ECP 2022 Abstract Book

Virchows Archiv (2022) 481 (Suppl 1):S1–S364 13 of glucose in whole blood by enzymatic colorimetric method with deproteinization - the result is negative. Conclusion: Taking into account the anamnestic and autopsy findings, the child was diagnosed with a congenital pathology of the pancreas - hyperplasia of the islets of Langerhans (nesidioblastosis) with severe metabolic disorders in the form of uncorrectable hypoglycemia, decompensated metabolic acidosis and multiple organ failure. In the genesis of this pathology, one cannot underestimate the role of a generalized intrauterine infection with damage to vital organs, including the pancreas. A post-mortem comprehensive approach to clarify this pathology is necessary. E-PS-20-022 Congenital interruption of aortic arch (IAA) – a foetal autopsy findings with literature review F. Soares Nogueira*, C. Dahlstedt Ferreira, D. Argyropoulou, H. Oliveira Coelho *Hospital Garcia de Orta, Portugal Background & objectives: Interruption of the aortic arch (IAA) is a rare and severe congenital heart disease, characterized by complete anatomic discontinuity between two adjacent segments of the aortic arch. It’s associated with other major intracardiac and noncardiac malformations. Methods: We present two foetal autopsies: A 33 week old male foetus that died in utero. The mother was 26 years old, without relevant medical history. An echocardiography revealed several heart defects. A 36-week-old female foetus that also died in utero, the mother was 33 years old, without relevant medical background, the CHD was only diagnose during the autopsy. Results: The first foetus had anthropometrical parameters compat- ible with 33-week-old gestation, without external malformations. The heart dissection revealed an interventricular communication and a complete interruption of aorta. Without other malformations. The second foetus had anthropometrical parameters compatible with 36-week-old gestation also without external malformations. The heart dissection revealed an interventricular communication, a third superior ostium in the posterior wall of the pulmonary artery that communicated with the aortic arch. The aorta emerged and branched as usually till the emerging of the left subclavian artery, where, it became atretic and communicate with the pulmonary artery, which turned out to be a systemic vessel into the remaining thorax and abdomen. Conclusion: Congenital aortic arch interruption is associated with coexisting intracardiac malformations, chromosomal anomalies and is the most common cardiac defect occurring in DiGeorge syndrome. We presented two cases of congenital interrupted aortic arch with other coexisting congenital heart defects but without association with a noncardiac malformations. E-PS-20-023 Foetal thrombotic vasculopathy: a case report S. Mabrouk*, T. Tlili, Z. Lajmi, S. Yacoub, A. Ben Abdelkader, B. Sriha, M. Mokni *Department of Pathology, Farhat Hached University Hospital, Tunisia Background & objectives: Foetal thrombotic vasculopathy (FTV) is a rare entity, defined by thrombosis of foetal vessels leading to fibrosis avascular downstream villi. These lesions occur at the end of the sec- ond and third trimester with a prevalence around 1%. Methods: A 28-year-old G2P1A0 pregnant women without any medical disease history. The pregnancy was normal without inci- dent. The patient presented a decrease in active foetal movements. On examination and abdominal ultrasonography, foetal death at 24 weeks was diagnosed. Foetal extraction was done. The foetus and placenta were referred to pathological diagnosis. There is no history of thrombophilia. Results: Macroscopically, foetal necropsy showed a macerated male foetus weighed 126 g, of an anatomical age of 18 weeks without any external or visceral malformations. The placenta had an oval shape, weighed 62 g, and measured 11,5cm x 8,5cm. The chorioamniotic membrane was translucent. The umbilical cord was hypercoiled with central insertion measuring 45cm. On section, the placental parenchyma had no macroscopically identifiable lesion, and no thrombi of chorionic vessels were visible. Histological examination of the placenta showed several endolu- minal chorionic vessel fibrosis with fibrosis villi and the pres- ence of groups of avascular villi. No visceral thrombi in necropsy specimens were found. These changes were deemed to be consistent with FTV. Conclusion: FTV diagnosis is histologic, with foetal thrombotic lesions: chorionic vessel thrombi, and avascular fibrosis villi. These changes are similar to those seen in intrauterine foetal demise but are focal rather than diffuse. The underlying aetiology of FTV is unknown though hypercoagulability(thrombophilia) and circulatory stasis implying chorioamnionitis and cord anomalies were reported in the literature. FTV may be related to adverse perinatal outcomes including foetal death. However, much studies about pathogenesis and criteria diag- nosis are desirable to change the unfavourable outcome. E-PS-21 | E-Posters Pulmonary Pathology E-PS-21-001 Pseudoprogression mimicking hyperprogressive disease after pembrolizumab treatment in a patient with lung cancer – his- topathological diagnostic clues K. Hashimoto, K. Kaira, O. Yamaguchi, A. Mouri, A. Shiono, Y. Miura, F. Nishihara, S. Shinomiya, T. Akagami, Y. Murayama, H. Imai, K. Kobayashi, H. Kagamu, H. Imada, T. Kawasaki* *Department of Pathology, Saitama Medical University Interna- tional Medical Center, Japan Background & objectives: Pseudoprogression after anti-programmed death-1 (PD-1) antibody therapy is a rare phenomenon in patients with non-small cell carcinoma. There is limited information about the pathological mechanism of pseudoprogression, especially regarding the relationship between intratumoral lymphocytes and exacerbation of pulmonary infiltrative shadow. Methods: The patient, a 51-year-old woman, with a history of smoking was referred to our hospital for abnormal shadow in chest radiograph and shortness of breath. Diagnostic bronchos- copy revealed pulmonary adenocarcinoma with cT4N3M1c, and programmed death-ligand 1 (PD-L1) was expressed in 75 % of the patient’s tumour specimen without any driver mutation. Therefore, only pembrolizumab was administered as the first- line treatment. Results: On the third day after pembrolizumab treatment, there was a sudden appearance of cough and sputum. Chest radiography showed extensive infiltrative shadow in the right lung field. On the eleventh day, the infiltrative shadow exhibited progressive exacerbation with severe symptoms, and S328