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Pain Reports 2021Low back pain is the leading cause for years lived in disability. Most people with acute low back pain improve rapidly, but 4% to 25% of patients become chronic. Since... (Review)
Review
Low back pain is the leading cause for years lived in disability. Most people with acute low back pain improve rapidly, but 4% to 25% of patients become chronic. Since the previous systematic reviews on the subject, a large number of new studies have been conducted. The objective of this article was to review the evidence of the prognostic factors behind nonspecific chronic low back pain. A systematic literature search was performed without date limitation from the MEDLINE, Cochrane library, and Medic databases. Specific inclusion criteria were used, and risk factors before the onset of chronic symptoms were searched. Study quality was assessed by 2 independent reviewers. One hundred eleven full articles were read for potential inclusion, and 25 articles met all the inclusion criteria. One study was rated as good quality, 19 studies were rated as fair quality, and 5 articles were rated as poor quality. Higher pain intensity, higher body weight, carrying heavy loads at work, difficult working positions, and depression were the most frequently observed risk factors for chronic low back pain. Maladaptive behavior strategies, general anxiety, functional limitation during the episode, smoking, and particularly physical work were also explicitly predictive of chronicity. According to this systematic review, several prognostic factors from the biomechanical, psychological and psychosocial point of view are significant for chronicity in low back pain.
PubMed: 33981936
DOI: 10.1097/PR9.0000000000000919 -
Frontiers in Immunology 2014Studies on monocyte and macrophage biology and differentiation have revealed the pleiotropic activities of these cells. Macrophages are tissue sentinels that maintain... (Review)
Review
Studies on monocyte and macrophage biology and differentiation have revealed the pleiotropic activities of these cells. Macrophages are tissue sentinels that maintain tissue integrity by eliminating/repairing damaged cells and matrices. In this M2-like mode, they can also promote tumor growth. Conversely, M1-like macrophages are key effector cells for the elimination of pathogens, virally infected, and cancer cells. Macrophage differentiation from monocytes occurs in the tissue in concomitance with the acquisition of a functional phenotype that depends on microenvironmental signals, thereby accounting for the many and apparently opposed macrophage functions. Many questions arise. When monocytes differentiate into macrophages in a tissue (concomitantly adopting a specific functional program, M1 or M2), do they all die during the inflammatory reaction, or do some of them survive? Do those that survive become quiescent tissue macrophages, able to react as naïve cells to a new challenge? Or, do monocyte-derived tissue macrophages conserve a "memory" of their past inflammatory activation? This review will address some of these important questions under the general framework of the role of monocytes and macrophages in the initiation, development, resolution, and chronicization of inflammation.
PubMed: 25368618
DOI: 10.3389/fimmu.2014.00514 -
Spine Mar 2002A systematic review of prospective cohort studies in low back pain. (Review)
Review
STUDY DESIGN
A systematic review of prospective cohort studies in low back pain.
OBJECTIVES
To evaluate the evidence implicating psychological factors in the development of chronicity in low back pain.
SUMMARY OF BACKGROUND DATA
The biopsychosocial model is gaining acceptance in low back pain, and has provided a basis for screening measurements, guidelines and interventions; however, to date, the unique contribution of psychological factors in the transition from an acute presentation to chronicity has not been rigorously assessed.
METHODS
A systematic literature search was followed by the application of three sets of criteria to each study: methodologic quality, quality of measurement of psychological factors, and quality of statistical analysis. Two reviewers blindly coded each study, followed by independent assessment by a statistician. Studies were divided into three environments: primary care settings, pain clinics, and workplace.
RESULTS
Twenty-five publications (18 cohorts) included psychological factors at baseline. Six of these met acceptability criteria for methodology, psychological measurement, and statistical analysis. Increased risk of chronicity (persisting symptoms and/or disability) from psychological distress/depressive mood and, to a lesser extent, somatization emerged as the main findings. Acceptable evidence generally was not found for other psychological factors, although weak support emerged for the role of catastrophizing as a coping strategy.
CONCLUSION
Psychological factors (notably distress, depressive mood, and somatization) are implicated in the transition to chronic low back pain. The development and testing of clinical interventions specifically targeting these factors is indicated. In view of the importance attributed to other psychological factors (particularly coping strategies and fear avoidance) there is a need to clarify their role in back-related disability through rigorous prospective studies.
Topics: Adaptation, Psychological; Chronic Disease; Cohort Studies; Confounding Factors, Epidemiologic; Depression; Disability Evaluation; Fear; Humans; Low Back Pain; Prospective Studies; Psychology; Risk Factors; Somatoform Disorders
PubMed: 11880847
DOI: 10.1097/00007632-200203010-00017 -
Kidney International Apr 2018C3 glomerulonephritis (C3GN) and dense deposit disease comprise the two classes of C3 glomerulopathy. Studies from Europe and Asia have aided our understanding of this... (Comparative Study)
Comparative Study
C3 glomerulonephritis (C3GN) and dense deposit disease comprise the two classes of C3 glomerulopathy. Studies from Europe and Asia have aided our understanding of this recently defined disorder, but whether these data apply to a diverse United States patient population remains unclear. We, therefore, reviewed clinical and histopathological data, including generation of a C3 Glomerulopathy Histologic Index to score biopsy activity and chronicity, to determine predictors of progression to end-stage renal disease (ESRD) and advanced chronic kidney disease (CKD) in 111 patients (approximately 35% non-white) with C3 glomerulopathy: 87 with C3GN and 24 with dense deposit disease. Complement-associated gene variants and autoantibodies were detected in 24% and 35% of screened patients, respectively. Our C3 Glomerulopathy Histologic Index denoted higher activity in patients with C3GN and higher chronicity in patients with dense deposit disease. Over an average of 72 months of follow-up, remission occurred in 38% of patients with C3GN and 25% of patients with dense deposit disease. Progression to late-stage CKD and ESRD was common, with no differences between C3GN (39%) and dense deposit disease (42%). In multivariable models, the strongest predictors for progression were estimated glomerular filtration rate at diagnosis (clinical variables model) and tubular atrophy/interstitial fibrosis (histopathology variables model). Using our C3 Glomerulopathy Histologic Index, both total activity and total chronicity scores emerged as the strongest predictors of progression. Thus, in a large, diverse American cohort of patients with C3 glomerulopathy, there is a high rate of progression to CKD and ESRD with no differences between C3GN and dense deposit disease.
Topics: Adolescent; Adult; Atrophy; Autoantibodies; Biomarkers; Biopsy; Complement C3; Complement Pathway, Alternative; Disease Progression; Female; Fibrosis; Glomerulonephritis, Membranoproliferative; Humans; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Remission Induction; Renal Insufficiency, Chronic; Retrospective Studies; Risk Factors; Time Factors; Treatment Outcome; United States; Young Adult
PubMed: 29310824
DOI: 10.1016/j.kint.2017.10.022 -
Animals : An Open Access Journal From... Sep 2021In chronic wounds in humans, biofilm formation and wound chronicity are linked, as biofilms contribute to chronic inflammation and delayed healing. Biofilms are... (Review)
Review
In chronic wounds in humans, biofilm formation and wound chronicity are linked, as biofilms contribute to chronic inflammation and delayed healing. Biofilms are aggregates of bacteria, and living as biofilms is the default mode of bacterial life; within these aggregates, the bacteria are protected from both antimicrobial substances and the immune response of the host. In horses, delayed healing is more commonly seen in limb wounds than body wounds. Chronic inflammation and hypoxia are the main characteristics of delayed wound healing in equine limbs, and biofilms might also contribute to this healing pattern in horses. However, biofilm formation in equine wounds has been studied to a very limited degree. Biofilms have been detected in equine traumatic wounds, and recent experimental models have shown that biofilms protract the healing of equine limb wounds. Detection of biofilms within wounds necessitates advanced techniques that are not available in routine diagnostic yet. However, infections with biofilm should be suspected in equine limb wounds not healing as expected, as they are in human wounds. Treatment should be based on repeated debridement and application of topical antimicrobial therapy.
PubMed: 34679846
DOI: 10.3390/ani11102825 -
Journal of Clinical Medicine Jun 2020Ph+ chronic myeloid leukemia (CML) is a clonal myeloproliferative disease whose clinical course is characterized by progression disease from the early chronic phase (CP)...
Ph+ chronic myeloid leukemia (CML) is a clonal myeloproliferative disease whose clinical course is characterized by progression disease from the early chronic phase (CP) to the fatal blastic phase (BP). This programmed course is closely related to the translocation t(9;22)(q22;q11) and the resulting BCR-ABL1 fusion protein (p210) that drives the leukemic transformation of hematopoietic stem cells. Therefore, the cure of CML can only pass through the abrogation of the Ph+ clone. Allogeneic stem cell transplantation (allo-SCT) and interferon-alpha (IFNα) have been proven to reduce the Ph+ clone in a limited proportion of CML population and this translated in a lower rate of progression to BP and in a significant prolongation of survival. Tyrosine-kinase inhibitors (TKIs), lastly introduced in 2000, by preventing the disease blastic transformation and significantly prolonging the survival in up to 90% of the patient population, radically changed the fate of CML. The current therapy with TKIs induces a chronicization of the disease but several criticisms still persist, and the most relevant one is the sustainability of long-term therapy with TKIs in terms of compliance, toxicity and costs. The perspectives concern the optimization of therapy according to the age, the risk of disease, the potency and the safety profiles of the TKIs. The prolongation of survival is the most important end point which should be guaranteed to all patients. The treatment free remission (TFR) is the new goal that we would like to give to an increasing number of patients. The cure remains the main objective of CML therapy.
PubMed: 32498406
DOI: 10.3390/jcm9061709 -
Nephrology, Dialysis, Transplantation :... Nov 2023Glomerulonephritis (GN) is a diverse group of immune-mediated disorders. Currently, GN is classified largely by histological patterns that are difficult to understand...
Glomerulonephritis (GN) is a diverse group of immune-mediated disorders. Currently, GN is classified largely by histological patterns that are difficult to understand and teach, and most importantly, do not indicate treatment choices. Indeed, altered systemic immunity is the primary pathogenic process and the key therapeutic target in GN. Here, we apply a conceptual framework of immune-mediated disorders to GN guided by immunopathogenesis and hence immunophenotyping: (i) infection-related GN require pathogen identification and control; (ii) autoimmunity-related GN, defined by presence of autoantibodies and (iii) alloimmunity-related GN in transplant recipients both require the suppression of adaptive immunity in lymphoid organs and bone marrow; (iv) autoinflammation-related GN, e.g. inborn errors of immunity diagnosed by genetic testing, requires suppression of single cytokine or complement pathways; and (v) Monoclonal gammopathy-related GN requires B or plasma cell clone-directed therapy. A new GN classification should include disease category, immunological activity to tailor the use of the increasing number of immunomodulatory drugs, and chronicity to trigger standard chronic kidney disease care including the evolving spectrum of cardio-renoprotective drugs. Certain biomarkers allow diagnosis and the assessment of immunological activity and disease chronicity without kidney biopsy. The use of these five GN categories and a therapy-focused GN classification is likely to overcome some of the existing hurdles in GN research, management and teaching by reflecting disease pathogenesis and guiding the therapeutic approach.
Topics: Humans; Glomerulonephritis; Biomarkers; Autoantibodies; Renal Insufficiency, Chronic; Nephrectomy
PubMed: 37218714
DOI: 10.1093/ndt/gfad067 -
Frontiers in Toxicology 2023Chronic ocular pain is a common, debilitating chronic pain condition with significant morbidity and negative impact in patients' quality of life. Several, diverse types... (Review)
Review
Chronic ocular pain is a common, debilitating chronic pain condition with significant morbidity and negative impact in patients' quality of life. Several, diverse types of insults to the ocular surface can lead to acute, and under certain conditions to chronic ocular pain, and these include toxic irritants. Exposure of ocular surface to toxic irritants, in addition to direct tissue injury, carries the capacity to generated intense immune and neuronal responses with hyper-excitability, sensitization and chronic pain. Because, chronic ocular pain subsequent to toxic exposures is relatively unrecognized clinical entity, this brief review highlights pertinent concepts of its epidemiology, pathogenesis/pathophysiology, clinical progression, with recommendations for its clinical management that clinicians may find helpful. Suppression of pain signaling, generating neuronal sensitization, and prevention of chronicity of neuropathic pain is particularly emphasized in this respect.
PubMed: 37637478
DOI: 10.3389/ftox.2023.1188152 -
Journal of Evaluation in Clinical... Oct 2017An authentic sickness history is the vantage point for juxtaposing a biomedical and a biographical-phenomenological reading. What, in a biomedical framework, appears to...
An authentic sickness history is the vantage point for juxtaposing a biomedical and a biographical-phenomenological reading. What, in a biomedical framework, appears to be a longstanding state of comorbidity of different and unrelated types of diseases is rendered transparent in a biographical reading. This particular reading, evidencing the shortcomings of a biomedical framework regarding identifying the social sources of an increasingly complex burden of disease, is reflected upon in light of recent research in the neurosciences. Thus, the biomedical contribution to a sickness history is demonstrated, with its resultant multimorbidity, chronification, and complete incapacitation of a woman despite the continuing and nearly excessive involvement of the health care system.
Topics: Chronic Pain; Comorbidity; Humans
PubMed: 28497485
DOI: 10.1111/jep.12715