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Neurology India 2023Melioidosis is a bacterial infection caused by Burkholderia pseudomallei that is endemic in Southeast Asia, northern Australia, and Africa. Neurological involvement is... (Review)
Review
BACKGROUND
Melioidosis is a bacterial infection caused by Burkholderia pseudomallei that is endemic in Southeast Asia, northern Australia, and Africa. Neurological involvement is rare and reported in 3-5% of total cases.
OBJECTIVE
The purpose of this study was to report a series of cases of melioidosis with neurological involvement and a brief review of the literature.
MATERIALS AND METHODS
We collected the data from six melioidosis patients having neurological involvement. Clinical, biochemical, and imaging findings were analyzed.
RESULT
All patients in our study were adults (age range 27 to 73 years). The presenting symptoms were fever of varying duration (range 15 days to 2 months). Altered sensorium was noted in five patients. Four cases had brain abscess, one had meningitis, and one had a spinal epidural abscess. All cases of brain abscesses were T2 hyperintense with an irregular wall showing central diffusion restriction and irregular peripheral enhancement. The trigeminal nucleus was involved in one patient, but there was no enhancement of the trigeminal nerve. Extension along the white matter tract was noted in two patients. Magnetic resonance (MR) spectroscopy done in two patients showed increased lipid/lactate and choline peak in both of them.
CONCLUSION
Melioidosis can present as multiple micro-abscesses in the brain. Involvement of the trigeminal nucleus and extension along the corticospinal tract may raise the possibility of infection by B. pseudomallei. Meningitis and dural sinus thrombosis, although rare, can be presenting features.
Topics: Adult; Humans; Middle Aged; Aged; Melioidosis; Magnetic Resonance Imaging; Brain Abscess; Brain; Lactic Acid
PubMed: 36861583
DOI: 10.4103/0028-3886.370442 -
International Journal of Molecular... Jun 2021ANCA-associated vasculitis (AAV) comprises granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis... (Review)
Review
ANCA-associated vasculitis (AAV) comprises granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA). While systemic vasculitis is a hallmark of all AAV, GPA is characterized by extravascular granulomatous inflammation, preferentially affecting the respiratory tract. The mechanisms underlying the emergence of neutrophilic microabscesses; the appearance of multinucleated giant cells; and subsequent granuloma formation, finally leading to scarred or destroyed tissue in GPA, are still incompletely understood. This review summarizes findings describing the presence and function of molecules and cells contributing to granulomatous inflammation in the respiratory tract and to renal inflammation observed in GPA. In addition, factors affecting or promoting the development of granulomatous inflammation such as microbial infections, the nasal microbiome, and the release of damage-associated molecular patterns (DAMP) are discussed. Further, on the basis of numerous results, we argue that, in situ, various ways of exposure linked with a high number of infiltrating proteinase 3 (PR3)- and myeloperoxidase (MPO)-expressing leukocytes lower the threshold for the presentation of an altered PR3 and possibly also of MPO, provoking the local development of ANCA autoimmune responses, aided by the formation of ectopic lymphoid structures. Although extravascular granulomatous inflammation is unique to GPA, similar molecular and cellular patterns can be found in both the respiratory tract and kidney tissue of GPA and MPA patients; for example, the antimicrobial peptide LL37, CD163 macrophages, or regulatory T cells. Therefore, we postulate that granulomatous inflammation in GPA or PR3-AAV is intertwined with autoimmune and destructive mechanisms also seen at other sites.
Topics: Animals; Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis; Antibodies, Antineutrophil Cytoplasmic; Autoimmune Diseases; Autoimmunity; Biomarkers; Cell Movement; Disease Management; Disease Susceptibility; Granulomatosis with Polyangiitis; Humans; Immunity, Innate; Immunohistochemistry; Organ Specificity
PubMed: 34204207
DOI: 10.3390/ijms22126474 -
Frontiers in Pediatrics 2022More than 400 single gene defects have been identified as inborn errors of immunity, including many arising from genes encoding proteins that affect NF-κB activity. We... (Review)
Review
More than 400 single gene defects have been identified as inborn errors of immunity, including many arising from genes encoding proteins that affect NF-κB activity. We summarise the skin phenotypes in this subset of disorders and provide an overview of pathogenic mechanisms. NF-κB acts cell-intrinsically in basal epithelial cells during differentiation of skin appendages, influences keratinocyte proliferation and survival, and both responses to and amplification of inflammation, particularly TNF. Skin phenotypes include ectodermal dysplasia, reduction and hyperproliferation of keratinocytes, and aberrant recruitment of inflammatory cells, which often occur in combination. Phenotypes conferred by these rare monogenic syndromes often resemble those observed with more common defects. This includes oral and perineal ulceration and pustular skin disease as occurs with Behcet's disease, hyperkeratosis with microabscess formation similar to psoriasis, and atopic dermatitis. Thus, these genotype-phenotype relations provide diagnostic clues for this subset of IEIs, and also provide insights into mechanisms of more common forms of skin disease.
PubMed: 36733767
DOI: 10.3389/fped.2022.1098426 -
Indian Journal of Otolaryngology and... Sep 2023Kimura Disease, an eosinophilic hyperplastic granulomatous disease of idiopathic origin is most commonly seen in young males. It mostly presents with deep subcutaneous...
UNLABELLED
Kimura Disease, an eosinophilic hyperplastic granulomatous disease of idiopathic origin is most commonly seen in young males. It mostly presents with deep subcutaneous tissue swelling along with enlargement of salivary glands and regional lymphadenopathy. Diagnosis is mainly based on histopathological findings and raised serum IgE and hypereosinophilia. The radiological investigation of choice is Magnetic Resonance Imaging. Management strategy includes surgery and steroid therapy. Chemotherapeutic agents are also frequently used by some centres. Relapse and recurrence stands to be a common problem with management of this disease process.
SUPPLEMENTARY INFORMATION
The online version contains supplementary material available at 10.1007/s12070-023-03817-y.
PubMed: 37636657
DOI: 10.1007/s12070-023-03817-y -
Reumatologia 2019Rheumatoid neutrophilic dermatitis is a rare extra-articular manifestation of rheumatoid arthritis, both seropositive and seronegative for rheumatoid factor. The...
Rheumatoid neutrophilic dermatitis is a rare extra-articular manifestation of rheumatoid arthritis, both seropositive and seronegative for rheumatoid factor. The condition most often presents as symmetric erythematous papules, nodules, plaques, and urticaria-like lesions in patients with severe, long-lasting rheumatoid arthritis. We report a case of a 65-year-old man with well-controlled rheumatoid arthritis, who developed rheumatoid neutrophilic dermatitis on the right lower leg. The biopsy of skin lesions revealed an intense, neutrophilic dermal infiltrate, microabscesses, and leukocytoclasis without vasculitis. The patient responded well to pulses of intravenous methylprednisolone. We present this patient due to the rarity of the disease and atypical unilateral manifestation involving the flexural surfaces of the lower leg.
PubMed: 32226170
DOI: 10.5114/reum.2019.90363 -
Intensive Care Medicine Experimental Jul 2019Sepsis is a highly lethal disorder. Organ dysfunction in sepsis is not defined as a clinicopathological entity but rather by changes in clinical, physiological, or... (Review)
Review
BACKGROUND
Sepsis is a highly lethal disorder. Organ dysfunction in sepsis is not defined as a clinicopathological entity but rather by changes in clinical, physiological, or biochemical parameters. Pathogenesis and specific treatment of organ dysfunction in sepsis are unknown. The study of the histopathological correlate of organ dysfunction in sepsis will help understand its pathogenesis.
METHODS
We searched in PubMed, EMBASE, and Scielo for original articles on kidney, brain, and liver dysfunction in human sepsis. A defined search strategy was designed, and pertinent articles that addressed the histopathological changes in sepsis were retrieved for review. Only studies considered relevant in the field were discussed.
RESULTS
Studies on acute kidney injury (AKI) in sepsis reveal that acute tubular necrosis is less prevalent than other changes, indicating that kidney hypoperfusion is not the predominant pathogenetic mechanism of sepsis-induced AKI. Other more predominant histopathological changes are apoptosis, interstitial inflammation, and, to a lesser extent, thrombosis. Brain pathological findings include white matter hemorrhage and hypercoagulability, microabscess formation, central pontine myelinolysis, multifocal necrotizing leukoencephalopathy, metabolic changes, ischemic changes, and apoptosis. Liver pathology in sepsis includes steatosis, cholangiolitis and intrahepatic cholestasis, periportal inflammation, and apoptosis. There is no information on physiological or biochemical biomarkers of the histopathological findings.
CONCLUSIONS
Histopathological studies may provide important information for a better understanding of the pathogenesis of organ dysfunction in sepsis and for the design of potentially effective therapies. There is a lack of clinically available biomarkers for the identification of organ dysfunction as defined by the histological analysis.
PubMed: 31346833
DOI: 10.1186/s40635-019-0236-3 -
The Lancet. Rheumatology Jan 2023Neutrophilic inflammation is a pervasive characteristic common to spondyloarthropathies and related disorders. This inflammation manifests as Munro's microabscesses of... (Review)
Review
Neutrophilic inflammation is a pervasive characteristic common to spondyloarthropathies and related disorders. This inflammation manifests as Munro's microabscesses of the skin and osteoarticular neutrophilic inflammation in patients with psoriatic arthritis, intestinal crypt abscesses in patients with inflammatory bowel disease, ocular hypopyon in anterior uveitis, and neutrophilic macroscopic and microscopic inflammation in patients with Behçet's disease. Strong MHC class I associations are seen in these diseases, which represent so-called MHC-I-opathies, and these associations indicate an involvement of CD8 T-cell immunopathology that is not yet well understood. In this Personal View, we highlight emerging data suggesting that the T-cell-neutrophil axis involves both a T-cell-mediated and interleukin (IL)-17-mediated (type 17) recruitment and activation of neutrophils, and also a sequestration of activated neutrophils at disease sites that might directly amplify type 17 T-cell responses. This amplification likely involves neutrophilic production of IL-23 and proteases as well as other feedback mechanisms that could be regulated by local microbiota, pathogens, or tissue damage. This crosstalk between innate and adaptive immunity offers a novel explanation for how bacterial and fungal microbes at barrier sites could innately control type 17 T-cell development, with the aim of restoring tissue homoeostasis, and could potentially explain features of clinical disease and treatment response, such as the fast-onset action of the IL-23 pathway blockade in certain patients. This axis could be crucial to understanding non-response to IL-23 inhibitors among patients with ankylosing spondylitis, as the axial skeleton is a site rich in neutrophils and a site of haematopoiesis with myelopoiesis in adults.
Topics: Adult; Humans; Interleukin-23; Neutrophils; Spondylarthropathies; Arthritis, Psoriatic; Abscess
PubMed: 38251507
DOI: 10.1016/S2665-9913(22)00334-4 -
Frontiers in Immunology 2022Munro's microabscess is a typical pathological feature in the early psoriatic lesion, mainly characterized by the accumulation of neutrophils in the epidermis. DNA...
INTRODUCTION
Munro's microabscess is a typical pathological feature in the early psoriatic lesion, mainly characterized by the accumulation of neutrophils in the epidermis. DNA methylation microenvironment of Munro's microabscess and the crosstalk with transcription and its effect on neutrophils have not yet been revealed.
METHODS
Performed genome-wide DNA methylation analysis and further differential methylation analysis of psoriatic skin lesions with and without Munro's microabscess from two batch samples consisting of 114 former samples in the discovery stage and 21 newly-collected samples in the validation stage. Utilized GO, MEME, and other tools to conduct downstream analysis on differentially methylated sites (DMSs). Correlation analysis of methylation level and transcriptome data was also conducted.
RESULTS
We observed 647 overlapping DMSs associated with Munro's microabscess. Subsequently, GO pathway analysis revealed that DNA methylation might affect the physical properties associated with skin cells through focal adhesion and cellsubstrate junction and was likely to recruit neutrophils in the epidermis. Via the MEME tool, used to investigate the possible binding transcription factors (TFs) of 20 motifs around the 647 DMSs, it was found that DNA methylation regulated the binding of AP1 family members and the recruitment of neutrophils in the epidermis through the TGF-beta pathway and the TH17 pathway. Meanwhile, combined with our earlier transcriptome data, we found DNA methylation would regulate the expressions of CFDP, SIRT6, SMG6, TRAPPC9, HSD17B7, and KIAA0415, indicating these genes would potentially promote the process of Munro's microabscess.
DISCUSSION
In conclusion, DNA methylation may affect the course of psoriasis by regulating the progression of Munro's microabscess in psoriatic skin lesions.
Topics: Humans; DNA Methylation; Epigenesis, Genetic; Psoriasis; Skin; Abscess; Sirtuins
PubMed: 36569916
DOI: 10.3389/fimmu.2022.1057839 -
Future Oncology (London, England) Jun 2016Idiopathic granulomatous mastitis (IGM) is a rare chronic inflammatory condition of the breast which although benign can mimic carcinoma. Establishing a diagnosis can be... (Review)
Review
Idiopathic granulomatous mastitis (IGM) is a rare chronic inflammatory condition of the breast which although benign can mimic carcinoma. Establishing a diagnosis can be challenging and requires a high index of suspicion with exclusion of infective and autoimmune breast diseases. IGM is characterized histologically by noncaseating granulomas which are of a lobulo-centric pattern and often associated with microabscess formation. Management of confirmed cases remains controversial with proponents of initial surgical or medical therapies - each has its associated problems which can be worse than the original symptoms of IGM. However, many patients require more than one modality of treatment to completely resolve IGM lesions and careful judgment is necessary to ensure optimal type and sequencing of treatments.
Topics: Female; Granulomatous Mastitis; Humans
PubMed: 27067146
DOI: 10.2217/fon-2015-0038 -
Comprehensive Physiology Dec 2015The importance of homocysteine in vascular function and arteriosclerosis was discovered by demonstration of arteriosclerotic plaques in children with homocystinuria... (Review)
Review
The importance of homocysteine in vascular function and arteriosclerosis was discovered by demonstration of arteriosclerotic plaques in children with homocystinuria caused by inherited enzymatic deficiencies of cystathionine synthase, methionine synthase, or methylene-tetrahydrofolate reductase. According to the homocysteine theory of arteriosclerosis, an elevated blood homocysteine level is an important risk factor for atherosclerosis in subjects without these rare enzymatic abnormalities. The homocysteine theory is supported by demonstration of arterial plaques in experimental animals with hyperhomocysteinemia, by discovery of a pathway for conversion of homocysteine thiolactone to sulfate in cell cultures from children with homocystinuria, and by demonstration of growth promotion by homocysteic acid in normal and hypophysectomized animals. Studies with cultured malignant cells revealed abnormal homocysteine thiolactone metabolism, resulting in homocysteinylation of proteins, nucleic acids, and glycosaminoglycans, explaining the abnormal oxidative metabolism, abnormalities of cellular membranes, and altered genetic expression observed in malignancy. Abnormal homocysteine metabolism in malignant cells is attributed to deficiency of thioretinamide, the amide synthesized from retinoic acid and homocysteine thiolactone. Two molecules of thioretinamide combine with cobalamin to form thioretinaco. Based on the molecular structure of thioretinaco, a theory of oxidative phosphorylation was proposed, involving oxidation to a disulfonium derivative by ozone, and binding of oxygen, nicotinamide adenine dinucleotide and phosphate as the active site of adenosine triphosphate synthesis in mitochondria. Obstruction of vasa vasorum by aggregates of microorganisms with homocysteinylated low-density lipoproteins is proposed to cause ischemia of arterial wall and a microabscess of the intima, the vulnerable atherosclerotic plaque.
Topics: Aging; Animals; Atherosclerosis; Homocysteine; Humans
PubMed: 26756640
DOI: 10.1002/cphy.c150021