Homelessness: cause and effects

Canoso, Juan J.

doi:10.1007/s10067-020-05517-2

Cited by 9 publications

(16 citation statements)

References 5 publications

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“…Additionally, recent retrospective studies have also demonstrated the effectiveness of RTX in patients with anti-MDA5 antibodies [ 64 , 65 , 91 , 92 , 93 ]. A case series of four patients with amyopathic DM (ADM) with rapidly progressive ILD who failed to respond to high-dose GCs and immunosuppressants reported that RTX treatments improved or stabilized respiratory symptoms, pulmonary function tests, and HRCT images in all patients after 6 months to 2 years of follow-up [ 64 ].…”

Section: Treatmentmentioning

confidence: 99%

Management of Myositis-Associated Interstitial Lung Disease

Fujisawa

2021

Medicina

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Idiopathic inflammatory myopathies, including polymyositis (PM), dermatomyositis (DM), and clinically amyopathic DM (CADM), are a diverse group of autoimmune diseases characterized by muscular involvement and extramuscular manifestations. Interstitial lung disease (ILD) has major pulmonary involvement and is associated with increased mortality in PM/DM/CADM. The management of PM-/DM-/CADM-associated ILD (PM/DM/CADM-ILD) requires careful evaluation of the disease severity and clinical subtype, including the ILD forms (acute/subacute or chronic), because of the substantial heterogeneity of their clinical courses. Recent studies have highlighted the importance of myositis-specific autoantibodies’ status, especially anti-melanoma differentiation-associated gene 5 (MDA5) and anti-aminoacyl tRNA synthetase (ARS) antibodies, in order to evaluate the clinical phenotypes and treatment of choice for PM/DM/CADM-ILD. Because the presence of the anti-MDA5 antibody is a strong predictor of a worse prognosis, combination treatment with glucocorticoids (GCs) and calcineurin inhibitors (CNIs; tacrolimus (TAC) or cyclosporin A (CsA)) is recommended for patients with anti-MDA5 antibody-positive DM/CADM-ILD. Rapidly progressive DM/CADM-ILD with the anti-MDA5 antibody is the most intractable condition, which requires immediate combined immunosuppressive therapy with GCs, CNIs, and intravenous cyclophosphamide. Additional salvage therapies (rituximab, tofacitinib, and plasma exchange) should be considered for patients with refractory ILD. Patients with anti-ARS antibody-positive ILD respond better to GC treatment, but with frequent recurrence; thus, GCs plus immunosuppressants (TAC, CsA, azathioprine, and mycophenolate mofetil) are often needed in order to achieve favorable long-term disease control. PM/DM/CADM-ILD management is still a therapeutic challenge for clinicians, as evidence-based guidelines do not exist to help with management decisions. A few prospective clinical trials have been recently reported regarding the treatment of PM/DM/CADM-ILD. Here, the current knowledge on the pharmacologic managements of PM/DM/CADM-ILD was mainly reviewed.

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Section: Treatmentmentioning

confidence: 99%

Management of Myositis-Associated Interstitial Lung Disease

Fujisawa

2021

Medicina

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“…Although there has been a significant improvement in both patient and renal survival in patients with LN with the advent of cyclophosphamide-based and mycophenolate mofetil-based treatment regimens, there is still a substantial treatment-related morbidity and mortality [ 6 ]. We have shown, in a study that included 101 patients with severe proliferative LN, that an initial high-dose oral corticosteroid regimen (≥0.5 mg/kg/day in the first month of induction therapy) increased the risk for serious infections by 7.5-fold (HR, 7.57; 95% CI 1.64–34.8) [ 6 ]. Accordingly, continuous efforts have been made to refine the immunosuppressive regimens, e.g., by limiting cyclophosphamide and corticosteroids exposure, by switching to CD20-depleting or multitarget-based regimens [ 6 ].…”

Section: Transition From Bench To Bedside—novel Therapies In Lupusmentioning

confidence: 99%

“…We have shown, in a study that included 101 patients with severe proliferative LN, that an initial high-dose oral corticosteroid regimen (≥0.5 mg/kg/day in the first month of induction therapy) increased the risk for serious infections by 7.5-fold (HR, 7.57; 95% CI 1.64–34.8) [ 6 ]. Accordingly, continuous efforts have been made to refine the immunosuppressive regimens, e.g., by limiting cyclophosphamide and corticosteroids exposure, by switching to CD20-depleting or multitarget-based regimens [ 6 ]. After decades of negative trials, in which several new agents added to the current standard of care regimens (both cyclophosphamide-based and mycophenolate mofetil-based) failed to show an improvement in the treatment response rates, recent years brought ground-breaking results to the LN treatment [ 10 ].…”

Section: Transition From Bench To Bedside—novel Therapies In Lupusmentioning

confidence: 99%

“…All renal compartments can be injured in SLE, but lupus nephritis (LN) is the most frequent pattern of injury encountered, affecting up to 60% of patients [ 3 , 4 ]. LN is associated with significant morbidity and mortality in SLE, these patients having a worse survival compared to those without nephritis, among the contributors to death being both disease-related and treatment-related factors [ 4 , 5 , 6 ]. In our experience, the 10-year and 20-year renal and/or patient survival is approximately 70% and 60%, respectively [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

“…In our experience, the 10-year and 20-year renal and/or patient survival is approximately 70% and 60%, respectively [ 4 ]. Additionally, we showed that the treatment-related morbidity is substantial, the incidence rate of infections and serious infections being 26.6 and 9.56 events per 100 patient-years, respectively [ 6 ]. Nevertheless, both patient and renal survival significantly improved over the past decades with the advent of newer treatment strategies [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

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Advances in Lupus Nephritis Pathogenesis: From Bench to Bedside

Obrișcă

Sorohan

Tuţă

et al. 2021

IJMS

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Systemic lupus erythematosus (SLE) is the prototype of autoimmune disorders caused by a loss of tolerance to endogenous nuclear antigens triggering an aberrant autoimmune response targeting various tissues. Lupus nephritis (LN), a major cause of morbidity and mortality in patients with SLE, affects up to 60% of patients. The recent insights into the genetic and molecular basis of SLE and LN paved the way for newer therapies to be developed for these patients. Apart from the traditional B-cell-centered view of this disease pathogenesis, acknowledging that multiple extrarenal and intrarenal pathways contribute to kidney-specific autoimmunity and injury may help refine the individual therapeutic and prognostic characterization of such patients. Accordingly, the formerly induction-maintenance treatment strategy was recently challenged with the exciting results obtained from the trials that evaluated add-on therapy with voclosporin, belimumab, or Obinutuzumab. The scope of this review is to provide an insight into the current knowledge of LN pathogenesis and future therapeutic strategies.

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Pressure changes in the Kager fat pad at the extremes of ankle motion suggest a potential role in Achilles tendinopathy

Malagelada

Stephen

Dalmau-Pastor

et al. 2019

Knee Surg Sports Traumatol Arthrosc

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Introduction The Kager fat pad is one of the largest soft tissue structures local to the ankle joint, yet it is poorly understood. It has been hypothesised to have a role in Achilles tendinopathy. This study aimed to investigate the pressure areas in the Kager fat pad adjacent to the Achilles tendon and to assess the anatomy and deformation of the Kager fat pad in cadavers. Methods Twelve fresh frozen cadaveric ankles (mean age 44 years, range 38–51) were mounted in a customized testing rig, enabling plantar flexion and dorsiflexion of the ankle, with the Achilles tendon loaded. A needle tipped pressure sensor was inserted in two areas of the Kager fat pad under ultrasound guidance (retrocalcaneal bursa and at 3 cm proximal from Achilles insertion). Pressure readings were recorded at different flexion angles. Following testing, the specimens were dissected to expose the Kager fat pad and retrieve it for analysis. MRI images were also taken from three healthy volunteers and the Kager fat pad deformation examined. Results Mean pressures significantly increased in all specimens at terminal ankle plantar and dorsi flexion in both regions (p < 0.05). The Kager fat pad was consistently adherent to the Achilles at its posterior aspect for a mean length of 7.7 cm (SD 0.27, 89% of KFP length). The most distal part of the Kager fat pad was the exception and it detached from the Achilles to give way to the retroalcaneal bursa for a mean length of 0.92 cm (SD 0.24, 11% of KFP length). The bursal space is partially occupied by a constant ‘wedge’ extension of Kager fat pad. The mean volume of the whole Kager fat pad was 10.6 ml (SD 3.37). Video and MRI demonstrated that the Kager fat pad undergoes significant deformation during plantar flexion as it is displaced superiorly by the Achilles, with the wedge being forced into the retrocalcaneal bursal space. Conclusion The Kager fat pad does not remain static during ankle range of motion, but deforms and its pressure also changes. This observation supports the theory that it acts as a shock‐absorber to the Achilles tendon and pathological changes to the fat pad may be clinically important in the development of Achilles tendinopathy.

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Homelessness: cause and effects

Cited by 9 publications

References 5 publications

Management of Myositis-Associated Interstitial Lung Disease

Management of Myositis-Associated Interstitial Lung Disease

Advances in Lupus Nephritis Pathogenesis: From Bench to Bedside

Pressure changes in the Kager fat pad at the extremes of ankle motion suggest a potential role in Achilles tendinopathy

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