UDC 616.155.392

Abstract

Introduction. Thrombotic thrombocytopenic purpura (TTP) is a rare but life-threatening thrombotic microangiopathy characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ ischemia due to microvascular thrombi. Its pathophysiology primarily involves a severe deficiency of the ADAMTS13 enzyme, leading to uncontrolled platelet aggregation and microthrombi formation. TTP presents with nonspecific symptoms: fatigue, petechiae, neurological disturbances, renal impairment, and fever, often mimicking other conditions. Advances in diagnosis, and targeted therapies like caplacizumab, plasma exchange, and immunosuppression have significantly reduced mortality rates from over 90.0 % to approximately 10.0-20.0 %. Still challenges remain in early diagnosis, treatment accessibility, and management.

The aim of the study. Using the case report of TTP to demonstrate the recent achievements in understanding of pathogenesis, and treatment of this severe condition.

Materials and methods. A systematic review was conducted for the period from 01.01.2014 to 01.11.2024 using methods of the National Library of Health (NIH). Filters applied: TTP, Free full text, Review. Of the 183 sources received, we selected and analyzed 17 and 2 articles (1982 and 1998) were used for historical reasons. The case report of complicated TTP is demonstrated.

Results. The increased frequency of TTP results in the risk for physicians of various specialties of encountering unrecognized or untimely diagnosed TTP, which, even with modern possibilities of verification and treatment, leads to exitus lethalis. The presented clinical case is an example of a sudden severe fatal course of the disease.

Conclusions. The presented case report demonstrates that even early detection of TTP and ensuring the timeliness of adequate treatment does not guarantee the success. Each case of thrombocytopenia should be considered as a possible TTP.

УДК 616.716.4-089.843-003-076.4/.5-092.9

This study aimed to investigate the dynamic changes in the histo-morphological architecture of bone-ceramic regeneration following the transplantation of natural collagen combined with lincomycin into an experimental defect of the rabbit mandible. 45 adult male rabbits aged 6-7 months and weighing 2.5-3 kg were used for the study. 20 animals were in control group and 20 animals in experimental. An additional 5 intact animals were used to study the normal structure of bone tissue in the studied area of the lower jaw. The control group consisted of animals with a bone defect that healed under a blood clot. The experimental group consisted of rabbits with the bone defect filled with natural collagen, with simultaneous intramuscular injections of lincomycin at a dose of 12 mg/kg body weight once a day for 6 days (Col-C-lincomycin). Post-traumatic bone tissue status within the defect area was monitored for 84 days. Ultrastructural changes were studied using scanning electron microscopy. To determine changes in the composition in the bone regeneration, three parameters were calculated – the relative volume of: 1) bone tissue, 2) osteoplastic material and 3) connective tissue in the bone regeneration. The data were analyzed using the Student's t-test, and a difference at p<0.05 was considered statistically significant. The research of the surface topography of the experimental bone defect in the rabbit mandible, following the implantation of Col-C material in combination with lincomycin, revealed numerous regenerative changes that occurred after injury and correlated with the dynamic changes in the relative volume of bone tissue, osteoplastic material, and connective tissue within the regeneration. Morphometric analysis of the relative volume of the constituent components of the regeneration in the experimental defect revealed a phased nature of the dynamics of the observed changes. The osteocyte lacuno-canalicular system that formed after material implantation acquired characteristics of typical structure. Foci of incomplete osteogenesis were not visualized. Unlike the control group, after the application of Col-C material in combination with lincomycin, the majority of osteons in the regeneration near the outer bone plate did not differ from the typical structure of the maternal bone in terms of both its structure and geometry.

Introductions. Inflammation plays a crucial role in the occurrence and progression of atherosclerosis. Recent studies have explored the clinical effects of inflammatory reactions in the development of coronary heart disease. They found that different subtypes of leukocytes—specifically neutrophils, lymphocytes, and monocytes—provide more predictive value for assessing the risk of cardiovascular disease than just the total leukocyte count. Additionally, several studies have reported hematological abnormalities in COVID-19 patients. These abnormalities include an increase in white blood cell count, as well as a decrease in red blood cell count and hemoglobin levels. Such alterations are associated with a higher risk of severe disease and poorer outcomes. Smoking is also a recognized risk factor, as noted in the Framingham Heart Study. Smokers face an increased risk of myocardial infarction or sudden cardiac events.

Aim. To evaluate the levels of leukocyte inflammatory markers in patients with unstable angina and post-COVID-19 syndrome, based on smoking status.

Materials and Methods. The study involved 147 patients with unstable angina aged between 35 and 76 years, with a mean age of 60.32 ± 0.66 years. Among the participants, 17.69% (n=26) were women, while 82.31% (n=121) were men. The presence of post-COVID syndrome was assessed using the POSTCOVID-19 Functional Status Scale, which allowed for the division of patients into two groups: group (I) comprised 87 patients (59.18%) with post-COVID syndrome, and group (II) included 60 individuals (40.81%) without post-COVID syndrome. Each group was further categorized into subgroups based on smoking status: subgroup IA and IIA consisted of smokers, while subgroup IB and IIB comprised non-smokers. The study measured several leukocyte inflammatory markers, including the Neutrophil-to-Lymphocyte Ratio (NLR), Monocyte-to-Lymphocyte Ratio (MLR), Systemic Immune Inflammation Index (SII), Systemic Inflammation Response Index (SIRI), and Aggregate Index of Systemic Inflammation (AISI). Comparisons were made between the subgroups: IA and IIB, IA and IIA, as well as IB and IIB, taking into account the presence or absence of post-COVID syndrome and smoking status.

Results and discussion. The data obtained revealed that mean Neutrophil-Lymphocyte Ratio (NLR) levels were significantly higher in the smoking subgroup experiencing post-COVID syndrome (designated as IA) compared to the non-smoking subgroup without post-COVID syndrome (designated as IIB). Specifically, NLR levels in subgroup IA were 50% greater, measuring 3.47±0.85×10⁹/L, compared to 1.73±0.12×10⁹/L in subgroup IIB (p<0.03). Additionally, the average Monocyte-Lymphocyte Ratio (MLR) was also significantly elevated in subgroup IA by 37.9%, with values of 0.29±0.04×10⁹/L for IA versus 0.18±0.02×10⁹/L for IIB (p<0.03).  The aggregate indices of leukocyte inflammation, including Systemic Inflammatory Index (SII), Systemic Inflammatory Response Index (SIRI), and Aggregate Immune Score Index (AISI), were significantly higher in subgroup IA, ranging from 52% to 62% compared to subgroup IIB. Specifically, SII was 52.7% higher (803.81±163.64×10⁹/L for IA vs. 380.42±34.78×10⁹/L for IIB, p<0.009), SIRI was 60.8% higher (2.02±0.60×10⁹/L for IA vs. 0.80±0.09×10⁹/L for IIB, p<0.02), and AISI was 62.7% higher (466.64±115.80×10⁹/L for IA vs. 174.06±24.32×10⁹/L for IIB, p<0.01). When comparing smokers with post-COVID syndrome (IA) to smokers without post-COVID syndrome (IIA), MLR was 37.93% higher in the IA subgroup (0.29±0.04×10⁹/L for IA vs. 0.18±0.02×10⁹/L for IIA, p<0.02). SIRI was 55.9% higher (803.81±163.64×10⁹/L for IA vs. 380.42±34.78×10⁹/L for IIA, p<0.05), and AISI was 53.99% higher (466.64±115.80×10⁹/L for IA vs. 174.06±24.32×10⁹/L for IIA, p<0.03). Among non-smokers, individuals with post-COVID syndrome (IB) exhibited significantly higher levels of inflammatory leukocyte markers compared to non-smokers without post-COVID syndrome (IIB), showing increases of 33% to 40%. Specifically, NLR was 34.2% higher (2.63±0.22×10⁹/L for IB vs. 1.73±0.12×10⁹/L for IIB, p<0.005), SII was 39.16% higher (625.26±57.12×10⁹/L for IB vs. 380.42±34.78×10⁹/L for IIB, p<0.001), SIRI was 33.88% higher (1.21±0.12×10⁹/L for IB vs. 0.80±0.09×10⁹/L for IIB, p<0.01), and AISI was 39.57% higher (288.05±32.20×10⁹/L for IB vs. 174.06±24.32×10⁹/L for IIB, p<0.006).

Conclusions. Patients with unstable angina who present with both post-COVID syndrome and a history of smoking (IA) demonstrate the highest average levels of leukocyte inflammatory markers. In comparison, smokers without post-COVID syndrome (IIA) and non-smokers in general (IB and IIB) exhibit lower levels. It is noteworthy that non-smokers with post-COVID syndrome (IB) still display elevated levels of leukocyte inflammatory markers relative to non-smokers without post-COVID syndrome (IIB). These results indicate that both post-COVID syndrome and smoking may independently exert pro-inflammatory effects, leading to a significantly enhanced inflammatory response, as reflected by increased average levels of leukocyte inflammatory markers in the affected subgroups. The interplay between these factors serves to amplify their individual effects, culminating in a markedly pronounced inflammatory response.

Keywords: ischemic heart disease, unstable angina, COVID-19, post-COVID syndrome, smoking, inflammation markers.

Background. Liver involvement secondary to multiple myeloma is a rare and uncommon radiologic finding. Such extraosseous secondary lesions as well as tongue involvement require pathohistological confirmation to prevent misdiagnosis. Clinical and laboratory diagnostics are challenging in patients with COVID-19 and underlying multiple myeloma and its secondary lesions, leading to difficulties in treatment and outcomes.
Case Report. A 64-year-old male patient, not vaccinated against COVID-19, with a history of multiple myeloma presented with symptoms of headache, fatigue, dyspnea, cough, and fever. The patient’s medical history was intricate, involving cholecystectomy and a diagnosis of multiple myeloma, which was
subsequently treated with chemotherapy and radiation therapy. Additionally, uncommon liver and tongue involvement secondary to multiple myeloma was found. Upon admission, the patient’s peripheral oxygen saturation was 90%, accompanied by increasing shortness of breath and a respiratory rate of 26 breaths per minute. A positive COVID-19 test was recorded. A lung computed tomography revealed bilateral multifocal areas of ground-glass opacity and consolidation, encompassing the entire pulmonary regions, corresponding to CO-RADS 6. The patient was admitted to the intensive care unit. Despite initiating oxygen support and symptomatic therapy, the patient’s death occurred. Autopsy confirmed the development of severe acute respiratory distress syndrome and bilateral hemorrhagic pneumonia, with multiple myeloma as a contributing factor.
Conclusions. This case report highlighted the rare occurrence of secondary liver involvement in multiple myeloma, characterized by nodules with distinct imaging features. It underscored the importance of identifying coexisting lesions, such as tongue involvement, and the diagnostic challenges they pose. Additionally, the case emphasized the need for comprehensive clinical assessment in patients with concurrent COVID-19 and underlying multiple myeloma, as it may lead to the development of acute respiratory distress syndrome.