Journal of Personalized Medicine

Background: Dialyzer-associated hypersensitivity reactions are rare but potentially life-threatening complications of hemodialysis (HD). Their pathophysiology is heterogeneous. Methods: We report a 49-year-old patient with end-stage chronic kidney disease (CKD G5), severe secondary hyperparathyroidism, poorly controlled arterial hypertension, a long history of heavy smoking, severe coronary and valvular disease, reduced left ventricular ejection fraction, renal anemia, and chronic volume overload. Results: Shortly after initiation of HD with a polysulfone dialyzer (Diacap Pro), she repeatedly developed severe dyspnea, hypoxemia, and marked hypertensive responses. Similar reactions occurred after switching to a cellulose triacetate dialyzer (Sureflux), necessitating temporary conversion to peritoneal dialysis (PD). Progressive PD ultrafiltration failure and loss of residual kidney function eventually required a return to HD. Severe reactions recurred within 15–30 min of treatment despite premedication. During the most severe episode, the patient developed profound hypoxemia (SpO₂ 55%), severe hypertension (up to 240/130 mmHg), ventricular tachycardia, and cardiac arrest requiring successful cardiopulmonary resuscitation. Immunological evaluation demonstrated normal total IgE (17 U/mL), decreased C3 (0.76 g/L), markedly reduced total hemolytic complement activity (CH50, 18%), and elevated IL-6 (87.5 pg/mL). Chronic HD was successfully reinitiated using an FX CorAL dialyzer with a Helixone^® hydro membrane. Since its introduction, no further hypersensitivity reactions have occurred, and corticosteroid, antihistamine, and bronchodilator premedication has been discontinued. This case demonstrates severe recurrent dialyzer-associated hypersensitivity with findings suggestive of complement involvement, complicated by cardiac arrest in a patient with markedly impaired cardiovascular reserve. Conclusions: Successful long-term treatment with a hydrophilic Helixone^® dialyzer highlights the importance of individualized dialyzer selection in patients with severe hypersensitivity reactions.

Cardiovascular fibrosis is a dynamic process that involves fibroblast activation, extracellular matrix production, and myocardial remodeling. While it can damage the heart through an unregulated and progressive response, it is also an essential component of the body’s repair mechanisms. Fibroblast activation protein (FAP) targeted positron emission tomography (PET) has emerged as a molecular imaging approach for showing FAP expression in association with activated fibroblasts, potentially providing complementary information to established and contemporary imaging techniques. This narrative review examines the biological basis, tracer development and emerging cardiovascular applications of FAP-targeted PET, with emphasis on the clinical applications and limitations of available evidence. Relevant publications were found through a PubMed/MEDLINE search and selected according to their relevance to cardiovascular FAP-targeted imaging and potential clinical applications. Recent developments include gallium-68-labeled tracers such as ⁶⁸Ga-FAPI-04, fluorine-18-labeled tracers such as ¹⁸F-FAPI-74, and high-affinity ligand platforms such as ONCOFAP. Current evidence consists of case reports, preclinical investigations, and mostly small exploratory clinical studies across many cardiovascular conditions. These studies report associations between cardiovascular FAP tracer uptake and measures of myocardial injury, remodeling and cardiac function, primarily in small exploratory cohorts. However, it is important to note that FAP expression reflects fibroblast activation and does not directly establish active collagen deposition, pathological fibrosis or tissue reversibility. Also, differences in tracer selection and imaging protocol, small study sizes and limited standardization restrict the ability to fully understand the clinical applications of existing findings. Cardiovascular FAP-targeted PET, although promising, remains investigational, and its clinical utility, prognostic value, and superiority over established imaging methods have not been fully demonstrated. More standardized, prospective studies are required to determine its exact role in cardiovascular disease assessment and management.

Introduction: Cleft lip and/or palate (CLP) is a defect caused by the failure of palatal shelf fusion and growth, which is heavily influenced by many environmental and biological factors. Transcription, growth, inflammation and antimicrobial factors modulate molecular events in clefted tissue and are, therefore, vital in the morphopathogenic assessment of CLP. The aim of this study is to determine the expression of immunomodulators and cellular signaling molecules (bone morphogenetic proteins (BMP), nuclear factor kappa beta (NF-κB), interleukin 10 (IL-10), galectin 10 (Gal-10), heat shock protein 70, Caspase 3, cathelicidin 37 (LL-37)) between sinistral (left), dextral (right) and bilateral cleft-affected tissue. Materials and Methods: Tissue samples were obtained from 19 patients—5 with CLP of the right side, 6 on the left side, and 8 bilateral. Five controls were used for comparison. Due to cohort size, this study was conducted as a preliminary pilot investigation. Data were evaluated with immunohistochemistry, semi-quantitative evaluation and the Mann–Whitney U test. Results: Epithelium of CLP presented with significant changes in Gal-10 (U = 3, p = 0.030); IL-10 (U = 3.0, p = 0.030), (U = 1.0, p = 0.002), (U = 2.0, p = 0.032); NF-kB p105 (U = 2.0, p = 0.017), (U = 14.5, p = 0.017). Connective tissue presented with significant differences in Gal-10 (U = 2.5, p = 0.032), (U = 5, p = 0.019), and HSP70 (U = 1.5, p = 0.016). Caspase 3, LL-37 and BMP2/4 showed no significant differences. Conclusions: CLP on the right side presented with a larger number of statistically significant differences than any other type of CLP. An increase in factor expression in the epithelium illustrates the conditions of chronic inflammation. An increase in factor expression in connective tissue suggests protective actions. Factors that showed no change in their distribution suggest unaffected osteogenesis and antimicrobial activity in CLP.