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Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice
Ellinor Kenne, Anna Erlandsson, Lennart Lindbom, Lars Hillered, Fredrik Clausen
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-17
Abstract: In this study we used controlled cortical impact (CCI) as a model for TBI and investigated the role of neutrophils in the response to injury. The outcome of mice that were depleted of neutrophils using an anti-Gr-1 antibody was compared to that in mice with intact neutrophil count. The effect of neutrophil depletion on blood-brain barrier function was assessed by Evan's blue dye extravasation, and analysis of brain water content was used as a measurement of brain edema formation (24 and 48 hours after CCI). Lesion volume was measured 7 and 14 days after CCI. Immunohistochemistry was used to assess cell death, using a marker for cleaved caspase-3 at 24 hours after injury, and microglial/macrophage activation 7 days after CCI. Data were analyzed using Mann-Whitney test for non-parametric data.Neutrophil depletion did not significantly affect Evan's blue extravasation at any time-point after CCI. However, neutrophil-depleted mice exhibited a decreased water content both at 24 and 48 hours after CCI indicating reduced edema formation. Furthermore, brain tissue loss was attenuated in neutropenic mice at 7 and 14 days after injury. Additionally, these mice had a significantly reduced number of activated microglia/macrophages 7 days after CCI, and of cleaved caspase-3 positive cells 24 h after injury.Our results suggest that neutrophils are involved in the edema formation, but not the extravasation of large proteins, as well as contributing to cell death and tissue loss following TBI in mice.The pathological response following traumatic brain injury (TBI) consists of the primary and secondary injury. The primary injury results in death of neurons and glial cells and widespread axonal damage at the moment of impact or acceleration/deceleration. This primary injury initiates a complex secondary injury cascade that includes intracranial inflammation and edema formation. Due to the non-expandable skull compartment, brain edema leads to increased intracranial pressure which in
Urine Biomarkers Neutrophil Gelatinase-Associated Lipocalin (NGAL) and Kidney Injury Molecule-1 (KIM-1) have Different Patterns in Heart Failure Exacerbation
Meyeon Park, Eric Vittinghoff, Kathleen D. Liu, Michael G. Shlipak, and Chi-yuan Hsu
Biomarker Insights , 2012, DOI: 10.4137/BMI.S11479
Abstract: Individuals with acute heart failure exacerbation often experience a deterioration in renal function. We sought to determine whether this deterioration is ischemic in nature and detectable by sensitive urine biomarkers neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). We measured serial biomarker levels and evaluated the associations of these biomarkers with renal recovery in a cohort of hospitalized patients with acute heart failure exacerbation.
Acute hemorrhagic edema of infancy  [PDF]
Sultan Ecer Mente?,Mustafa Ta?kesen,Selahattin Katar,M.Emin Günel
Dicle Medical Journal , 2009,
Abstract: Acute hemorrhagic edema of infancy is a rare form of leukocytoclastic vasculitis. Mostly it appears under three years of age and is characterized by purpuric skin lesions, fever and edema. A three years-old boy, who has cough and coryzea was admitted to our clinic for fever and red spots on legs and arms. In physical examination; ecimotic skin lesions on right ear, face, arms, dorsal of the hands, buttocks, legs and dorsal of the feet were found. In the laboratory tests acute phase reactants were elevated and blood coagulation tests were in normal range. Hepatit A,B,C and TORCH markers were negative. Punch biopsy obtained from gluteal area showed leukositoclastic vasculity. Focal fibrinogen accumulation was detected by immun fluorescent microscopy. Regression on lesions was not observed despite supportive therapy, so prednisolone (1 mg/kg/day) therapy was started. On the third day of the steroid therapy, complete recovery was achived.
Kowsalya R, Jagatheesh K, Pavan Kumar Padarthi, Elangovan N*
International Journal of Bioassays , 2013,
Abstract: Lipocalins as biochemical markers of disease have been extensively used. The clinical indications relate to almost any field of medicine, such as inflammatory disease, cancer, lipid disorders, liver and kidney function. Lipocalins are mainly extracellular carriers of lipophilic molecules, though exceptions with properties like prostaglandin synthesis and protease inhibition are observed for specific lipocalins. Lipocalin 2, a member of the lipocalin family that carries small lipophilic ligands, has gained recent attention as both a potential biomarker and a modulator of human cancers. Neutrophil gelatinase-associated lipocalin, also known as lipocalin 2, has been originally identified as a 25 kDa protein covalently linked to neutrophil gelatinase B. It is an acute phase protein involved in diverse physiological processes with an important role in intracellular iron transport. Moreover, lipocalin 2 is involved in the physiopathology of neoplastic process. Lipocalin 2 is a protein that has garnered a great deal of interest in multidisciplinary fields over the last two decades since its discovery. This review focuses on lipocalin 2 and its function.
Neutrophil gelatinase-associated lipocalin levels in right and left heart failure: an observational study  [cached]
Fatih Koca,?brahim Halil Tanbo?a,Mehmet Mustafa Can,Alper ?zkan
Anadolu Kardiyoloji Dergisi , 2011,
Abstract: Objective: Neutrophil gelatinase-associated lipocalin (NGAL) is a novel marker for early detection of renotubular deterioration. Despite the limited data concerning the NGAL in heart failure (HF), significance of NGAL in right-sided HF remains unknown. We assessed serum and urinary NGAL in left and right-sided HF due to non-ischemic cardiomyopathy (NICMP) and severe pulmonary arterial hypertension (PAH). Methods: In this cross-sectional observational study, we compared three groups; 35 patients with NICMP, 28 patients with PAH and 27 healthy controls. None had a serum creatinine ≥1.5 mg/dL. Plasma brain natriuretic peptide (BNP) levels, estimated glomerular filtration rate (eGFR) by Cockroft-Gault (CG) and Modification of Diet in Renal Disease Study formulas, echocardiographic measures of left and right ventricles (LV, RV) and non-invasive measurement of cardiac index (CI) by echocardiography and impedance cardiography were assessed. Differences among the groups for continuous variables were evaluated by the ANOVA and the Kruskal-Wallis test as appropriate. The Chi-square test was used for comparison of categorical variables.Results: Despite eGFR with CG formula was lower in NICMP and PAH subsets as compared to those in controls (102±27 and 99.4±29.4 vs 122.4±25.9 mL/min, p<0.05 and p<0.005 in order), serum NGAL [141 (113-151), 174 (130-192) and 132 (95-181) ng/mL] and urinary NGAL [15 (12-18), 15 (12-22) and 13 (8-18) ng/mL] levels were not different among groups (p=0.15 and p=0.35, respectively). Conclusion: Despite the mildly impaired eGFR in left-sided HF due to NICMP and right-sided HF due to PAH, neither serum, nor urinary NGAL levels are elevated in these patients.
Neutrophil gelatinase-associated lipocalin in dehydrated patients: a preliminary report
Constantine N Antonopoulos, Alexandros Kalkanis, Georgios Georgakopoulos, Theodoros N Sergentanis, Dimitrios N Rigopoulos
BMC Research Notes , 2011, DOI: 10.1186/1756-0500-4-435
Abstract: A total of twelve patients presented with symptoms of mild dehydration defined by history of diarrheas or vomiting and orthostatic (postural) hypotension and an age and sex matched group of twelve control patients were included. The two groups of patients did not seem to differ in basic clinical and laboratory parameters. Serum Ngal was higher in dehydrated patients when compared to control group (Ngal = 129.4 ± 25.7 ng/mL vs 60.6 ± 0.4 ng/mL, p = 0.02). Ngal was not correlated with age, hemoglobin, white blood cell count, red blood cell count, urea or creatinine.The presence of elevated Ngal levels in dehydrated patients may suggest its role as a very sensitive biomarker in even minimal and "silent" prerenal kidney dysfunctionRenal impairment may be the result of a variety of renal or systemic diseases and may lead to renal failure [1]. Although the gold standard of renal failure's diagnosis is serial measurements of serum creatinine (Cr) [2,3], this biomarker is of little clinical importance in very early stages of renal disease. A novel biomarker, neutrophil gelatinase-asssociated lipocalin (Ngal), has been promising in evidencing renal impairment, even when changes in serum Cr level are undetectable [1].In order to explore the possible role of Ngal in subclinical renal dysfunction, such as renal hypoperfusion, we prospectively evaluated twelve patients aged>18 years with medical history suggesting mild dehydration, accompanied by orthostatic hypotension. A group of twelve apparently healthy individuals with no history of dehydration and no evidence of orthostatic hypotension were treated as controls. Ethical approval was obtained by the Ethics Committee of the "401 General Army Hospital" in Athens, Greece and all patients gave informed consent.Dehydrated and controls were similar in age and gender (75% males in each group) and in terms of basic laboratory tests (Hemoglobin; Hb, White blood cells; Wbc, Red blood cells; Rbc, Urea; Ur and Cr). Although no laborator
Edema hemorrágico agudo del lactante Infant acute hemorrhagic edema
Lilian Pérez C,Alicia Benavides M,Bárbara Barrientos F,Cristian Deza E
Revista chilena de pediatría , 2006,
Abstract: El edema hemorrágico agudo del lactante (EHAL) es una variante de vasculitis leucocitoclástica confinada a la piel que se caracteriza por placas purpúricas y edema de las extremidades, en un ni o en buenas condiciones generales. Durante una o dos semanas previas al inicio del cuadro se describen infecciones, uso de drogas o inmunizaciones los que gatillarían un proceso inmunológico mediado por inmunocomplejos. Su principal diagnóstico diferencial es el púrpura de Sch nlein-Henoch. Es de evolución benigna y autolimitada. Objetivo: Presentar un caso de EHAL, dando a conocer la enfermedad y entregar herramientas de diagnóstico. Caso clínico: Lactante de 8 meses que presenta edema y lesiones purpúricas extensas en cara y extremidades asociadas un cuadro respiratorio intercurrente. No había compromiso del estado general, los exámenes de laboratorio fueron normales y la biopsia de piel fue compatible con EHAL. Se descartaron los diagnósticos diferenciales más importantes. No se realizó ningún tratamiento específico y el cuadro remitió en forma espontánea sin recurrencias posteriores. Este caso representa el cuadro típico del edema hemorrágico agudo del lactante, el cual es poco frecuente, pero sus manifestaciones cutáneas son muy alarmantes y pueden originar confusión en el diagnóstico Background: Acute hemorrhagic edema of infancy (AHEI) is a cutaneous small vessel leukocytoclastic vasculitis characterized by purpuric plaques and edema of limbs, in a healthy infant. Clinical presentation consists in a recent history of upper respiratory tract infection and/or use of antibiotics or immunizations that triggers an immunologic response mediated by immune complexes. The main differential diagnosis is Sch nlein-Henoch Purpura and it is a benign self-limited disease. Objective: To inform about this disease and therefore increase its diagnosis. Case-report: An 8 months-old healthy infant with edema and purpura in the face and limbs, associated with respiratory disease. Laboratory exams were normal and skin biopsy was compatible with AHEI. He didn’t receive any specific treatment and the disease improved spontaneously without recurrence. This child presents a typical case of acute hemorrhagic edema of infancy. Although it is unfrequent, skin manifestations are alarming and can mistake the diagnosis
Methylprednisolone Therapy in Acute Hemorrhagic Edema of Infancy  [PDF]
Jeyanthini Risikesan,Uffe Koppelhus,Torben Steiniche,Mette Deleuran,Troels Herlin
Case Reports in Dermatological Medicine , 2014, DOI: 10.1155/2014/853038
Abstract: We present a case of an 18-month-old boy who showed severe clinical signs indicative of acute hemorrhagic edema of infancy (AHEI) with painful purpuric skin affection primarily of the face and marked edema of the ears. The histological findings were diagnostic for leukocytoclastic vasculitis and thus met the histological criteria for AHEI. Indicative of infection as causative agent for the condition were symptoms of gastroenteritis. High-dose intravenous corticosteroids led to a fast resolution of symptoms and normalization of laboratory parameters. AHEI is usually not described as being very responsive to corticosteroids. The case presented here indicates that severe cases of AHEI can be treated with high-dose intravenous corticosteroids resulting in significant relief and shortening of the symptoms. Clinical followup showed no underlying malignancy or other severe chronic systemic diseases thus confirming earlier reports that AHEI is not associated with such conditions. The differential diagnoses with AHEI are discussed. 1. Introduction Acute hemorrhagic edema of infancy (AHEI) is an uncommon benign form of cutaneous small-vessel leukocytoclastic vasculitis, which typically affects children from 4 to 24 months of age [1]. AHEI was first described by Snow in 1913 [2]. A case series and systematic review by Fiore et al. [3] has reported approximately 300 patients with AHEI, with a male predominance. The pathogenesis is not fully understood, but a prodromal phase with various infections has been documented in children with AHEI. These include upper respiratory infections, pharyngitis, conjunctivitis, otitis media, bronchitis, urinary tract infections, and pneumonia [4]. AHEI is characterized by the clinical triad of fever; edema of the face, auricles, and extremities; and rosette-shaped purpura. Unlike Henoch-Sch?nlein purpura (HSP) visceral involvement is infrequent [1]. A correct diagnosis of the disorder is important to distinguish it from other vasculitides. The clinical features of AHEI may be confused with the symptoms seen in (HSP), erythema multiforme (EM), meningococcemia, and septicemia. The diagnostic criteria for AHEI are (1) age younger than 2 years; (2) purpuric or ecchymotic “bruise-like” skin lesions with edema of the face, auricles, and extremities with or without mucosal involvement; (3) lack of systemic disease or visceral involvement and spontaneous recovery within a few days or weeks [5]. AHEI is self-limiting (lasting from one to three weeks) and is not usually considered responsive to corticosteroids [1]. We present a severe case
Acute Hemorrhagic Edema of Infancy: A Case Report Case Report  [cached]
Hakan Turan,Ay?egül Turan
Güncel Pediatri , 2011,
Abstract: Introduction: Acute hemorrhagic edema of infancy is a rare subtype of leukocytoclastic vasculitis. It is characterized by target-like hemorrhagic plaques with edema. Lesions are localized to face and distal extremities. It usually heals spontaneously without any sequelae.Case Report: Herein, an 8-month-old girl infant with acute hemorrhagic edema of infancy was presented. Conclusion: Both dermatologists and pediatricians must be familiar with this rare type of leukocytoclastic vasculitis. We believe that this familiarity will eliminate unnecessary treatment and anxiety about the disease (Journal of Current Pediatrics 2011; 9: 50-2)
Effects of Angiopoietin-1 on Hemorrhagic Transformation and Cerebral Edema after Tissue Plasminogen Activator Treatment for Ischemic Stroke in Rats  [PDF]
Kunio Kawamura, Tetsuya Takahashi, Masato Kanazawa, Hironaka Igarashi, Tsutomu Nakada, Masatoyo Nishizawa, Takayoshi Shimohata
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0098639
Abstract: An angiogenesis factor, angiopoietin-1 (Ang1), is associated with the blood-brain barrier (BBB) disruption after focal cerebral ischemia. However, whether hemorrhagic transformation and cerebral edema after tissue plasminogen activator (tPA) treatment are related to the decrease in Ang1 expression in the BBB remains unknown. We hypothesized that administering Ang1 might attenuate hemorrhagic transformation and cerebral edema after tPA treatment by stabilizing blood vessels and inhibiting hyperpermeability. Sprague-Dawley rats subjected to thromboembolic focal cerebral ischemia were assigned to a permanent ischemia group (permanent middle cerebral artery occlusion; PMCAO) and groups treated with tPA at 1 h or 4 h after ischemia. Endogenous Ang1 expression was observed in pericytes, astrocytes, and neuronal cells. Western blot analyses revealed that Ang1 expression levels on the ischemic side of the cerebral cortex were decreased in the tPA-1h, tPA-4h, and PMCAO groups as compared to those in the control group (P = 0.014, 0.003, and 0.014, respectively). Ang1-positive vessel densities in the tPA-4h and PMCAO groups were less than that in the control group (p = 0.002 and <0.001, respectively) as well as that in the tPA-1h group (p = 0.047 and 0.005, respectively). These results suggest that Ang1-positive vessel density was maintained when tPA was administered within the therapeutic time window (1 h), while it was decreased when tPA treatment was given after the therapeutic time window (4 h). Administering Ang1 fused with cartilage oligomeric protein (COMP) to supplement this decrease has the potential to suppress hemorrhagic transformation as measured by hemoglobin content in a whole cerebral homogenate (p = 0.007) and cerebral edema due to BBB damage (p = 0.038), as compared to administering COMP protein alone. In conclusion, Ang1 might be a promising target molecule for developing vasoprotective therapies for controlling hemorrhagic transformation and cerebral edema after tPA treatment.
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