Showing papers on "Fibrinoid necrosis published in 2019"

The pathological features of regulated necrosis.

Abstract: Necrosis of a cell is defined by the loss of its plasma membrane integrity. Morphologically, necrosis occurs in several forms such as coagulative necrosis, colliquative necrosis, caseating necrosis, fibrinoid necrosis, and others. Biochemically, necrosis was demonstrated to represent a number of genetically determined signalling pathways. These include (i) kinase-mediated necroptosis, which depends on receptor interacting protein kinase 3 (RIPK3)-mediated phosphorylation of the pseudokinase mixed lineage kinase domain like (MLKL); (ii) gasdermin-mediated necrosis downstream of inflammasomes, also referred to as pyroptosis; and (iii) an iron-catalysed mechanism of highly specific lipid peroxidation named ferroptosis. Given the molecular understanding of the nature of these pathways, specific antibodies may allow direct detection of regulated necrosis and correlation with morphological features. Necroptosis can be specifically detected by immunohistochemistry and immunofluorescence employing antibodies to phosphorylated MLKL. Likewise, it is possible to generate cleavage-specific antibodies against epitopes in gasdermin protein family members. In ferroptosis, however, specific detection requires quantification of oxidative lipids by mass spectrometry (oxylipidomics). Together with classical cell death markers, such as TUNEL staining and detection of cleaved caspase-3 in apoptotic cells, the extension of the arsenal of necrosis markers will allow pathological detection of specific molecular pathways rather than isolated morphological descriptions. These novel pieces of information will be extraordinarily helpful for clinicians as inhibitors of necroptosis (necrostatins), ferroptosis (ferrostatins), and inflammasomes have emerged in clinical trials. Anatomical pathologists should embrace these novel ancillary tests and the concepts behind them and test their impact on diagnostic precision, prognostication, and the prediction of response to the upcoming anti-necrotic therapies. Copyright © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Anti-MOG encephalitis mimicking small vessel CNS vasculitis.

Abstract: Objective To report 2 patients with anti–myelin oligodendrocyte glycoprotein (MOG)-associated encephalitis who were initially misdiagnosed with small vessel primary CNS vasculitis. Methods Review of symptoms, MRI and neuropathologic features, and response to treatment. MOG antibodies were determined in serum and CSF using a cell-based assay. Results Symptoms included fever, headache, and progressive mental status changes and focal neurologic deficits. CSF studies revealed lymphocytic pleocytosis, and both patients had abnormal brain MRIs. Brain biopsy samples showed prominent lymphocytic infiltration of the wall of small vessels; these findings initially suggested small vessel CNS vasculitis, and both patients were treated accordingly. Although 1 patient had a relapsing-remitting course not responsive to cyclophosphamide, the other one (also treated with cyclophosphamide) did not relapse. Retrospective assessment of serum and CSF demonstrated MOG antibodies in both cases, and review of biopsy specimens showed absence of fibrinoid necrosis (a pathologic requirement for small vessel CNS vasculitis). Conclusions Anti–MOG-associated encephalitis can be mistaken for small vessel CNS vasculitis. This is important because the diagnosis of anti–MOG-associated encephalitis does not require brain biopsy and can be established with a serologic test.

Radiologic and Pathological Investigation of Pseudarthrosis in Ankylosing Spondylitis: Distinguishing Between Inflammatory and Traumatic Etiology

Abstract: Objective To investigate the pathogenesis of pseudarthrosis in ankylosing spondylitis (AS) based on the pathological analysis of specimens harvested during surgery Methods Radiographic and clinical data for 17 consecutive AS patients with pseudarthrosis were retrospectively analyzed Meanwhile, the pathological analysis of specimens obtained during surgery was also performed Results In total, 18 extensive Andersson lesions were included Pseudarthrosis located at the apical region were noted in 12 patients Complete ossified anterior longitudinal ligaments above or below pseudarthrosis and fracture through posterior elements or facet joints were observed in 7 and 6 lesions, respectively The most definitive pathological characteristic in all cases was proliferating hypovascular edematous fibrous tissue involving disc, bone-disc border, and vertebral body Fibrinoid necrosis, necrotic bone fragments, hemosiderin deposits, and active subchondral osteogenesis were found, indicating trauma process Mild perivascular collections of inflammatory cells were detected in only 2 cases Conclusion AS-related pseudarthrosis is more likely to originate from mechanical trauma than inflammation The above-mentioned radiological and histological findings showed that multiple mechanisms lead to the formation of pseudarthrosis These mechanisms include excessive stress, insufficiency fracture, and an acute fracture involving a 3-column structure

Lead Intoxication in Free-Ranging Bald Eagles ( Haliaeetus leucocephalus).

Abstract: Lead toxicity due to ingestion of spent ammunition is an ongoing cause of mortality in bald eagles. While gross and histologic lesions of lead intoxication have been described in a few individuals of this species, the prevalence of lesions is underreported. A retrospective study of 93 bald eagles with severe lead intoxication was performed to describe the associated lesions and their prevalence and to compare the lesions with blood, liver, kidney, and/or bone lead concentrations. Gross lesions associated with lead toxicity were most frequent within the heart (51/93 birds) and consisted of multifocal myocardial pallor and rounding of the apex. Within the brain, gross lesions included petechiae or hemorrhagic necrosis (13/93 birds). Histologic lesions compatible with lead toxicity occurred within the heart (76/93 birds), brain (59/93 birds), and eyes (24/87 birds). Lead toxicity in bald eagles is characterized by fibrinoid necrosis of small- to medium-caliber arteries, most commonly affecting the heart, brain, and eyes. Gross and histologic lesions are consistent with ischemia caused by a primary vascular injury. A blood lead concentration of greater than 4 ppm and markedly elevated liver lead concentrations were associated with a greater likelihood of lesions in the heart. Severe lead intoxication is frequently associated with lesions that are histologically detectable in bald eagles. The presence of fibrinoid arterial necrosis and parenchymal degeneration, necrosis, and/or hemorrhage within the heart, brain, and/or eyes is suggestive of lead toxicity in bald eagles and warrants evaluation of liver or bone lead concentrations.

Mast cell chymase degrades fibrinogen and fibrin

Abstract: Background The accumulation of immunoreactants and fibrinoid necrosis of postcapillary vessel walls are common pathological features of cutaneous immune complex vasculitis. In more advanced lesions, these immunoreactants are subject to proteolysis. Mast cell chymase is a powerful enzyme that can degrade several substrates including the extracellular matrix. Heparin can influence the catalytic properties of chymase. Objectives To study the effects of recombinant human (rh) chymase on fibrinogen, coagulation and fibrinolysis, and to relate these effects to the pathogenesis of vasculitis. Methods The colocalization of chymase and fibrin in vasculitis specimens was analysed by immunohistochemical double staining. Fibrinogen and fibrin were treated with rh-chymase and the effects were studied in vitro by sodium dodecylsulfate polyacrylamide gel electrophoresis and a variety of clotting and fibrin gel experiments. The effects of rh-chymase on vasculitis cryosections were analysed by direct immunofluorescence. Results Chymase-positive mast cells were associated with fibrin-positive vessels in vasculitis cryosections. Rh-chymase degraded the alpha-, beta- and gamma-chains of fibrinogen, while heparin enhanced the degradation of the beta-chain. Rh-chymase pretreatment of fibrinogen prolonged thrombin-induced clotting time. Fibrinogen degradation products induced by rh-chymase increased the clotting time of human plasma. Rh-chymase degraded fibrin gel prepared from fibrinogen or human plasma. Immunofluorescence staining positivity of fibrin in vasculitis cryosections decreased after pretreatment with rh-chymase for 24 h, and heparin enhanced this effect. Conclusions Mast cell chymase may constitute a previously unrecognized endogenous anticoagulant and fibrinolytic enzyme, and may be involved in the clearance of fibrin from vessel walls in aged vasculitis lesions.

A Case of Cerebral Amyloid Angiopathy-Related Inflammation With the Rare Apolipoprotein ε2/ε2 Genotype.

Abstract: Cerebral amyloid angiopathy (CAA)-related inflammation (CAA-RI) is a rare CAA variant characterized by acute or subacute encephalopathy, headache, epilepsy, or focal neurological deficits. Radiologically, CAA-RI presents with widespread white matter lesions on brain magnetic resonance imaging (MRI) in addition to the hemorrhagic imaging features of CAA. Previous studies have found that the apolipoprotein E (ApoE) e4 allele and e4/e4 genotype were over-represented in CAA-RI. The role of the ApoE e2 allele in CAA-RI, however, is largely unknown, partly due to the rarity of the e2/e2 genotype in the general population. The authors report the first case of CAA-RI with the rare ApoE e2/e2 genotype. The patient presented with mild clinical symptoms but striking neuroimaging abnormalities. The response to small-dose glucocorticoids was satisfactory. Because ApoE e2 promotes amyloid β accumulation and fibrinoid necrosis in the cerebral vasculature, the e2/e2 genotype, similar to e4/e4, may also be a precipitating factor for CAA-RI. To clarify the role of ApoE e2 in CAA-RI, studies with large sample sizes investigating whether e2 is more common in patients with CAA-RI than in those with CAA only are warranted.

Rheumatoid Arthritis Complicated with Nasal Septum Perforation Due to Methotrexate-associated Lymphoproliferative Disorder.

Abstract: A 44-year-old female with rheumatoid arthritis treated with methotrexate (MTX) and tocilizumab (TCZ) was admitted to our hospital with nasal pain. Nasal fiberscopy revealed septum perforation, while a membrane biopsy indicated granuloma and fibrinoid necrosis of the small artery. The patient was treated with prednisolone 30 mg/day after discontinuation of MTX and TCZ. Inguinal lymph node biopsy revealed diffuse infiltrations of atypical T-cells and Epstein-Barr virus-positive B cells. The patient was diagnosed with peripheral T-cell lymphoma due to MTX-associated lymphoproliferative disorder (MTX-LPD). We herein describe the case of a patient with nasal septum perforation due to MTX-LPD mimicking granulomatosis with polyangiitis.

Vascular fibrinoid necrosis in the urinary bladder of ketamine abusers: A new finding that may provide a clue to the pathogenesis of ketamine-induced vesicopathy.

Abstract: Two 31-year-old women who had abused ketamine, 1 for 8 years and 1 for 5 years, presented with ketamine-induced vesicopathy with urinary frequency, decreased bladder capacity, and detrusor overactivity. An enterocystoplasty was performed in both cases. The pathology of the urinary bladders in both women showed ulcerative cystitis and fibrinoid necrosis of vessels; the latter was confirmed by Masson trichrome staining. Fibrinoid necrosis of vessels is a kind of immune complex-mediated vasculitis that induces the release of inflammatory mediators, with subsequent thrombosis, ischemic injury, and eventual tissue necrosis in localized areas, the so-called Arthus reaction. The new finding of fibrinoid necrosis in the urinary bladders of ketamine abusers may provide a new clue to the pathogenesis of ketamine-induced vesicopathy.

Sudden unexpected death due to coronary thrombosis associated with isolated necrotizing vasculitis in the coronary arteries of a young adult.

Abstract: Coronary arteritis is an uncommon cause of sudden death in non-atherosclerotic coronary diseases, and is mostly associated with systemic vasculitis or systemic autoimmune diseases; therefore, sudden death due to isolated coronary arteritis rarely occurs. The case described in this report is that of a 34-year-old man with no significant personal medical history who died suddenly after presenting with nausea. Postmortem examination revealed a significant infiltration of lymphocytes predominantly on the adventitia and periadventitial tissues of the coronary arteries in the epicardium. The lymphocytic infiltrate partially extended to the thickened intima with fibrosis, destructing the media and internal elastic lamina, and the lumen was occluded by a thrombus in the left main stem and left anterior descending branch. The arterial walls exhibited focal fibrinoid necrosis with regression in the intima and fibrous scars with angiogenesis in the media and adventitia. Focal myocardial infarction was detected in the left ventricle as a fibrotic change of the myocardium. No findings associated with vasculitis were discerned in the aorta, other peripheral arteries, or major organs. Laboratory tests of postmortem blood samples returned negative results for antinuclear antibodies, cryoglobulin, immunoglobulin G4, and cytoplasmic anti-neutrophil cytoplasmic antibodies for myeloperoxidase and proteinase 3. These autopsy findings suggest that the sudden death was caused by isolated necrotizing vasculitis that is assumed to be polyarteritis nodosa localized at the coronary arteries. However, pathological characteristics may not be exactly the same between isolated necrotizing vasculitis in the coronary arteries and polyarteritis nodosa.

Vascularites médicamenteuses : à propos d’une série de 13 cas

Abstract: Summary Introduction Drug-induced vasculitis is reported in almost 10–20 % of vasculitis. Several drugs may be incriminated in their occurrence. Our study aimed to study the epidemiological, clinical, histopathological and evolutionary characteristics of drug-indced vasculitis from a series of cases and to specify the different drugs involved. Methods We conducted a retrospective study during the period from January 2006 to December 2015 from the cases notified to the regional pharmacovigilance center of Sousse, Tunisia. The diagnosis was established according to the criteria proposed by the group of the American college of rheumatology (ACR). Results Our study included thirteen cases of drug-induced vasculitis over a ten-year period, with an mean incidence of 1.3 new cases per year. Mean age of patients was 40.84 years. The mean delay from the treatment onset was 14.46 days with extremes ranging from 5 days to six weeks. Most patients had pure skin involvement. Association with other extracutaneous complaints was present in five cases. Cutaneous biopsy was performed in all patients showing a pathological pattern of leukocytoclastic vasculitis, associated with fibrinoid necrosis, extravasation of red blood cells and allergic capillaritis. The outcome was favorable for all patients. The offending drugs in our series were amoxicillin, pristinamycin, rifampicin, fluconazole, metformin, glimepiride, phenobarbital, gabapentin, fenofibrate, ibuprofen, allopurinol, rituximab and tinzaparin. Conclusion Anamnestic, clinical, biological and histopathological findings allow the early recognition of drug-induced vasculitis. Adequate treatment prevents systemic spreading and a worse prognosis.

Correlations between clinical and placental histopathological and immunohistochemical features in women with and without hereditary thrombophilia.

Abstract: Aim The primary objective of this study was to correlate hereditary thrombophilia (high- or low-risk) with specific placental histopathological (HP) and∕or immunohistochemical (IHC) changes, for confirming∕ruling out a possible linkage between these two biological parameters. Patients, materials and methods We present a 3-year prospective study conducted between 2016 and 2019 that enrolled 90 women registered in two Clinics of Obstetrics and Gynecology in Craiova, Romania, with personal thrombotic and/or pathological obstetrical history. The HP and IHC analysis of the placenta was performed using monoclonal anti-cluster of differentiation 34 (CD34) antibody, anti-hypoxia-inducible factor-1 alpha (HIF-1α) and anti-endothelial nitric oxide synthase (eNOS) antibody. Results There was a high incidence of all thrombophilia (TPh) mutations in Caucasian women with thrombotic and obstetrical complications. Among them, both HP and IHC examination revealed significant changes. These were more severe in the placentas of patients with homozygous Factor V Leiden (FVL) gene mutation and double heterozygous FVL∕PII gene mutation. Multiple placental infarctions with massive fibrinoid necrosis and an increase in syncytial knots are common findings. In the same group, we found by means of IHC examination - intense positive HIF-1α and eNOS immunoexpression, and low positive CD34 expression, especially in fibrinoid necrosis and thrombosis areas. We found no correlation between clinical, HP and IHC changes in patients with low-risk TPh or without TPh. Conclusions Among patients with obstetric and thrombotic complications, there is a high prevalence of TPh. It appears that hypercoagulability reported in high-risk thrombophilia (HR-TPh) has major effects on placental tissue (fibrinoid necrosis, multiple thromboses, hypoxia and oxidative stress). Significant placental changes were found predominantly in women with HR-TPh. Strategies for TPh screening based on HP/IHC pattern would be, most probably, more cost-effective compared with the extended TPh testing offered in large populations. This way, a smaller number of patients will be tested and in this group a higher proportion of patients will be found as having HR-TPh mutations.

A Child Diagnosed With Treatment-Resistant Polyarteritis Nodosa: Can the Clinical Diagnosis Be Different?

Abstract: Polyarteritis nodosa (PAN) is a necrotizing systemic vasculitis involving the wall of small and medium sized arteries. The histological aspect is defined by the presence of fibrinoid necrosis and an infiltrate rich in neutrophil polynuclears in the artery wall and rare granulomas. CECR1 (Cat Eye Syndrome Chromosome Region 1) gene mutation causing adenosine deaminase 2 (ADA2) deficiency is also associated with systemic inflammation, vasculopathy, and frequently PAN. Strokes, neurological involvement, and gastrointestinal involvement have poor prognosis in the cases with ADA2 deficiency particularly in early stage. In this article, we report a 17-year-old male patient diagnosed with PAN who had severe gastrointestinal system involvement that was resistant to intensive and conventional immunosuppressive treatment and showed a fatal course despite the emergency surgical intervention. After the patient was exitus, he was detected to have a heterozygous mutation (V276A) of familial Mediterranean fever (FMF) and also a homozygous ADA2 mutation. The aim of this article is to highlight that ADA2 deficiency may be present in treatment-resistant PAN cases who apply due to severe systemic involvement. In this case, accompanying FMF mutation was also observed.

Cerebral Vasculitis in Ulcerative Colitis Is Predominantly Venular: Case Report and Review of the Literature.

Abstract: Extraintestinal complications of ulcerative colitis include isolated case reports of cerebral vasculitis. In this case report, we describe autopsy findings in a 50-year-old female who died as a result of massive multifocal cerebral hemorrhage. Microscopic examination of the left colon showed findings typical for ulcerative colitis. Examination of the brain showed an extensive vasculitis. More affected vessels were noted in grey matter than in white matter. Many showed fibrinoid necrosis, invasion by neutrophils and thrombosis. There was extensive perivascular hemorrhage with associated infarction. Vessel analysis shows most of the vessels to have been venous rather than arterial. There were no perivascular sleeves of demyelination to suggest a primary demyelinating disorder, such as acute hemorrhagic leucoencephalitis. Our analysis shows that veins are the likely target of cerebral vasculitis in ulcerative colitis. This has clinical implications because venous occlusion generally causes massive intracerebral hemorrhage with a high mortality.

Study of placental shape and histopathological changes in pregnant ladies with preeclampsia

Abstract: Objective: To discover the morbid changes (macroscopic and microscopic) in placenta in cases of preeclampsia and to correlate the findings with birth weight and outcome of new born babies in comparison with normotensive mothers. Methods: A case control study carried out in Babylon teaching for maternity and children Hospital, in a period of 12 months from Jan. 2017 to the end of Dec. 2017. One hundred twenty pregnant women were enrolled in the current study 60 normotensive pregnant women and 60 patients with preeclampsia. The placenta of the participants was studied (morphologically and hist/opathologically), fetal outcome whether alive or dead was recorded and neonatal birth weight was assessed. Results: In the present study, it was observed that weight and dimensions of placenta were less in study group when compared with control group while retroplacental clots are more significantly common in study group more than control group. The mean neonatal birth weight was more in normal pregnant ladies also fetal outcome is significantly better in normotensive group due to normal placental conditions. Histopathological study showed significant number of syncytial knots, trophoblastic basement membrane thickness, cytotrophoblastic cell proliferation, areas of fibrinoid necrosis, hyalinization, calcification and areas of infarction. Conclusion: Preeclampsia has effects on the patient's placenta by decrease its dimension and weight in addition to presence of retroplacental clots, that is due to several histopathological changes that affect the normal functions of it which lead to reduce the neonatal birth weight and may result in intra uterine death, so we must screen about this disease as early as possible to discover and manage it earlier and decrease its complications in high risk pregnancies.

Association between histopathological changes and expression of selected microRNAs in skin of adult patients with IgA vasculitis.

Abstract: AIMS IgA vasculitis (IgAV) is a common small-vessel systemic vasculitisthat is histologically characterised by granulocyte infiltration and IgA deposition in vessel walls. Information on microRNA (miRNA) involvement inIgAVis limited. The aim of this study was to analyse the association between histopathological changes and expression profiles of 14 miRNAs in the affected skin of 70 adult patients with IgAV. METHODS AND RESULTS miRNA expression analysis was performed by quantitative real-time polymerase chain reaction and evaluation of histopathological changes by light and immunofluorescence microscopy on formalin-fixed paraffin-embedded skin excision samples. In IgAV-affected skin, granulocyte infiltration was significantly associated with vessel fibrinoid necrosis. Of the analysed miRNAs, four showed two-fold increased expression (let-7d, let-7f, miR-21-5p, and miR-203-3p), five showed five-fold increased expression (let-7b, miR-17-5p, miR-155-5p, miR-423-5p, and miR-451a), and threeshowed 15-fold increased expression (let-7a, miR-21-3p, miR-223-3p), as compared with controls (all P < 0.001). miR-146a-5p and miR-148b-3p showed three-fold decreased expression (P = 0.981 and P < 0.001). The expression of miR-223-3p also showed a significant positive association with granulocyte infiltration and fibrinoid necrosis. CONCLUSIONS Altered miRNA expression, especially of miRNA-223-3p, may be associated with the skin inflammatory state in IgAV. The majority of aberrantly expressed miRNAs in IgAV-affected skin are known to influence the nuclear factor-κB signalling pathway, which is crucial for activation of key proinflammatory genes, including those encoding tumour necrosis factor-α, interleukin (IL)-6, and IL-8. Furthermore, miR-146a-5p and miR-148b-3p, which are negative regulators of inflammatory gene expression, showed decreased expression and could contribute to the exaggerated inflammation. Further investigation of miRNA expression in the affected tissues could improve our knowledge of IgAV pathogenesis, and possibly help to identify novel biomarkers in body fluids.

Histopathological study of placental changes associated with pre-eclampsia and eclampsia in a tertiary care centre of Puducherry

Abstract: Introduction: Foetal development mainly depends on normal placental development. Mother, Placenta and Foetus are related to each other during the course of the pregnancy. Pregnancy induced hypertension shows considerable changes in the histopathology of placenta. Therefore the main aim of the present study is to evaluate the morphological changes of placenta in case of Pregnancy Induced Hypertension (PIH) and to correlate the findings with severity of toxaemia of pregnancy. Materials and Methods: The present study includes 61cases of placenta out of which 51 are in the study group and 10 cases are in the control group. Our study was descriptive study conducted in the Department of Pathology, Mahatma Gandhi Medical College and Research Institute, Sri Balaji Vidhyapeeth University, Puducherry during the period of July 2015-June 2018. The study group were further divided into four categories. All the placenta are grossed according to the institute protocol and the slides were examined for various morphological changes and correlated with the severity of pre-eclampsia and eclampsia. Descriptive statistics were used to evaluate the results. Results: The most prominent lesion seen in the toxaemia of pregnancy were villous cytotrophoblastic proliferation and villous fibrinoid necrosis which accounts to 78% and 75% respectively. Villous stromal fibrosis constitutes 71% of the study group cases. Increased villous vascularity was seen in 39% of the placenta of toxaemia of pregnancy. 69% of the cases shows villous basement membrane thickening in the study group placenta. Conclusion: Our study helps in evaluating the various morphological changes in placenta in the hypertensive disorder of pregnancy. This study helps in anticipating the occurrence of changes in the subsequent pregnancy induced hypertension cases. Keywords: Pregnancy, Eclampsia, Cytotrophoblastic cell proliferation, Fibrinoid necrosis.

Acute kidney injury due to acute cortical necrosis following vivax malaria.

Abstract: Malaria is a parasitic infection of global importance but has a high prevalence in the developing countries. Renal failure is a common complication of severe Plasmodium falciparum malaria and has been reported in up to 40% of all cases. Acute kidney injury (AKI), however, is not commonly associated with Plasmodium vivax infection. In those patients who develop AKI following P. vivax infection, the cause is commonly attributed to mixed undiagnosed falciparum infection or coexistent sepsis, dehydration, or hypotension. Infrequently, an association of P. vivax infection with thrombotic microangiopathy (TMA) has been reported. The purpose of this report is to describe renal failure due to TMA following malaria caused by P. vivax. A 24-year-old female presented with a history of fever and jaundice of two weeks duration followed by progressive oliguria and swelling of the face and feet five days after the onset of fever. The evaluation revealed normal blood pressure, anemia, thrombocytopenia, azotemia, unconjugated hyperbilirubinemia with mildly elevated transaminases, and elevated lactate dehydrogenase. Peripheral smear was positive for P. vivax, and schistocytes were seen. She was given intravenous artesunate followed by oral primaquine for 14 days. Urine examination showed proteinuria and microscopic hematuria. She remained oliguric and dialysis dependent, and her kidney biopsy revealed patchy cortical necrosis involving 40% of sampled cortex with widespread fibrinoid necrosis of the vessel wall, red blood cell fragmentation, and luminal thrombotic occlusion. Hemodialysis was discontinued after three weeks when there was the improvement of renal function over time, and her serum creatinine decreased to 2.2 mg/dL by six weeks. Patients with P. vivax malaria developing renal failure may have TMA. Renal biopsy, if performed early in the course of the disease, may identify TMA and institution of plasma exchange in such patients could help in early recovery.

Cutaneous necrotizing small‐vessel vasculitis induced by acute hepatitis E

Abstract: Hepatitis E virus is a new emergent virus causing acute self-limiting hepatitis, but may also cause extrahepatic manifestations. Hepatitis E virus should be systematically considered in patients with cutaneous small-vessel vasculitis and cytolytic hepatitis.

Fri0259 serological immune abnormalities associate with specific pathological active lesions in lupus nephritis

Abstract: Background: Serological immune abnormalities such as anti-double strand DNA (dsDNA) antibodies (Abs) and hypocomplementemia (HC) are characteristic of lupus nephritis (LN). International Society of Nephrology/Renal Pathology Society (ISN/RPS) Classification of LN defines pathological active lesions (ALs) as including endocapillary hypercellularity, karyorrhexis, fibrinoid necrosis, cellular/fibrocellular crescents, and wire-loop lesion/hyaline thrombi [Reference 1]. Few reports have focused on the clinicopathological impact of serological immune abnormalities on pathological ALs. Objectives: To identify the clinicopathological association between serological immune abnormalities and pathological ALs in LN. Methods: We enrolled 126 Japanese LN patients who were subjected to renal biopsy in 11 hospitals from 2000 to 2018. We determined various clinical parameters at the time of renal biopsy, including creatinine (Cr), estimated glomerular filtration rate (eGFR), total protein (TP), IgG, IgA, IgM, C3, C4, CH50, anti-nuclear antibodies (Abs), anti-double strand DNA (dsDNA) Abs, anti-Sm Abs, anti-RNP Abs in the sera, urinalysis findings, presence of comorbidities (antiphospholipid antibody syndrome, hypertension, hyperlipidemia, diabetes mellitus, and hyperuricemia), and use of any immunosuppressive medications before renal biopsy. Renal biopsy findings were classified by ISN/RPS Classification including ALs. Immune deposits were evaluated by immunofluorescence. Elevation of serum anti- dsDNA Abs level [dsDNA Abs (+)] was defined as >12 IU/mL. HC was defined by C3 Results: Of 126 patients (104 females; mean age 41.8 years), dsDNA Abs (+) and HC (+) were found in 83 (65.9%) and 80 (63.5%), respectively. There were no significant differences in renal function, comorbidities, immune deposits or immunosuppressive medications before renal biopsy between dsDNA Abs (+) and dsDNA Abs (-), or between HC (+) and HC (-) patients. In pathological study, endocapillary hypercellularity, karyorrhexis, fibrinoid necrosis, cellular or fibrocellular crescents, and wire-loop lesion/hyaline thrombi were found in 81 (64.3%), 33 (26.2%), 19 (15.1%), 51 (40.5%), and 41 (32.5%), respectively. dsDNA Abs (+) had a higher frequency of endocapillary hypercellularity, karyorrhexis, fibrinoid necrosis, and wire-loop lesion/hyaline thrombi than dsDNA Abs (-). HC (+) had a higher frequency of endocapillary hypercellularity, karyorrhexis, fibrinoid necrosis, cellular or fibrocellular crescents, and wire-loop lesion/hyaline thrombi than HC (-). On multiple regression analysis dsDNA Abs and C3 associated with fibrinoid necrosis and karyorrhexis, respectively (β=0.25, p=0.049; β=-0.31 p=0.01). Conclusion: Serum anti-dsDNA Abs and HC were associated with fibrinoid necrosis and karyorrhexis, respectively. These results document that individual serological immune abnormalities associate with specific AL, suggesting that pathophysiological differences underlie each AL. References: [1] J Am Soc Nephrol. 2004;15:241-50. Disclosure of Interests: None declared

Surgery of Intracerebral Hemorrhage

Abstract: Spontaneous intracerebral hemorrhage (ICH) due to uncontrolled hypertension is a common clinical entity that affects up to four million people annually [1]. Hemodynamic injury to perforating end arteries (100–400 μm) results in pathological lesions such as lipohyalinosis, fibrinoid necrosis, and Charcot-Bouchard microaneurysm which may predispose to rupture. Common locations where these hemorrhages may occur include the basal ganglia, pons, thalamus, cerebellum, or subcortical white matter (lobar) [2].

Pregnancy-Induced Uterine Vascular Remodelling and the Pathophysiology of Decidual Vasculopathy

Abstract: Maternal vasculopathy encompasses several related lesions, including incomplete physiologic remodelling, fibrinoid necrosis, and atherosis, that occur within the maternal blood vessels feeding the placenta. These lesions are thought to develop early in gestation, but their effects do not generally arise until the latter half of pregnancy. The alterations in the maternal vasculature change both the volume and flow characteristics of the blood entering the placenta, resulting in hypoxic/oxidative damage. Maternal vasculopathy is associated most closely with the hypertensive disorders of pregnancy but can also be found in several other adverse pregnancy outcomes.

Miscellaneous Lesions of the Villous Parenchyma

Abstract: In this chapter, some rare and some more common findings are discussed. Calcification in the placenta is a frequent finding. Although frequently it does not have any known clinical consequences, it is a sign of significant pathology in some cases. Presence of heterotopic tissue in the placental parenchyma is rare, but these interesting lesions underline our limited knowledge of the development of the placenta.

The effect of syphilitic infection on fetal growth and development

Abstract: Aim : to study the fetal development during the early gestational period (7-9 weeks) in women with syphilitic infection who chose to terminate the pregnancy with the help of artificial abortions. Materials and methods . Women with a history of syphilitic infection and a physiological pregnancy of 7-9 weeks underwent ultrasound examination of the fetus. Following the abortion procedure, histological sections of the abortive material were analyzed. Results . During the ultrasound examination of these women at the gestation period of 7-9 weeks, the thickness of the collar space was 1.5-1.6 mm, the yolk sac was 4.4-4.6 mm, and the coccygeal-parietal size - 54-56 mm, with no significant differences from the control group. In the decidual tissue, foci of fibrinoid necrosis and leukocyte infiltration of the stroma were significantly more common in women with primary or anamnestic syphilis as compared with the control group. Conclusion . In the early stages of pregnancy on the background of syphilitic infection, there were no sonographic differences from non-infected pregnant women; though inflammatory and other abnormalities were found in a histological analysis of the abortion material.

Recurrent Febrile Attacks, Myalgia and Livedo Reticularis

Abstract: Polyarteritis nodosa (PAN) is characterized by fibrinoid necrosis of the vessel wall of small to medium sized arteries Diagnosis of PAN in children requires demonstration of necrotizing vasculitis by histopathology, aneurysm formation, stenosis, or occlusion by angiography in medium or small -sized arteries, plus one of the following: Cutaneous findings such as livedo reticularis, nodules, infarcts Myalgia or tenderness upon palpation Hypertension (>95th percentile for height) Peripheral neuropathy Renal involvement The following extra features in a PAN patient should direct clinicians to deficiency of adenosine deaminase type 2: Early-onset manifestations Presence of consanguinity Presence of a relative with same clinical picture Ischemic or hemorrhagic stroke

Патоморфологическая гетерогенность вульварного склероатрофического лихена

Abstract: Vulvar lichen sclerosus (LS) is a common chronic mucocutaneous disease, which is usually underdiagnosed and tend to progress without adequate treatment. Morphological characteristics of vulvar LS with unusual histological features. Vulvar biopsy material ( n = 83) with morphologically diagnosed LS was examined histologically and statistically. Often saw-toothed modification of the epithelium, fibrinoid necrosis, cytoid bodies, satellite cell necrosis, hemorrhages, papillomatosis, milia, predominantly plasma cell inflammatory infiltrate, lymphoid follicles, elastosis, angiokeratoma-like vasculare change were found on the background vulvar LS. Saw-tooth epidermal change, multiple cytoid bodies and satellite cell necrosis are histological features of LS described for the first time in this study, the former being a frequent presentation of vulvar LS. The mentioned above histological changes cannot appear as features in favor of lichen planus in the differential diagnosis of these diseases.

Pathomorphology of cats with myocardial infectious peritonitis

Abstract: The article presents the results of macroscopic and microscopic examinations of myocardial cats in wet and mixed forms of FIP. A pathoanatomical study of 19 cat carcasses, aged from 3 months to 7 years, was diagnosed with infectious peritonitis during life (on the basis of anamnesis, clinical features, morphological and biochemical blood test, ultrasound, Rivalt test and FCVetx rapid test VetE.) All animals were kept at home. For the microstructural study, samples of cats' hearts were selected, which were fixed in 10% aqueous formalin neutral solution, Carnua, Buen solutions and 96 ° ethyl alcohol. Histogram sections were stained with hematoxylin and eosin staining, picrofuxin (Van Gizon), PAS reaction (McManus), methyl green pyronin (Brache), Malory, and examined under a microscope. Histological examination of the cardiac muscle of cats in various forms of infectious peritonitis revealed changes of non-inflammatory and inflammatory nature. In the exudative form, non-inflammatory processes prevailed. In the myocardium, the most severe changes occurred in the capillaries, the walls of the arterial vessels and the stroma, which were characterized by diapedic hemorrhage, mucoid and fibrinoid swelling and necrosis of the walls of the arterioles. Disorganization of connective tissue was accompanied by stratification of connective tissue fibers and impregnation of weakly oxyphilic, PAS-positive compounds of the intermuscular lumen, which was combined with dystrophic changes in cardiomyocytes. In the mixed form, proliferative-destructive vasculitis, diffuse or focal lymphoid-histiocytic infiltrates in the myocardium prevail. The revealed optical changes in the structural elements of the heart indicated a sharp weakening of the contractile function of cardiomyocytes and heart failure. In addition, it should be noted that the characteristic morphological manifestation for immunocomplex diseases is the development of vasculitis, which is preceded by fibrinoid necrosis of the walls of the arterial vessels and intensive infiltration of their circulatory elements, and these changes occurred in infectious peritonitis of cats.

Necrosis of the small intestine leading to a diagnosis of polyarteritis nodosa: a case report.

Abstract: Polyarteritis nodosa is a disease that presents with necrotizing vasculitis in small and medium-sized arteries. It may occur in various organs, but approximately half of cases have gastrointestinal involvement. Prognosis is not favorable once organ dysfunction begins as evidenced by gastrointestinal symptoms; thus, treatment with steroids should be promptly initiated. We report the case of a patient who presented with necrosis of the small intestine, which was pathologically diagnosed as polyarteritis nodosa and treated successfully with steroids. An 18-year-old Japanese woman reported a sudden onset of abdominal pain and vomiting that led her to visit our emergency department, where she was evaluated by a physician. On physical examination, tenderness to palpation in the upper umbilical region was noted, and diagnostic imaging with computed tomography showed emphysema of the wall of her small intestine. She was diagnosed as having necrosis of the small intestine requiring urgent surgery. No strangulations were noted intraoperatively but approximately 20 cm of her small intestine was necrotized. The surrounding arteries were examined and no palpable pulse was observed; therefore, segmentectomy of the necrotized regions was performed. Pathological findings revealed active vasculitis with fibrinoid necrosis, as well as destruction, fibrogenesis, and luminal stenosis of the elastic lamina found in the muscular arteries. A diagnosis of polyarteritis nodosa was confirmed as the cause of the necrosis of her small intestine. No recurrence of polyarteritis nodosa symptoms was observed when she was administered 40 mg of prednisolone daily. In cases of idiopathic intestinal necrosis or perforation, systemic diseases such as polyarteritis nodosa should be considered in the differential diagnosis.