treatment approach aiming to balance between the risk of tumor recurence and the risks related to hypertyhroidism in view of pateints age, risk factors and comorbidities is essential. Close folow-up is therefore necessary with frequent dose adjustments according to target TSH values published in American Thyroid Association guidelines.

Gut microbiome research has been a surge of interest in many branches of medicine in the last decade. Our main aim is to show ability of microbes to infuence the functions of human body, especially in the immune system, and on the other hand to clarify changes in composition of gut microbiome in the post-transplantation period and their function for the long-term survival of the graft and the patient in the context of the occurrence of a wide range of complications. Kidney transplantation with the subsequent use of immunosuppressants and antibiotics affects the composition of gut microbiome. The subsequent development of dysbiosis significantly increases the risk of acute rejection, interstitial fibrosis and tubular atrophy of the graft, post-transplant diarrhoea, organ´s infections and metabolic complications such as post-transplant diabetes mellitus. Also important is the influence of the microorganisms of the gut microbiome on metabolism of immunosuppressants with the production of less effective components and the subsequent necessity of modifying their levels with a higher risk of underdosing and the occurrence of graft rejection. Support of the composition of the gut microbiome in the post-transplantation period in favor of bacteria producing short chain fatty acids (SCFA) is possible by changing of diet with predominance of fiber, the application of probiotics, prebiotics. According to available studies, it can lead to benefits in term of metabolic compensation, to the induction of donor-specific tolerance and many others, with an overall improvement in the quality of patient and graft survival.