Interferon system in acute transient synovitis.

Leibowitz, E; Levin, Stanley; Torten, Judith

doi:10.1136/adc.60.10.959

Cited by 13 publications

(7 citation statements)

References 7 publications

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“…Tolat et al [23] identified that interferon levels were raised in 28 of 65 children with TS, but they did not use a control group. Similar observations were made by Leibowitz et al [10] in an unadjusted analysis using a control group formed from individuals of all ages. However, whilst this provides some evidence to support a viral hypothesis, the finding of raised interferon levels is not universal, not specific to a virus, and is not made in comparison with a wellformed control group.…”

Section: Introductionsupporting

confidence: 78%

“…Uncertainty has led to various hypotheses to explain the aetiopathogenesis of the condition. The common notion of a viral aetiology is based on five primary research papers, of which three measured immunological parameters and two investigated clinical evidence of a preceding viral illness [3,5,10,11,23]. Tolat et al [23] identified that interferon levels were raised in 28 of 65 children with TS, but they did not use a control group.…”

Section: Introductionmentioning

confidence: 99%

“…However, whilst this provides some evidence to support a viral hypothesis, the finding of raised interferon levels is not universal, not specific to a virus, and is not made in comparison with a wellformed control group. Additionally, searches for the viral pathogen have failed to produce a consistent result, with a range of viruses isolated in a variable number of children with TS, a finding which is perhaps consistent with any group of infants [10]. Clinical enquiries of viral illness are also inconclusive, with some suggesting a higher rate of preceding gastroenteritis or upper respiratory tract infection [5], though these studies are similarly inconsistent and flawed by recall bias.…”

Section: Introductionmentioning

confidence: 99%

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The epidemiology of transient synovitis in Liverpool, UK

Harrison

Vooght

Singhal

et al. 2014

Journal of Children's Orthopaedics

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BackgroundThe epidemiology of transient synovitis is poorly understood, and the aetiology is unknown, although a suggestion of a viral association predominates.PurposeThis population-based study investigated the epidemiology in order to formulate aetiological theories of pathogenesis.Patient and methodsCases in Merseyside were identified between 2004 and 2009. Incidence rates were determined and analysed by age, sex, season and region of residence. Socioeconomic deprivation scores were generated using the Index of Multiple Deprivation, allocated by postcode. Poisson confidence intervals were calculated and Poisson regression was used to check for trends.ResultsTwo hundred and fifty-nine cases were identified over 5.5 years. The annual incidence was 25.1 (95 % CI 22.1–28.5) per 100,000 0–14 year-olds. Male to female ratio was 3.2:1 (p < 0.001). Mean age at presentation was 5.4 years (95 % CI 5.0–5.8), which demonstrated a near-normal distribution. No relationship was identified between seasonality and incidence (p = 0.64). A correlation was identified with socioeconomic deprivation in Merseyside: incidence rate ratio 1.16 (95 % CI 1.06–1.26, p < 0.001), although further analysis within the subregion of Liverpool did not confirm this finding (p = 0.35).ConclusionsThe normal distribution for age at disease presentation suggests a specific disease entity. The absence of seasonality casts some doubt on the popular theory of a viral aetiology. The absence of a consistent socioeconomic gradient in both Merseyside and Liverpool challenges a previous suggestion of an association with Perthes’ disease. This paper provides ecological evidence that may challenge existing aetiological theories, though transient synovitis remains an enigma.

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Section: Introductionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The epidemiology of transient synovitis in Liverpool, UK

Harrison

Vooght

Singhal

et al. 2014

Journal of Children's Orthopaedics

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“…But IFNs have a short half-life in blood, suggesting that the IFN concentrations in blood and the IFN-α-2b concentrations used in this study should not be simply compared. Moreover, it has been reported that peripheral blood mononuclear cells significantly produce IFN-α via stimulation by polyribonucleotides in vitro (Leibowitz et al 1985). Thus, IFN-α, which is produced from the mononuclear cells, must show considerably high concentrations in the adjacent tissues in vivo.…”

Section: The Effect Of Ifn-α On Nervous Systemsmentioning

confidence: 99%

Interferon-α reduces catecholamine secretion from bovine adrenal chromaffin cells stimulated by acetylcholine

Tachikawa

Kondo

Takahashi

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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A long-term pretreatment (72 h) of bovine adrenal chromaffin cells with recombinant human interferon (IFN) -alpha-2b (1500 units/ml) produced a decrease in the secretion of catecholamines from the cells stimulated by acetylcholine (ACh) (25 micromol/l) but not that with human fibloblast IFN-beta (3000 units/ml) or recombinant human IFN-gamma (3000 units/ml). IFN-alpha-2b inhibited the ACh-induced secretion in a concentration- (30-1500 units/ml) and time-dependent manner (18-72 h). The content of catecholamines in the cells treated with IFN-alpha-2b for 72 h did not change. The inhibitory effect of IFN-alpha-2b on the secretion was abolished when the cells were simultaneously treated with anti-IFN-alpha antibody, and it was overcome by the increase in the external ACh concentration. IFN-alpha-2b also inhibited ACh-induced Ca2+ influx into the cells in a concentration-dependent manner similar to that of the IFN-alpha-2b inhibiting ACh-induced secretion. On the other hand, IFN-alpha-2b failed to reduce the secretion from the cells induced by high K+. These results strongly suggest that IFN-alpha-2b reduces the ACh-induced secretion of catecholamines from bovine adrenal chromaffin cells due to modulating the gene expression of the nicotinic ACh receptor-operated cation channels rather than due to directly affecting the channels. The results further indicate that the IFN-alpha-2b inhibition may be associated with the psychiatric side effects of IFN-alpha (depression, neurasthenica and somnolence, etc.), and that immune systems may regulate the function of (autonomic) nervous systems or adrenal medulla via IFN-alpha in vivo.

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“…A viral aetiology is further supported by the finding of raised blood and synovial fluid interferon levels [12,13].…”

Section: Discussionmentioning

confidence: 92%