Publications by authors named "E Pillebout"

63 Publications

[Who can pretend knowing how to treat adult IgA vasculitis? What are the futures challenges?]

Rev Med Interne 2021 Nov 11. Epub 2021 Nov 11.

Service de Néphrologie, Hôpital Saint Louis, AP-HP, France.

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http://dx.doi.org/10.1016/j.revmed.2021.10.326DOI Listing
November 2021

Maintenance of a Gastric Pacemaker in the Excluded Stomach During a Roux-en-Y Gastric Bypass Procedure in a Patient with Obesity, Type 1 Diabetes and Refractory Gastroparesis.

Obes Surg 2021 Dec 6;31(12):5497-5499. Epub 2021 Oct 6.

Centre Hospitalier Universitaire Ambroise Paré, Service d'Endocrinologie Diabétologie et Nutrition, Assistance Publique-Hôpitaux de Paris, 9 avenue Charles De Gaulle, 92100, Boulogne Billancourt, France.

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http://dx.doi.org/10.1007/s11695-021-05726-xDOI Listing
December 2021

IgA vasculitis.

Semin Immunopathol 2021 Oct 25;43(5):729-738. Epub 2021 Jun 25.

Department of Dermatology and Venereology, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120, Halle/Saale, Germany.

IgA vasculitis (IgAV) is an inflammation of small vessels caused by perivascular deposition of IgA and activation of neutrophils. It may present as systemic vasculitis (IgAV - Henoch-Schönlein purpura) or as a variant restricted to the skin (skin-limited IgAV), while IgA nephropathy presents a variant restricted to the kidneys. Systemic IgAV affects children more frequently than adults (150 to 200 for 1; incidence 1 in 1 million/year). In the latter, disease more often leads to chronic renal disease. The dominant clinical features include round or oval and retiform palpable purpura predominantly on the lower legs, arthralgia or arthritis, gastrointestinal bleeding or pain and glomerulonephritis with mesangial IgA deposits (IgAVN). Pulmonary, cardiac, genital and neurological involvement occurs, but is rare. Immune complexes containing galactose-deficient IgA1 play a pivotal role in the pathophysiology of IgAV; via the Fc alpha receptor (CD89), they induce neutrophilic inflammation around cutaneous vessels and mesangial proliferation and inflammation in the glomerulus. In case of self-limited disease, only symptomatic treatment is recommended. Treatment of severe IgAV, nephritis or gastrointestinal manifestations, is not established, but some studies reported a benefit of corticosteroids, combined with immunosuppressive drugs. Short-term outcome depends on the severity of gastrointestinal manifestations, while long-term prognosis depends on the severity of nephritis.
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http://dx.doi.org/10.1007/s00281-021-00874-9DOI Listing
October 2021

IgA Vasculitis and IgA Nephropathy: Same Disease?

J Clin Med 2021 May 25;10(11). Epub 2021 May 25.

Nephrology Unit, Saint-Louis Hospital, 75010 Paris, France.

Many authors suggested that IgA Vasculitis (IgAV) and IgA Nephropathy (IgAN) would be two clinical manifestations of the same disease; in particular, that IgAV would be the systemic form of the IgAN. A limited number of studies have included sufficient children or adults with IgAN or IgAV (with or without nephropathy) and followed long enough to conclude on differences or similarities in terms of clinical, biological or histological presentation, physiopathology, genetics or prognosis. All therapeutic trials available on IgAN excluded patients with vasculitis. IgAV and IgAN could represent different extremities of a continuous spectrum of the same disease. Due to skin rash, patients with IgAV are diagnosed precociously. Conversely, because of the absence of any clinical signs, a renal biopsy is practiced for patients with an IgAN to confirm nephropathy at any time of the evolution of the disease, which could explain the frequent chronic lesions at diagnosis. Nevertheless, the question that remains unsolved is why do patients with IgAN not have skin lesions and some patients with IgAV not have nephropathy? Larger clinical studies are needed, including both diseases, with a common histological classification, and stratified on age and genetic background to assess renal prognosis and therapeutic strategies.
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http://dx.doi.org/10.3390/jcm10112310DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8197792PMC
May 2021

[Contrast-induced acute kidney injury].

Nephrol Ther 2021 Jun 11;17(3):191-198. Epub 2021 May 11.

Service de transplantation, hôpital Necker, 149, rue de Sèvre, 75015 Paris, France.

The nephrotoxicity of iodinated contrast agent/media is defined by acute renal failure occurring within 48 to 72 hours after injection of iodized contrast product, in the absence of other etiology. The risk factors for contrast agent renal injury must systematically be sought before the exam. The presence of risk factors, including the existence of a renal failure defined by a creatinine clearance (eGFR) of less than 60 mL/min/1.73 m, requires to take prevention measures including hydration. If eGFR is less than 30 mL/min/1.73 m, the advice of a nephrologist is necessary.
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http://dx.doi.org/10.1016/j.nephro.2021.04.001DOI Listing
June 2021
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