Infectious and inflammatory disorders might increase the risk of developing idiopathic intracranial hypertension – a national case-control study

Abstract

Objective To investigate whether conditions causing inflammatory activation are associated with increased risk of idiopathic intracranial hypertension. Methods All newly diagnosed idiopathic intracranial hypertension patients (cases) in Sweden between 2000–2016 were identified using pre-determined algorithms (n = 902) and matched with five controls from the general population and five individuals with an obesity diagnosis (n = 4510) for age, sex, region, and vital status. National health registers provided information on infections, inflammatory disorders and dispensed medications. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals. Results Compared to general population controls, the cases had fourfold increased odds of having an infection (odds ratio = 4.3, 95% confidence interval 3.3–5.6), and threefold increased odds of an inflammatory disorder the year prior to idiopathic intracranial hypertension diagnosis (odds ratio = 3.2, 95% confidence interval 2.4–4.3). Organ specific analyses showed that odds were increased for the study diseases in the respiratory organ, kidney organ and gastrointestinal tract, but not for female genital infections. Similar results were found when comparing idiopathic intracranial hypertension with obese controls though the odds ratios were of lower magnitude. Sub-analyses on exposure to anti-infectious and anti-inflammatory drugs confirmed the increased odds ratios for idiopathic intracranial hypertension patients. Conclusions These findings suggest that major inflammatory activation may be a risk factor in idiopathic intracranial hypertension development.

A national Swedish case-control study investigating incidence and factors associated with idiopathic intracranial hypertension

“…In that study we found an increased OR on the proxy analysis of drug dispensation of antibiotics, even when the risk factor antibiotics (tetracyclines, sulphonamides, quinolones) were excluded. Still, the OR of exposure prior to IIH development in this study was slightly higher for tetracycline and sulphonamide antibiotics compared to all other antibiotics in the previous analysis (31), which supports the argument that there may be an effect from the drug itself. We also found increased OR for lithium and corticosteroid treatments.…”

“…When discussing pharmacological treatments as risk factors one must consider the indication why they are used. For antibiotics, the underlying infections might explain the increased risk seen as proposed in our previous study (31). In that study we found an increased OR on the proxy analysis of drug dispensation of antibiotics, even when the risk factor antibiotics (tetracyclines, sulphonamides, quinolones) were excluded.…”

“…The underlying pathophysiological cause of why uraemia is associated with IIH is unknown. End stage kidney failure with uraemia is associated with inflammation in the adipose tissue regardless of adiposity level (30) and we have previously proposed that possibly inflammatory activation could be involved as an underlying mechanism (31). Kidney failure is also associated with arterial hypertension which might be part of the pathophysiological process.…”

Characteristics and Outcomes of the Idiopathic Intracranial Hypertension Treatment in Intrinsic and Extrinsic Stenosis: A Single-Center Experience in China

“…Enlarged arachnoid granulations can potentially obstruct the sinus lumen as well as organized chronic thrombus. There were various inducing factors for these changes, including metabolism, endocrine disorders, inflammatory change, and female-related comorbidities [2,7,[22][23][24][25][26][27]. There is still controversy about the precipitating factors causing the initial elevation in ICP leading to secondary venous hypertension.…”

Commentary: The role of inflammation in idiopathic intracranial hypertension

“…Exposure to an infectious or inflammatory disorder in the year preceding IIH diagnosis was significantly associated with increased odds of developing IIH supporting the hypothesis that a major inflammatory activation could act as a trigger factor to IIH development. [ 20 ]…”