Features Of Acute Inflammation Research Articles

Dirofilarial nodule as a differential diagnosis for subcutaneous lumps in children

Subcutaneous nodules in children are commonly caused by pilomatrixoma, dermoid cysts, soft tissue tumors, etc. Parasitic infections are reported to cause subcutaneous nodules and are infrequently described, mostly in the adult literature. We aim to describe the clinicopathological features of subcutaneous lumps caused by dirofilarial infestation in children in an endemic country. A retrospective analysis was performed of all patients presenting with the above condition to Lady Ridgeway Hospital from 2018 to 2022 and their relevant details were captured in a proforma. There were 55 patients with a male to female ratio of 2:1. The mean age at presentation was 50months (7-156months). The mean duration was 97days (1-820days). The common sites involved were scrotum (30.9%), back (14.5%), abdominal wall (102.7%) and face (10.9%). The majority had a painless nodule (70.9%), while ten (18.2%) had features of acute inflammation. Thirty (55.5%) had preoperative ultrasonography which showed features of parasitic nodules in 26 (47.3%). Parasite was demonstrated in histopathological analysis only in 30 patients (54.5%). Dirofilarial nodule should be considered in the differential diagnosis of subcutaneous lumps in children, especially in the endemic areas.

Efficacy and safety of temelimab in multiple sclerosis: Results of a randomized phase 2b and extension study

Background: The envelope protein of human endogenous retrovirus W (HERV-W-Env) is expressed by macrophages and microglia, mediating axonal damage in chronic active MS lesions. Objective and Methods: This phase 2, double-blind, 48-week trial in relapsing-remitting MS with 48-week extension phase assessed the efficacy and safety of temelimab; a monoclonal antibody neutralizing HERV-W-Env. The primary endpoint was the reduction of cumulative gadolinium-enhancing T1-lesions in brain magnetic resonance imaging (MRI) scans at week 24. Additional endpoints included numbers of T2 and T1-hypointense lesions, magnetization transfer ratio, and brain atrophy. In total, 270 participants were randomized to receive monthly intravenous temelimab (6, 12, or 18 mg/kg) or placebo for 24 weeks; at week 24 placebo-treated participants were re-randomized to treatment groups. Results: The primary endpoint was not met. At week 48, participants treated with 18 mg/kg temelimab had fewer new T1-hypointense lesions (p = 0.014) and showed consistent, however statistically non-significant, reductions in brain atrophy and magnetization transfer ratio decrease, as compared with the placebo/comparator group. These latter two trends were sustained over 96 weeks. No safety issues emerged. Conclusion: Temelimab failed to show an effect on features of acute inflammation but demonstrated preliminary radiological signs of possible anti-neurodegenerative effects. Current data support the development of temelimab for progressive MS. Trial registration: CHANGE-MS: ClinicalTrials.gov: NCT02782858, EudraCT: 2015-004059-29; ANGEL-MS: ClinicalTrials.gov: NCT03239860, EudraCT: 2016-004935-18

English

BACKGROUND Appendicitis is the most common indication for intra-abdominal surgery, especially in adolescents and young adults. In about 15 – 25 % of appendices removed at surgery because of suspected symptoms, histological features of acute appendicitis are absent. The cause of acute abdominal pain in these patients can be due to mast cells which may play a role in pathogenesis of appendicitis-like pain. Demonstration of mast cell in tissue can be done by toluidine blue staining or immunohistochemistry (IHC) marker CD 117. We wanted to evaluate whether the degree of distribution of mast cells has any relation with clinical findings and evaluate its usefulness as a diagnostic marker for histological diagnosis of acute appendicitis. METHODS This is a descriptive study done in 120 cases of appendicectomy specimens from clinically diagnosed cases of acute appendicitis received in a tertiary care center in South India in which 60 where histology positive and others were histology negative. Mast cell distribution in each group was compared using toluidine blue stain and CD 117. Collected data was entered in Microsoft excel and analysed using the statistical software SPSS version 16. RESULTS Mast cell distribution was significant in all layers of histologically negative acute appendicitis in comparison with histology positive cases. Mucosa has maximum mast cells distribution. CONCLUSIONS Mast cells play an important role in the clinical symptoms of patients even when there were no features of acute inflammation. In those cases, mast cells can be demonstrated by simple toluidine blue staining or IHC markers. This is one of the less studied areas, and the clinicopathological discrepancy can be solved by giving mast cell distribution along with histopathology diagnosis. KEYWORDS Appendicitis, Histologically Negative Acute Appendicitis, Mast Cells, Toluidine Blue, CD 117

Septic arthritis is a mimicker of rheumatic fever

Septic arthritis is an uncommon form of arthritis in children. A five years old boy presented with pain and swelling of both knee joints for 7 days. His joints swellings were disproportionate to pain. He had no history of trauma to the joints. On examination, there was soft tissue swelling of both knee joints. Investigation showed features of acute inflammation. Plain radiograph showed soft tissue swelling. Ultrasonography showed fluid accumulation in joints space. After 7 days of antistaphylococcal therapy, the child improved significantly. Physicians treating the children need to be aware of taking proper history and doing physical examination and checking laboratory findings of the children with septic arthritis for appropriate case management.
 Mediscope Vol. 6, No. 1: Jan 2019, Page 41-43

Primary cutaneous lymphoplasmacytic lymphoma-like B-cell neoplasm with features of acute inflammation and epidermal atypical cells

Primary cutaneous lymphoplasmacytic lymphoma (LPL) is rare. The author herein reports a case of LPL-like B-cell neoplasm with acute inflammation and epidermal cell atypia. A 69-year-old man presented skin ulcer of neck. The lesion appeared granulation tissue with surface fibrin deposition; an inflammatory process was suggested. Peripheral blood data showed no abnormalities, including the segments of leukocytes. No plasmacytosis was seen. No M-proteins, macroglubulins, or cryoglobulins were noted in serum and urine. The clinical diagnosis was non-specific skin ulcer. A wide biopsy was taken. It showed a destructive proliferation of atypical small lymphocytes, atypical plasmacytoid lymphocytes, and atypical plasma cells in dermis and subcutaneous tissue. The biopsy also showed acute inflammatory features; foci of many neutrophils were scattered in neoplastic cells. Some of them showed microabscesses. In addition, foci of atypical squamous cells were seen in the epidermis. Immunohsitochemically, the tumor cell showed B-cell lineage. The tumor cells were diffusely positive for vimentin, CD45, CD20, CD79, bcl-2, CD38, and CD138. The tumor cells were only focally positive for CD3 and CD45RO. A few tumor cells were positive for CD30, CD56, and CD10. Some of the tumor cells were positive for p53 and Ki-67 antigen (labeling index = 35%). The tumor cells were negative for pancytokeratin AE1/3, pancytokeratin CAM5.2, CD5, CD23, CD43, and cyclinD1. The tumor cells were positive for κ-chain but negative for λ-chain, indicating that the tumor cells have plasmacytic characteristics and that there was a light chain restriction which indicates monoclonal nature of the tumor plasma cells. The tumor cells were negative for Epstein-Barr virus (EBV) associated molecules such as EBV latent membrane protein-1 (LMP-1) and EBV early RNAs (EBER). A pathological diagnosis made by the author was cutaneous LPL-like B-cell malignant tumor. The author thought that this tumor could not be definitely diagnosed a primary cutaneous LPL, because other small-sized B-cell lymphomas with plasmacytoid differentiaton could not be excluded. The current tumor was also characterized by acute inflammatory features and epidermal squamous cell atypia suggestive of squamous cell carcinoma. Imaging modalities including CT identified no other tumors and lymphoadenopathy in the body. The systemic bones were free of myeloma features. No bone marrow study was performed after the pathological diagnosis. The tumor cured and the patient discharged from the hospital 3 months after the first presentation.

Molecular and Cellular Mediators of the Inflammatory Response

Inflammation is a highly complex process involving vascular, neurogenic, humoral, and cellular responses. Although the descriptive features of acute inflammation have long been known (i.e., heat, redness, pain, swelling), a single satisfactory definition of this phenomenon is still lacking. Successful therapy for inflammation rests not only on investigating the type of injury, but also on the timing of the intervention. This review focuses on humoral and cellular responses to injury, defining essential and interrelated inflammatory pathways. Systemic inflammatory response system (SIRS), in relation to sepsis syndrome, is defined by the global proinflammatory physiologic response to a stimulus. In contrast, compensatory antiinflammatory response (CARS) results from a predominant antiinflammatory response to an insult, also causing immunosuppression and increased susceptibility to infection. Also discussed are the roles of cytokines, adhesion molecules, inflammatory cells such as neutrophils, mast cells, and lymphocytes, extracellular vesicles, sphingolipids, reactive oxygen metabolites, nitric oxide, the complement cascade, and eicosanoids. Therapeutic implications and trials are examined in relation to cytokines in SIRS and CARS, activated protein C, and inflammatory bowel disease. This review contains 11 figures, 4 tables, and 79 references.

Molecular and Cellular Mediators of the Inflammatory Response

Inflammation is a highly complex process involving vascular, neurogenic, humoral, and cellular responses. Although the descriptive features of acute inflammation have long been known (i.e., heat, redness, pain, swelling), a single satisfactory definition of this phenomenon is still lacking. Successful therapy for inflammation rests not only on investigating the type of injury, but also on the timing of the intervention. This review focuses on humoral and cellular responses to injury, defining essential and interrelated inflammatory pathways. Systemic inflammatory response system (SIRS), in relation to sepsis syndrome, is defined by the global proinflammatory physiologic response to a stimulus. In contrast, compensatory antiinflammatory response (CARS) results from a predominant antiinflammatory response to an insult, also causing immunosuppression and increased susceptibility to infection. Also discussed are the roles of cytokines, adhesion molecules, inflammatory cells such as neutrophils, mast cells, and lymphocytes, extracellular vesicles, sphingolipids, reactive oxygen metabolites, nitric oxide, the complement cascade, and eicosanoids. Therapeutic implications and trials are examined in relation to cytokines in SIRS and CARS, activated protein C, and inflammatory bowel disease. This review contains 11 figures, 4 tables, and 79 references.

254 A Multicenter Study to Evaluate Magnetic Resonance Enterography (MRE) for Selection of Crohn's Disease Patients for Inclusion Into a Therapeutic Clinical Trial

Conclusions: The majority of strictures in CD patients treated by surgery are consistent with a mixed type inflammation (acute inflammation plus fibrosis). The presence of stratified BS pattern shows a significantly higher degree of fibrosis while the evidence of high mural signal intensity on T2-weighted fatsaturated images on MRI reflects histological features of acute inflammation. Even if the ideal definition of the type of the strictures in CD still remains significantly far to be obtained, the combined use of BS and MRI can offer useful information in a sub-group of patients needing surgery for complicating CD.

995 Feasibility, Precision and Reproducibility of MR Enterography for Detection of Inflammation in Crohn's Disease in a Multicenter Clinical Trial

Conclusions: The majority of strictures in CD patients treated by surgery are consistent with a mixed type inflammation (acute inflammation plus fibrosis). The presence of stratified BS pattern shows a significantly higher degree of fibrosis while the evidence of high mural signal intensity on T2-weighted fatsaturated images on MRI reflects histological features of acute inflammation. Even if the ideal definition of the type of the strictures in CD still remains significantly far to be obtained, the combined use of BS and MRI can offer useful information in a sub-group of patients needing surgery for complicating CD.

Very low birthweight placenta: clustering of morphologic characteristics.

Our objective was to use factor analysis as a data reduction tool to organize a large number of placental pathologic features into useful aggregates. We examined 1146 placentas of live-born infants with a birth weight of 500-1500 g. We then conducted analyses of pairs of characteristics and multiple characteristics to identify "associated groups" and "factors," respectively. We found an associated group and factor that had placental features associated with acute inflammation and another associated group and factor that had features associated with vasculopathy. Acute umbilical vasculitis had the strongest correlation with other features of the acute inflammation associated group and factor. Gross evidence of acute inflammation (opacification and green appearance of membrane) was eliminated in the reduction from associated group to factor. Infarcts and syncytial knots were strongly dissociated with features of acute inflammation. The multiple pathologic features of the very low birthweight placenta can be aggregated into two associated groups or two factors. Lack of membrane opacification cannot be used as a criterion for declining microscopic examination. The absence of infarcts and syncytial knots should prompt a search for features of acute inflammation. If a placenta has two or more findings from the acute inflammation factor or the vasculopathy factor, it is unlikely to demonstrate features from the other factor.

Endosonographic and color doppler flow imaging alterations observed within irradiated rectal cancer

Purpose : To correlate the endosonographic and color Doppler flow imaging alterations observed in irradiated rectal cancers with the pathologic features of radiation response, and to evaluate the potential impact of altered blood flow on the integrity of the surgical anastamosis. Methods and Materials : Endosonography with color and pulsed wave Doppler was performed on 20 rectal cancer masses before and after high dose preoperative radiation (XRT). Pre- and post-XRT observations indices. Comparisons were made with pathologic findings in the irradiated specimens and with the incidence of anastomotic failure. Results : Compared to pre-XRT observations, irradiated rectal cancers decreased in size and became either mixed in echogenicity with less apparent color Doppler flow (16 of 20) or unchanged in color Doppler flow and echotexture (4 of 20). Those with less flow (16 of 20) were imaged later (mean = 90.2 ± 12.1 days) than those without change in color Doppler flow (mean = 21.7 ± 2.7 days). Pathologically, the group of four without change in color Dopper signal had features of acute inflammation which were not observed in 16 of 20 imaged later. Based on pulsatility index measurements, both high and low resistance vessels were detected and confirmed by immunohistochemical staining, and features of postradiation obliterative vasculitis were observed. Only one primary anastomosis in 14 patients with decreased flow failed. Conclusions : The sonographic and color Doppler flow imaging alterations observed within irradiated rectal cancer correlated with changes of postradiation obliterative vasculitis. The apparent diminished local blood flow within high and low resistance vessels post-XRT did not result in an increased incidence of anastomotic failures.

Gastric mucosal hydrophobicity and Helicobacter pylori: response to antimicrobial therapy.

The hydrophobic properties of the gastric mucosa are reduced by NSAIDs and by Helicobacter pylori infection. Our investigation was to determine whether this abnormality was due to the bacteria or to the inflammatory response. Contact angle measurements were made on gastric antral and corpus biopsies taken from 10 H. pylori-infected volunteers before eradication therapy, after 2 and 14 days of therapy, and 4 weeks after therapy. The contact angle improved steadily and statistically throughout the 2 weeks of therapy (for day 0, 3, 14, respectively) antral mucosa 54.2 +/- 2, 59.3 +/- 2, and 63.2 +/- 2; corpus mucosa 55 +/- 1, 57.8 +/- 3, and 66.6 +/- 1. After 2 days of therapy, H. pylori bacteria were no longer evident, and yet the contact angle continued to improve, suggesting that bacteria and bacterial products (e.g., lipases) may not be critical factors. H. pylori was eradicated in five and failed in five. One month after ending therapy, the contact angles of those with recrudescence of infection and those with eradication were similar and higher (p < 0.05) than before therapy (antrum: 69.8 +/- 1 vs. 71.1 +/- 2, corpus: 66.4 +/- 4 vs. 70.8 +/- 2) (p > 0.25 for both). We conclude that gastric surface hydrophobicity abnormalities do not appear to be directly related to the presence of H. pylori organisms or the histologic features of acute inflammation, but are responsive to antimicrobial therapy.

Differences in the onset of the inflammatory response to cutaneous leishmaniasis in resistant and susceptible mice.

Sites of cutaneous infection with Leishmania major in genetically susceptible (BALB/c) and resistant (C57B1/6) mice were investigated for the early inflammatory response (6 h to 12 days) by electron microscopy combined with enzyme-histochemical methods. Susceptible BALB/c mice spontaneously recruited only polymorphonuclear leukocytes (PMNs) at the site of infection. Infiltrating mononuclear phagocytes (and eosinophils) were first observed at day 1 in a ratio equal to the influx of PMNs (about 40%). This pattern persisted during the following 11 days of infection. In the resistant C57/B16 mice, the first cellular infiltrate at the infected site contained mononuclear phagocytes (25%) and eosinophils (15%) besides PMNs (60%). Within 3 days after infection, mononuclear phagocytes became the dominant population of cells in cutaneous lesions (up to 80%). It was found in situ that L. major accumulated and replicated in immature macrophages, that is, intermediate stages between monocytes and resident macrophages, which were found in lesions of both strains. The burden of parasites was, however, degraded more rapidly by the infiltrating cells of the resistant mice than by those of the susceptible ones. Within the first 4 days of infection, the parasites were found in PMNs, mononuclear phagocytes, and extracellular spaces in both strains. In susceptible mice this distribution pattern persisted up to 12 days after infection; in resistant C57B1/6 mice parasites accumulated inside mononuclear phagocytes within this period. It is concluded that the features of acute inflammation during leishmaniasis in BALB/c mice are sustained over a prolonged period that is ineffective in the elimination of L. major.

Glycoconjugates in the Colons of New World Monkeys With Spontaneous Colitis

Abstract A spontaneously occurring experimental model of chronic colitis has been described in three closely related species of New World monkeys. One species, Saguinus oedipus oedipus, has the additional feature of developing adenocarcinoma of the colon in this setting. Pathological and lectin histochemistry studies were undertaken in 50 such colonic specimens to determine if pathological or histochemical features were associated with the concomitant development of cancer. Chronic inflammation was found in all of the colons examined, and 14% had features of acute inflammation, which was significantly associated with those animals that developed cancer. An oncofetal glycoconjugate structure has been defined in human colons by the ability to bind peanut lectin. A similar glycoconjugate, probably a mucin, was expressed in the colons of 65% of these animals. A marked degree of expression of the mucin was significantly associated with those animals that developed cancer. A highly significant association was found between the presence of acute inflammation and the expression of the mucin. These studies demonstrate similarities in glycoconjugate expression between the human colon and the New World monkey model of spontaneous colitis. A form of mucin is expressed in these animals that is highly associated with both the presence of acute inflammation and the development of cancer elsewhere in the colon. In addition, an association between acute inflammatory activity and neoplasia was found, suggesting a potential etiologic linkage between the two.

Glycoconjugates in the colons of New World monkeys with spontaneous colitis: Association between inflammation and neoplasia

A spontaneously occurring experimental model of chronic colitis has been described in three closely related species of New World monkeys. One species, Saguinus oedipus oedipus, has the additional feature of developing adenocarcinoma of the colon in this setting. Pathological and lectin histochemistry studies were undertaken in 50 such colonic specimens to determine if pathological or histochemical features were associated with the concomitant development of cancer. Chronic inflammation was found in all of the colons examined, and 14% had features of acute inflammation, which was significantly associated with those animals that developed cancer. An oncofetal glycoconjugate structure has been defined in human colons by the ability to bind peanut lectin. A similar glycoconjugate, probably a mucin, was expressed in the colons of 65% of these animals. A marked degree of expression of the mucin was significantly associated with those animals that developed cancer. A highly significant association was found between the presence of acute inflammation and the expression of the mucin. These studies demonstrate similarities in glycoconjugate expression between the human colon and the New World monkey model of spontaneous colitis. A form of mucin is expressed in these animals that is highly associated with both the presence of acute inflammation and the development of cancer elsewhere in the colon. In addition, an association between acute inflammatory activity and neoplasia was found, suggesting a potential etiologic linkage between the two.

Clinical features of acute inflammation of the pancreas; analysis of ninety-four attacks in seventy-eight patients.

This report is based on a study of 78 patients admitted to the Graduate Hospital with the diagnosis of primary acute pancreatitis or recurrent acute pancreatitis. Since several patients were admitted more than one time, there are a total of 94 separate admissions between 1941 and 1954. Unfortunately, not all patients with this diagnosis during these years could be used, because of inadequate objective data in some of the charts of patients seen in the earlier years. The incidence of acute pancreatitis has been increasing progressively in recent years, with 50% of the patients herein reported being admitted during the years 1952-1954. In part, this may be the result of a greater awareness of the disease and the more frequent employment of the serum pancreatic enzyme determinations. The purpose of this study was to evaluate the cumulative clinical experience with acute pancreatitis. Consideration has been given to a critical appraisal