Acute autonomic neuropathy associated with a high serum bradykinin level and positive anti-nuclear and anti-DNA antibodies titers.

Otokida, Koroku; Yoshida, Hiroaki; Sato, Norio; Kutsuzawa, Shigeo; Isagozawa, Shigeaki; Yamada, Michio; Kato, Masataka

doi:10.2169/internalmedicine1962.29.560

Cited by 6 publications

(2 citation statements)

References 11 publications

(10 reference statements)

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“…[11][12][13][14][15] An autoimmune mechanism has been suggested as a causal mechanism in both POTS and CFS, 2,3,7,14,16 due to frequent findings of autoantibodies (including ANA) in POTS/CFS patients. [17][18][19][20][21][22] More specifically, ganglionic A3 acetylcholine receptor antibodies are found in at least one in seven POTS patients. 7 Moreover, various autoantibodies, including those directed against cardiac proteins, 21 b1/2-adrenergic, M2/3 muscarinic 23 and N-type acetylcholine receptors, 7 have been identified in POTS patients, strengthening the idea of POTS as member of the autoimmune autonomic neuropathies family.…”

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confidence: 99%

Postural Orthostatic Tachycardia Syndrome (POTS) – A novel member of the autoimmune family

Dahan

Tomljenovic

Shoenfeld

2016

Lupus

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Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous disorder of the autonomic nervous system in which a change from the supine position to an upright position causes an abnormally large increase in heart rate or tachycardia (30 bpm within 10 min of standing or head-up tilt). This response is accompanied by a decrease in blood flow to the brain and hence a spectrum of symptoms associated with cerebral hypoperfusion. Many of these POTS-related symptoms are also observed in chronic anxiety and panic disorders, and therefore POTS is frequently under- and misdiagnosed.

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confidence: 99%

Postural Orthostatic Tachycardia Syndrome (POTS) – A novel member of the autoimmune family

Dahan

Tomljenovic

Shoenfeld

2016

Lupus

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“…BK was further investigated and reported to reduce blood pressure and cause the slow contraction of the gut and was hence named BK (brady = slow, and kinin = move) (15). Previously, increased levels of BK were reported in patients with acute autonomic neuropathy (16), and the authors suggested its association with SLE. Several studies reported the role of angiotensin-converting enzyme (ACE) gene polymorphisms in SLE, but thus far, no study has directly measured the levels of BK and BK-des-arg-9 in SLE or RA (17).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Proinflammatory Bradykinin Peptides in Systemic Lupus Erythematosus and Rheumatoid Arthritis

Vanarsa

Henderson

Soomro

et al. 2020

The Journal of Immunology

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Our recent study has implicated bradykinin (BK) signaling as being of pathogenic importance in lupus. This study aims to investigate the biomarker potential of BK peptides, BK and BK-des-arg-9, in lupus and other rheumatic autoimmune diseases. Sera from systemic lupus erythematosus (SLE) patients and healthy subjects were screened for BK and BK-des-arg-9 by liquid chromatography-mass spectrometry metabolomics. Serum from 6-mo-old C57BL/6 mice and three murine lupus strains were also screened for the two peptides by metabolomics. Given the promising initial screening results, validation of these two peptides was next conducted using multiple reaction monitoring in larger patient cohorts. In initial metabolomics screening, BK-des-arg-9 was 22-fold higher in SLE serum and 106-fold higher in mouse lupus serum compared with healthy controls. In validation assays using multiple reaction monitoring and quadrupole time-of-flight mass spectrometry, BK and BK-des-arg-9 showed significant elevations in SLE serum compared with controls (p < 0.0001; area under the curve = 0.79-0.88), with a similar but less pronounced increase being noted in rheumatoid arthritis serum. Interestingly, increased renal SLE disease activity index in lupus patients was associated with reduced circulating BK-des-arg-9, and the reasons for this remain to be explored. To sum, increased conversion of BK to the proinflammatory metabolite BK-des-arg-9 appears to be a common theme in systemic rheumatic diseases. Besides serving as an early marker for systemic autoimmunity, independent studies also show that this metabolic axis may also be a pathogenic driver and therapeutic target in lupus.

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Autonomic involvement in Guillain–Barre syndrome: A review

1994

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Autonomic neuropathy is an important and common complication of Guillain-Barré syndrome (GBS). Manifestations be present in cardiovascular, sudomotor, gastrointestinal and other systems involving both sympathetic and parasympathetic fibers. Some apparently selective acute autonomic neuropathies may be subvarieties of GBS. Experimental work in animal models, pathological studies of GBS patients, and autonomic function studies have provided some help in the understanding of this complication. In managing GBS patients with autonomic dysfunction there are important practical considerations that can improve their care. In this article we review the literature on autonomic neuropathy in GBS and propose a management scheme to accommodate it in the overall treatment of the neuropathy.

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Acute autonomic neuropathy associated with a high serum bradykinin level and positive anti-nuclear and anti-DNA antibodies titers.

Cited by 6 publications

References 11 publications

Postural Orthostatic Tachycardia Syndrome (POTS) – A novel member of the autoimmune family

Postural Orthostatic Tachycardia Syndrome (POTS) – A novel member of the autoimmune family

Upregulation of Proinflammatory Bradykinin Peptides in Systemic Lupus Erythematosus and Rheumatoid Arthritis

Autonomic involvement in Guillain–Barre syndrome: A review

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