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Caution in blaming nasal steroids in causing 'Benign' intracranial hypertension
- Oliver Backhouse (25 April 2001)
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Drug Points: This is the Weakest Link – goodbye!
- Michael Oko, Andrew Johnston, Iain R C Swan (1 May 2001)
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Oliver Backhouse, SpR Ophthalmology York District Hospital. UK
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Editor - I would like to sound a note of caution regarding the conclusions drawn in the article by Bond et al on the causation of Benign intracranial hypertension with nasal fluticasone propionate usage [1] Despite many compelling case reports suggesting a causation of Idiopathic intracranial hypertension (IIH) with steroid administration or withdrawl, the validity of these cases is often in doubt due to the poor adherence to the modified Dandy criteria needed for diagnosis [2], which are being continually updated. The link is also not supported by case- controlled trials [3]. Many of their referenced cases do not meet these criteria and had various associated illnesses including active inflammatory disease (SLE, Crohn's) and nephrotic syndrome which are conditions that may cause IIH independent of steroid use by a proposed mechanism of aseptic arachnoiditis [4] or an imbalance in hydrostatic forces. Some previous cases of raised intracranial pressure, which would have been diagnosed as idiopathic, are now identified by Magnetic resonance venography as having cerebral venous sinus thrombosis which is associated with a prothrombotic state [5]. Steroids are known to be prothrombotic and this, together with their weight gain effect and frequent use in inflammatory conditions that can affect the cerebral vasculature may be why they are frequently labelled as a cause of IIH. Although the patients symptoms and signs may be due to raised intracranial pressure, bilateral disc swelling, fluorescein dye optic nerve head leakage and cranial nerve palsies may be caused by inflammatory conditions and therefore an LP opening pressure measurement (not done in the case presented) is needed to help confirm the disc swelling as papilloedema. I therefore feel it a little premature to blame nasal steroids as a cause of IIH in this patient with Chron's disease and do not agree that 'the occurence of Benign intracranial hypertension is well documented with corticosteroids. [1]Bond D, Charlton C, Gregson R. benign intracranial hypertension secondary to nasal fluticasone propionate. BMJ 2001;322:897. [2]Smith J. Whence pseudotumour cerebri? J Clin Neuro Ophthalmol 1985;5:55-6. [3]Giuseffi V, Wall M, Siegel P et al. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumour cerebri). A case-control study. Neurol 1991;41:239-44. [4]Green L, Vinker S, Amital H et al. Pseudotumour Cerebri in Systemic Lupus erythematosus. Sem Arthritis Rheum 1995;25(2):103-8. [5]DeBruijn S, Stam J, Koopman M et al. Case-control study of risk of cerebral sinus thrombosis in oral contraceptive users and in carriers of hereditery prothrombotic conditions. The Cerebral Venous Sinus Thrombosis Study Group. BMJ 1998;316:589-92. No conflict of interest. |
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Michael Oko, 1.SpR 2.Consultant. 3.Senior Lecturer Otolaryngology 1&2.Monklands Hospital, Monkscourt Avenue Airdrie. ML6 OJS. 3.Glasgow Royal Infirmary16 Alexandra Pa, Andrew Johnston, Iain R C Swan
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Editor – Bond et al proposed that nasal fluticasone propionate caused benign intracranial hypertension (BIH) in a 13 year old boy with a history of Crohn’s disease1 and subsequently reported this to the Committee on Safety of Medicines. We however have a number of problems with this hypothesis. Firstly, they clearly failed to confirm the diagnosis of intracranial hypertension as the cerebrospinal fluid pressure, which should be markedly elevated2, was not measured on any occasion. Hence their conclusions at best can only be based on papilloedema, headache and backache. Our ENT colleagues were involved but no mention was made of the presence or absence of the otological manifestations, which include objective pulsatile tinnitus and low frequency hearing loss, which can be the major or only manifestation of this syndrome3. Other recognised associated conditions were not excluded such as hypervitaminosis A, systemic lupus erythromatosis, hypothyroidism and its correction, malnutrition and renutrition4 (not unheard of in Crohn’s, and the patient was in remission hence both factors could have been at work). We have to surmise that this teenage patient was not receiving any other drugs such as tetracyclines or isotretinoin (commonly used in the treatment of acne in adolescents) which also have been implicated in the development of BIH. The natural history of the condition tends to be self-limiting, with a course of less than 12 months in most cases5 and recurrence in 10%; hence we were concerned that the temporal relationship the authors describe may just be the normal course for the condition. It is paradoxical that steroids are implicated as an aetiological factor and are also an accepted treatment. Would the authors suggest that nasal steroids could in different circumstances be a useful treatment? In these days of evidence based medicine there are several tests of causation that a hypothesis/ proposal should be subjected to and we feel that authors have clearly failed to do this. We would however encourage all clinicians to be observant of adverse drug reactions with particular reference to topical nasal steroids and children. 1.Bond DW, Charlton CPJ. Benign intracranial hypertension secondary to nasal fluticasone propionate. BMJ 2001;322:897 (14 April) 2. Susman JL. Benign intracranial hypertension. Journal of Family Practice 1990;30(3):290-2. 3. Sismanis A. Otologic manifestations of benign intracranial hypertension syndrome: diagnosis and management. Laryngoscope 1987; 97(8 Pt 2 Suppl 42):1-17. 4.Lessell S. Pediatric pseudotumor cerebri (idiopathic intracranial hypertension). Survey of Ophthalmology 1992; 37(3): 155-66. 5. Cody CM. Benign intracranial hypertension. American Family Physician 1992; 45 Authors 1.Michael Oko
2. Andrew Johnston
3.Iain R.C.Swan
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