Inflammation

Rheumatoid Arthritis in Adults

Nathan Hinkle — Fri, 11 Sep 2026 05:00:00 +0000

Date Added:

September 11, 2026

Journal/Publication:

JAMA

Publisher:

The American Medical Association

Publication Date:

September 10, 2026

Pages:

E1-E15

URL:

Rheumatoid Arthritis in Adults A Review

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

doi: 10.1001/jama.2026.15455

Keywords

Arthritis, Rheumatoid

MeSH

RPR Commentary: A review of what we currently understand about rheumatoid arthritis in adults. James W. Mold, MD, MPH

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Importance Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation and destruction of cartilage and adjacent bone and can lead to irreversible disability. Rheumatoid arthritis affects 0.53% of adults worldwide and 0.74% of US adults.

Observations Rheumatoid arthritis is more common among females than males (2:1) and has a peak incidence at ages 55 to 75 years. Rheumatoid arthritis can affect all synovial joints, and extra-articular involvement may include rheumatoid nodules, vasculitis, and rheumatoid lung disease. At diagnosis, approximately 40% to 60% of patients have autoantibodies (eg, rheumatoid factor and/or anticitrullinated peptide antibodies). There are no formal diagnostic criteria for RA, so the diagnosis is based on clinical history, characteristic joint swelling in proximal interphalangeal, metacarpophalangeal, and/or wrist joints and often presence of autoantibodies and elevated C-reactive protein levels. Early diagnosis, ideally within 6 weeks of symptom onset, allows rapid initiation of therapy with disease-modifying antirheumatic drugs (DMARDs), which inhibit inflammation and decrease the risk of joint destruction. The goal of treatment is to achieve at least 50% improvement in disease activity by 3 months and remission or low disease activity at 6 months, measured by validated indexes such as the Clinical Disease Activity Index (CDAI). The European Alliance of Associations for Rheumatology recommends starting treatment with methotrexate, 7.5 mg to 10 mg orally weekly, increasing to 20 mg to 25 mg weekly within 4 to 8 weeks, and considering addition of short-term glucocorticoids (eg, prednisone, 5-7.5 mg/d), tapered and discontinued within 3 months, or 1 intramuscular injection of 80 mg to 160 mg depot methylprednisolone. For patients with contraindications to methotrexate, sulfasalazine (2-4 g/d) or leflunomide (20 mg/d) is recommended. With treatment, about 40% of patients with newly diagnosed RA achieve CDAI remission within 6 months. Patients who do not achieve remission with first-line DMARDs should be prescribed biological DMARDs (eg, tumor necrosis factor α inhibitors, costimulation inhibitors, interleukin 6 receptor inhibitors, anti-CD20–targeting B cells), or Janus kinase (JAK) inhibitors (in patients not at high risk of thromboembolism, cardiovascular disease, or malignancy). With addition of biological DMARDs or JAK inhibitors to first-line DMARDs, overall remission or low disease activity rates increase to approximately 80%.

Conclusions and Relevance Rheumatoid arthritis is a chronic autoimmune disease that causes joint destruction. First-line initial therapy is methotrexate, with consideration of glucocorticoids as additive therapy. For patients who do not achieve remission with this initial treatment, adding biological DMARDs or JAK inhibitors increases overall remission or low disease activity rates to 80%.

Author/s:

Josef S. Smolen, Andreas Kerschbaumer, Daniel Aletaha

IgA Nephropathy in Adults: A Review

Megan George — Wed, 04 Mar 2026 18:10:22 +0000

Date Added:

March 4, 2026

Journal/Publication:

JAMA

Publication Date:

January 26, 2026

URL:

IgA Nephropathy in Adults: A Review

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

doi:10.1001/jama.2025.25020

Keywords

Antigen-Antibody Complex

IgA Nephropathy

Renal Insufficiency

Angiotensin Receptor Antagonists

renin-angiotensin system

MeSH

Glomerulonephritis

IGA

Antigen-Antibody Complex

Inflammation

Scarring

renal insufficiency

Angiotensin Receptor Antagonists

renin-angiotensin system

blood pressure

Adults

Humans

A comprehensive review of what we know about IgA nephropathy. James W. Mold, MD, MPH

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Importance IgA nephropathy (IgAN) is a chronic kidney disease involving deposition of IgA-containing immune complexes in the glomerulus, causing glomerular inflammation and scarring. It is the most common immune-mediated glomerular disease worldwide, and affects an estimated 198 887 to 208 184 persons in the US. Up to 50% of patients with IgAN develop kidney failure within 10 years of diagnosis.

Observations IgAN typically presents with nephritic syndrome and usually occurs in younger adults, with a mean age at diagnosis of 34 to 45 years. Incidence is highest in East Asia. Approximately 60% of cases are detected incidentally with hematuria or proteinuria on urinalysis. Up to 30% of patients present with episodic visible hematuria, often concomitantly with an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria). Less common presentations include nephrotic syndrome (<5%) and rapidly progressive glomerulonephritis (<5%). When IgAN is suspected (due to hematuria, proteinuria, or reduced kidney function), initial workup should include quantification of proteinuria and assessment for other causes of nephritic syndrome (eg, lupus nephritis). Adults with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy. The diagnosis of primary IgAN is based on presence of IgA-dominant immune deposits in the glomerular mesangium after excluding other causes of this histologic appearance, ie, IgA vasculitis, IgA-dominant infection-related glomerulonephritis, and secondary IgAN from diseases such as cirrhosis, inflammatory bowel disease, celiac disease, infection (eg, viral hepatitis), and autoimmune diseases (eg, axial spondyloarthritis). Based on the Kidney Disease: Improving Global Outcomes 2025 clinical practice guideline for the management of IgAN, treatment for patients with proteinuria greater than 0.5 g per day includes behavioral modifications (eg, dietary sodium <2 g/d, smoking cessation, weight control, exercise), antihypertensive medications for goal blood pressure less than 120/70 mm Hg, and therapies to reduce the formation of IgA-containing immune complexes (eg, targeted-release budesonide), decrease glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage existing IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor or dual endothelin angiotensin receptor antagonist [eg, sparsentan] alone or in combination with a sodium-glucose cotransporter 2 inhibitor).

Conclusions and Relevance IgAN is the leading cause of immune-mediated glomerular disease worldwide. Patients with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy to confirm the diagnosis. Treatment of IgAN includes behavioral modifications, blood pressure management, and therapies to decrease formation of IgA-containing immune complexes (eg, targeted-release budesonide), reduce immune complex–mediated glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor, dual endothelin angiotensin receptor antagonist, and sodium-glucose cotransporter 2 inhibitor).

Author/s:

Sinead Stoneman, Jia Wei Teh, Michelle Marie O’Shaughnessy

Calcium pyrophosphate deposition disease

Megan George — Mon, 02 Feb 2026 15:53:10 +0000

Date Added:

February 2, 2026

Journal/Publication:

Canadian Medical Association Journal

Publication Date:

February 2, 2026

URL:

Calcium pyrophosphate deposition disease

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

https://doi.org/10.1503/cmaj.250933

Keywords

pseudogout

calcium pyrophosphate deposition disease

MeSH

Calcium Pyrophosphate

adrenal cortex hormones

Inflammation

Adults

Humans

Calcium Pyrophostphate Deposition Disease

Pseudogout

A concise review of calcium pyrophosphate deposition disease ("pseudogout"). James W. Mold, MD, MPH

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Calcium pyrophosphate deposition (CPPD) disease is caused by CPP crystal accumulation in musculoskeletal tissues, leading to inflammation
Symptomatic CPPD disease (formerly known as “pseudogout”) is more common in older than younger adults and typically affects joints with previous damage. Chondrocalcinosis visible on radiographs affects 10% of adults and 50% of those older than 80 years, but most people are asymptomatic and findings are noted incidentally.1

The most common presentation is acute inflammatory monoarthritis affecting the wrists or knees, which resolves within 4 weeks
Extra-articular structures can also be affected, leading to acute inflammatory tendinitis. Crowned dens syndrome comprises 5% of CPPD disease presentations and can mimic bacterial meningitis, manifesting with acute cervical neck pain, fever, and elevated inflammatory markers with CPPD at C1 to C2, seen on computed tomography. The chronic (> 3 mo) inflammatory phenotype presents with hand or wrist symmetric polyarthritis, or with recurrent flares, and can be misdiagnosed as seronegative rheumatoid arthritis. Calcium pyrophosphate deposition disease and osteoarthritis can co-exist — underlying CPPD disease should be considered in patients with osteoarthritis at atypical locations (e.g., metacarpophalangeal joints, wrists, ankles, shoulders, elbows).2

Diagnosis can be confirmed with CPP crystals identified from synovial fluid, or the presence of the crowned dens syndrome
Although used for research, the 2023 Classification Criteria have high sensitivity (99.2%) and specificity (92.5%), thereby providing a diagnostic framework.2 Supportive diagnostic features include acute knee or wrist inflammatory arthritis in an older adult, osteoarthritis at atypical areas, or CPPD on imaging.3

Patients younger than 60 years at diagnosis should be assessed for associated metabolic diseases
Investigations for secondary causes of CPPD disease include calcium (hypercalcemia), parathyroid hormone (hyperparathyroidism), ferritin, transferrin saturation (hemochromatosis), magnesium (hypomagnesemia), and alkaline phosphatase (hypophosphatasia).2

Corticosteroids, colchicine, and nonsteroidal antiinflammatory drugs can treat acute flares4
Inflammatory arthritis lasting more than 3 months or recurrent flares (> 2/yr) should prompt rheumatology referral for consideration of chronic suppressive colchicine, hydroxychloroquine, or methotrexate (Appendix 1, available at www.cmaj.ca/lookup/doi/10.1503/cmaj.250933/tab-related-content).5

Author/s:

Timothy S.H. Kwok, Gregory Choy

What Is Diverticulitis?

Megan George — Fri, 14 Nov 2025 19:07:17 +0000

Date Added:

November 14, 2025

Journal/Publication:

JAMA Patient Page

Publication Date:

November 13, 2025

URL:

What Is Diverticulitis?

Type:

Patient Education Materials

Format:

Poster

DOI (1):

10.1001/jama.2025.17403

Keywords

Gastroenterology

Diverticulitis

Diverticulum

PMID (1):

41231515

MeSH

diabetes mellitus, type 2

Analgesics

analgesics, opioid

Anti-Inflammatory Agents

Anti-Inflammatory Agents, Non-Steroidal

Diverticulitis

Diverticulitis, Colonic

risk factors

Diverticulum, colon

Inflammation

Ehlers-Danlos Syndrome

Information for patients about diverticulitis. James W. Mold, MD, MPH

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Diverticulitis involves inflammation of outpouchings of the intestinal wall, a condition known as diverticulosis.

Risk factors for diverticulosis include being older than 65 years, obesity (body mass index [BMI] of 30 or more), high blood pressure, type 2 diabetes, certain medications (such as opioids, steroids, and nonsteroidal anti-inflammatory drugs [NSAIDs]), connective tissue diseases (such as polycystic kidney disease, Marfan syndrome, and Ehlers-Danlos syndrome), and specific genetic variants.1

By age 60 years, nearly 60% of people have diverticulosis, most often on the left side of the colon. About 1% to 4% of people with diverticulosis develop diverticulitis in their lifetime. Acute diverticulitis affects about 180 per 100 000 people in the US each year, resulting in approximately 200 000 hospitalizations annually.

Author/s:

Shreya Narayanan, Christopher D. Jackson, MD

The effectiveness and safety of methotrexate in the intervention of osteoarthritis: A systematic review and meta-analysis of randomized controlled trials

Megan George — Tue, 14 Oct 2025 13:08:01 +0000

Date Added:

October 14, 2025

Journal/Publication:

Medicine

Publication Date:

October 10, 2025

URL:

The effectiveness and safety of methotrexate in the intervention of osteoarthritis: A systematic review and meta-analysis of randomized controlled trials

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

10.1097/MD.0000000000044994

Keywords

MeSH

The findings of this meta-analysis suggest that methotrexate is both safe and effective for treatment of pain and joint stiffness in patients with osteoarthritis. James W. Mold, MD, MPH

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Background:
Osteoarthritis (OA) is a prevalent chronic joint disorder among middle-aged and older adults, characterized by progressive cartilage degeneration, subchondral bone remodeling, and osteophyte formation, leading to joint pain, stiffness, dysfunction, and reduced quality of life. With the global aging population, OA imposes a growing socioeconomic burden, yet no disease-modifying therapy is currently available—particularly for moderate-to-severe stages. Emerging evidence implicates synovial inflammation as a central contributor to OA symptoms and progression, raising interest in methotrexate (MTX), a well-established, low-dose anti-inflammatory agent used safely in rheumatoid arthritis. Preliminary studies suggest MTX may alleviate OA-related pain, but findings from randomized controlled trials (RCTs) have been inconsistent and limited in number. Given recent new RCTs and the heterogeneity of existing outcomes, an updated systematic review and meta-analysis is urgently needed to clarify the efficacy and safety of MTX in OA and inform future clinical trial design.

Methods:
PubMed, ClinicalTrials, Web of Science, Cochrane Library and other databases were searched to find randomized controlled trials (RCT) of MTX treatment of OA. Methodological quality was assessed using the Cochrane "risk of bias" assessment tool, and the meta-analysis was conducted using Review Manager (RevMan) version 5.3 (The Cochrane Collaboration, London, UK).

Results:
Fifteen RCTs involving 1591 participants were included in this review. The meta-analysis results showed that the ineffective rate in the experimental group was lower [RR: 0.40 (0.24, 0.67), P = .004]; the VAS in the experimental group was lower [WMD: −0.66 (−1.08, −0.24), P = .002]; the WOMAC score-stiffness in the experimental group was lower [WMD: −0.72 (−1.04, −0.41), P < .00001]; the WOMAC score-function in the experimental group was lower [WMD: −7.72 (−13.56, −1.87), P = .01]. The adverse events in the experimental group were not statistically significant compared with the control group [RR: 1.04 (0.77, 1.42), P = .78].

Conclusion:
MTX demonstrates potential in effectively alleviating pain, improving joint function, and slowing disease progression in patients with OA. Its safety profile is comparable to that of control treatments, making it a viable and reliable therapeutic option worthy of broader clinical application.

Author/s:

Wan, Lifei, Yang, Qianyue, Yang, Kailin, Zeng, Liuting, Sun, Lingyun

Prostatitis: A Review

Megan George — Tue, 12 Aug 2025 13:07:09 +0000

Date Added:

August 12, 2025

Journal/Publication:

JAMA

Publication Date:

August 11, 2025

URL:

Prostatitis: A Review

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

10.1001/jama.2025.11499

Keywords

PMID (1):

40788632

MeSH

urinary tract infections

anti-bacterial agents

Escherichia coli

Urinary Retention

A review of our current understanding of prostatitis. James W. Mold, MD, MPH

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Importance Prostatitis is defined as infection, inflammation, or pain of the prostate gland and affects approximately 9.3% of men in their lifetime.

Observations Acute bacterial prostatitis consists of a urinary tract infection (UTI) that includes infection of the prostate, typically associated with fever or chills and caused by gram-negative bacteria, such as Escherichia coli, Klebsiella, or Pseudomonas, in 80% to 97% of cases. First-line therapy for acute prostatitis is broad-spectrum intravenous or oral antibiotics, such as intravenous piperacillin-tazobactam, ceftriaxone, or oral ciprofloxacin, which has a 92% to 97% success rate when prescribed for 2 to 4 weeks for people with febrile UTI and acute prostatitis. Chronic bacterial prostatitis is defined as a persistent bacterial infection of the prostate, typically presenting as recurrent UTIs from the same strain. Up to 74% of chronic bacterial prostatitis diagnoses are due to gram-negative organisms, such as E coli. First-line therapy for chronic bacterial prostatitis is a minimum 4-week course of levofloxacin or ciprofloxacin. Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) presents as pelvic pain or discomfort for at least 3 months and is associated with urinary symptoms, such as urinary frequency. CP/CPPS is diagnosed when evaluation, including history and physical examination, urine culture, and postvoid residual measurement, does not identify other causes for the symptoms, such as infection, cancer, urinary obstruction, or urinary retention. The National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) measures symptom severity (scale of 0-43), with a 6-point change considered clinically meaningful. First-line oral therapy for CP/CPPS with urinary symptoms is α-blockers (eg, tamsulosin, alfuzosin; ΔNIH-CPSI score difference vs placebo = −10.8 to −4.8). Other oral therapies are associated with modest changes in NIH-CPSI score compared with placebo, including anti-inflammatory drugs (eg, ibuprofen; ΔNIH-CPSI score difference = −2.5 to −1.7), pregabalin (ΔNIH-CPSI score difference = −2.4), and pollen extract (ΔNIH-CPSI score difference = −2.49).

Conclusions and Relevance Prostatitis includes acute bacterial prostatitis, chronic bacterial prostatitis, and CP/CPPS, each of which is diagnosed and treated differently. First-line treatments are broad-spectrum antibiotics for acute bacterial prostatitis (such as piperacillin-tazobactam, ceftriaxone, or ciprofloxacin), at least 4 weeks of fluoroquinolones for chronic bacterial prostatitis, and α-blockers for CP/CPPS with urinary symptoms.

Author/s:

Benjamin J Borgert, Eric M Wallen, Minh N Pham

Uveitis in Adults

Hope Smashey — Tue, 01 Jul 2025 17:07:23 +0000

Date Added:

July 1, 2025

Journal/Publication:

JAMA

Publication Date:

May 28, 2025

URL:

Uveitis in Adults

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

10.1001/jama.2025.4358

Keywords

human leukocyte antigen

PMID (1):

40434762

MeSH

human leukocyte antigen

corticosteroid

antimicrobial

Inflammation

An evidence-based review of the diagnosis, causes, and treatment of uveitis in adults. James W. Mold, MD, MPH

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Importance: Uveitis is characterized by inflammation of the uvea—the middle portion of the eye composed of the iris, ciliary body, and choroid—causing eye redness, pain, photophobia, floaters, and blurred vision. Untreated uveitis may cause cataracts, glaucoma, macular edema, retinal detachment, optic nerve damage, and vision loss.

Observations: Uveitis predominantly affects individuals aged 20 to 50 years. Anterior uveitis affects the iris and ciliary body (41%-60% of cases); intermediate uveitis affects the pars plana (attachment point of vitreous humor) and peripheral retina (9%-15%); posterior uveitis involves the choroid and/or retina (17%-23%); and panuveitis involves all uveal layers (7%-32%). Uveitis is classified as noninfectious or infectious, with toxoplasmosis, herpes, tuberculosis, and HIV comprising 11% to 21% of infectious cases in high-income countries and 50% in low- and middle-income countries. Incidence and prevalence of uveitis are influenced by genetic factors (eg, human leukocyte antigen–B27), environmental factors (eg, air pollution), and infection rates. In the US and Europe, 27% to 51% of uveitis cases are idiopathic, and 37% to 49% are associated with systemic disease, such as axial spondyloarthritis. Treatment goals are to induce and maintain remission while minimizing corticosteroid use to reduce corticosteroid-related adverse effects. Infectious uveitis requires systemic antimicrobial treatment. Active inflammatory disorders associated with uveitis should be treated by the appropriate specialist (eg, rheumatologist). Treatment for uveitis depends on subtype; anterior uveitis is treated with topical corticosteroids, and mild intermediate uveitis may be monitored without initial treatment. Patients with moderate to severe intermediate uveitis, posterior uveitis, and panuveitis are at high risk of sight-threatening complications and require systemic and/or intravitreal corticosteroids and immunosuppressive agents. For posterior uveitis, first-line therapy with disease-modifying antirheumatic drugs such as methotrexate achieved remission of inflammation in 52.1% (95% CI, 38.6%-67.1%) of patients, and mycophenolate mofetil controlled inflammation in 70.9% (95% CI, 57.1%-83.5%). In patients who do not improve or worsen with first-line therapy, adalimumab extended time to treatment failure to 24 weeks vs 13 weeks with placebo and reduced frequency of treatment failure from 78.5% to 54.5% (P < .001).

Conclusions and Relevance: Uveitis is characterized by inflammation of the uvea and primarily affects adults aged 20 to 50 years. For noninfectious anterior uveitis, corticosteroid eyedrops are first-line treatment. For posterior noninfectious uveitis, disease-modifying antirheumatic drugs are first-line therapy; biologics such as adalimumab are second-line treatment for patients with inflammation refractory to treatment. Uveitis caused by systemic infection should be treated with antimicrobials, and local or systemic steroids may be used depending on the severity of uveitis and the specific microorganism.

Author/s:

Panayiotis Maghsoudlou, Simon J. Epps, Catherine M. Guly

Dupilumab for COPD with Blood Eosinophil Evidence of Type 2 Inflammation

Alex Haga — Sun, 30 Jun 2024 18:27:10 +0000

Date Added:

June 30, 2024

Journal/Publication:

New England Journal of Medicine

Publication Date:

May 20, 2024

Issue:

Volume:

390

URL:

Dupilumab for COPD with Blood Eosinophil Evidence of Type 2 Inflammation

Type:

Clinical Research Results

Format:

Article

DOI (1):

10.1056/NEJMoa2401304

Keywords

PMID (1):

38767614

MeSH

Antibodies

Monoclonal

Humanized* / adverse effects

Humanized* / therapeutic use

Eosinophils*

Forced Expiratory Volume / drug effects

Inflammation

Leukocyte Count

Pulmonary Disease

Chronic Obstructive* / blood

Dupilumab (Dupixent) appears to reduce exacerbations and improve FEV1 in patients with COPD with elevated blood eosinophil counts. James W. Mold, MD, MPH

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Background: Dupilumab, a fully human monoclonal antibody that blocks the shared receptor component for interleukin-4 and interleukin-13, key and central drivers of type 2 inflammation, has shown efficacy and safety in a phase 3 trial involving patients with chronic obstructive pulmonary disease (COPD) and type 2 inflammation and an elevated risk of exacerbation. Whether the findings would be confirmed in a second phase 3 trial was unclear.

Methods: In a phase 3, double-blind, randomized trial, we assigned patients with COPD who had a blood eosinophil count of 300 cells per microliter or higher to receive subcutaneous dupilumab (300 mg) or placebo every 2 weeks. The primary end point was the annualized rate of moderate or severe exacerbations. Key secondary end points, analyzed in a hierarchical manner to adjust for multiplicity, included the changes from baseline in the prebronchodilator forced expiratory volume in 1 second (FEV1) at weeks 12 and 52 and in the St. George's Respiratory Questionnaire (SGRQ; scores range from 0 to 100, with lower scores indicating better quality of life) total score at week 52.

Results: A total of 935 patients underwent randomization: 470 were assigned to the dupilumab group and 465 to the placebo group. As prespecified, the primary analysis was performed after a positive interim analysis and included all available data for the 935 participants, 721 of whom were included in the analysis at week 52. The annualized rate of moderate or severe exacerbations was 0.86 (95% confidence interval [CI], 0.70 to 1.06) with dupilumab and 1.30 (95% CI, 1.05 to 1.60) with placebo; the rate ratio as compared with placebo was 0.66 (95% CI, 0.54 to 0.82; P<0.001). The prebronchodilator FEV1 increased from baseline to week 12 with dupilumab (least-squares mean change, 139 ml [95% CI, 105 to 173]) as compared with placebo (least-squares mean change, 57 ml [95% CI, 23 to 91]), with a significant least-squares mean difference at week 12 of 82 ml (P<0.001) and at week 52 of 62 ml (P = 0.02). No significant between-group difference was observed in the change in SGRQ scores from baseline to 52 weeks. The incidence of adverse events was similar in the two groups and consistent with the established profile of dupilumab.

Conclusions: In patients with COPD and type 2 inflammation as indicated by elevated blood eosinophil counts, dupilumab was associated with fewer exacerbations and better lung function than placebo.

Author/s:

Surya P Bhatt, Klaus F Rabe, Nicola A Hanania, Claus F Vogelmeier, Mona Bafadhel, Stephanie A Christenson

Systemic Lupus Erythematosus: A Review

Alex Haga — Tue, 16 Apr 2024 18:50:07 +0000

Date Added:

April 16, 2024

Journal/Publication:

JAMA

Publisher:

JAMA

Publication Date:

April 8, 2024

URL:

Systemic Lupus Erythematosus: A Review

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

10.1001/jama.2024.2315

Keywords

A review of current knowledge about the diagnosis and management of systemic lupus erythematosus. James W. Mold, MD, MPH

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Importance
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by inflammation and immune-mediated injury to multiple organ systems, including the mucocutaneous, musculoskeletal, hematologic, and kidney systems. Approximately 3.4 million people worldwide have received a diagnosis of SLE.

Observations
Approximately 90% of people with SLE are female. Although there are no uniformly accepted diagnostic criteria for SLE, the 2019 European Alliance of Associations for Rheumatology (formerly the European League Against Rheumatism)/American College of Rheumatology classification criteria developed for scientific study are an estimated 96.1% sensitive and 93.4% specific for SLE. These classification criteria include both clinical factors, such as fever, cytopenia, rash, arthritis, and proteinuria, which may be indicative of lupus nephritis; and immunologic measures, such as SLE-specific autoantibodies and low complement levels. Approximately 40% of people with SLE develop lupus nephritis, and an estimated 10% of people with lupus nephritis develop end-stage kidney disease after 10 years. The primary goal of treatment is to achieve disease remission or quiescence, defined by minimal symptoms, low levels of autoimmune inflammatory markers, and minimal systemic glucocorticoid requirement while the patient is treated with maintenance doses of immunomodulatory or immunosuppressive medications. Treatment goals include reducing disease exacerbations, hospitalizations, and organ damage due to the disease or treatment toxicity. Hydroxychloroquine is standard of care for SLE and has been associated with a significant reduction in mortality. Treatments in addition to hydroxychloroquine are individualized, with immunosuppressive agents, such as azathioprine, mycophenolate mofetil, and cyclophosphamide, typically used for treating moderate to severe disease. Three SLE medications were recently approved by the Food and Drug Administration: belimumab (for active SLE in 2011 and for lupus nephritis in 2020), voclosporin (for lupus nephritis), and anifrolumab (for active SLE).

Conclusions and Relevance
Systemic lupus erythematosus is associated with immune-mediated damage to multiple organs and increased mortality. Hydroxychloroquine is first-line therapy and reduces disease activity, morbidity, and mortality. When needed, additional immunosuppressive and biologic therapies include azathioprine, mycophenolate mofetil, cyclophosphamide, belimumab, voclosporin, and anifrolumab.

Author/s:

Siegel, C.H., Sammaritano, L.R.

What Is Ulcerative Colitis?

Erin Blanchette — Mon, 12 Feb 2024 16:55:58 +0000

Date Added:

February 12, 2024

Journal/Publication:

JAMA

Publisher:

American Medical Association

Publication Date:

February 2, 2024

Issue:

Volume:

330

Pages:

951-965

URL:

What Is Ulcerative Colitis?

Type:

Patient Education Materials

Format:

Article

DOI (1):

10.1001/jama.2023.23814

Keywords

ulcerative colitis

Diarrhea

Gastroenterology

Inflammatory Bowel Disease

PMID (1):

38306113

MeSH

Information for patients about ulcerative colitis. James W. Mold, MD, MPH

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This JAMA Patient Page describes the condition of ulcerative colitis and its symptoms, diagnosis, and treatment options.

Author/s:

Rebecca Voelker

Allopurinol Prevents Cirrhosis-Related Complications: A Quadruple Blind Placebo-Controlled Trial

Erin Blanchette — Tue, 05 Dec 2023 20:09:29 +0000

Date Added:

December 5, 2023

Journal/Publication:

The American Journal of Medicine

Publisher:

Elsevier

Publication Date:

October 11, 2023

URL:

Allopurinol Prevents Cirrhosis-Related Complications: A Quadruple Blind Placebo-Controlled Trial

Type:

Clinical Research Results

Format:

Article

DOI (1):

10.1016/j.amjmed.2023.09.016

Keywords

PMID (1):

37832758

MeSH

Allopurinol dramatically reduces the rate of complications from hepatic cirrhosis. James W. Mold, MD, MPH

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Background: Complications associated with liver cirrhosis are various and potentially fatal. The treatment options to counteract hepatic decompensation are limited. Therefore, the study aimed to explore the use of allopurinol in preventing the recurrence of liver cirrhosis-related complications.

Methods: One hundred patients with hepatic decompensation were randomized into 1:1 ratio to receive either allopurinol 300 mg or placebo tablets once daily for 6 months. The primary endpoint was the incidence of cirrhosis-related complications (overt ascites, spontaneous bacterial peritonitis, variceal bleeding, hepatorenal syndrome, and hepatic encephalopathy).

Results: Six months following treatment, allopurinol reduced the relative risk (RR) of any first complication experienced after enrollment by 56% (hazard ratio [HR] 0.44; 95% confidence interval [CI], 0.27-0.62); P ˂ .001). Allopurinol decreased the RR of overt ascites by 67% (HR 0.33; 95% CI, 0.0098-0.94); P = .039] and reduced the RR of spontaneous bacterial peritonitis by about 75% (HR 0.25; 95% CI, 0.05-0.76; P = .01). Likewise, allopurinol was linked to an 80% reduction in the RR of developing hepatorenal syndrome (HR 0.2; 95% CI, 0.04-0.87; P = .033).

Conclusion: Allopurinol significantly decreased the recurrence of overall liver cirrhosis-related complications. Therefore, allopurinol may constitute a promising agent for patients with hepatic decompensation. These positive outcomes could be a result of its ability to reduce bacterial translocation and inflammation.

Author/s:

Khadija A M Glal, Sahar M El-Haggar, Sherief M Abd-Elsalam, Tarek M Mostafa

COVID-19–Associated Multisystem Inflammatory Syndrome in Children — United States, March–July 2020

Brian Desmarais — Tue, 11 Aug 2020 16:18:53 +0000

Date Added:

August 11, 2020

Journal/Publication:

Morbidity and Mortality Weekly Report

Publisher:

Centers for Disease Control and Prevention

Publication Date:

August 7, 2020

URL:

COVID-19–Associated Multisystem Inflammatory Syndrome in Children — United States, March–July 2020

Type:

Clinical Research Results

Format:

Article

DOI (1):

http://dx.doi.org/10.15585/mmwr.mm6932e2

MeSH

health personnel

Early Diagnosis

Public Health Practice

A summary from the CDC of what is currently known about COVID-19-related Multisystem Inflammatory Syndrome in Children (MIS-C) in the U.S. James W. Mold, MD, MPH

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Summary

What is already known about this topic?

Multisystem inflammatory syndrome in children (MIS-C) is a rare but severe condition that has been reported approximately 2–4 weeks after the onset of COVID-19 in children and adolescents.

What is added by this report?

Most cases of MIS-C have features of shock, with cardiac involvement, gastrointestinal symptoms, and significantly elevated markers of inflammation, with positive laboratory test results for SARS-CoV-2. Of the 565 patients who underwent SARS-CoV-2 testing, all had a positive test result by RT-PCR or serology.

What are the implications for public health practice?

Distinguishing MIS-C from other severe infectious or inflammatory conditions poses a challenge to clinicians caring for children and adolescents. As the COVID-19 pandemic continues to expand in many jurisdictions, health care provider awareness of MIS-C will facilitate early recognition, early diagnosis, and prompt treatment.

Author/s:

Godfred-Cato, S., Bryant, B., Leung, J.

Interventions for hand eczema

Brian Desmarais — Wed, 05 Jun 2019 20:27:09 +0000

Date Added:

June 5, 2019

Journal/Publication:

Cochrane Systematic Review

Publication Date:

April 26, 2019

URL:

Interventions for hand eczema

Type:

Meta-analyses, Reviews, and Guidelines

Format:

Article

DOI (1):

10.1002/14651858.CD004055.pub2.

Keywords

MeSH

Calcineurin Inhibitors/therapeutic use

Eczema/drug therapy

Emollients/therapeutic use

Immunosuppressive Agents/therapeutic use

Severity of Illness Index

Emollients

A Cochrane review of current RCT evidence regarding treatment of hand eczema. James W. Mold, MD, MPH

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Abstract

BACKGROUND:

Hand eczema is an inflammation of the skin of the hands that tends to run a chronic, relapsing course. This common condition is often associated with itch, social stigma, and impairment in employment. Many different interventions of unknown effectiveness are used to treat hand eczema.

OBJECTIVES:

To assess the effects of topical and systemic interventions for hand eczema in adults and children.

SEARCH METHODS:

We searched the following up to April 2018: Cochrane Skin Group Specialised Register, CENTRAL, MEDLINE, Embase, AMED, LILACS, GREAT, and four trials registries. We checked the reference lists of included studies for further references to relevant trials.

SELECTION CRITERIA:

We included randomised controlled trials (RCTs) that compared interventions for hand eczema, regardless of handeczema type and other affected sites, versus no treatment, placebo, vehicle, or active treatments.

DATA COLLECTION AND ANALYSIS:

We used standard methodological procedures expected by Cochrane. Primary outcomes were participant- and investigator-rated good/excellent control of symptoms, and adverse events.

Author/s:

Christoffers, W.A., Coenraads, P.J., Svensson, Å., Diepgen, T.L., Dickinson-Blok, J.L., Williams, H.C., Xia, J.