ZEITSCHRIFT FUR RHEUMATOLOGIE

[Switching Biologics: this is how I proceed]
Aries P
Implementation of the new DGRh S2e guideline on diagnostics and treatment of adult-onset Still's disease in Germany : Implications for clinical practice in rheumatology
Friedrich R, Kernder A, Blank N, Ernst D, Henes J, Keyßer G, Klemm P, Krusche M, Meinecke A, Rech J, Schulz N, Schomburg D, Vordenbäumen S and Feist E
Adult-onset Still's disease (AOSD) is a rare autoinflammatory disease. Since it can lead to variable organ involvement, including life-threatening complications, and due to newly available therapeutic approaches, the German Society for Rheumatology and Clinical Immunology (Deutsche Gesellschaft für Rheumatologie und klinische Immunologie; DGRh) issued a newly developed S2e guideline in December 2022.
[Not Available]
Global prevalence and solutions for burnout among rheumatologists
Takefuji Y
Burnout among rheumatologists is globally prevalent, driven by low personal accomplishment, younger age, dissatisfaction with the specialty, low income, long hours, emotional exhaustion, and depersonalization. Mitigation strategies include addressing modifiable risk factors, implementing organizational measures, investing in well-being, assessing individual grit, and managing workload with virtual care platforms.
[T-cell large granular lymphocytic leukemia and Felty's syndrome in rheumatoid arthritis]
Gernert M, Schwaneck EC and Schmalzing M
Neutropenia in rheumatoid arthritis (RA) is a problem that often needs to be addressed. Side effects of basic antirheumatic treatment, infections or substrate deficiencies are common causes; however, T‑cell large granular lymphocytic (T-LGL) leukemia, a mature T‑cell neoplasm, can also lead to autoimmune cytopenia. The T‑LGL leukemia can be associated not only with RA but also with other autoimmune diseases or neoplasms. Correspondingly, increases in clonal T cells, natural killer T (NKT) cells and LGL cells are found in the peripheral blood. A T‑cell receptor PCR and flow cytometry (or at least a blood smear) are therefore necessary to diagnose T‑LGL leukemia. The presence of clonal T cells alone is usually not pathological. A distinction must be made from Felty's syndrome (consisting of the clinical triad of arthritis, leukopenia, splenomegaly), which does not require the two T‑LGL leukemia criteria mentioned. The treatment for both entities (with underlying RA) is methotrexate and, if insufficiently effective, rituximab.
[Not Available]
[Not Available]
[Criteria for the authorization of training in medical specialist competence in internal medicine and rheumatology-A position paper of the German Society for Rheumatology and Clinical Immunology]
Pfeil A, Fleck M, Aringer M, Baraliakos X, Ernst D, Haase I, Hillebrecht C, Hoyer BF, Keyßer G, Kötter I, Krause A, Krusche M, Lorenz HM, Proft F, Schuch F, Vossen D, Voormann A, Wagner U, Wollenhaupt J, Specker C, and
The model advanced training regulations define the content of advanced training to achieve the qualification of medical specialist in internal medicine and rheumatology. There are currently no criteria for issuing the authorization in advanced training. This position paper describes the criteria proposed by the German Society for Rheumatology and Clinical Immunology (DGRh), which should be the foundation for the issuance of authorization for advanced training in the field of internal medicine and rheumatology and for the assessment of the duration. The model advanced training regulations 2018 and the advanced training plan recommended by experts function as the basis for this. Based on the criteria, the authorization for advanced training to advanced specialist training in internal medicine and rheumatology can be allocated in a standardized, graded and transparent manner throughout Germany. This enables an optimal quality of advanced training in rheumatology, which can be adapted to the future developments in the discipline.
[Chronic pain syndrome in musculoskeletal diseases-how different are fibromyalgia and long Covid?-Part 1]
Braun J
Chronic pain is a common problem in rheumatology. Nociceptive pain is distinguished from neuropathic and nociplastic pain. Mechanistically, the former is explained by persistent inflammation, for example. Included in the second category is nerve damage of various causes. In contrast, nociplastic pain is not caused by tissue damage or a lesion in the somatosensory nerve system. It is caused by an altered sensation of pain through the modulation of stimulus processing. The concept of central sensitization, together with further neurobiological and psychosocial mechanisms, best explains such pain conditions. Fibromyalgia (FM) plays a big part in rheumatology - on the one hand, as a differential diagnosis, and on the other, because the management of inflammatory rheumatic conditions is made more difficult by the simultaneous occurrence of FM. In the context of the coronavirus pandemic, persistent pain syndromes with similarities to FM have been described after COVID-19 infection. There is an increasing scientific controversy whether the so-called long Covid syndrome is an actual entity or "only" a variant of FM. This discussion and the current state of knowledge on the problem are the subject of this review.
[Quintessence of the new guidelines on physical training and fracture prophylaxis]
Lange U, Reißhauer A and Kemmler W
The guidelines on physiotherapy and exercise for osteoporosis from 2008 have recently been extensively revised on the basis of new scientific findings and possible applications. The S3 guidelines have not yet been approved by consensus and the planned completion date (Association of the Scientific Medical Societies in Germany, AWMF online, registry number 183-002) is autumn 2024. Based on the publication in Issue 3 Osteology (August 2023), key points of the guidelines on physical training and fracture prophylaxis are summarized in abridged form. These are practice-oriented, evidence-based recommendations for optimal training for fracture prevention.
[Influencing fracture healing by specific osteoporosis medications]
Stumpf U, Schmidmaier R, Taipaleenmäki H, Böcker W, Kurth A and Hesse E
Osteoporosis is a widespread disease defined by a reduction in bone mass and structure, thereby increasing the risk of fragility fractures. Treatment typically involves specific medications, which either inhibit bone resorption (antiresorptive) or stimulate bone formation (anabolic) and may potentially influence the healing of osteoporotic fractures. On the other hand, metabolic disorders, immune system dysfunctions or circulatory problems can impair fracture healing. Therefore, the targeted use of osteoporosis medications could be a strategy to promote the healing of impaired fractures.
[Indications and limitations of conservative and invasive treatment of the inflammatory shoulder joint and the shoulder girdle]
Hassel K
An inflammatory rheumatic shoulder can be assessed as a forgotten joint. Apparent problems and deformities of the hands and feet are prioritized in the perception of rheumatic patients. In contrast, however, involvement of the shoulder joint in the context of an inflammatory rheumatic disease is very high with up to 85% [2]. Loss of shoulder function and pain can be well compensated for a long time. This means that further diagnostics are only carried out when the joint is already destroyed and joint-preserving treatment options are obsolete. The various tools of evidence-based conservative treatment can be used to relieve pain and improve function. The cause of joint destruction, inflammatory synovitis, must be treated with medication or, if there is no response to basic immunomodulatory treatment, invasively. In order to contain further destruction of the joint, injections of glucocorticoids and radiosynoviorthesis are initially carried out. This should be followed by arthroscopic synovectomy of the shoulder joint due to better results, especially in early stages of destruction (LDE 0-3).
[Septic musculoskeletal complications under immunomodulating treatment]
Kernder A and Kneitz C
Infections are an important cause of morbidity and mortality in patients with inflammatory rheumatic diseases. Among these, musculoskeletal infections represent a relevant proportion as patients with rheumatoid arthritis face an increased risk of developing septic arthritis and prosthesis infections. The causes are multifactorial. In addition to immunosuppressive treatment, risk factors of infection in rheumatoid arthritis (RA) patients include repeated intra-articular joint punctures, an increased rate of joint replacement surgery, damaged joint structure and comorbidities. The use of glucocorticoids and tumor necrosis factor alpha (TNF-alpha) inhibitors, especially in the first 6 months of treatment, increase the risk of septic arthritis and periprosthetic joint infections. In addition, an increased disease activity could also be identified as a risk factor. Under immunosuppressive therapy rare pathogens such as Candida and mycobacteria can cause the infection and should be considered when there is a lack of clinical response to antibiotic treatment.
[Chronic pain syndrome in musculoskeletal diseases-how different are fibromyalgia and long COVID?-Part 2]
Braun J
Acute and chronic pain play an important part in the care of patients with musculoskeletal diseases. For rheumatologists this represents a frequent challenge. For the management of chronic pain conditions in rheumatology those that cannot be explained by objective tissue damage are particularly important-which makes patients' subjective assessment of pain a central building block of the diagnosis. For the diagnosis of fibromyalgia (FM) standardized questionnaires such as the Widespread Pain Index (WPI) and the Symptom Severity Score (SSS) are used. In connection with the recent global SARS-CoV‑2 pandemic protracted courses and health problems have been described, which have been termed long COVID syndrome and have some similarities but, as is shown in the following, also demonstrate some differences from FM. There has recently been an interesting scientific controversy that culminated in a pros and cons session at the EULAR congress 2024, following several publications. The arguments and citations exchanged have served as the basis for the overview produced here, which is intended to offer rheumatologists confronted with such clinical pictures assistance with the assessment of these diseases, even if the results of the studies presented are definitely controversial.
[Not Available]
[Not Available]
[Not Available]
[Histopathological diagnostics of infections in rheumatology]
Blümke L, Renz N and Krenn V
The histopathological differential diagnoses of inflammatory infectious and inflammatory noninfectious diseases of the musculoskeletal system, particularly infectious and noninfectious arthritis, soft tissue inflammation and osteomyelitis in rheumatology are presented with a focus on the differential diagnostic possibilities and limitations; however, a diverse spectrum of pathogenic mechanisms underly these diseases, which can present with similar inflammatory response patterns. This wide spectrum of inflammatory pathogenesis of infectious and noninfectious diseases includes diseases such as rheumatoid arthritis, gouty arthritis, osteomyelitis and pyoderma gangrenosum, which cannot clinically be manifested thus necessitating a histopathological clarification. In terms of tissue sampling the following general principle applies: the larger the tissue sample and the more diverse the sites of tissue extraction, the more conclusive are the histopathological diagnostics. This diagnostic approach to infections, especially in a rheumatological context, is generally considered complementary and even supplementary to microbiological diagnostics. Furthermore, consideration of the virulence-resistance relationship, which can alter the inflammatory pattern, is of additional relevance. Consequently, definitive causal diagnostics are only achievable within the clinical, rheumatological, microbiological, laboratory medical and infectiological context.
Effect of urate-lowering therapy on all-cause and CVD-specific mortality in gout and hyperuricemia: a meta-analysis
Lee YH and Song GG
The aim of this study was to assess the relationships between urate-lowering therapy (ULT) and both all-cause and cardiovascular disease (CVD)-specific mortality in patients diagnosed with gout or hyperuricemia.
[Influence of the treatment setting on the treatment of patients with rheumatoid arthritis or psoriatic arthritis within the delegation to rheumatological specialist assistants - A post hoc analysis of the StärkeR study]
Shabani R, Mai A, Denz R, Timmesfeld N, Braun J and Krause D
The StärkeR study has shown the non-inferiority of a team-based form of care with delegation to rheumatological specialist assistants (RFA) compared to standard care in patients with rheumatoid arthritis (RA) or psoriatic arthritis (PsA).
History of antineutrophil cytoplasmic autoantibodies : Milestones in rheumatology
de Groot K, Csernok E and van der Woude D
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are autoimmune inflammatory small-vessel disorders with potentially life-threatening organ manifestations. Recent disease definitions and classification criteria allow distinction between granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and non-granulomatous microscopic polyangiitis (MPA). The discovery of ANCA-autoantibodies directed against proteolytic enzymes of neutrophil granules-has enabled earlier diagnosis of AAV and paved the way to stage-adapted treatments. ANCA testing initially relied on different immunofluorescence patterns, i.e., cytoplasmic ANCA (C-ANCA) vs. perinuclear ANCA (P-ANCA), in ethanol-fixed neutrophils. This is nowadays outperformed by well-standardized immunoassays against the ANCA target antigens proteinase 3 (PR3) and myeloperoxidase (MPO) for the diagnosis of small-vessel vasculitides. The discovery of ANCA has contributed substantially to unravelling the pathogenesis of AAV, which comprises neutrophil degranulation, NETosis with concurrently amplified ANCA antigen presentation, and intra- and transmural vascular inflammation involving the alternative complement system in susceptible individuals. There is a genetic disposition concerning certain HLA alleles and polymorphisms of the proteinase 3 gene. Furthermore, epigenetic modifications impact on disease activity and relapse. During follow-up, the ANCA titer is not a reliable mirror of disease activity; however, PR3-ANCA positivity is associated with a greater likelihood of relapse and a better treatment response to rituximab as compared to cyclophosphamide/azathioprine. Within the past 60 years, the discovery of ANCA has revolutionized the ability to diagnose, understand, classify, and treat AAV in a targeted manner.