Showing papers on "Fibrinoid necrosis published in 2015"
TL;DR: Treatment of severe involvement in IgA vasculitis remains controversial, with no evidence that corticosteroids or immunosuppressive agents improved long-term outcome, and Prospective, randomized, controlled trials are needed to analyze the benefit-risk ratio of such treatments.
161 citations
TL;DR: Acute atherosis is rare in normal pregnancy, and occurs more frequently in patients with pregnancy complications, including preeclampsia, sPTL, preterm PROM, midtrimester spontaneous abortion, fetal death and SGA.
Abstract: Objective: Acute atherosis is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis and perivascular lymphocytic infiltration. This lesion is generally confined to non-transformed spiral arteries and is frequently observed in patients with preeclampsia. However, the frequency of acute atherosis in the great obstetrical syndromes is unknown. The purpose of this study was to determine the frequency and topographic distribution of acute atherosis in placentas and placental bed biopsy samples obtained from women with normal pregnancy and those affected by the “great obstetrical syndromes”. We also examined the relationship between acute atherosis and pregnancy outcome in patients with preeclampsia.Material and methods: A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted to examine 16 345 placentas. Patients were classified into the following groups: (1) uncomplicated pregnancy...
80 citations
TL;DR: Early pauci-immune necrotizing GN is characterized by a selective localization of CD163(+) M2 macrophages at sites of glomerular fibrinoid necrosis and in normal-appearing glomeruli.
Abstract: Background and objectives This study examined kidney biopsies with focal segmental glomerular fibrinoid necrosis to identify early features of pauci-immune necrotizing GN and the primary effector cells mediating initial capillary injury. Design, setting, participants, & measurements Seventeen consecutive kidney biopsies with focal pauci-immune necrotizing GN, obtained over a 6-year period (2007–2012), were studied. Neutrophils and CD68 + , CD163 + , CD3 + , CD56 + , and CD20 + cells were scored in paraffin sections counterstained with periodic acid–Schiff. Electron microscopy was performed in 15 of 17 biopsies and additional examples of pauci-immune necrotizing GN ( n =25). Biopsies with thin basement membrane nephropathy ( n =5) served as immunohistologic normal controls. Results Biopsies with pauci-immune necrotizing GN had a mean of 10 (range=3–25) normal-appearing glomeruli, a mean of 2 (range=1–5) glomeruli with segmental fibrinoid necrosis, and a mean of 2 (range=1–11) glomeruli with cellular crescents. CD68 + and CD163 + macrophages predominated at sites of fibrinoid necrosis in pauci-immune necrotizing GN, exceeding the quantity of neutrophils and T cells (mean scores [SD]=2.5 [0.7] and 2.2 [0.75] versus 0.6 [0.5] and 0.1 [0.3], respectively; P + and CD163 + macrophages than the controls (CD68 + , 0.9 [0.3] versus 0.4 [0.3]; CD163 + , 1 [0.4] versus 0.4 [0.3]; P r =0.74 and r =0.71, respectively; P =0.001) but did not correlate with the extent of fibrinoid necrosis ( r =0.36). Macrophages were localized at minute perforations and attenuations of the capillary basement membrane by electron microscopy. Conclusions Early pauci-immune necrotizing GN is characterized by a selective localization of CD163 + M2 macrophages at sites of glomerular fibrinoid necrosis and in normal-appearing glomeruli. These observations indicate that alternatively activated macrophages are positioned as potential effectors of glomerular injury in the early stages of pauci-immune necrotizing GN and may be potential targets for therapeutic intervention.
71 citations
TL;DR: There is substantial clinical overlap in the phenotypes of I-CAA, ABRA, and PACNS, and a proper diagnosis of these 3 conditions is necessary because their individual treatment differ.
Abstract: Cerebral amyloid angiopathy (CAA) results from deposition of amyloid-β fibrils in the wall of the small and medium-sized blood vessels, mostly arteries of the leptomeninges and cerebral cortex. Architectural disruption of amyloid-β laden vessels, occasionally with fibrinoid necrosis, leads to perivascular leakage. Vascular rupture causes lobar microbleeds or hematomas and high-convexity subarachnoid hemorrhages. The accumulation of amyloid-β causes vessel lumen obliteration, thereby leading to ischemic leukoencephalopathy and cerebral infarction. Varying amounts of perivascular inflammation may be present, involving multinucleated giant cells in the most severe cases.1 However, frank vasculitic destruction of the vessel wall such as is found in amyloid-β–related angiitis (ABRA)2 and primary angiitis of the central nervous system (PACNS)3 is absent in the inflammatory form of CAA (I-CAA). There is substantial clinical overlap in the phenotypes of I-CAA, ABRA, and PACNS. A proper diagnosis of these 3 conditions is necessary because their individual treatment differ. Through 3 cases, we summarize similarities and differences between I-CAA, ABRA, and PACNS.
A 52-year-old woman complained about limb paresthesias lasting 3 days. She reported cognitive decline and fatigue lasting 3 months, a relentless headache that had lasted for a year, in addition to episodic migraine and tension-type headaches. Past medical history was unremarkable, except for active cigarette smoking. Physical and neurological examination was normal. Brain magnetic resonance imaging (MRI) showed nonspecific lobar, white matter, nonenhancing hyperintensities on T2-weighted sequences. No treatment was initiated in the absence of a specific diagnosis. Blood tests, including inflammatory and prothrombotic work-up, cardiac ultrasound, Holter monitoring, digital subtraction cerebral angiography, and cerebrospinal fluid (CSF) analysis were normal. She remained stable clinically. Three months later, repeat brain MRI revealed new lobar T2-hyperintensities (Figure 1A) and several lobar microbleeds on gradient-echo sequences. CNS biopsy revealed extensive amyloid-β deposits in the wall of small leptomeningeal and cortical …
47 citations
TL;DR: Testing whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion (MVU), amniotic fluid infection (AFI), fetal vascular thrombo-occlusive disease (FVTOD) or chronic inflammation found to be true found it to be yes.
Abstract: Objective: Acute atherosis is a lesion of the spiral arteries characterized by fibrinoid necrosis of the vessel wall, an accumulation of fat-containing macrophages, and a mononuclear perivascular infiltrate, which can be found in patients with preeclampsia, fetal death, small-for-gestational age, spontaneous preterm labor/premature prelabor rupture of membrane, and spontaneous mid-trimester abortion. This lesion is thought to decrease blood flow to the intervillous space which may lead to other vascular lesions of the placenta. The objective of this study was to test whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion (MVU), amniotic fluid infection (AFI), fetal vascular thrombo-occlusive disease (FVTOD) or chronic inflammation.Material and methods: A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted examine 16 ...
44 citations
TL;DR: Direct targeting of the graft vasculature may create new opportunities for preventing allograft injury and loss.
44 citations
TL;DR: The presence and deeper location of acute atherosis is associated with poorer pregnancy outcomes, more severe disease, earlier onset of preeclampsia, and a greater frequency of SGA neonates in patients with preeClampsia.
Abstract: Acute atherosis is unique vascular changes of the placenta associated with poor placentation. It is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis of the arterial wall, perivascular lymphocytic infiltration, and it is histologically similar to early-stage atherosclerosis. Acute atherosis is rare in normal pregnancies, but is frequently observed in non- transformed spiral arteries in abnormal pregnancies, such as preeclampsia, small for gestational age (SGA), fetal death, spontaneous preterm labor and preterm premature rupture of membranes. In preeclampsia, spiral arteries fail to develop physiologic transformation and retain thick walls and a narrow lumen. Failure of physiologic transformation of spiral arteries is believed to be the main cause of uteroplacental ischemia, which can lead to the production of anti-angiogenic factors and induce endothelial dysfunction and eventually predispose the pregnancy to preeclampsia. Acute atherosis is more frequently observed in the spiral arteries of the decidua of the placenta (parietalis or basalis) than in the decidual or myometrial segments of the placental bed. The presence and deeper location of acute atherosis is associated with poorer pregnancy outcomes, more severe disease, earlier onset of preeclampsia, and a greater frequency of SGA neonates in patients with preeclampsia. Moreover, the idea that the presence of acute atherosis in the placenta may increase the risk of future cardiovascular disease in women with a history of preeclampsia is of growing concern. Therefore, placental examination is crucial for retrospective investigation of pregnancy complications and outcomes, and accurate placental pathology based on universal diagnostic criteria in patients with abnormal pregnancies is essential for clinicopathologic correlation.
31 citations
TL;DR: The inflammatory responses observed in kidney and liver in the present study were presumably suppuration and were attributed to the potential virulence factors of E. tarda.
Abstract: Edwardsiella tarda is one of the serious fish pathogens infecting both cultured and wild fish species. This study aimed to assess the phenotypic characterization and pathogenicity of E. tarda isolated from Clarias gariepinus (Burchell) with dropsy and histopathological alterations. The causative agent was identified with Vitek 2, and its pathogenicity was determined by intramuscular injection. The challenged catfish exhibited vertical hanging, frothing, excess mucus production, listing, swollen abdomen, anorexia, fin and tail rot, and reddish operculum. The LD50 of E. tarda PBB and PBP strains was found to be 8.52 x 10 6 and 1.68 x 10 7 cells fish -1 , respectively. Histopathological observations on catfish infected naturally revealed lymphocyte infiltration in muscle and focal necrosis, hyperplasia, edema, and swelling of the gill lamellar epithelium. The kidney of diseased fish exhibited ischemic type tubulopathy, necrosis of nephritic tubules, hyperplastic hematopoietic tissue, rupture of the tubular basement membrane, hydropic dystrophy of nephritic cells, neutrophil infiltration, fibrinoid necrosis of nephretic tubules, hemosiderin deposition, and edema. The liver sections revealed lymphocyte infiltration, dilation of hepatic sinusoids, expansion of space between hepatic sinusoids, and focal necrosis. The inflammatory responses observed in kidney and liver in the present study were presumably suppuration and were attributed to the potential virulence factors of E. tarda.
26 citations
TL;DR: The asthma like lung lesions induced in these models is preceded by immune complex-mediated eosinophilic vasculitis and iBALT formation, which is unlikely that mast cell-activated atopic mechanisms are responsible.
19 citations
TL;DR: Elevated serum IgG4 levels and infiltration of IgG 4-positive plasma cells were observed in a subgroup of patients with inflammatory neuropathy, particularly in patients diagnosed with primary systemic vasculitis, including microscopic polyangiitis.
Abstract: Objective: To evaluate the pathologic significance of immunoglobulin G4 (IgG4) in patients with inflammatory peripheral neuropathy. Methods: We clinicopathologically examined 149 consecutive patients with peripheral neuropathy who had clusters of inflammatory cells with or without vasculitis in sural nerve biopsy specimens and in whom we were able to assess the serum IgG4 levels. Results: Elevation of serum IgG4 levels and infiltration of IgG4-positive plasma cells, which are currently defined as the diagnostic criteria for IgG4–related disease, were found in 35 and 29 patients, respectively. In the 44 patients exhibiting either elevated serum IgG4 levels or IgG4-positive cell infiltration, the diagnoses prior to the examination of IgG4 in serum and pathologic samples included microscopic polyangiitis (12 patients) and eosinophilic granulomatosis with polyangiitis, or Churg-Strauss syndrome (19 patients). Thirty-four patients (77%) had findings of vasculitis as indicated by the destruction or obstruction of the vessel walls. Sixteen (36%) of these patients had fibrinoid necrosis. Axonal degeneration without evidence of demyelination was observed irrespective of the presence of vasculitis. The extent of fibrosis, assessed as the fibrotic area in the epineurium, significantly correlated with the grade of IgG4-positive cell infiltration ( p Conclusions: Elevated serum IgG4 levels and infiltration of IgG4-positive plasma cells were observed in a subgroup of patients with inflammatory neuropathy, particularly in patients diagnosed with primary systemic vasculitis, including microscopic polyangiitis. Epineurial IgG4-positive plasma cell infiltration correlated with the extent of epineurial fibrosis.
18 citations
Journal Article•
TL;DR: MRI, MR spectroscopy, positron emission tomography, and perfusion-weighted MR imaging have been used to evaluate RN and are discussed, and no definitive non-invasive diagnostic study exists to differentiate post-SR RN from recurrent metastatic tumor.
Abstract: Stereotactic radiosurgery (SR) is a standard therapy for brain metastases. Radiation necrosis (RN) of the brain is a syndrome of brain coagulative and fibrinoid necrosis and cortical irritation that occurs following radiotherapy. RN following SR peaks in a delayed fashion at 9-12 months postprocedure. Vasogenic cerebral edema secondary to necrosis occurs and can affect surrounding brain function. No definitive non-invasive diagnostic study exists to differentiate post-SR RN from recurrent metastatic tumor. Magnetic resonance (MR) imaging, MR spectroscopy, positron emission tomography, and perfusion-weighted MR imaging have been used to evaluate RN and are discussed. Treatment options for post-SR brain metastases include observation, corticosteroids, pentoxifylline and vitamin E, bevacizumab, radiotherapy, laser-interstitial thermal therapy, and surgical resection.
TL;DR: Diffuse alveolar hemorrhage was the most frequent presentation of lung involvement in children with MPA, and tachypnea, cough, hemoptysis and anemia were the common clinical symptoms.
Abstract: Kidneys and lungs are the most common organs involved in microscopic polyangiitis (MPA). A retrospective analysis of pediatric MPA patients with pulmonary lesions over the past 10 years was performed to investigate clinical features of MPA in children with pulmonary lesions. There were 9 patients enrolled in our study, including 2 boys and 7 girls, with a median age of 6.6 years at the time of disease onset and a median disease course of 2 months. All of the patients exhibited tachypnea, and 7 exhibited cough and hemoptysis. The most common presentation on pulmonary imaging was ground glass or patchy shadows, which were observed in 6 cases. Seven patients manifested with hematuria and proteinuria, with renal histopathology of fibrinoid necrosis/exudation of the glomerular capillaries. All of the patients presented with normocytic normochromic anemia. Of the 9 patients, 7 were positive for perinuclear antineutrophil cytoplasmic antibody (p-ANCA) and/or myeloperoxidase (MPO), and 2 were positive for p-ANCA/MPO and cytoplasmic ANCA/proteinase 3. Eight patients had normal complement 3 (C3) levels, and one had an elevated C3 level. Five of the 9 patients were positive for antinuclear antibody ANA, and 4 were positive for double strand DNA (ds-DNA) antibody (3 were positive for both). The 7 patients who exhibited renal involvement received steroid plus cyclophosphamide (CTX) treatment. Of these patients, 4 achieved various degrees of remission, 2 were at the beginning of induction therapy, and one was lost to follow-up. Two patients with isolated pulmonary involvement received steroid plus leflunomide treatment and achieved complete remission. Diffuse alveolar hemorrhage was the most frequent presentation of lung involvement in children with MPA, and tachypnea, cough, hemoptysis and anemia were the common clinical symptoms. The majority of these patients exhibited hematuria, proteinuria and renal insufficiency. The efficacy of steroid plus CTX or leflunomide was evident in these patients.
TL;DR: A case of 45-year-old female patient with the diagnosis of seropositive rheumatoid arthritis, who was admitted to the hospital with exacerbation of the disease, and treated with rituximab, with significant improvement.
Abstract: We present a case of 45-year-old female patient with the diagnosis of seropositive rheumatoid arthritis, who was admitted to our rheumatology department with exacerbation of the disease. The patient's disease activity score (DAS 28) was 6.9. Physical examination revealed changes in the lung auscultation as a rough breathing sound at the middle and lower lobe of the right lung. Chest X-ray revealed multiple nodular densities in both lungs. Lung biopsy was performed for the diagnosis and revealed necrotizing granulomas with central fibrinoid necrosis surrounded by epithelioid cells. Such a histopathological picture is typical for rheumatoid nodules. Finally the patient was treated with rituximab, with significant improvement.
TL;DR: Presentation of clinical cases in this series was variable, and there did not appear to be well-defined vasculitic syndromes as described in people.
Abstract: Inflammation of the blood vessel wall has been reported infrequently in dogs, and it may occur without apparent cause (primary vasculitis) or as a pathologic reaction to a range of initiating insults (secondary vasculitis). The aims of our study were to report histologic, clinical, and survival data from a large series of cases with primary and secondary vasculitis, and to compare the clinical parameters and outcome data between groups. Clinical data was collected retrospectively from the medical records of 42 client-owned dogs with a histologic diagnosis of primary or secondary vasculitis, and follow-up information was obtained. Cases were grouped according to clinical and histologic descriptors, and biochemical, hematologic, and survival data was compared between groups. Several forms of primary vasculitis were observed, and vascular inflammation was observed in conjunction with numerous other diseases. Female dogs were more likely to develop primary vasculitis, and serum globulin concentration was greater in dogs with primary vasculitis compared to those with underlying disease. All dogs with primary vasculitis of the central nervous system died or were euthanized shortly after presentation, but other forms of primary vasculitis could be managed effectively. In conclusion, presentation of clinical cases in this series was variable, and there did not appear to be well-defined vasculitic syndromes as described in people.
Journal Article•
TL;DR: In this paper, a case of 45-year-old female patient with the diagnosis of seropositive rheumatoid arthritis, who was admitted to the hospital with exacerbation of the disease.
Abstract: We present a case of 45-year-old female patient with the diagnosis of seropositive rheumatoid arthritis, who was admitted to our rheumatology department with exacerbation of the disease. The patient's disease activity score (DAS 28) was 6.9. Physical examination revealed changes in the lung auscultation as a rough breathing sound at the middle and lower lobe of the right lung. Chest X-ray revealed multiple nodular densities in both lungs. Lung biopsy was performed for the diagnosis and revealed necrotizing granulomas with central fibrinoid necrosis surrounded by epithelioid cells. Such a histopathological picture is typical for rheumatoid nodules. Finally the patient was treated with rituximab, with significant improvement.
TL;DR: A 67-year-old man with an 11-month history of ANCAnegative eosinophilic granulomatosis with polyangiitis (EPGA) was evaluated in the authors' department for weight loss of 5 kg over 2 months and progressive fatigue.
05 Dec 2015
TL;DR: The introduction of ANCA testing in routine clinical practice has increased the ability of disease suspicion and recognition, resulting in earlier establishment of diagnosis by seeking a tissue confirmation of pauci-immune vasculitis, which results in timely diagnosis.
Abstract: Background: Pauci-immune glomerulonephritis is the most common cause of aggressive glomerulonephritis and occurs as a renal-limited disease or as a component of systemic necrotizing small-vessel vasculitis. It is characterized by paucity of staining for immunoglobulins, by immunofluorescence along with fibrinoid necrosis and crescent formation by light microscopy, while the vast majority of patients have anti-neutrophil cytoplasmic antibodies (ANCA) in their circulation, which also participate in the pathogenesis of the disease. Summary: Pauci-immune glomerulonephritis often manifests with rapidly deteriorating kidney function, which may be accompanied by distinctive clinical features of systemic necrotizing small-vessel vasculitis of one the following clinical phenotypes: microscopic polyangiitis, granulomatosis with polyangiitis or eosinophilic granulomatosis with polyangiitis. These are associated with a wide spectrum of vasculitic manifestations in different organ systems at clinical presentation and during the course of the disease. ANCA specificity is associated with distinct clinical syndromes and different prognostic profiles among patients. The key element of the management of patients with pauci-immune glomerulonephritis, with or without systemic vasculitis, is the clinical acumen, which results in timely diagnosis. Speed in diagnosis is crucial for the quick institution of immunosuppressive therapy aimed at removing circulating autoantibodies and quelling the inflammatory process. Key Messages: The introduction of ANCA testing in routine clinical practice has increased the ability of disease suspicion and recognition, resulting in earlier establishment of diagnosis by seeking a tissue confirmation of pauci-immune vasculitis. ANCA specificity is associated with distinct clinical syndromes and different prognostic profiles among patients. The management of patients with ANCA glomerulonephritis and/or vasculitis includes two major elements: prompt diagnosis and institution of immunosuppressive therapy to avoid irreversible kidney damage or death, and consideration of the predictors, which are associated with relapsing disease for planning of therapy in the long term. Facts from East and West: Treatment options for ANCA-associated vasculitis are shared between the East and West, with corticosteroid combined with cyclophosphamide being the standard regimen for inductive therapy and switching to azathioprine after remission. The major cause of death in treated patients is infection related to immunosuppressive therapy within the first year after diagnosis, and this rate might be higher in China than in Western countries. Western studies demonstrated the efficacy and safety of rituximab for induction of remission in cases with relatively mild disease and maintenance therapy, but this agent is rarely used in China.
TL;DR: It is concluded that, in view of the apparent self-limited nature of this lesion, additional treatment may not be required in these patients, and awareness of thisLesion may spare patients unwarranted further intervention.
TL;DR: In this paper, the clinical and pathological characteristics of 10 cases of cerebral amyloid angiopathy (CAA)-related cerebral lobar hemorrhage (CLH) that was diagnosed at autopsy were investigated to facilitate the diagnosis of this condition.
Abstract: Objective The clinical and pathological characteristics of 10 cases of cerebral amyloid angiopathy (CAA)-related cerebral lobar hemorrhage (CLH) that was diagnosed at autopsy were investigated to facilitate the diagnosis of this condition. Methods The clinical characteristics of 10 cases of CAA-related CLH were retrospectively reviewed, and a neuropathological examination was performed on autopsy samples. Results The 10 cases included two with a single lobar hemorrhage and eight with multifocal lobar hemorrhages. In all of the cases, the hemorrhage bled into the subarachnoid space. Pathological examinations of the 10 cases revealed microaneurysms in two, double barrel-like changes in four, multifocal arteriolar clusters in five, obliterative onion skin-like intimal changes in four, fibrinoid necrosis of the vessels in seven, neurofibrillary tangles in eight, and senile plaques in five cases. Conclusion CAA-related CLHs were located primarily in the parietal, temporal, and occipital lobes. These hemorrhages normally consisted of multiple repeated CLHs that frequently bled into the subarachnoid space. CAA-associated microvascular lesions may be the pathological factor underlying CLH.
TL;DR: A single mass was found on the left submandibular salivary gland at necropsy of a 15-month-old male commercially bred laboratory Beagle dog from a control dose group from a repeat toxicity study.
Abstract: A single mass was found on the left submandibular salivary gland at necropsy of a 15-month-old male commercially bred laboratory Beagle dog from a control dose group from a repeat toxicity study. Microscopically, the mass was composed of a well-demarcated area of coagulative necrosis surrounded and separated from the normal salivary gland tissue by a thick fibrovascular capsule. Necrosis was admixed with areas of hemorrhage, fibrin, edema, fibrinoid necrosis of the vascular tunica media, and thrombosis of small and large vessels. Within the necrotic tissue, there was marked ductal hyperplasia, and squamous metaplasia of duct and acinar epithelium. The mass was diagnosed as necrotizing sialometaplasia of the submandibular gland. Hyperplastic ductal elements and squamous metaplasia can be mistaken microscopically with squamous cell carcinoma. Therefore, pathologists should be aware of this lesion as to avoid errors in the diagnosis of this benign pathologic condition.
TL;DR: The presence of above parameters in a renal biopsy report of a patient (in absence of facilities of autoimmune serology and immunofluoresence) can alert both nephrologist and nephropathologist to keep a possibility of renal symptoms arising out of systemic vasculitis.
Abstract: Objectives: Pauci-immune glomerulonephritis is the commonest cause of rapidly progressive glomerulonephritis (RPGN) which is associated with increased mortality and morbidity. More than 90% of these patients have serological presence of either antineutrophil cytoplasmic antibodies (ANCA), of cytoplamic (C) or perinuclear (P) type. "Immunofluoresence studies" exhibiting minimal or no fluorescence is diagnostic in all such cases. The present study aims to study the differences between renal biopsies of serologically ANCA negative versus ANCA positive individuals. Materials and Methods: One hundred and twenty renal biopsies (of clinically suspected cases of systemic vasculitis) were sub-divided sub-divided under the heading of serologically ANCA positive and serologically ANCA negative; and scoring them by means of a semi-quantitative scoring system devised at the beginning of the study to identify statistically significant, specific light microscopic features in the sub-components of renal biopsy. Results: Fifteen parameters were found to be statistically significantly (p-value < 0.05) in ANCA positive serological cases. These were glomerular capillary loop infiltration by neutrophils, cellular crescents, fibro-cellular crescents, glomerular fibrinoid necrosis, glomerular sclerosis, peri-glomerular infiltration, interstitial oedema, interstitial eosinophils, tubular atrophy, tubular necrosis, tubulitis, arterial hyalinization, arterial necrosis, arterial vessel wall polymorpho nuclear infiltrate and myointimal hypertrophy. Conclusion: The presence of above parameters in a renal biopsy report of a patient (in absence of facilities of autoimmune serology and immunofluoresence) can alert both nephrologist and nephropathologist to keep a possibility of renal symptoms arising out of systemic vasculitis.
TL;DR: Porcine circovirus type 2 (PCV2) associated reproductive disease was diagnosed in a herd containing only gilts and a single case of abortion occurred and no other disorder was evident in the herd.
Abstract: Porcine circovirus type 2 (PCV2) associated reproductive disease was diagnosed in a herd containing only gilts. A single case of abortion occurred and no other disorder was evident in the herd. PCV2 antigen and/or DNA were detected in two aborted fetuses. One of the fetuses, revealing both PCV2 DNA and antigen, presented multinucleated giant cells, severe vascular lesions (intramural oedema, fibrinoid necrosis, mild lympho-histiocytic vasculitis, fibrin thrombi) and mild non-suppurative inflammation in the lungs. Other abortifacient infections were not found. This is the only report of PCV2-induced abortion in Hungary since 1999, when PCV2-associated disease was first discovered in the country.
TL;DR: A case of 36-year-old man who presented with a swelling in the left epididymis and was diagnosed to be single organ variant of PAN, which is a systemic necrotizing vasculitis that typically affects medium-sized muscular arteries, with occasional involvement of small muscular arteries is reported.
Abstract: Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis that typically affects medium-sized muscular arteries, with occasional involvement of small muscular arteries. Unlike some other vasculitides (e.g. microscopic polyarteritis, Wegener's granulomatosis) PAN is not associated with antineutrophil cytoplasmic antibodies. Patients typically present with systemic symptoms such as fever, weight loss, and malaise. The kidneys, skin, joints, muscles, nerves, and gastrointestinal tract are commonly involved, usually in some combination. PAN can affect any organ, but usually spare the lungs. Clinical variants or subsets of PAN include single-organ disease and cutaneous-only PAN. Scrotal involvement is rarely the first presenting sign. We herein report a case of 36-year-old man who presented with a swelling in the left epididymis, which was surgically removed. The swelling histopathologically showed necrotizing inflammation, fibrinoid necrosis of the medium-sized arteries of the epididymis and was diagnosed to be single organ variant of PAN.
TL;DR: A 34-year-old woman with SLE and LETM of the whole spine is presented, with rapid progression despite intensive treatment, and immunohistochemistry showed CD3-positive T-lymphocytes in the wall of the spinal blood vessels, and a prominent D2-40 immunostaining.
TL;DR: A highly significant increase in the villous abnormalities in the PIH group was found as compared to full term placenta which could attribute towards reduced uteroplacental flow.
Abstract: Background: Hypertension is one of the common complications seen in pregnancies in the developing countries which contribute significantly to the maternal and fetal morbidity and mortality. Objective: The present study was undertaken to analyse the histomorphologic changes of the placenta in pregnancy induced hypertension by looking for any significant differences in the villous abnormalities between the PIH group and the control group. Study Design: Placentae from fifty mothers with uncomplicated pregnancy and fifty mothers with pregnancy induced hypertension (PIH) were divided as control and study group respectively. The microscopic features were compared between the control and PIH group. Place and Duration of study: Department of Pathology, MVJ Medical College and Research Hospital, Bangalore, between 2011 and 2013. Methodology: The microscopic features such as syncytial knots, vasculo-syncytial membrane (VSM), fibrinoid necrosis, basement membrane thickening and villous stromal fibrosis were compared between the placentae of the control and the PIH group. About four hundred villi were Original Research Article Jena and Shalini; BJMMR, 9(9): 1-9, 2015; Article no.BJMMR.17899 2 counted for each placenta and the mean was calculated for all the microscopic features. A ‘p’ value less than 0.05 was taken to be statistically significant. Gross abnormalities such as infarction and calcification were noted. Results: The villous abnormalities observed in the study (PIH) group were increased syncytial knots (66%), paucity of vasculo-syncytial membrane (80%), fibrinoid necrosis (100%), basement membrane thickening (76%) and villous stromal fibrosis (90%). A ‘p’ value <0.001 of statistical significance was noted in the microscopic abnormalities of the villi in the placentae of the PIH group. Conclusion: A highly significant increase in the villous abnormalities in the PIH group was found as compared to full term placenta which could attribute towards reduced uteroplacental flow.
01 Jan 2015
TL;DR: In this paper, the authors describe the cases of three patients who developed a symmetrical purpuric rash on the legs, after long walks on hot days, and diagnosed exercise-induced vasculitis.
Abstract: We describe the cases of three patients who developed a symmetrical purpuric rash on the legs, after long walks on hot days. Histological examination of one lesion showed signs of leukocytoclastic vasculitis without fibrinoid necrosis. The cases were diagnosed exercise-induced vasculitis. The treatment consisted in oral antihistamines and topical corticosteroids with favorable outcome. Exercise-induced vasculitis is a self-limiting process with good prognosis that can be differentiated from other forms of leukocytoclastic vasculitis.
TL;DR: Vasculitis are a heterogeneous group of disorders characterized by inflammation of the blood vessels of different caliber and sometimes fibrinoid necrosis with vessel wall destruction.
Abstract: Vasculitis are a heterogeneous group of disorders characterized by inflammation of the blood vessels of different caliber and sometimes fibrinoid necrosis with vessel wall destruction [1].
Vasculitis are divided into cutaneous and systemic forms, primary and secondary to hypertension, immunosuppression therapy, metabolic complications. The classification is based on the affected vessel size (Table (Table1).1). They may have neurological manifestations at the onset and during the desease development. These are more common in systemic forms such as SLE and Nodose Polyarteritis (PAN).
Table 1
Vasculitis: classification (Adapted from EULAR/PReS endorsed criteria for the classification of childhood vasculitis) 2006; 65:936-41
The Schonlein-Henoch purpura and Kawasaki disease, the most frequent vasculitisin childhood, rarely can have neurological disorders. There are forms of mild to moderate intensity like headache, irritability, mood disorders and behavioral and forms of severe as seizures and sensory disturbance up to coma.
In the course of SLE, neuropsychiatric manifestations, headache and chorea are common, with an incidence of 20-40% (also 80% with cognitive disorders and asymptomatic alterations RMN). The neuropsychiatric manifestations involve 40-56% of children; headache the 22-64%; convulsions the 20-31%; chorea 4-10%; peripheral neuropathy 5-6%; myelopathy 1%. Heterogeneity in their neurological symptoms are important for prognostic purposes.
In antiphospholipid syndrome, primary or secondary, the following are common: transient cerebral ischemia and ischemic stroke, memory loss, chorea, seizures, vision problems [2].
The PAN is a necrotizing vasculitis histo-pathological examination, rarely aneurysm, stenosis or occlusion (not caused by fibro-muscular dysplasia, or by other causes not inflammatory) artery of small and medium caliber. In addition, at least one of the following signs/symptoms: skin involvement (livedo, nodules or heart attacks); myalgia; hypertension; peripheral neuropathy (sensory or motor); renal involvement (proteinuria, haematuria, renal impairment).
The primary central nervous system vasculitis is a brain vessels inflammation not associated with vasculitis of other organs. The classification is based on the vessel size: small (with normal angiography) and medium-large (progressive and non-progressive). This form, responsible for 40-60% of arterial ischemic stroke, affects 3-8/100.000 children/year. Symptoms are characterized by acute severe headache (80%), focal neurological deficit (78%), motor deficit (62%), cognitive disorders (54%), cranial nerve involvement (59%), seizures (small vessel vasculitis).
Peripheral neuropathies are characteristic of the Churg-Strauss disease.
The clinical diagnosis is often difficult (Table (Table22).
Table 2
Vasculitis: diagnosis
Neurological complications are diagnosed early because the treatment must be immediate and aggressive.
TL;DR: The goal of this work was to study the kinetic and pattern of infiltration of these cells in the synovial tissue during the course of arthritis to find any real switch M1/M2 over time but a “cohabitation” of these two macrophages sub-types.
Abstract: Background Macrophages play a major role in the pathogenesis of rheumatoid arthritis (RA). There are professional phagocytic cells present in all organs to maintain tissue integrity, clear debris, and respond rapidly to initiate repair after injury. These cells can produce inflammatory cytokine such as TNF α. They can differentiate into two sub-populations: the proinflammatory M1 and anti-inflammatory M2 macrophages. It has been suggested that chronic inflammation could be enhanced by an imbalance between these two subpopulations with and excess of M1 over M2 polarization. Objectives The goal of our work was to study the kinetic and pattern of infiltration of these cells in the synovial tissue during the course of arthritis. Methods We used a murine animal model of antigen-induced arthritis (AIA), which is characterized by an acute arthritis followed by a spontaneous resolution of inflammation over time. Sixteen C57BL/6 mice aged 7 weeks were used. They were sacrificed at various clinical stages of arthritis: early (D3), peak (D7), stabilization (D10) and decline (D14). Expression of M1 and M2 markers within the joint was studied by RT-qPCR using the following markers: CD11b (myeloid cells), CD64 and CD86 (M1), CD163, IL-10 and CD200R (M2). The different macrophage subtypes were studied by immunohistochemistry (IHC) using the following markers: Iba-1 (pan-macrophage or M0), iNOS (M1), CD206 (M2). Finally, human synovial samples from RA patients (n=19) were using the following markers: CD68 (M0), iNOS (M1), CD163 (M2). Results In the AIA model, the expression of CD11b was significantly increased over time. M1 markers expression was significantly increased early, on D3 (4 and 7 times for CD86 and CD64, respectively) then slowly decreased without returning to baseline (2.5 and 4 times on day 14 for CD86 and CD64, respectively; p≤0.05). Expression of the M2 markers (IL-10, CD200r1 and CD163) was modulated differently. CD163 marker decreased by 5 times at D3 (p=0.05), and quickly returned to its basal expression. The IL-10 marker increased more gradually with maximum expression of 5.5 times on D7 (p≤0.05). Finally, the marker CD200r1 increased in the early phase D3 (p≤0.05), stabilized and then decreased in decline D14. On IHC, INOS staining (M1) was maximal on D7 (score 10, p≤0.05) and decreased over time. The CD206 marking (M2) increased progressively to its maximum on D14 (score 7; p≤0.05). In human synovial biopsies intensity iNOS marking (M1) but not CD163 (M2) was correlated with the histological inflammation (p=0.0091; r =0.5806). In contrast, presence of M2 macrophages was associated with fibrinoid necrosis (p=0.002 and correlation coefficient r =0.7606). Conclusions We did not find any real switch M1/M2 over time but a “cohabitation” of these two macrophages sub-types. However, an earlier increase in the M1 population and an inversion of the ratio M1/M2 in the resolution phase of arthritis as been observed in the AIA model. In human synovial tissues the correlation between the fibrinoid necrosis and the presence of subpopulation M2 might be linked to the functional role of these cells in tissue repair and cleaning of debris. Disclosure of Interest None declared
01 Jan 2015
TL;DR: The Henoch-Schonlein purpura is an immunoglobulin A (IgA)-mediated small- vessel systemic vasculitis, rare in adults, and physicians should be aware of it.
Abstract: ABSTRACT Introduction: The Henoch-Schonlein purpura (HSP) is an immunoglobulin A (IgA)-mediated small- vessel systemic vasculitis, rare in adults. The association with solid tumours has been described, especially with lung cancer. Case Report: We present the case of a 60-year-old Caucasian male, diag- nosed with lung adenocarcinoma that underwent surgical resection without (neo)adjuvant theraphy. Two months latter he was admitted for abdominal pain, purpuric rash on his lower extremities and acute kidney injury, with serum creatinine (Scr) of 2 mg/dl. Urinalysis revealed haematuria and 24h proteinuria (P24h) of 1.5 g. The serum protein electrophoresis, complement components C3 and C4, circulating immune complexes, cryoglobulins, ANCA, ANA, anti-dsDNA and the remaining immunologic study as screening for viral infections (HCV, HBV and HIV) were negative. Renal ultrasound was normal and kidney biopsy revealed mild mesangial proliferation; 2 cellular glomerular crescents and 1 fibrinoid necrosis lesion; large amounts of red blood cell casts; lymphocytic infiltration in the intertubular inter- stitial capillaries; moderate arteriolar hyalinosis. Immunofluorescence demonstrated mesangial and parietal deposits of IgA. The diagnosis of HSP was assumed, and the patient started prednisolone 1 mg/kg/day. Ten months after diagnosis the patient's baseline Scr is 1.4 mg/dl with P24h of 0.18g, without haematuria. Conclusion: Although this is a rare association and the exact mechanism behind the disease is yet unknown, physicians should be aware of it. The early recognition and treatment may prevent renal disease progression.
Journal Article•
TL;DR: Cerebral lobar hemorrhage related with CAA is mainly located in the parietal, temporal and occipital lobes, readily breaking into the subarachnoid space, and it is often multiple and recurrent.
Abstract: Objective To summarize the clinical data and pathological features of 10 cases of cerebral lobar hemorrhage related with cerebral amyloid angiopathy (CAA) diagnosed pathologically, thereby to improve the knowledge and diagnosis of the disease. Methods The clinical data of 10 cases of cerebral lobar hemorrhage related with CAA, collected in the General Hospital of Shenyang Command from 1983 up to now, were retrospectively analyzed, and the clinical and neuropathological features of these cases were summarized. Results Of the 10 patients, 2 suffered from single lobar hemorrhage and 8 multiple lobar hemorrhage, all of them were confirmed pathologically to have ruptured into the subarachnoid space. Pathological examination revealed microaneurysm in 2 cases, "double barrel" change in 4 cases, multiple arteriolar clusters in 5 cases, obliterative onion-liked intima change in 4 cases, and fibrinoid necrosis of vessel wall in 7 cases. In addition, neurofibrillary tangles were found in 8 cases, and senile plaque was observed in 5 cases. Conclusions Cerebral lobar hemorrhage related with CAA is mainly located in the parietal, temporal and occipital lobes, readily breaking into the subarachnoid space, and it is often multiple and recurrent. The CAA associated microvasculopathy was found frequently in the autopsy sample of CAA related cerebral lobar hemorrhage, and it may contribute to the pathogenesis of cerebral hemorrhage.
DOI: 10.11855/j.issn.0577-7402.2015.07.04