Data on neuro-Behçet’s disease in North Africa remain limited and fragmented. We conducted a systematic review and meta-analysis to estimate the frequency of neurologic involvement in North African patients with Behçet’s disease and to summarize the main clinical, cerebrospinal fluid, and imaging characteristics. PubMed, Scopus, and Web of Science databases were searched for studies reporting neuro-Behçet’s disease in North Africa. Proportions were pooled using a random-effects meta-analysis model to estimate overall pooled proportions (OPP). Heterogeneity was assessed using I2 statistics. The review protocol was registered in PROSPERO (CRD420261303759). Thirteen studies were included. Among 4262 patients with Behçet’s disease, the pooled proportion of Neuro-Behçet’s disease was 18.54

Introduction: Hantavirus infection is an uncommon zoonosis in Europe but remains an important cause of acute kidney injury, particularly in patients with environmental exposure to rodents. Renal involvement is the hallmark of the disease, although pulmonary manifestations may coexist and mimic immune-mediated pulmonary–renal syndromes, leading to diagnostic challenges in internal medicine. Case description: A 46-year-old previously healthy man living in a rural area was admitted for acute febrile illness with asthenia and myalgia. Initial investigations revealed severe thrombocytopenia and acute kidney injury with proteinuria and microscopic haematuria. A computed tomography scan of the chest and abdomen showed bilateral pulmonary abnormalities, consistent with an acute pulmonary–renal syndrome. Extensive immunological and infectious investigations excluded autoimmune disease and alternative infectious causes. Hantavirus infection was confirmed by positive IgM and IgG serology, with molecular identification of Puumala virus. Renal biopsy demonstrated moderate acute tubular necrosis with minimal interstitial inflammation and preserved glomeruli. The patient was treated with supportive care only, resulting in rapid clinical improvement and complete recovery of renal function. Conclusion: Hantavirus infection should be considered in patients presenting with acute pulmonary–renal syndrome, thrombocytopenia, and compatible epidemiological exposure. Early diagnosis allows appropriate supportive management, avoids unnecessary immunosuppressive therapy, and is associated with an excellent renal prognosis in Puumala virus infection.

Introduction: Lymphocytic-variant of hypereosinophilic syndrome (L-HES) is a clonal T-cell disorder driven by an aberrant Th2 response, typically featuring CD3- CD4+ T-cell expansion, eosinophil-mediated tissue injury, most commonly skin lesions, and lymphadenopathy. Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma of follicular helper T-cell origin; it can present with similar clinical features such as lymphadenopathy, rash and eosinophilia. Histological and immunophenotypic features may also be common in both diseases, thus creating a diagnostic overlap. Case description: We report the case of a 53-year-old man with a medical history of allergic rhinitis who developed a diffuse, persistent maculopapular rash with pruritis. Physical examination revealed inguinal lymphadenopathy without organomegaly, laboratory investigations demonstrated marked eosinophilia, and hypergammaglobulinemia, while additional testing excluded any infectious or autoimmune aetiologies. Lymphocytic immunophenotyping on peripheral blood and skin biopsy revealed a high proportion of CD3-CD4+ cells exhibiting a classic TH2 phenotype, consistent with L-HES. However, lymph node histology demonstrated architectural remodelling with intrafollicular infiltration by atypical T lymphocytes showing a T-cell follicular helper phenotype, findings indicative of AITL. The coexistence of L-HES and AITL was established. The patient underwent polychemotherapy, resulting in rapid clinical improvement of skin lesions with sustained remission at 6 months of follow up. Conclusion: L-HES and AITL may coexist, or L-HES may precede overt lymphoma, suggesting clonal evolution within a shared biological spectrum. This case highlights diagnostic pitfalls and emphasizes the need for integrated clinical, pathological, flow cytometric and molecular evaluation.

Behçet's disease (BD) is a chronic, multisystemic inflammatory vasculitis affecting veins and arteries. Its etiopathogenesis remains unclear but is thought to result from genetic predisposition combined with environmental triggers. Recent genome-wide association studies (GWAS) have linked various genetic polymorphisms (e.g., HLA*B51, ERAP1) to an increased risk of BD, with particular focus on cytokine-related gene variants. Infectious agents, such as Streptococcus species and herpes simplex virus, along with oral and intestinal dysbiosis and molecular mimicry, are key environmental triggers of innate immune inflammation, which is further amplified by adaptive immune responses. The innate immune system's primary cells, including neutrophils and NK cells, are upregulated, leading to an overproduction of proinflammatory cytokines. Additionally, an imbalance in T cell populations, characterized by a decrease in Tregs and expansion of Th1 and Th17 cells, contributes to disease pathogenesis. This review provides an overview of recent advances in understanding BD's etiopathogenesis.

Cogan Syndrome (CS) is a rare autoimmune systemic vasculitis affecting the inner ear and the eye with systemic manifestations affecting mainly young adults. The clinical presentation is historically classified in two subtypes. Typical CS associated interstitial keratitis with audio-vestibular symptoms with a 2-year maximum delay between these 2-organ involvements. Atypical CS subgroup associated inflammatory ocular disease in the absence of interstitial keratitis, audio-vestibular impairment, and systemic manifestations in a delay longer than 2 years between different organ manifestations. Neither diagnostic criteria nor specific biomarkers could lead to definite diagnosis. Cogan syndrome is a diagnosis of exclusion after a meticulous appropriate investigation to rule out other conditions. Disease prognosis is related to the risk of deafness and/or blindness as well as complications related to systemic vasculitis. Early recognition of this condition and early intervention can minimize disabling and irreversible damage. Treatment of CS is challenging, and the only available data comes from case reports and series. The aim of this review is to describe the clinical spectrum and outcome of CS through a summary of published case series, the differential diagnosis, and the therapeutic approaches with a special focus on the recent novel therapeutic options in the biological era.

BACKGROUND:The FIP1L1-PDFGRA (F/P)-associated hypereosinophilic syndrome (HES) is a rare condition. The F/P fusion gene testing is one of the first-line investigations in patients with unexplained eosinophilia and yields poor diagnostic performance. OBJECTIVE:To build and validate the factor interacting with PAPOLA and CPSF1 (FIP) score: a set of weighted criteria warranting testing for the F/P fusion gene. METHODS:We merged data from 151 patients with F/P-associated HES and 320 patients with either F/P-negative HES (n = 279) or hypereosinophilia of undetermined significance (n = 41). Training and validation cohorts (comprising, respectively, 90% and 10% of all patients) were randomly dichotomized. Variables with a P value less than .20 in univariate analysis were included in the multivariable forward-backward logistic regression model to assess their independent contribution to testing positive for the F/P fusion gene. Beta coefficients from multivariable logistic regression were used to assign points for the construction of the score. RESULTS:Age younger than 66 years, male sex, splenomegaly, lymphomatoid papulosis, absence of gastrointestinal involvement, high serum vitamin B12, high serum tryptase, and normal serum immunoglobulin E levels were the 8 variables retained in the model. The best cutoff value was greater than 48. The model yielded a sensitivity, specificity, positive predictive value, negative predictive value, and area under the curve, respectively, of 88.3%, 93.7%, 87.1%, 94.4%, and 0.962 in the training dataset and of 85.7%, 97.0%, 85.7%, and 97.0%, 0.986 in the validation dataset. CONCLUSIONS:The FIP score highlights the need for closely selecting patients with hypereosinophilia for whom F/P fusion gene testing should be performed, resulting in medical time reduction and substantial cost-savings.

La péricardite est une complication souvent asymptomatique au cours de la polyarthrite rhumatoïde. Elle évolue rarement vers la tamponnade ou vers la chronicité. Il existe peu de données sur la prise en charge thérapeutique de cette complication sérieuse. Récemment, quelques rares données évaluant la place de la biothérapie dans la péricardite rhumatoïde ont été publiées. Nous rapportons l'observation d'un patient avec une polyarthrite rhumatoïde immunopositive échappant à plusieurs lignes de traitement de fond qui développe une tamponnade qui récidive après drainage chirurgical. Seul une combothérapie par rituximab et anakinra a permis l'induction d'une rémission rhumatologique et une disparition de la péricardite.

Sarcoidosis is an inflammatory multisystemic granulomatosis of unknown cause, with a wide range of clinical features, characterized by the presence of non-caseating granulomas. Liver is the third involved organ after lungs and lymph nodes, with a reported prevalence of hepatic involvement in 5 to 25

Sarcoidosis is a chronic granulomatous inflammatory disease that primarily affects the lungs and skin. Cutaneous involvement occurs in approximately 30

BACKGROUND:Hypereosinophilic syndromes (HES) are a heterogenous group of eosinophilic disorders. To date, only retrospective studies of limited sample-size and/or follow-up duration are available. METHODS:The COHESion study is a national prospective multicenter multidisciplinary cohort recruiting both adults or children with the spectrum of eosinophilic disorders (including reactive HE/HES [HE/HES-R], idiopathic HES [HES-I], lymphocytic HES [HES-L], neoplastic HE/HES [HE/HES-N], HE of unknown significance [HE-US], as well as IgG4-related disease [IgG4RD] or ANCA-negative eosinophilic granulomatosis with polyangiitis [EGPA] overlaps). Patients are followed-up yearly. All data about final diagnosis, organ involvement assessments, and outcome profiles in HES-I were captured and analyzed centrally by HES expert centers. RESULTS:From May 2019 to November 2023, 779 patients were included. For this preliminary analysis, 550 cases were available for centralized review (mean ± SD age: 56 ± 18 years, 42% of female patients). The final diagnoses were HES-I (47%), HE/HES-R (16%), HE-US (15%), HE/HES-N (7%), HE/HES-L (6%), IgG4RD (2%), and ANCA-negative EGPA (7%). In the 258 HES-I patients, outcome profiles were classified as follows: 16.3% had a "single-flare" without further relapse, 28.3% had a "relapsing-remitting" disease when there was at least a 6-month period free of symptoms between two flares, 46.1% had a "persistent disease" requiring continuous treatment to avoid relapses (9.3% remained unclassified because of insufficient follow-up). CONCLUSIONS:The COHESion cohort is the first nationwide prospective multicenter study collecting data on the full spectrum of HE/HES disorders. This preliminary analysis confirms that idiopathic HES patients have various outcome profiles, suggesting different underlying pathophysiological mechanisms and the need of patient-specific management. TRIAL REGISTRATION:ClinicalTrials.gov identifier: NCT04018118.

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Background: The treatment and prognosis of cryoglobulinemia vasculitis (CryoVas) depend on etiology. Rituximab (RTX) and corticosteroids (CS) are the first line treatment for mixed essential (ME) CryoVas and connective tissue disease (CTD)-related CryoVas. The prognosis and long term outcomes of these forms of CryoVas are as yet unknown. Objectives: The aim of this study was therefore to describe the risk of relapse and treatment-related morbidities in patients with ME and CTD-related CryoVas. Methods: A retrospective study was conducted of 63 patients in remission of ME or CDT-related CryoVas after RTX-CS therapy, with a median follow-up time of 58 months (interquartile range, 33–88 months). Results: Thirty-nine out of 63 patients (62%) had a relapse a median of 42 (23–65) months after the initial flare. The relapse incidence was 38% at 2 years and 46% at 3 years. The factors associated with relapse were purpura at the time of the qualifying flare (HR, 2.2; 95% confidence interval (CI), 1.1–4.4; p = 0.002) and prior history of CryoVas flares (HR, 1.9; 95% CI, 1.0–3.7; p = 0.04). Maintenance therapy was associated with a lower risk of relapse 6–24 months after the initial flare (HR, 0.27; 95% CI, 0.09–0.78; p = 0.02), but not thereafter (HR, 2.0; 95% CI, 0.7–5.7; p = 0.21). The most common form of maintenance therapy was 500 mg RTX every 6 months. The most frequent complication was infection, and maintenance RTX therapy was associated with a higher risk of severe infection (HR, 2,2; 95% CI, 0.9–5,6; p = 0.08). Conclusion: In this group of patients in RTX-CS remission of ME and CTD-related CryoVas, relapses were common and the risk of relapse was significantly associated with purpura during the qualifying flare and a prior history of relapse. Maintenance RTX was associated with a lower risk of relapse but was also associated with an increased risk of severe infection. REFERENCES: [1] Saadoun D, Sellam J, Ghillani-Dalbin P, Crecel R, Piette JC, Cacoub P. Increased Risks of Lymphoma and Death Among Patients With Non–Hepatitis C Virus–Related Mixed Cryoglobulinemia. Arch Intern Med. 2006 Oct 23;166(19):2101–8. [2] Cacoub P, Comarmond C, Domont F, Savey L, Saadoun D. Cryoglobulinemia Vasculitis. Am J Med. 2015 Sep 1;128(9):950–5. [3] Terrier B, Krastinova E, Marie I, Launay D, Lacraz A, Belenotti P, et al. Management of noninfectious mixed cryoglobulinemia vasculitis: data from 242 cases included in the CryoVas survey. Blood. 2012 Jun 21;119(25):5996–6004. [4] Terrier B, Carrat F, Krastinova E, Marie I, Launay D, Lacraz A, et al. Prognostic factors of survival in patients with non-infectious mixed cryoglobulinaemia vasculitis: data from 242 cases included in the CryoVas survey. Ann Rheum Dis. 2013 Mar 1;72(3):374–80. [5] Quartuccio L, Bortoluzzi A, Scirè CA, Marangoni A, Del Frate G, Treppo E, et al. Management of mixed cryoglobulinemia with rituximab: evidence and consensus-based recommendations from the Italian Study Group of Cryoglobulinemia (GISC). Clin Rheumatol. 2023 Feb 1;42(2):359–70. [6] Terrier B, Marie I, Launay D, Lacraz A, Belenotti P, de Saint-Martin L, et al. Predictors of early relapse in patients with non-infectious mixed cryoglobulinemia vasculitis: Results from the French nationwide CryoVas survey. Autoimmun Rev. 2014 Jun 1;13(6):630–4. [7] Foessel L, Besancenot JF, Blaison G, Magy-Bertrand N, Jaussaud R, Etienne Y, et al. Clinical Spectrum, Treatment, and Outcome of Patients with Type II Mixed Cryoglobulinemia without Evidence of Hepatitis C Infection. J Rheumatol. 2011 Apr 1;38(4):716–22. [8] Visentini M, Tinelli C, Colantuono S, Monti M, Ludovisi S, Gragnani L, et al. Efficacy of low-dose rituximab for the treatment of mixed cryoglobulinemia vasculitis: Phase II clinical trial and systematic review. Autoimmun Rev. 2015 Oct;14(10):889–96. [9] Colantuono S, Mitrevski M, Yang B, Tola J, Carlesimo M, De Sanctis GM, et al. Efficacy and safety of long-term treatment with low-dose rituximab for relapsing mixed cryoglobulinemia vasculitis. Clin Rheumatol. 2017 Mar 1;36(3):617–23. Acknowledgements: NIL. Disclosure of Interests: Claire POGGI: None declared, Eric Hachulla BOEHRINGER INGELHEIM, GSK, SANOFI,, JANSSEN-CILAG, Bayer HealthCare SAS, GSK, BRISTOL MYERS SQUIBB, IQVIA Operations France, United Therapeutics Corporation, NOVARTIS PHARMA SAS, CHUGAI PHARMA FRANCE, ASTRAZENECA, MSD, JANSSEN-CILAG, Bayer HealthCare SAS, GSK, BRISTOL MYERS SQUIBB,, GENZYME, SANOFI, RE-IMAGINE Health Agency, Otsuka Pharmaceutical France SAS, AXONAL, PFIZER SAS, LIVE! BY GL EVENTS, SHIRE France S.A., Cemka, ROCHE SAS, Galapagos SASU, PATIENTYS, Alexandre Karras Alnylam France SAS, BOEHRINGER INGELHEIM FRANCE, NOVARTIS PHARMA SAS, ASTRAZENECA, Otsuka Pharmaceutical France SAS, LABORATOIRE GLAXOSMITHKLINE, PFIZER SAS, Vertex Pharmaceuticals Incorporated, TRAVERE THERAPEUTICS, INC., Retrophin, Inc, Antoine BRIANTAIS BOEHRINGER INGELHEIM FRANCE,, ROCHE SAS, LABORATOIRE GLAXOSMITHKLINE, Genzyme, Camille Ravaiau: None declared, Pierre GOBERT Alexion Pharma France, MENARINI FRANCE, SANOFI AVENTIS FRANCE, Alban Deroux VIFOR FRANCE, EUSA Pharma (France) SAS, BOEHRINGER INGELHEIM FRANCE, LABORATOIRE GLAXOSMITHKLINE, SANOFI AVENTIS FRANCE, EXELTIS SANTE, Celltrion Healthcare France SAS, SWEDISH ORPHAN BIOVITRUM, Sarah Nicolas HD MEDICAL, MSD FRANCE, Hélène François SANOFI AVENTIS FRANCE,, Matthieu Groh SANOFI AVENTIS FRANCE, LABORATOIRE GLAXOSMITHKLINE, ASTRAZENECA, CSL BEHRING SA, CHUGAI PHARMA FRANCE, BRISTOL-MYERS SQUIBB, Jonathan London AMICUS THERAPEUTICS SAS, CORIN FRANCE, AMICUS THERAPEUTICS SAS, CORIN FRANCE, JANSSEN-CILAG, AbbVie, Julien Campagne SHIRE France S.A., SANOFI AVENTIS FRANCE,, BOEHRINGER INGELHEIM FRANCE,, VIFOR FRANCE SA, SANDOZ, Alnylam France SAS, AMGEN, Jean-Sébastien Allain LEO Pharma, LABORATOIRE GLAXOSMITHKLINE, Emmanuelle Dernis BRISTOL-MYERS SQUIBB, LILLY FRANCE, MSD France, JANSSEN-CILAG, Galapagos SASU, AbbVie, NORDIC PHARMA SAS, UCB Pharma SA, CHUGAI PHARMA FRANCE, FRESENIUS KABI FRANCE, MSD France, BRISTOL-MYERS SQUIBB,, NOVARTIS PHARMA SAS, AMGEN SAS, MEDAC SAS, RE-IMAGINE Health Agency, Cécile-Audrey Durel VIFOR FRANCE, NOVARTIS PHARMA SAS, Genzyme, NOVARTIS PHARMA SAS, Genzyme, Takeda France, SHIRE France S.A., BOEHRINGER INGELHEIM FRANCE, Thomas Le Gallou NOVARTIS PHARMA SAS, LABORATOIRE GLAXOSMITHKLINE, Alexandre Curie PFIZER SAS, LABORATOIRE GLAXOSMITHKLINE, SHIRE France S.A., Philippe Kerschen: None declared, Noémie Gensous Alnylam France SAS, SWEDISH ORPHAN BIOVITRUM, NOVARTIS PHARMA SAS, AMGEN SAS, ASTRAZENECA, AMGEN SAS, Anne-Hélène Reboux: None declared, Hélène Béhal: None declared, Benjamin Terrier VIFOR, ASTRAZENECA, GSK, ASTRAZENECA, LFB BIOMEDICAMENTS, BRISTOL-MYERS SQUIBB, PFIZER SAS, Lilly France SAS, GRIFOLS France, Oséus, Terumo BCT Europe SA, SANOFI-AVENTIS RECHERCHE & DEVELOPPEMENT, BOEHRINGER INGELHEIM FRANCE, FRESENIUS KABI FRANCE, SWEDISH ORPHAN BIOVITRUM, BRISTOL-MYERS SQUIBB, NOVARTIS PHARMA SAS, ROCHE SUISSE, JANSSEN-CILAG, MSD France, RE-IMAGINE Health Agency, LFB BIOMEDICAMENTS, Thomas Quéméneur VIFOR, LEO Pharma, ASTRAZENECA, VIFOR, OVERCOME,, VIFOR, SANOFI, GENZYME, GSK.

Behcet disease (BD) is a systemic vasculitis which can involve many different organ systems. Neurological involvement (NBD) occurs in 5.3% to 59% of BD patients. The diagnosis is challenging especially in case of inaugural neurological presentation, and is based on a constellation of clinical, laboratory, and neuroimaging findings. NBD can be subdivided into parenchymal NBD through an immune mediated meningoencephalitis with a predilection to the brainstem, basal ganglia, thalamus, cranial nerves, and spinal cord involvement, and extraparenchymal NBD encompassing cerebral veinous thrombosis and intracranial arterial involvement. Brain magnetic resonance shows ill-defined areas of oedema with high signal intensity on T2-FLAIR images, isointense or hypointense in T1-weighted images in the basal ganglia area or in the brainstem, which may extend to the diencephalic structures. Swelling might be noticed. Hemorrhages can be seen, such as contrast enhancement (blood brain barrier disruption). Magnetic resonance venography and computerized tomographic angiography can be used to diagnose extraparenchymal NBD. Treatment of parenchymatous forms is based on glucocorticoids associated with oral immunosuppressants (azathioprine, mycophenolate mofetil or methotrexate) in mild forms, and intravenous cyclophosphamide or infliximab in severe forms. The management of cerebral thrombosis consists of steroids course associated with an oral anticoagulation. An early recognition of this condition is mandatory to initiate adequate therapies in order to improve outcomes and limit the risk of sequelae, relapses, or death. The aim of this review is to summarize a comprehensive review on the various neurological presentations of BD with emphasizes on diagnostic tools, prognosis, and therapeutic issues.

Introduction Le dupilumab est un anticorps monoclonal dirigé contre la sous-unité alpha du récepteur de l’interleukine (IL)-4, bloquant ainsi la signalisation induite par l’interleukine (IL)-4 et l’IL-13. Il a une autorisation de mise sur le marché pour la dermatite atopique modérée à sévère, l’asthme modéré à sévère, la polypose naso-sinusienne, l’œsophagite à éosinophiles et le prurigo nodulaire. Plusieurs cas de développement ou de rechute de maladies inflammatoires sous dupilumab ont été décrits à la suite de sa mise sur le marché. L’objectif de cette étude est de décrire les maladies inflammatoires systémiques survenant sous dupilumab. Patients et méthodes Nous avons réalisé une étude multicentrique rétrospective par un appel à observations afin de recueillir les observations de patients présentant une maladie inflammatoire systémique apparue ou ayant rechuté suite à la mise sous dupilumab. Nous avons ensuite effectué une étude de pharmacovigilance à l’aide de la base de données Vigibase (base de données mondiale de l’OMS) afin confirmer ou non certains signaux de pharmacovigilance. Nous avons étudié les Reporting Odds Ratios (ROR) des différentes pathologies suspectées en considérant comme un signal de pharmacovigilance celles dont le ROR était supérieur à 1. Résultats Nous avons recueilli par l’appel à observations 18 cas de maladies inflammatoires apparues sous dupilumab (âge médian 62,5 ans (écart interquartile 49–72,3), hommes 39 %, femmes 61 %). Un seul cas sur les 18 était une rechute (GEPA) de maladies systémiques, les autres cas étant des maladies nouvellement diagnostiquées. Il s’agissait par ordre décroissant de GEPA (n=6), artérite à cellules géantes (n=4), granulomatoses (n=2, une cutanée et une sarcoïdose), deux polyarthrites inclassées, un rhumatisme psoriasique, une maladie d’Addison, un purpura thrombopénique immunologique et une vascularite à éosinophiles. Le délai de survenue de la maladie après le début de traitement par dupilumab était de 5,5 mois en médiane (EIQ 3–-21).La survenue de ces maladies a conduit à l’arrêt du dupilumab dans 15/18 cas (83 %). Une corticothérapie orale seule a été introduite dans 11/18 cas (61 %), et dans 5 cas la prise en charge a reposé sur une corticothérapie associée à un autre traitement (rituximab dans 2 cas, mepolizumab dans 2 cas, benralizumab dans un cas et méthotrexate dans un cas). Un cas de sarcoïdose a régressé spontanément sans arrêter le dupilumab.L’analyse de la base de pharmacovigilance Vigibase a retrouvé un signal de pharmacovigilance pour les pathologies suivantes (par ordre décroissant) : la granulomatose éosinophilique avec polyangéite (ROR 27,9, IC95 % 20,4–38,2), les arthrites séronégatives (ROR 6,30, IC95 % 2,76–14,3), les granulomatoses cutanées (ROR 5,49, IC95 % 1,33–22,7), la maladie d’Addison (ROR 3,35, IC95 % 1,24–9,05), le syndrome de Sjögren (ROR 2,88, IC95 % 1,70–4,9), la sarcoïdose (ROR 2,36, IC 95 % 1,42–3,95), l’artérite à cellules géantes (ROR 2,2, IC95 % 1,19–4,16) et le lupus érythémateux disséminé (ROR 1,9, IC95 % 1,33–2,8). Conclusion Le dupilumab semble être associé à la survenue de novo ou la rechute de maladies inflammatoires systémiques. Il s’agit essentiellement de la granulomatose éosinophilique avec polyangéite, d’arthrites séronégatives, de granulomatoses cutanées, de la sarcoïdose, de l’artérite à cellules géantes, de la maladie d’Addison, du syndrome de Sjögren, ou du lupus érythémateux disséminé.