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Introduction: The coronavirus disease 2019 (COVID-19) infection, caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), involves several organs through participation of angiotensin-conversion enzyme 2 (ACE2) receptors. The presence of ACE2 receptors in the liver renders this organ a potential target for the novel coronavirus. Methods: We performed 14 complete autopsies of patients infected with SARS-CoV-2. In each case we stained liver tissue sections with haematoxylin/eosin, Masson blue trichrome stain, periodic acid-Schiff (PAS), Perls, and performed cytokeratin-7 (CK7) immunochemistry. Results: Macroscopically, livers were pale and yellowish in 8 of 14 (57%) patients, and had a nutmeg appearance in the other 6 cases (42%). Histologically, centrolobular necrosis was observed in 12 cases (86%), and was associated with discreet to moderate lobular or portal inflammation. Steatosis was seen in 8 cases (57%), but fibrosis was rare. Cholestasis and discrete bile duct proliferation was observed in 5 cases (36%). Discussion/Conclusion: The main histological changes can be explained by the hypoxic status as a result of severe hypoxemic pneumonia leading to death. Drug toxicity may also play a role in certain cases. Other histological changes may be explained by previous hepatic conditions or underlying hepatic diseases. We concluded that COVID-19 infection was not associated with a specific histopathological pattern of the liver.

Background Type IIIb dysplasia is a subtype of focal cortical dysplasia associated with a tumor, most frequently with gangliogliomas then with dysembryoplastic neuroepithelial tumors (DNETs). Their preoperative diagnosis often remains equivocal since specific features are missing. The functional results (i.e., seizure free) is good with 81%–87% of Engel Ia at 5-year follow-up. Case Description A 4-year-old boy presented with a 1-year history of severe, invalidating, drug-resistant epilepsy. Imaging workup demonstrated a huge left limbic lesion, of which diagnosis remained speculative. Because of worsening neurological status, resective surgery was recommended after multidisciplinary discussion. The resection was performed through left transtemporal approach under neuronavigation (C.R.). Postoperative magnetic resonance imaging assessed uncomplicated near-total resection. Histopathological analysis showed combined features of a DNET of nonspecific type and a focal cortical dysplasia. Conclusion We describe a rare condition of type IIIb dysplasia combining a focal cortical dysplasia with a DNET. Preoperative diagnosis of the lesion was of utmost difficultly, thereby rendering mandatory a thorough histopathological examination of resected specimen in the vast majority of cases. Increased recognition of the condition brings up the hypothesis of a genetic continuum or linkage between the 2 conditions. Functional results on seizure activity after ablative surgery are good and maximal safe resection should be the goal.

A 78-year-old woman was admitted for acute dyspnoea. One year before, she had been treated with cisplatin and gemcitabine for a high grade urothelial carcinoma. Immunotherapy was discussed 9 months later due the progression of bone metastases but could not be administered before this episode of respiratory distress. There was a major discrepancy between the findings of a limited pulmonary embolism at thoracic tomodensitometry and the severity of a recently developed pulmonary hypertension at echocardiography. The patient presented cardiac arrest on day 6 and post-mortem findings were consistent with diffuse pulmonary tumor thrombotic microangiopathy, a rare complication of urothelial carcinoma.

A middle-aged man with an addiction to alcohol met with sudden death at home. Additional clinical information was not available. In particular, there was no radiological examination prior to death. The local authorities requested an autopsy because the deceased had been involved in a car accident 3 days before, which was presumed to be related to his excessive alcohol consumption. Two forensic pathologists performed a medico-legal autopsy. No abnormalities were found at autopsy of the major organs (heart, lungs, liver, kidneys, and spleen). Signs of tuberous sclerosis were lacking. More specifically, characteristic skin lesions, renal cysts, angiomyolipomas, cardiac rhabdomyomas, or cystic pulmonary formations were absent. A certified neuropathologist performed the brain exam. External examination of the brain did not show any particularities, except for an insignificant temporal and cerebellar pressure cone, probably caused by hypoxia during agony [...]

Highlights • With adrenocortical carcinoma, tumoral secretion is present in 25 to 75% of the cases. • In the absence of excessive hormonal production, the diagnosis is often delayed. • Isolated liver metastatic lesion may develop after several years of follow-up. • Resection of a large intrahepatic malignant lesion may be complicated by a secondary capillary leak syndrome., Introduction Adrenocortical carcinoma is a rare type of malignant adrenal tumor with a possibility of delayed metastases. Diagnosis may be delayed with a non-secreting tumor or metastasis, and even in this case, surgical management may be complicate. Presentation of case A 55-year-old man underwent elective surgery for the resection of a large intra-hepatic mass from an undetermined type according to a recent liver biopsy. He had a previous history of a non-secreting adrenal tumor that was operated ten years before. Pre-operatively, he was poorly symptomatic, with a normal arterial blood pressure. Anesthesia induction was uneventful, but at the time of tumor resection and removal, he developed extreme vasoplegia and shock with anuric renal failure, lactic acidosis, four-limb and abdominal compartment syndrome. The patient died on day 9 from delayed septic complications. According to the pathological findings, the tumor was a non-secreting adrenocortical carcinoma. Discussion Adrenocortical carcinoma (ACC) is rare condition with diverse clinical manifestations due to excessive hormonal production when the tumor is secreting and mimicking pheochromocytoma. Our patient underwent the resection a large intrahepatic non-secreting metastasis more than ten years after the initial lesion. Peri-operative and post-operative management was complicated by a refractory shock with the characteristics of a secondary systemic capillary leak syndrome. The role of endothelial lesions may be discussed. Conclusion Surgery of metastatic adrenocortical carcinoma may be complicated by severe hemodynamic complications, even in the absence of hormonal secretion.

Tryptophan catabolism is used by tumors to resist immune attack. It can be catalyzed by indoleamine 2,3-dioxygenase (IDO1) and tryptophan 2,3-dioxygenase (TDO). IDO1 is frequently expressed in tumors and has been widely studied as a potential therapeutic target to reduce resistance to cancer immunotherapy. In contrast, TDO expression in tumors is not well characterized. Several human tumor cell lines constitutively express enzymatically active TDO. In human tumor samples, TDO expression has previously been detected by transcriptomics, but the lack of validated antibodies has precluded detection of the TDO protein and identification of TDO-expressing cells. Here, we developed novel TDO-specific monoclonal antibodies and confirmed by immunohistochemistry the expression of TDO in the majority of human cancers. In all hepatocarcinomas (10/10), TDO was expressed by most tumor cells. Some glioblastomas (10/39) and kidney carcinomas (1/10) also expressed TDO in tumor cells themselves but only in focal tumor areas. In addition, all cancers tested contained foci of nontumoral TDO-expressing cells, which were identified as pericytes by their expression of PDGFRβ and their location in vascular structures. These TDO-expressing pericytes belonged to morphologically abnormal tumor vessels and were found in high-grade tumors in the vicinity of necrotic or hemorrhagic areas, which were characterized by neoangiogenesis. We observed similar TDO-expressing pericytes in inflammatory pulmonary lesions containing granulation tissue, and in chorionic villi, two tissue types that also feature neoangiogenesis. Our results confirm TDO as a relevant immunotherapeutic target in hepatocellular carcinoma and suggest a proangiogenic role of TDO in other cancer types.See article by Schramme et al., p. 32. ispartof: Cancer Immunology Research vol:8 issue:1 pages:19-31 ispartof: location:United States status: published

Background In spite of aggressive multimodal treatment, survival for patients with glioblastoma (GBM) remains short. Nevertheless, some patients survive much longer than expected and become long-term survival patients. The extent of resection (EoR), Karnofsky Performance Scale (KPS), age and methyl-guanine methyltransferase gene (MGMT) methylation are well-defined prognostic factors, but the characteristics of patients with long-term survival (LTS, survival of at least three years after diagnosis) has not been fully determined yet. That is the reason why we analyzed the GBM patients with LTS at our center. Methods We retrospectively reviewed all consecutive patients who underwent surgery for GBM between January 2002 and November 2011, including patients treated with surgical resection under neuronavigation with or without intraoperative MRI (ioMRI) and those who had stereotactic biopsy. We identified and further analyzed those patients with LTS. Results A total of 127 patients underwent surgery for GBM during the study period. 101 (79.6%) of whom had surgical resection and 26 (20.4%) of whom had stereotactic biopsy. Of the 101 patients who were treated with surgical resection, 12 had LTS. After two other pathologists reviewed the patients' cases, they confirmed that 11 (11%) of the 12 patients had a GBM (female/male ratio 4.5; average age 50 years; preoperative Karnofsky Score 82%), and one patient had an anaplastic glioma. The mean survival in the LTS patients with confirmed GBM was 74 (36-150) months. Seven of the LTS patients (63.6%) had a gross total resection (GTR), including two with an additional resection after ioMRI. Three (27.3%) had a near total resection (NTR: residue ≤5%) and one (9.1%) had a partial resection. Ten (90.9%) patients had a methylation of MGMT, only two (18.8%) had an IDH1 mutation, and seven (63.6%) received a full Stupp protocol. Conclusions Among patients with a GBM who were treated with one or more resections, 11% had LTS with 90.9% with at least a near total resection (36% with ioMRI) and a methylated MGMT. 50% of the patients with a second surgery survived at least two years postoperatively. Those encouraging observations emphasize the importance of maximizing the resection by using, if possible, an intraoperative guidance method like ioMRI with an analysis of biomarkers such as MGMT and if necessary, multiple surgical procedures.

IntroductionAdditional robust criteria to predict early postoperative recurrence of non-functioning pituitary macroadenomas (NFMAs) are needed. Recently, a new classification of pituitary tumors has been proposed, which is based on both radiological and histological criteria and allows the grading into 5 groups of different potential aggressiveness. The aim of this study was to use this classification to further characterize predictive factors of recurrence in an independent series of NFMA.Cases and methods120 patients operated for a NFMA were analyzed retrospectively. For each of them, the invasion of the cavernous and/or sphenoidal sinuses by the tumor was studied on the preoperative MRI and the proliferative character was based on precise histological and immunohistological examination.Results26% (n = 31) of the adenomas were proliferative and 57% (n = 68) were invasive. The invasive lesions were larger (P P DiscussionThe new clinicopathological classification proves to be very useful in predicting the risk of recurrence of non-functioning pituitary macroadenomas after a first surgery. In particular, grade 2b lesions showed an overall likelihood of recurrence that was 8.6 times greater than those of grade 1a.

Summary A 26-year-old woman presented with severe postpartum headaches. Magnetic resonance imaging (MRI) revealed a symmetric, heterogeneous enlargement of the pituitary gland. Three months later, she developed central diabetes insipidus. A diagnosis of postpartum hypophysitis was suspected and corticosteroids were prescribed. Six months later, the pituitary mass showed further enlargement and characteristics of a necrotic abscess with a peripheral shell and infiltration of the hypothalamus. Transsphenoidal surgery was performed, disclosing a pus-filled cavity which was drained. No bacterial growth was observed, except a single positive blood culture for Staphylococcus aureus, considered at that time as a potential contaminant. A short antibiotic course was, however, administered together with hormonal substitution for panhypopituitarism. Four months after her discharge, severe headaches recurred. Pituitary MRI was suggestive of a persistent inflammatory mass of the sellar region. She underwent a new transsphenoidal resection of a residual abscess. At that time, the sellar aspiration fluid was positive for Staphylococcus aureus and she was treated with antibiotics for 6 weeks, after which she had complete resolution of her infection. The possibility of a pituitary abscess, although rare, should be kept in mind during evaluation for a necrotic inflammatory pituitary mass with severe headaches and hormonal deficiencies. Learning points: The possibility of a pituitary abscess, although rare, should be kept in mind during evaluation for a necrotic inflammatory pituitary mass with severe headaches and hormonal deficiencies. In a significant proportion of cases no pathogenic organism can be isolated. A close follow-up is necessary given the risk of recurrence and the high rate of postoperative pituitary deficiencies.

Rasmussen encephalitis is a rare, devastating condition, typically presenting in childhood. Cases of adult-onset Rasmussen have also been described, but the clinical picture is less defined, rendering final diagnosis difficult. We present a case of adult-onset Rasmussen encephalitis with dual pathology, associated with focal cortical dysplasia and encephalitis. We interpreted the Rasmussen encephalitis to be caused by severe and continuous epileptic activity due to focal cortical dysplasia. The best therapeutic approach for such cases remains unclear.

A 75-year-old man was admitted to the Department of internal medicine because of a 2-month history of neurological deterioration. During the previous year, he complained of recurrent sinusitis, asthma, arthralgias, myalgias and asthenia. Later on, an oculomotor palsy, weakness and disturbance of the sensibility of the right upper limb appeared. Blood sample showed 6510 eosinophils per microlitre. The cerebral magnetic resonance demonstrated bilateral frontal and left parietal subcortical lesions from which the most voluminous presented large haemorrhagic areas. A cerebral biopsy showed small vessel's vasculitis, fibrinoid necrosis and extravascular eosinophilic encroachment. A diagnosis of oculomotor palsy secondary to eosinophilic granulomatosis with polyangeitis was then made, which was successfully treated with corticosteroids and cyclophosphamide.