Antifibroblast growth factor receptor 3 antibodies identify a subgroup of patients with sensory neuropathy

Antoine, Jean‐Christophe; Boutahar, Nadia; Lassablière, François; Reynaud, Evelyne; Férraud, Karine; Rogemond, Véronique; Paul, Stéphane; Honnorat, Jérôme; Camdessanché, Jean‐Philippe

doi:10.1136/jnnp-2014-309730

Cited by 52 publications

(69 citation statements)

References 35 publications

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“…Length‐dependent SFN had IENFD that was more reduced at distal sites (ankle or calf) than at proximal sites (lower or upper thigh). For non–length‐dependent SFN, IENFD was prominently reduced at proximal sites . Clinical characterizations of patients were as follows: length‐dependent, if the symptoms were present initially only in the feet, although the symptoms may have spread over time; and non–length dependent, if symptoms began in the arms, trunk, or face.…”

Section: Methodsmentioning

confidence: 99%

Cryptogenic small‐fiber neuropathies: Serum autoantibody binding to trisulfated heparan disaccharide and fibroblast growth factor receptor‐3

et al. 2019

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Introduction Causes of small‐fiber peripheral neuropathies (SFN) are often undefined. In this study we investigated associations of serum autoantibodies, immunoglobulin G (IgG) vs fibroblast growth factor receptor‐3 (FGFR‐3), and immunoglobulin M (IgM) vs trisulfated heparan disaccharide (TS‐HDS) in cryptogenic SFN. Methods One hundred fifty‐five patients with biopsy‐proven SFN and no identified cause for their neuropathy were blindly tested for serum IgM vs TS‐HDS and IgG vs FGFR‐3. Results Forty‐eight percent of SFN patients had serum antibodies, 37% with IgM vs TS‐HDS and 15% with IgG vs FGFR‐3. TS‐HDS antibodies were more frequent in SFN patients than in controls (P = .0012). Both antibodies were more common in females, and with non–length‐dependent nerve pathology. Nintey‐two percent of patients with acute‐onset SFN had serum IgM vs TS‐HDS. Discussion Autoantibodies directed against TS‐HDS and FGFR‐3 suggest an immune disorder in otherwise idiopathic SFN. Serum IgM vs TS‐HDS may be a marker for SFN with an acute onset.

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Section: Methodsmentioning

confidence: 99%

Cryptogenic small‐fiber neuropathies: Serum autoantibody binding to trisulfated heparan disaccharide and fibroblast growth factor receptor‐3

et al. 2019

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“…The disease has been slowly progressing over the last three years even though the patient is still responding to periodic immunoglobulin infusions. The autoantibodies that are reactive to the sensory neurons identified in paraneoplastic SG are well known as biological markers capable of distinguishing immune-mediated SG from other aetiologies [7]. Antoine JC et al (2015) have recently described the diagnostic accuracy of serum antibodies against the intracellular domains of fibroblast growth factor receptor 3 (FGFR3; anti-FGFR3 Abs) to identify a patient subgroup that has developed a sensory neuron disorder, which suggests that in the future other immune markers could be detected in patients that initially appear to have idiopathic SG.…”

Section: Discussionmentioning

confidence: 99%

“…Even when clinical criteria aid in differentiating SG from other neuropathies, an etiological diagnosis remains elusive. Thus, there is a need for biological markers than can distinguish immune-mediated SG from other etiologies [7].…”

Section: Introductionmentioning

confidence: 99%

Paraneoplastic and Idiopathic Ganglionopathy: Importance of Differential Diagnosis

Gasque¹,

Schmidt²,

Carvalho³

2015

J Neurol Neurophysiol

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Sensory ganglionopathies (SG) may occur in association with different diseases and are characterized by the degeneration of the primary sensory neurons located in the dorsal root ganglia. The most important associated conditions are paraneoplastic SG, HIV infection, Sjogren's syndrome, and cisplatin or pyridoxine toxicity. Even when clinical criteria help differentiate SG from other neuropathies, an etiological diagnosis remains elusive. Thus, there is a need to identify biological markers than can distinguish immune-mediated SG from other etiologies. Objectives: The present study of two cases of SG compares their neurological outcomes with their treatment responses in accordance with the etiology of each one. Methods: evaluate the clinical presentation and examination results to be able to define the etiology and institute early treatment. Results: To differentiate paraneoplastic and idiopathic causes, more precise imaging techniques and paraneoplastic antibody tests are required. These diagnostic tools might be helpful in early diagnosis and treatment, thus affording the best chance of stabilizing the neurological symptoms. Conclusions: The identification of paraneoplastic antibodies before the onset of cancer can reduce the percentage of cases misdiagnosed as idiopathic, leading to early treatment and perhaps a more favorable prognosis.

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“…Dann kann eine immunsuppressive Therapie erfolgreich sein [2]. immunentzündliche ursache Die Vermutung eines spezifischen immunentzündlichen Mechanismus als Ursache einer Neuronopathie wurde kürzlich mit den Nachweis von Antikörpern gegen den Fibroblasten Wachstumsfaktorrezeptor 3 weiter bestätigt [9]. Toxisch Pyridoxin (B6) kann selten auch in niedriger Dosis von 200 mg/Tag eine Neuronopathie mit schwere Ataxie verursachen [11].…”

Section: Ursachenunclassified

Sensible Neuronopathie – Fallberichte und Review

Büchner

2017

Klin Neurophysiol

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ZusammenfassungDie sensible Neuronopathie ist klinisch gekennzeichnet durch Sensibilitätsstörungen dominant des Vibrations- und Lageempfindens, verursachend eine sensible Ataxie. Neurophysiologisch ist sie charakterisiert durch den Ausfall der sensiblen Nervenleitung bei normaler motorischer Neurografie. Neuropathologisch besteht eine Degeneration der Hinterstrangganglien. Eine „small fibre“ Neuropathie mit neuropathischen Schmerzen ist häufig. Neben hereditären und toxischen Ursachen sind Tumorerkrankungen (paraneoplastisch) und das Sjögren-Syndrom häufig, allerdings bleibt in rund der Hälfte aller Fälle die Ursache ungeklärt. Ist die Ursache behandelbar kann eine Verschlechterung verhindert werden und in wenigen Fällen kommt es zu Verbesserungen. An Fallberichten wird die sehr variable klinische Präsentation und der Verlauf der Erkrankung vorgestellt. Die Kriterien zur Differenzialdiagnose einer Polyneuropathie werden erklärt. Ein pragmatisches Vorgehen für die Suche nach der Ursache wird vorgeschlagen.

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Antifibroblast growth factor receptor 3 antibodies identify a subgroup of patients with sensory neuropathy

Abstract: A anti-FGFR3 Abs identify a subgroup of patients with SN in whom an underlying autoimmune disorder affecting sensory neurons in the dorsal root and trigeminal nerve ganglia is suspected.

Cited by 52 publications

References 35 publications

Cryptogenic small‐fiber neuropathies: Serum autoantibody binding to trisulfated heparan disaccharide and fibroblast growth factor receptor‐3

Cryptogenic small‐fiber neuropathies: Serum autoantibody binding to trisulfated heparan disaccharide and fibroblast growth factor receptor‐3

Paraneoplastic and Idiopathic Ganglionopathy: Importance of Differential Diagnosis

Sensible Neuronopathie – Fallberichte und Review

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