Unlike classic APS, CAPS causes multiple microthrombosis due to an increased inflammatory response, known as a “thrombotic storm”. CAPS typically develops after infection, trauma, or surgery and begins with the following symptoms: fever, thrombocytopenia, muscle weakness, visual and cognitive disturbances, abdominal pain, renal failure, and disseminated intravascular coagulation. Although the presence of antiphospholipid antibodies in the blood is one of the diagnostic criteria, the level of these antibodies can fluctuate significantly, which complicates the diagnostic process and can lead to erroneous interpretation of rapidly developing symptoms. Triple therapy is often used to treat CAPS, which includes the use of anticoagulants, plasmapheresis, and high doses of glucocorticosteroids and, in some cases, additional intravenous immunoglobulins. The use of LMWH is recommended as the drug of choice due to its anti-inflammatory and anticoagulant properties. CAPS is a multifactorial disease that requires not only an interdisciplinary approach but also highly qualified medical care, adequate and timely diagnosis, and appropriate prevention in the context of relapse or occurrence of the disease. Improved new clinical protocols and education of medical personnel regarding CAPS can significantly improve the therapeutic approach and reduce mortality rates.

Newborns are the most vulnerable patients for thrombosis development among all children, with critically ill and premature infants being in the highest risk group. The upward trend in the rate of neonatal thrombosis could be attributed to progress in the treatment of severe neonatal conditions and the increased survival in premature babies. There are physiological differences in the hemostatic system between neonates and adults. Neonates differ in concentrations and rate of synthesis of most coagulation factors, turnover rates, the ability to regulate thrombin and plasmin, and in greater variability compared to adults. Natural inhibitors of coagulation (protein C, protein S, antithrombin, heparin cofactor II) and vitamin K-dependent coagulation factors (factors II, VII, IX, X) are low, but factor VIII and von Willebrand factor are elevated. Newborns have decreased fibrinolytic activity. In the healthy neonate, the balance is maintained but appears more easily converted into thrombosis. Neonatal hemostasis has less buffer capacity, and almost 95% of thrombosis is provoked. Different triggering risk factors are responsible for thrombosis in neonates, but the most important risk factors for thrombosis are central catheters, fluid fluctuations, liver dysfunction, and septic and inflammatory conditions. Low-molecular-weight heparins are the agents of choice for anticoagulation.

The results of recent studies show that tumor biology, coagulation activation, and inflammatory reactions profoundly contribute to the thrombosis pathogenesis in cancer as well as tumor progression, metastasis, and developing chemoresistance. Cancer is an independent predictor of thrombosis. During carcinogenesis, tumor cells express proinflammatory cytokines, proangiogenic and procoagulant factors, and also stimulate other cells to express various components promoting emerging thromboinflammation. The discovery of neutrophil extracellular traps (NETs) provides an opportunity to take a new look at biology and a role neutrophils may play in thromboinflammation and tumorigenesis. The close interplay between tumor cells, tumor-associated neutrophils and NETs as well as other players in the tumor microenvironment underlies activation of thromboinflammation in cancer patients not only resulting in thrombus formation, but also promoting tumor growth and dissemination.

Antiphospholipid syndrome in neonates and children is a rare, but in some cases life-threatening condition with arterial and/or venous thrombosis and/or non-thrombotic neurological, skin, ophthalmological and other manifestations. This review highlights the available information about the features of pediatric APS, including the rare catastrophic form, the differences between pediatric and adult APS, and the role of genetic thrombophilia in APS manifestation. The clinical manifestations and treatment options for APS in children may differ from those in adults, and prescribing therapy can be challenging due to the unique clinical and morphological characteristics of the pediatric patient. Pediatric APS may be a predictor of the development of certain autoimmune diseases and classic manifestations of APS in adulthood, therefore, a revision of the existing criteria for the diagnosis and treatment of APS in children is necessary.

Hepatogenic diabetes (HepD) is a form of diabetes where the primary pathogenesis is a liver disease, usually cirrhosis, complicated by the development of portal hypertension with the formation of porto-caval shunts. In the development of HepD, in addition to traditional risk factors for carbohydrate metabolism disorders, the pathogenetic features of liver diseases play a significant role. However, the exact mechanism of HepD development remains unclear, and several questions are still open for discussion. Despite having distinct pathophysiological and clinical features, hepatogenic diabetes is currently not considered as an independent disease. This is likely due to the difficulties in differentiating between types of diabetes due to the bidirectional relationship between glucose metabolism disorders and chronic liver diseases. It is known that diabetes negatively affects the development and progression of chronic liver diseases of various etiologies, and their combination is associated with worse clinical outcomes in terms of mortality, the occurrence of liver decompensation, and the development of hepatocellular carcinoma (HCC). Unfortunately, early diagnosis and the selection of optimal therapeutic strategies for diabetes may be challenging due to the lack of established clinical guidelines and the presence of comorbidities in patients with HepD.