ABSTRACT
BACKGROUND: Neutrophilic myocarditis often stems from bacterial or fungal infections, and it is typically detectable through blood cultures or analyses of the primary infection site. However, research specifically addressing the morphological features of acute myocarditis in complex sepsis cases is scarce, with existing studies primarily dating back to the pre-antibiotic era. METHODS: This study constitutes a retrospective and descriptive analysis encompassing 22 forensic cases. We collected data from forensic reports emphasising clinical details, disease history, gross observations, and histopathological findings. RESULTS: The results show that using positive-air-pressure ventilation could be related to cardiac inflammation (45.45%, 10/22). Despite large-spectrum antibiotic therapy, the blood samples were positive for Staphylococcus aureus (MRSA strain), Klebsiella pneumoniae (ESBL strain), Acinetobacter baumannii, and Pseudomonas aeruginosa. Colonies developed in the myocardium of 36% of the patients (8/22), where 4 of them had septic emboli. Fungal myocarditis accompanied bacterial infections (2/8) and were unsuspected clinically. Background changes, such as interstitial fibrosis and arteriosclerosis, were associated with a greater degree of inflammation and septic embolism. CONCLUSION: Neutrophilic myocarditis in patients with emerging sepsis is linked to fatal virulent infections, where bacteria and/or fungi contaminate and impair the myocardium syncytium. Prolonged hospitalisation and positive-air-pressure ventilation may be a risk factor for this condition and needs further research.
ABSTRACT
CD30, also known as TNFRSF8 (tumor necrosis factor receptor superfamily member 8), is a protein receptor that is heavily glycosylated inside the Golgi apparatus, as well as a tumor marker that is found on the surface of specific cells in the body, including certain immune cells and cancer ones. This review aims to shed light on the critical importance of CD30, from its emergence in the cell to its position in diagnosing various diseases, including Hodgkin lymphoma, where it is expressed on Hodgkin and Reed-Sternberg cells, as well as embryonal carcinoma, anaplastic large cell lymphoma (ALCL), and cutaneous T-cell lymphoma (CTCL). In addition to its role in positive diagnosis, targeting CD30 has been a promising approach treating CD30-positive lymphomas, and there is ongoing research into the potential use of CD30-targeted therapies for autoimmune disorders. We aim to elaborate on CD30's roles as a tumor marker, supporting thus the hypothesis that this receptor might be the aim of cytostatic treatment.
Subject(s)
Hodgkin Disease , Lymphoma, Large-Cell, Anaplastic , Lymphoma , Humans , Hodgkin Disease/metabolism , Lymphoma/metabolism , Lymphoma, Large-Cell, Anaplastic/diagnosis , Lymphoma, Large-Cell, Anaplastic/drug therapy , Reed-Sternberg Cells/metabolism , Reed-Sternberg Cells/pathology , Ki-1 Antigen/metabolism , Biomarkers, Tumor/metabolismABSTRACT
A rare entity of non-hiatal type transdiaphragmatic hernias, which must be clearly differentiated from paraoesophageal hernias, are the phrenic defects that bear the generic name of congenital hernias-Bochdalek hernia and Larey-Morgagni hernia, respectively. The etiological substrate is relatively simple: the presence of preformed anatomical openings, which either do or do not enable transit from the thoracic region to the abdominal region or, most often, vice versa, from the abdomen to the thorax, of various visceral elements (spleen, liver, stomach, colon, pancreas, etc.). Apart from the congenital origin, a somewhat rarer group is described, representing about 1-7% of the total: an acquired variant of the traumatic type, frequently through a contusive type mechanism, which produces diaphragmatic strains/ruptures. Apparently, the symptomatology is heterogeneous, being dependent on the location of the hernia, the dimensions of the defect, which abdominal viscera is involved through the hernial opening, its degree of migration, and whether there are volvulation/ischemia/obstruction phenomena. Often, its clinical appearance is modest, mainly incidental discoveries, the majority being digestive manifestations. Severe digestive complications such as strangulation, volvus, and perforation are rare and are accompanied by severe shock, suddenly appearing after several non-specific digestive prodromes. Diagnosis combines imaging evaluations (plain radiology, contrast, CT) with endoscopic ones. Surgical treatment is recommended regardless of the side on which the diaphragmatic defect is located or the secondary symptoms due to potential complications. The approach options are thoracic, abdominal or combined thoracoabdominal approach, and classic or minimally invasive. Most often, selection of the type of approach should be made taking into account two elements: the size of the defect, assessed by CT, and the presence of major complications. Any hiatal defect that is larger than 5 cm2 (the hiatal hernia surface (HSA)) has a formal recommendation of mesh reinforcement. The recurrence rate is not negligible, and statistical data show that the period of the first postoperative year is prime for recurrence, being directly proportional to the size of the defect. As a result, in patients who were required to use mesh, the recurrence rate is somewhere between 27 and 41% (!), while for cases with primary suture, i.e., with a modest diaphragmatic defect, this is approx. 4%.