The DOI matches its Crossref record; 59 of the 71 references it cites were found in a registry or an index; none of the 12 sources its claims cite is checked for support yet.
Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamic-pituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems
Open accessAbstract
Objective To study in parallel the outflow of the sympathetic nervous system (SNS) and the hypothalamic-pituitary adrenal (HPA) axis tone in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).Methods 32 patients with SLE, 62 with RA, and 65 healthy subjects (HS) were included. To measure the tone of the HPA axis, plasma ACTH and serum cortisol were determined. Serum neuropeptide Y (NPY) was used to evaluate the sympathetic outflow.Results Patients with SLE had increased NPY levels in comparison with HS, irrespective of prior prednisolone treatment (p<0.001). For patients with RA, only those with prednisolone treatment had increased NPY levels in comparison with HS (p = 0.016). Daily prednisolone dose correlated positively with serum NPY in RA (R(Rank) = 0.356, p = 0.039). In contrast, plasma ACTH levels were generally decreased significantly in comparison with HS in SLE with prednisolone, and in RA with/without prednisolone. Similarly, serum cortisol levels were also decreased in SLE with/without prednisolone, and in RA with prednisolone. The NPY/ACTH ratio was increased in SLE and RA, irrespective of prior prednisolone treatment. The NPY/cortisol ratio was increased in SLE with/without prednisolone, and in RA with prednisolone. Twelve weeks' anti-TNF antibody treatment with adalimumab did not decrease NPY levels in RA, irrespective of prednisolone treatment.Conclusions An increased outflow of the SNS was shown and a decreased tone of the HPA axis in patients with SLE and RA. Low levels of cortisol in relation to SNS neurotransmitters may be proinflammatory because cooperative anti-inflammatory coupling of the two endogenous response axes is missing.
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TL;DR
In patients with SLE and RA, serum neuropeptide Y indicated increased sympathetic outflow while ACTH/cortisol indicated reduced hypothalamic-pituitary-adrenal axis tone, producing increased NPY/ACTH and NPY/cortisol ratios. This uncoupling was present with or without prednisolone in SLE and mainly in prednisolone-treated RA, and 12 weeks of adalimumab did not reduce NPY levels.
Key findings
- Patients with SLE had increased NPY levels versus healthy subjects, irrespective of prior prednisolone treatment (p<0.001); in RA, only prednisolone-treated patients had increased NPY versus healthy subjects (p=0.016), and daily prednisolone dose correlated positively with serum NPY in RA (R Rank=0.356, p=0.039).
- Plasma ACTH was decreased versus healthy subjects in SLE with prednisolone and in RA with or without prednisolone; serum cortisol was decreased in SLE with or without prednisolone and in RA with prednisolone.
- The NPY/ACTH ratio was increased in SLE and RA irrespective of prior prednisolone treatment; the NPY/cortisol ratio was increased in SLE with or without prednisolone and in RA with prednisolone.
- Twelve weeks of anti-TNF treatment with adalimumab did not decrease NPY levels in RA, irrespective of prednisolone treatment, and neither NPY/ACTH nor NPY/cortisol ratios changed during treatment.
Methods
- The study included 32 patients with SLE, 62 patients with RA, and 65 healthy subjects; subgroups were matched according to age and sex. Blood was drawn between 08:00 and 10:00, and serum NPY, plasma ACTH, and serum cortisol were measured by immunoassays.
- Some patients with RA (16 with and 16 without parallel prednisolone) received adalimumab 40 mg subcutaneously every other week for 12 weeks plus stable methotrexate; blood was drawn at baseline and at weeks 2, 6, and 12.
- Group medians were compared by Mann-Whitney tests, correlations by Spearman rank analysis, and changes over time by Friedman tests; p<0.05 was significant.
Limitations
- Stated in the paper: norepinephrine was not measured because of expected strong bias from prolonged storage, since norepinephrine is more labile than NPY; the authors also note that NPY may not be the ideal measure in older patients when SNS activity is only increased to a small extent.
- Evident from the text: the main SLE/RA versus healthy-subject comparisons are cross-sectional, so temporal or causal direction cannot be established; prednisolone groups were not randomized, and the adalimumab analysis was a small RA subset (16 with and 16 without prednisolone) with no placebo control described in this paper.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Daily prednisolone dose correlated positively with serum NPY in RA (R Rank = 0.356, p = 0.039).”
- Also stated in: § DISCUSSION · boosted
“Clearly, the prednisolone dose correlated with NPY serum levels in patients with RA but not in patients with SLE (figs 1C and D).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Also stated in: § DISCUSSION · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For patients with RA, only those with prednisolone treatment had increased NPY levels in comparison with HS (p = 0.016).”
- Also stated in: § DISCUSSION · plain
“In RA, only patients with prior prednisolone had increased NPY serum levels in comparison with healthy subjects (fig 1B).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § DISCUSSION · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Twelve weeks' anti-TNF antibody treatment with adalimumab did not decrease NPY levels in RA, irrespective of prednisolone treatment.”
- Also stated in: § DISCUSSION · plain
“Using the Friedman test statistics, 12 weeks of anti-TNF treatment did not change NPY serum levels, irrespective of prednisolone treatment (fig 4).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § DISCUSSION · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Patients with SLE had increased NPY levels in comparison with HS, irrespective of prior prednisolone treatment (p,0.001).”
- Also stated in: § DISCUSSION · boosted
“Figure 1 demonstrates higher NPY serum levels in patients with SLE than in HS, irrespective of prednisolone treatment (fig 1A).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § DISCUSSION · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The NPY/cortisol ratio was increased in SLE with/without prednisolone, and in RA with prednisolone.”
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
“The ratio of NPY/cortisol was increased in both SLE patient groups, irrespective of prednisolone treatment (fig 3C).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In patients with RA, prednisolone treatment increased this particular ratio (fig 2D).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Relation of NPY serum levels and HPA axis hormones
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The NPY/ACTH ratio was increased in SLE and RA, irrespective of prior prednisolone treatment.”
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
“The ratio of NPY/ACTH was significantly higher in patients with SLE and RA than in healthy controls, irrespective of prior prednisolone treatment (figs 2C and D).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, serum cortisol levels were also decreased in SLE with/without prednisolone, and in RA with prednisolone.”
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
“In RA, only those patients with prior prednisolone treatment had decreased cortisol serum levels (fig 3B).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, plasma ACTH levels were generally decreased significantly in comparison with HS in SLE with prednisolone, and in RA with/without prednisolone.”
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
“In addition, patients with RA without prior prednisolone treatment also had decreased ACTH levels in comparison with healthy subjects (fig 2B).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, serum cortisol levels were also decreased in SLE with/without prednisolone, and in RA with prednisolone.”
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · boosted
“For cortisol, patients with SLE demonstrated decreased serum levels, irrespective of prior prednisolone treatment (fig 3A).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Relation of NPY serum levels and HPA axis hormones · boosted
- Probably not a substantial claim. 8
- It may state two separate claims as one. 8
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Plasma NPY levels did not differ between male and female patients with or without prednisolone (data not shown).”
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
“The above-mentioned ratios did not differ between male and female patients with or without prednisolone (data not shown).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > RESULTS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Also stated in: § Relation of NPY serum levels and HPA axis hormones · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, neither the ratio of serum NPY/plasma ACTH nor the ratio of serum NPY/serum cortisol changed during 12 weeks of anti-TNF treatment (data not shown).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > DISCUSSION
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“None of the patients without prednisolone received glucocorticoids during a period of 6 months before study entry, whereas patients with prednisolone had stable treatment over several weeks before study entry.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > PATIENTS AND METHODS
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, an increased SNS tone would support atherosclerosis in patients with chronic inflammatory diseases.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > DISCUSSION
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“This permissive effect of cortisol is due to b adrenoceptor up regulation and stabilisation of the cyclic AMP (cAMP)/protein kinase A/ cAMP responsive element binding protein signalling pathway.30”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > D
What the sources say
- Not checked yetcites [30] Schramm, 2000, beta-Adrenergic relaxation of rabbit tracheal smooth muscle: a receptor deficit that improves with corticosteroid administration, J Pharmacol Exp Ther source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The study was approved by the ethics committee of the University Hospital of Regensburg, Germany, and for the adalimumab study, approval was obtained from the ethics committee of L Sacco University Hospital, Italy.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > PATIENTS AND METHODS
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For all assays, intraassay and interassay coefficients of variation were below 10%.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Laboratory variables
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An increased outflow of the SNS was shown and a decreased tone of the HPA axis in patients with SLE and RA.”
- Also stated in: § DISCUSSION · boosted
“Using NPY as a reliable read-out measure of the SNS activity, we were able to demonstrate an increased SNS outflow in relation to the HPA axis tone in all patients with SLE and in patients with RA treated with prednisolone.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Abstract
Load-bearingStrength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § DISCUSSION · boosted
None of the sources cited for this claim have been checked yet.
In the paper
“In chronic inflammatory diseases such as systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) the HPA axis alters markedly : (a) secretion of adrenocorticotropic hormone (ACTH) relative to circulating cytokines is inadequate 7 ; (b) patients have inappropriately low sponta- neous and stimulated cortisol secretion in relation to inflammation”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > D
What the sources say
- Not checked yetcites [7] Straub, 2002, Inadequately low serum levels of steroid hormones in relation to IL-6 and TNF in untreated patients with early rheumatoid arthritis and reactive arthritis, Arthritis Rheum source
- Not checked yetcites [8] Gudbjornsson, 1996, Intact adrenocorticotropic hormone secretion but impaired cortisol response in patients with active rheumatoid arthritis. Effect of glucocorticoids, J Rheumatol
- Not checked yetcites [9] Crofford, 1997, Circadian relationships between interleukin (IL)-6 and hypothalamic- pituitary-adrenal axis hormones: failure of IL-6 to cause sustained hypercortisolism in patients with early untreated rheumatoid arthritis, J Clin Endocrinol Metab source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“NPY is an excellent indicator of sympathetic activity, 34 which is more stable and has a significantly longer half life in plasma.35”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > D
What the sources say
- Not checked yetcites [34] Morris, 1986, Increases in plasma neuropeptide Y concentrations during sympathetic activation in man, J Auton Nerv Syst source
- Not checked yetcites [35] Pernow, 1986, Plasma neuropeptide Y-like immunoreactivity and catecholamines during various degrees of sympathetic activation in man, Clin Physiol source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The subgroups were matched according to age and sex (table 1).”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > PATIENTS AND METHODS
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Some studies have indicated that patients with chronic inflammatory diseases have an increased activity of the SNS.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > D
What the sources say
- Not checked yetcites [16] Leden, 1983, Autonomic nerve function in rheumatoid arthritis of varying severity, Scand J Rheumatol source
- Not checked yetcites [17] Kuis, 1996, The autonomic nervous system and the immune system in juvenile rheumatoid arthritis, Brain Behav Immun source
- Not checked yetcites [18] Perry, 1989, Altered autonomic function in patients with arthritis or with chronic myofascial pain, Pain source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Release of cortisol is typically coupled to release of norepinephrine, which leads to stronger signalling through the b adrenoceptor; several studies have shown cooperation of cortisol and norepinephrine at a molecular level.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > D
What the sources say
- Not checked yetcites [22] Oikarinen, 1984, Modulation of glucocorticoid receptor activity by cyclic nucleotides and its implications on the regulation of human skin fibroblast growth and protein synthesis, Biochim Biophys Acta source
- Not checked yetcites [23] Gruol, 1986, Cyclic AMP-dependent protein kinase promotes glucocorticoid receptor function, J Biol Chem source
- Not checked yetcites [24] Nakada, 1987, Glucocorticoid regulation of beta-adrenergic receptors in 3T3-L1 preadipocytes, Mol Pharmacol
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In all subjects, blood was drawn between 08:00 and 10:00 in the morning when the patients visited the outpatient clinic.”
§ Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamicpituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems > Laboratory variables
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Serum levels of adrenal hormones are largely independent of sex.
“Because serum levels of adrenal hormones are largely independent of sex, male and female subjects were not further separated into subgroups.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“There seems to be a dissociation between high activity of the SNS and relatively normal activity of the HPA axis in CIDs [114,115].”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [115]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Adalimumab administration is described as both injection and infusion
MinorThe methods specify subcutaneous self-injections every other week, but the next sentence says the anti-TNF antibodies were infused. These describe different administration routes for the treatment.
“Patients were assigned to receive single self injections of adalimumab 40 mg subcutaneously every other week.”
“Anti-TNF antibodies were infused on weeks 0, 2, 4, 6, 8, 10, and 12.”
Claimed age- and sex-matching conflicts with the RA control group
MinorThe RA group was 84% female and had a mean age of 57.7 years, whereas its purportedly matched healthy-subject group was 52% female with a mean age of 51.5 years. These reported characteristics do not support the statement that the groups were matched on both age and sex.
“The subgroups were matched according to age and sex (table 1).”
“| Age (years) | 38.1 (2.1) | 37.1 (1.5) | 57.7 (1.7) | 51.5 (0.8) | | Sex, female/male (%) | 24/8 (75/25) 25/17 (60/40) 52/10 (84/16) 12/11 (52/48) | | | |”
Citations
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Research works printed but not linked: 2
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Cited by
Sorted by citations
Understanding the dynamics: pathways involved in the pathogenesis of rheumatoid arthritis.
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Brain–Gut Interactions in Inflammatory Bowel Disease
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“This pattern has been observed in inflammatory diseases of several different types of tissues including the skin (Buske-Kirschbaum et al., 2006; Buske-Kirschbaum et al., 2002), joints (Härle et al., 2006), and gut (Straub et al., 2002).”
BackgroundThe Spectrum of Achalasia: Lessons From Studies of Pathophysiology and High-Resolution Manometry
Kahrilas, P. J., & Boeckxstaens, G. E. (2013) · Gastroenterology · doi:10.1053/j.gastro.2013.08.038 · Cited by 236
Etiology and Risk Factors for Rheumatoid Arthritis: A State-of-the-Art Review
Romão, V. C., & Fonseca, J. E. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2021.689698 · Cited by 228
“Moreover, there is an increased systemic sympathetic tone, which is thought to be a physiological response to the decreased HPA axis function and that results in the uncoupling of these two systems (119, 130).”
BackgroundKoopman, F. A., Stoof, S. P., Straub, R. H., van Maanen, M. A., Vervoordeldonk, M. J., & Tak, P. P. (2011) · Molecular Medicine · doi:10.2119/molmed.2011.00065 · Cited by 159
Self-citationNovel insights into an “old” phenomenon: the no reflow
Durante, A., & Camici, P. G. (2015) · International Journal of Cardiology · doi:10.1016/j.ijcard.2015.03.359 · Cited by 126
Autonomic function and rheumatoid arthritis—A systematic review
Adlan, A., Lip, G. Y. H., Paton, J. F. R., Kitas, G. D., & Fisher, J. P. (2014) · Seminars in Arthritis and Rheumatism · doi:10.1016/j.semarthrit.2014.06.003 · Cited by 122
“Eighteen studies utilized clinical cardiovascular tests (CCTs) of ANS function;(51, 53, 54, 58, 60, 62, 69, 74-83, 85) 15 studies assessed heart rate variability (HRV)(49-51, 55, 57, 59, 61, 65, 68, 71, 73, 77, 86-88) of which 5 assessed HRV in combination with clinical cardiovascular reactivity;(51, 68, 77, 86, 87) a…”
BackgroundMethodInfluentialInteraction of the endocrine system with inflammation: a function of energy and volume regulation
Straub, R. H. (2014) · Arthritis Research & Therapy · doi:10.1186/ar4484 · Cited by 121
“[114,115].”
Self-citationAutonomic Dysfunction Precedes Development of Rheumatoid Arthritis: A Prospective Cohort Study
Koopman, F. A., Tang, M. W., Vermeij, J., de Hair, M. J. H., Choi, I. Y. K., Vervoordeldonk, M. J., Gerlag, D. M., Karemaker, J. M., & Tak, P. P. (2016) · EBioMedicine · doi:10.1016/j.ebiom.2016.02.029 · Cited by 117
“SNSrelated hormones are not influenced by DMARD or NSAID use, but prednisone use may lower (nor)epinephrine levels (Harle et al., 2006; Golczynska et al., 1995), and prednisone was included as an additional confounder in the analysis of these parameters.”
BackgroundStress hormones collaborate to induce lymphocyte apoptosis after high level spinal cord injury
Lucin, K. M., Sanders, V. M., & Popovich, P. G. (2009) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2009.06232.x · Cited by 102
“Interestingly, in individuals with systemic lupus erythematosus (SLE) and systemic sclerosis, b2AR expression and signaling are impaired in B cells (Wahle et al. 2001).”
BackgroundInfluentialCognitive dysfunction in systemic lupus erythematosus: Past, present, and future
Kozora, E., Hanly, J. G., Lapteva, L., & Filley, C. M. (2008) · Arthritis & Rheumatism · doi:10.1002/art.23991 · Cited by 100
The intriguing mission of neuropeptide Y in the immune system
Dimitrijević, M., & Stanojević, S. (2011) · Amino Acids · doi:10.1007/s00726-011-1185-7 · Cited by 86
“Similarly, rheumatoid arthritis and Sjogren's syndrome are associated with increased NPY levels in synovial fluid and saliva, respectively (Harle et al. 2006; Santavirta et al. 1997).”
BackgroundStraub, R., Bijlsma, J., Masi, A., & Cutolo, M. (2013) · Seminars in Arthritis & Rheumatism · doi:10.1016/j.semarthrit.2013.04.008 · Cited by 83
Self-citationDurante, A., & Bronzato, S. (2015) · Journal of Clinical Medicine Research · doi:10.14740/jocmr2122w · Cited by 83
“outflow [45] and increased endothelin-1 [46] in SLE, both of”
BackgroundEffects of smoking cessation on β-cell function, insulin sensitivity, body weight, and appetite
Stadler, M., Tomann, L., Storka, A., Wolzt, M., Peric, S., Bieglmayer, C., Pacini, G., Dickson, S. L., Brath, H., Bech, P., et al. (2013) · European Journal of Endocrinology · doi:10.1530/eje-13-0590 · Cited by 84
Immune‐Neuroendocrine Interactions and Autoimmune Diseases
Jara, L. J., Navarro, C., Medina, G., Lastra, O. L. V., & Blanco, F. (2006) · Journal of Immunology Research · doi:10.1080/17402520600877059 · Cited by 71
Haas, S., & Straub, R. H. (2012) · Arthritis Research & Therapy · doi:10.1186/ar3852 · Cited by 71
Self-citationDisrupted brain–immune system–joint communication during experimental arthritis
del Rey, A., Wolff, C., Wildmann, J., Randolf, A., Hahnel, A., Besedovsky, H. O., & Straub, R. H. (2008) · Arthritis & Rheumatism · doi:10.1002/art.23869 · Cited by 68
Self-citationStraub, R. H. (2011) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2010.08.002 · Cited by 69
Self-citationImpact of heart rate variability, a marker for cardiac health, on lupus disease activity
Thanou, A., Stavrakis, S., DYER, J. W., Munroe, M. E., James, J. A., & Merrill, J. T. (2016) · Arthritis Research & Therapy · doi:10.1186/s13075-016-1087-x · Cited by 69
Straub, R. H., Buttgereit, F., & Cutolo, M. (2011) · PubMed · Cited by 65
Self-citationMicrovascular Disease and Small-Vessel Disease: The Nexus of Multiple Diseases of Women
Patel, H. N., Aggarwal, N. T., Rao, A., Bryant, E., Sanghani, R. M., Byrnes, M., Kalra, D. K., Dairaghi, L., Braun, L. T., Gabriel, S. E., et al. (2020) · Journal of Women s Health · doi:10.1089/jwh.2019.7826 · Cited by 68
Microcirculatory Hemodynamics and Endothelial Dysfunction in Systemic Lupus Erythematosus
Wright, S., O’Prey, F. M., Rea, D. J., Plumb, R., Gamble, A., Leahey, W. J., Devine, A. B., McGivern, R. C., Johnston, D., Finch, M. B., et al. (2006) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000238351.82900.7f · Cited by 58
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How stress contributes to autoimmunity—lessons from Sjögren's syndrome
Skopouli, F., & Katsiougiannis, S. (2018) · FEBS Letters · doi:10.1002/1873-3468.12933 · Cited by 50
A neuropeptide in immune-mediated inflammation, Y?
Prod’homme, T., Weber, M. S., Steinman, L., & Zamvil, S. S. (2006) · Trends in Immunology · doi:10.1016/j.it.2006.02.003 · Cited by 55
“In particular, elevated serum levels of NPY have been detected in the serum of patients with asthma and systemic lupus erythematosus [13, 14 ], two inflammatory diseases associated with Th2 immunity.”
BackgroundStraub, R. H., Härle, P., Sarzi‐Puttini, P., & Cutolo, M. (2006) · Arthritis & Rheumatism · doi:10.1002/art.21946 · Cited by 51
Self-citationCytokines and the immune–neuroendocrine network: What did we learn from infection and autoimmunity?
Correa, S. G., Maccioni, M., Rivero, V. E., Iribarren, P., Sotomayor, C. E., & Riera, C. M. (2007) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2007.01.011 · Cited by 52
“[79] Harle P, Straub RH, Wiest R, Mayer A, Scholmerich J, Atzeni F, et al.”
BackgroundZhou, J., Xu, Z. Q., & Jiang, C. (2008) · Neuroscience Bulletin · doi:10.1007/s12264-008-0130-6 · Cited by 53
“Elevated serum level of NPY has also been detected in the patients with asthma and systemic lupus erythematosus[9].”
BackgroundPlasma neuropeptide Y: a biomarker for symptom severity in chronic fatigue syndrome
FLETCHER, M. A., Rosenthal, M., Antoni, M. H., Ironson, G. H., Zeng, X. R., Barnes, Z. M., Harvey, J. M., Hurwitz, B. E., Levis, S., Broderick, G., et al. (2010) · Behavioral and Brain Functions · doi:10.1186/1744-9081-6-76 · Cited by 52
“Plasma levels of NPY are reported to be elevated in other complex multi-symptom illnesses associated with immunologic dysfunction, including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) [33].”
BackgroundDimitrijević, M., Stanojević, S., Mitić, K. V., et al. (2008) · Peptides · doi:10.1016/j.peptides.2008.08.017 · Cited by 50
Hoff, P., Belavý, D. L., Huscher, D., Lang, A., Hahne, M., Kuhlmey, A.-K., Maschmeyer, P., Armbrecht, G., Fitzner, R., Perschel, F. H., et al. (2014) · Cellular and Molecular Immunology · doi:10.1038/cmi.2014.106 · Cited by 49
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Innervation of the Joint and Role of Neuropeptides
Konttinen, Y. T., Tiainen, V., Gómez‐Barrena, E., Hukkanen, M., & SALO, J. (2006) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1351.013 · Cited by 41
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“We believed that the elevated serum levels of NPY in patients with asthma and systemic lupus erythematosus (Groneberg et al., 2004; Harle et al., 2006) might play a crucial role on the onset and exacerbation of these diseases.”
Uncoupling of sympathetic nervous system and hypothalamic‐pituitary‐adrenal axis in cirrhosis
Wiest, R., Moleda, L., Zietz, B., Hellerbrand, C., Schölmerich, J., & Straub, R. H. (2008) · Journal of Gastroenterology and Hepatology · doi:10.1111/j.1440-1746.2008.05456.x · Cited by 37
Self-citationSanaee, F., Clements, J. D., Waugh, A. W. G., et al. (2011) · British Journal of Clinical Pharmacology · doi:10.1111/j.1365-2125.2011.04019.x · Cited by 36
Jung, J., Nam, J., Kim, H., & Suh, C. (2015) · Medicine · doi:10.1097/md.0000000000001184 · Cited by 34
Chronic Effects of the Sympathetic Nervous System in Inflammatory Models
Pongratz, G., & Straub, R. H. (2023) · NeuroImmunoModulation · doi:10.1159/000530969 · Cited by 29
“On a systemic level, however, sympathetic relative to parasympathetic activity is increased as indicated, e.g., by increased chromogranin A or neuropeptide Y levels in patients with RA [90, 102] and also by respective data from measurements of HRV or altered cardiac parameters [103, 104].”
BackgroundSelf-citationStraub, R. H., Pongratz, G., Hirvonen, H., Pohjolainen, T., Mikkelsson, M., & Leirisalo‐Repo, M. (2008) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2008.089458 · Cited by 28
Self-citationThe link between post-traumatic stress disorder and systemic lupus erythematosus
Goldschen, L., Ellrodt, J., Amonoo, H. L., Feldman, C. H., Case, S., Koenen, K. C., Kubzansky, L. D., & Costenbader, K. H. (2022) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2022.12.012 · Cited by 33
Drug-disease interaction: Clinical consequences of inflammation on drugs action and disposition
Abdallah, Y. E. H., Chahal, S., Jamali, F., & Mahmoud, S. H. (2023) · Journal of Pharmacy & Pharmaceutical Sciences · doi:10.3389/jpps.2023.11137 · Cited by 31
Botte, D. A. C., Noronha, I. L., Malheiros, D. M. A. C., et al. (2014) · Clinical & Experimental Immunology · doi:10.1111/cei.12336 · Cited by 25
Rastmanesh, R., Salehi‐Abargouei, A., Shadman, Z., Ebrahimi, A. A., & Weber, C. E. (2008) · Journal of Pain · doi:10.1016/j.jpain.2008.03.006 · Cited by 24
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Montero-López, E., Santos-Ruiz, A., González, R., Navarrete-Navarrete, N., Ortego-Centeno, N., Martínez-Augustín, O., Rodríguez-Blázquez, M., & Peralta-Ramírez, M. I. (2017) · Stress · doi:10.1080/10253890.2017.1369524 · Cited by 22
Schwemmer, S., Beer, P., Schölmerich, J., Fleck, M., & Straub, R. H. (2006) · PubMed · Cited by 21
Self-citationRibeiro-da-Silva, M., Vasconcelos, D. M., Alencastre, I. S., Oliveira, M. J., Linhares, D., Nevès, N., Costa, G., Henrique, R., Lamghari, M., & Alves, C. J. (2018) · Scientific Reports · doi:10.1038/s41598-018-33360-8 · Cited by 20
Vlček, M., Rovenský, J., Blazicek, P., Rádiková, Ž., Penesová, A., Kerlik, J., Květňanský, R., & Imrich, R. (2008) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1410.026 · Cited by 19
Neuroendocrine immune pathways in chronic arthritis
Capellino, S., & Straub, R. H. (2008) · Best Practice & Research Clinical Rheumatology · doi:10.1016/j.berh.2008.01.010 · Cited by 18
Self-citationFitzgerald, P. J. (2013) · Medical Hypotheses · doi:10.1016/j.mehy.2013.01.018 · Cited by 18
“eral diseases, such as SLE [71,72].”
Suarez, E. C., & Schramm‐Sapyta, N. L. (2013) · Nutrition Research · doi:10.1016/j.nutres.2013.10.001 · Cited by 17
Cardiovascular and Autonomic Dysfunction in Murine Ligature-Induced Periodontitis
Ribeiro, A. B., Santos-Júnior, N. N., Luiz, J. P. M., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-63953-1 · Cited by 17
Straub, R. H. (2014) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12409 · Cited by 14
Self-citationRamírez-Villafaña, M., Saldaña-Cruz, A. M., Aceves-Aceves, J. A., et al. (2020) · Journal of Immunology Research · doi:10.1155/2020/8982163 · Cited by 13
“Härle et al. identi fi ed higher concentrations of RA and SLE compared to controls, although Härle et al. found no correlation between NPY levels and disease activity in RA patients [11].”
InfluentialImpaired hypothalamo-pituitary-adrenal axis in patients with ankylosing spondylitis
Kebapçılar, L., Bilgir, O., Alacacıoğlu, A., Yıldız, Y., Taylan, A., Günaydın, R., Yüksel, A., Karaca, B., & Sarı, İ. (2009) · Journal of Endocrinological Investigation · doi:10.1007/bf03346548 · Cited by 13
STRAUB, R. H., DEL REY, A., & BESEDOVSKY, H. O. (2007) · Psychoneuroimmunology · doi:10.1016/b978-012088576-3/50014-9 · Cited by 14
Self-citationPires, A. L. P. V., Simoura, J. A. D. S., Cerqueira, J. D. M., Lima‐Arsati, Y. B. D. O., Arsati, F., dos Santos, J. N., & Freitas, V. S. (2020) · Oral Surgery Oral Medicine Oral Pathology and Oral Radiology · doi:10.1016/j.oooo.2020.10.004 · Cited by 13
Pan, Q., Chen, X., Liao, S., Chen, X., Zhao, C., Xu, Y., & Liu, J. (2019) · PeerJ · doi:10.7717/peerj.7179 · Cited by 11
“A multitude of studies revealed that an increased level of neuropeptides decreases the hypothalamic-pituitary-adrenal axis tone, giving rise to abnormalities of immune function and inflammatory processes, thereby contributing to the development of SLE both in patients and animal models (Bracci-Laudiero et al., 1998, 1…”
BackgroundZhang, G., Wu, Y., Liu, F., Chen, Q., Sun, X., Qu, Q., Fu, H., Huang, X., & Zhang, X. (2023) · Journal of Thrombosis and Haemostasis · doi:10.1016/j.jtha.2023.02.030 · Cited by 11
Greene, E. R., Yonan, K. A., Sharrar, J. M., et al. (2011) · Lupus · doi:10.1177/0961203311428458 · Cited by 10
Suppression of the physiological stress response is not stress
Makuya, L., Pillay, N., Rimbach, R., et al. (2023) · Trends in Ecology & Evolution · doi:10.1016/j.tree.2023.06.007 · Cited by 9
Enhanced pain perception in rheumatoid arthritis: Novel considerations
Wood, P. B. (2009) · Current Pain and Headache Reports · doi:10.1007/s11916-009-0071-4 · Cited by 9
Clements, J. D., & Jamali, F. (2009) · Journal of Pharmacy & Pharmaceutical Sciences · doi:10.18433/j3d012 · Cited by 9
Kreiner, F. F., & Galbo, H. (2012) · Arthritis Research & Therapy · doi:10.1186/ar4017 · Cited by 9
“The effect of anti-TNF-a treatment was studied in the latter patients; NPY concentrations were not influenced by the treatment, a finding which is not surprising considering the fact that concentrations were not increased before treatment [32].”
BackgroundInfluentialMolina, E., Gould, N. F., Lee, K., Krimins, R. A., Hardenbergh, D., & Timlin, H. (2022) · Lupus · doi:10.1177/09612033221122980 · Cited by 8
“Such that, while the HPA axis is depleted and unable to produce the anti-inflammatory glucocorticoids in chronic stress, the SNS pathway is hyperresponsive, resulting in these systems becoming uncoupled.(91) In fact, in patients with other chronic rheumatic diseases, there is evidence of an impaired sympathetic respon…”
BackgroundR–R interval variation and sympathetic skin response in systemic lupus erythematosus
Tekataş, A., Koca, S. S., Tekatas, D. D., Aksu, F., Doğru, Y., & Pamuk, Ö. N. (2013) · Clinical Rheumatology · doi:10.1007/s10067-013-2391-3 · Cited by 8
“Apart from cardiovascular reflex tests, some biochemical tests have also been used to evaluate autonomic functions in SLE patients [20, 29].”
BackgroundMethodMaggio, M. C., Miniaci, A., Gallizzi, R., & Civino, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241713192 · Cited by 7
“low levels of cortisol in relation to hyperactivity of CNS neurotransmitters may play a proinflammatory role, since a joining of the two endogenous response axes is lacking [7].”
BackgroundA History of Psycho-Neuro-Endocrine Immune Interactions in Rheumatic Diseases
Straub, R. H., & Cutolo, M. (2024) · NeuroImmunoModulation · doi:10.1159/000540959 · Cited by 12
Self-citationNeuropeptide Analysis of Oral Mucosa in Diabetic Rats
Kispélyi, B., Lohinai, Z. M., Altdorfer, K., et al. (2014) · NeuroImmunoModulation · doi:10.1159/000356949 · Cited by 7
Quisi, A., & Alıcı, G. (2018) · Journal of Clinical Laboratory Analysis · doi:10.1002/jcla.22598 · Cited by 7
Rastmanesh, R. (2009) · Medical Hypotheses · doi:10.1016/j.mehy.2009.05.035 · Cited by 6
“creased in RA patients who are taking prednisolone [31].”
BackgroundInfluentialThe Sensory and Sympathetic Nervous System in Cartilage Physiology and Pathophysiology
Grässel, S., Straub, R. H., & Jenei‐Lanzl, Z. (2017) · Springer eBooks · doi:10.1007/978-3-319-45803-8_9 · Cited by 6
Self-citationButts, C. L., & Sternberg, E. M. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4377-1893-5.00013-3 · Cited by 7
Malysheva, O., Wagner, U., Wahle, M., Pierer, M., Wagner, U., Stalla, G. K., & Baerwald, C. (2011) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2011.151340 · Cited by 5
Neuropeptide Y, a potential marker for lupus, promotes lupus development
Wang, D., Xu, W., Tang, Y., et al. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.111272 · Cited by 5
Up-regulation of NPY gene expression in hypothalamus of rats with experimental chronic renal failure
Sucajtys-Szulc, E., Karbowska, J., Kochan, Z., Wołyniec, W., Chmielewski, M. S., Rutkowski, B., & Świerczyński, J. (2006) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2006.08.008 · Cited by 5
“We have not analyzed some factors frequently associated with uremia, including proinflammatory cytokine [33–35], sympathetic overactivity [36], hyperinsulinemia and hyperleptinemia (21) which may influence the NPY gene expression in hypothalamus and liver.”
BackgroundCatallani, B., Palma, B. D., Gil, F. Z., & Suchecki, D. (2007) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2007.08.010 · Cited by 5
Functional disturbance of the stress-adaptation system in patients with scleroderma
Matsuura, E., Ohta, A., Suematsu, R., Inoue, H., Koarada, S., Tada, Y., Sherriff-Tadano, R., Kuroki, T., Ikeda, D., & Nagasawa, K. (2011) · Modern Rheumatology · doi:10.3109/s10165-010-0412-5 · Cited by 9
“However, in systemic rheumatic diseases other than RA or SLE, there have been few reports indicating a possible relationship between stress and the pathomechanism of the disease.”
BackgroundInfluentialHardcastle, S. L., Brenu, E., Johnston, S., Staines, D., & Marshall‐Gradisnik, S. (2014) · Health Care For Women International · doi:10.1080/07399332.2014.962139 · Cited by 5
“…illness and in supporting the idea of defining such distinct severity subgroups (Baraniuk et al., 2013; Brenu et al., 2013; Friedberg & Krupp, 1994; Härle et al., 2006; Joyce, Hotopf, & Wessely, 1997; Kerr et al., 2008; Peckerman et al., 2003a; Rangel, Garralda, Levin, & Roberts, 2000; Stringer…”
BackgroundZhou, J., Lu, F., Li, S., Xie, M., Lu, H., Xie, Z., Wu, D., Wang, S., Wen, C., & Xu, Z. (2019) · Inflammopharmacology · doi:10.1007/s10787-019-00668-4 · Cited by 4
Baqai, T., Isenberg, D. A., & Ioannou, Y. (2014) · Rheumatology Reports · doi:10.4081/rr.2013.e6 · Cited by 4
Chapter 27 Modulation of Hormone Axes by Anti-TNF Therapy
Atzeni, F., Sarzi‐Puttini, P., Cutolo, M., & Straub, R. H. (2008) · Technical report · doi:10.1016/s1571-5078(07)00227-9 · Cited by 3
Self-citationNeuropeptide Y: The Story, the Players, the Outcomes
Dimitrijević, M., & Stanojević, S. (2012) · Springer eBooks · doi:10.1007/978-3-7091-0888-8_8 · Cited by 3
Origin of Typical Disease Sequelae
Straub, R. H. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-803321-0.00005-7 · Cited by 3
Self-citationLiu, S., Wu, J., Lin, Y., Liang, H., Cai, Y., Wang, L., Wang, Z., & Sang, H. (2025) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2025.08.003 · Cited by 3
“Elevated NPY levels serve as an independent marker of disease activity in rheumatoid arthritis and correlate with accelerated disease progression [22,23].”
The impact of the metabolic syndrome on cardiovascular risk and disease in rheumatoid arthritis
Dessein, P. H., González-Gay, M. Á., Woodiwiss, A. J., Joffe, B. I., Norton, G. R., & Solomon, A. (2008) · Future Rheumatology · doi:10.2217/17460816.3.4.335 · Cited by 2
Effect of thoracic Kinesio taping on acute lumbar and leg pain in a pregnant woman: A case report
Shahbazi, M., Sarrafzadeh, J., Fatemi, T. S., et al. (2021) · Sports Orthopaedics and Traumatology · doi:10.1016/j.orthtr.2021.06.004 · Cited by 2
Causas biológicas de depressão em doentes com lupus eritematoso sistémico: um estudo de revisão
Braga, J. C. F. F. (2014) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) · doi:10.34626/v2xh-me81 · Cited by 2
Warum gibt es analoge Krankheitsmechanismen bei chronisch entzündlichen Krankheiten?
Straub, R. H., Besedovsky, H. O., & del Rey, A. (2007) · Wiener klinische Wochenschrift · doi:10.1007/s00508-007-0834-z · Cited by 2
Self-citationGiri, P. S., Parmar, M., Ezhuthachan, D. D., Desai, T., & Dwivedi, M. (2023) · Human Gene · doi:10.1016/j.humgen.2023.201251 · Cited by 1
Li, B., Zhao, J., Liu, Z., Li, B., Chen, Z., Li, Z., Lyu, X., Guo, Z., Wu, W., Tan, L., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-31031-z · Cited by 1
Chapter 1 Neuroendocrine Immune Control Mechanisms and their Influence on Autoimmune Disease
Capellino, S., & Straub, R. H. (2008) · Technical report · doi:10.1016/s1571-5078(07)00201-2 · Cited by 1
Self-citationNeuroendocrine Involvement in Immune-Mediated Rheumatic Diseases
Cutolo, M., & Trombetta, A. C. (2019) · Endocrinology · doi:10.1007/978-3-319-66362-3_9-1 · Cited by 1
Self-citationNeuroendocrine Involvement in Immune-Mediated Rheumatic Diseases
Cutolo, M., & Trombetta, A. C. (2020) · Endocrinology · doi:10.1007/978-3-319-68729-2_9 · Cited by 1
Self-citationPathogenesis and Neuroendocrine Immunology
Straub, R. H. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-803321-0.00002-1 · Cited by 1
Self-citation", S., Khramenko, N., Velychko, L. M., Bogdanova, O. V., Konovalova, N., & Zhuravok, I. O. (2022) · Oftalmologicheskii Zhurnal · doi:10.31288/oftalmolzh20224311 · Cited by 1
Metadata
- Authors
- Härle, P., Straub, R. H., Wiest, R., Mayer, A., Schölmerich, J., Atzeni, F., Carrabba, M., Cutolo, M., & Sarzi-Puttini, P.
- Affiliations
- University Hospital Regensburg (DE)
- Luigi Sacco Hospital (IT)
- University of Genoa (IT)
- Corresponding author
- Straub, R H
- ORCID
- Cutolo, M
- Venue
- Annals of the Rheumatic Diseases
- Publisher
- Elsevier BV
- Published
- 2006-01
- Volume
- 65
- Issue
- 1
- Pages
- 51-56
- ISSN
- 0003-4967 (ISSN-L)
- PMC
- PMC1797997
- OpenAlex
- W2103734979
- Semantic Scholar
- 481ff5edd6e0c0423286f6e3f087c7d8f982432f
- Cited by
- 114
- References
- 71
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 8 · 2022: 4 · 2021: 2 · 2020: 5 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 4 · 2015: 9 · 2014: 10 · 2013: 11 · 2012: 7
- FWCI
- 3.48
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of the Rheumatic Diseases (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- University of Regensburg Publication Server (University of Regensburg) (acceptedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- HighWire Press Open Archive (submittedVersion)
- University of Regensburg Publication Server (University of Regensburg)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- sympathetic nervous system, neuropeptide Y, hypothalamic-pituitary-adrenal axis, systemic lupus erythematosus, rheumatoid arthritis, prednisolone, ACTH, cortisol, adalimumab, anti-TNF therapy, proinflammation, autoimmunity
- MeSH terms
- Adalimumab, Adrenocorticotropic Hormone, Adult, Antibodies, Monoclonal, Arthritis, Rheumatoid, Female, Glucocorticoids, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Lupus Erythematosus, Systemic, Male, Middle Aged, Neuropeptide Y, Pituitary-Adrenal System, Prednisolone, Severity of Illness Index, Sympathetic Nervous System, Tumor Necrosis Factor-alpha, Antibodies, Monoclonal, Humanized
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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