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| Year : 2001 | Volume
: 49
| Issue : 4 | Page : 404-6 |
Hypersensitivity to glucocorticoids in patients with raised ICP : report of two cases.
Sharma RR, Pawar SJ, Dev EJ, Ebenezer S, Mahapatra AK
The National Neurosurgery Centre, Khoula Hospital, Post Box - 90, Postal Code - 116, Mina-Al-Fahal, Sultanate of Oman.
Correspondence Address:
The National Neurosurgery Centre, Khoula Hospital, Post Box - 90, Postal Code - 116, Mina-Al-Fahal, Sultanate of Oman.
[email protected]
Corticosteroids are widely used in patients with raised intracranial pressure associated with cerebral neoplasms, cerebral vascular malformations, cerebral ischaemia and benign intracranial hypertension. In general clinical practice, anti-allergic, anti-inflammatory and immuno-suppressive properties of corticosteroids are commonly utilised in the management of allergic and immunological diseases. However in exceptionally rare circumstances, steroids may be the cause of hypersensitive reactions. Authors report two patients with raised intracranial pressure who developed steroid hypersensitivity. A review of the relevant literature is discussed.
How to cite this article:
Sharma R R, Pawar S J, Dev E J, Ebenezer S, Mahapatra A K. Hypersensitivity to glucocorticoids in patients with raised ICP : report of two cases. Neurol India 2001;49:404 |
How to cite this URL:
Sharma R R, Pawar S J, Dev E J, Ebenezer S, Mahapatra A K. Hypersensitivity to glucocorticoids in patients with raised ICP : report of two cases. Neurol India [serial online] 2001 [cited 2023 Mar 30];49:404. Available from: https://www.neurologyindia.com/text.asp?2001/49/4/404/1210 |
Corticosteroids are commonly used in the management of allergic and immunological conditions. In acute hypersensitivity reactions such as angioneurotic oedema of the larynx and anaphylactic shock, corticosteroids are used as an adjunct to emergency treatment, along with adrenaline. In neurosurgical practice, steroids are generally used in patients with raised intracranial pressure due to cerebral neoplasms, cerebral ischaemia, temporal arteritis and benign intracranial hypertension. However despite their anti-inflammatory, antioedema, and immunosuppressive properties, corticosteroids may also be the cause of hypersensitive reactions.[1],[2],[3],[4] Two cases with raised intracranial pressure who developed severe hypersensitive reactions when treated with corticosteroids, are reported.
Case 1 : A 24 year old lady was admitted with complaints of intermittent severe headaches and visual deterioration in both eyes, immediately following the delivery of her second child, six months back. Neurological examination revealed bilateral enlargement of the blind spots, reduction of the peripheral visual fields and bilateral papilloedema. Computed tomographic (CT) scans showed findings suggestive of intracranial ideopathic hypertension.
Lumbar puncture using 25 G needle showed CSF pressure of 290 mm of water. She was given dexamethasone 4 mg six hourly. Within 24 hours, she developed diffuse erythematous wheals over the trunk and the face with severe itching associated with swelling of the face and lips (angioedema). She, however, felt partly relieved of her headaches. As she was on no other medication, dexamethasone was discontinued. She was given chlorpheniramine maleate, 4 mgs six hourly with calcium gluconate and local application of calamine lotion. She was also given furesemide (40 mgs twice daily) and acetazolamide (250 mg thrice daily) for IIH with favourable results. She recovered from her hypersensitive reaction within a period of 3-4 days. She was referred to the dermatology where a skin test was positive with dexamethasone and therefore she was warned about her steroid hypersensitivity.
Case 2 : A 23 years old lady presented with complaints of severe parietal headaches for the past one year and recent onset focal sensory seizures in the left upper and lower limbs. No history suggestive of allergy, hay fever or asthma was noted. Her general physical and neurological examination was essentially normal except a subtle left facial paresis. CT scan (plain and contrast) suggested vascular malformation involving the right parietal region, which was confirmed on CT angiography and DSA studies. While awaiting embolisation procedure, she developed an episode of left sensory -motor seizures involving face and limbs along with post-ictal weakness. CT scan of brain showed right parietal perilesional oedema. She was put on dexamethasone 4 mg, six hourly. She developed erythematous rashes over her chest and hands on the same day. Dexamethasone hypersensitivity was considered and the same was discontinued. She was treated with chlorpheniramine maleate, cimetidine hydrochloride, calcium gluconate and calamine lotion. She responded very well and within a period of five days she recovered well. Thereafter, she was referred to another centre for embolisation of cerebral arteriovenous malformation with instructions regarding dexamethasone hypersensitivity.
One year following embolisation she suddenly developed left sided seizures and developed left hemiparesis. A plain and contrast CT scan at this stage showed obliteration of arteriovenous malformation spontaneously, with acutely severe left parietal cerebral oedema. Inadvertently, she was started on dexamethasone with resultant urticarial wheals all over the body within 24 hours. Prompt withdrawal of dexamethasone resulted in a good response, but her left hemiparesis persisted. A trial of hydrocortisone was given which also resulted in reappearance of the rashes, which was also discontinued. The patient was treated successfully with furesemide and acetazolamide. She was discharged two weeks later with improvement in her left hemiparesis with an advice regarding a regular OPD follow-up.
Drug reactions[5] can be classified into three groups : a) non- immunological (predictable and unpredictable) b) immunological (unpredictable) which include IgE dependent drug reactions, immune complex dependent drug reactions, cytotoxic drug induced reactions, cell mediated reactions, and c) miscellaneous-e.g. jarisch herxheimer reaction, infectious mononucleosis - ampicillin reaction.
The skin has a limited repertoire of morphological reaction patterns in response to a wide variety of stimuli, and it is often impossible to identify an offending drug, or pathological mechanism involved, on the basis of clinical appearance alone. We, therefore, remain relatively ignorant about the mechanisms underlying many clinical drug eruptions. Both the patients reacted with urticarial type of skin lesions which is the cutaneous manifestation of a type I reaction, mediated by lgE antibodies or a type III reaction, in which the antigen forms a complement fixing complex with antibody. Immediate reactions occur within minutes of drug administration; accelerated reactions may occur within hours or days and generally include urticaria but may involve laryngeal oedema. In vivo cross linkage by polyvalent drug protein conjugates of specific lgE molecules, fixed to sensitised tissue mast cells or circulating basophil leucocytes, triggers the cell to release a variety of chemical mediators including histamine, peptides such as eosinophil chemotactic factor of anaphylaxis and lipids such as leukotrienes or prostaglandins. Clinically, this may produce pruritus, urticaria, bronchospasm, laryngeal oedema and in severe cases anaphylactic shock with hypotension and possible death.[6]
In the first case, the patient developed the skin lesions following administration of dexamethasone tablets and since there were no other drugs being given concomitantly, the reactions can be attributed to that being caused by dexamethasone itself. In the second case, the fact that provocation with dexamethasone after recovery resulted in reappearance of the skin rash, proves that the patient was sensitive to the drug. A drug suspected of causing a drug eruption may be reliably incriminated by the reaction in response to a test dose administered after recovery. The same patient reacting to hydrocortisone with similar skin lesions, suggests cross sensitivity of the patient to dexamethasone and hydrocortisone. It is well known that the unwitting substitution of a drug which is chemically closely related, may perpetuate a reaction.
Investigations which could help in the diagnosis are skin tests including prick and intra-dermal testing and patch testing. These are for the most part unreliable even when apparently appropriate antigens are used and may be hazarduous. In vitro tests like lymphocyte transformation tests, macrophage migration inhibition tests and lymphocyte toxicity assay are not widely available and are essentially research tools.[5],[7]
Steroid Hypersensitivity : Corticosteroids are often used to treat allergic reactions. However, it appears that patients can also have allergic-type reactions to these agents.[12] The severity of the reactions can vary from a rash to anaphylaxis or death. Both immediate and delayed reactions can occur.[13],[14] These reactions are more often reported when glucocorticoids are applied topically as compared to systemically administered glucocorticoids. Glucocorticoids may lead to dangerous allergic complication if administered systemically.[6],[9] Rasanen and Hasan[11] in their study of five patients who had developed a rash when treated with systemic or intralesional hydrocortisone, methyl prednisolone, prednisolone or betamethasone, were challenged with oral or intraarticular corticosteroid preparations and skin tests. Upon provocations, the patients reacted with diffuse erythema principally on the trunk or on the face. The erythema appeared within a period ranging from a few hours to 24 hours and faded in 1-3 days. On patch testing, one patient reacted to prednisolone and methyl prednisolone which induced a positive response upon provocation. Patients who were sensitive to hydrocortisone or methyl prednisolone reacted to these corticosteroids in the intradermal tests. A combination of intradermal and patch tests is recommended when allergy to systemic or intralesional corticosteroids is suspected. If these skin tests remain negative, provocation is the method of choice. Alexiou et al[1] reported a crisis reaction to prednisolone and dexamethasone in one of their four patients with steroid allergy. In these cases renewed application of prednisolone hemisuccinate was well tolerated, when histamine-1 and histamine-2 receptors were blocked (with the use of cimetidine hydrochloroide, 200 mg twice per day and dimethindene maleate 4 mg twice per day) and calcium was given for membrane stabilisation.
Awareness of corticosteroid hypersensitivity reactions is important. Steroid hypersensitivity carries morbidity and mortality and therefore must be vigourously treated. Confirmatory dermatological tests indicated should be carried out later. Patients should be given steroid hypersensitivity cards as a reminder.
| 1. | Alexiou C, Kau RJ, Luppa P et al : Allergic type reactions after systemic administration of glucorticosteroid therapy. Arch Otolaryngol Head Neck Surg 1998; 124 : 1260-1264.  |
| 2. | Kamm GL, Hagmeyer KO : Allergic- type reactions to corticosteroids. Ann Pharmacother1999; 33 : 451-460. |
| 3. | Murrieta-Aguttes M, Michelen V, Leynadier F et al : Systemic allergic reactions to corticosteroids. J Asthma 1991; 28 : 329-339. |
| 4. | Peller JS, Bardana EJ Jr : Anaphylactoid reaction to corticosteroid : case report and review of literature. Ann Allergy 1985; 54 : 302-305. |
| 5. | Breathnach SM : Drug Reactions. In : Rook, Wilkinson, Ebling - Textbook of dermatology. Champion RH, Burton IC, Ebling FJG. (eds) 5th ed. vol 4 Ch. 74. Blackwell Scientific publication, Newyork. 1992; 2961-3035. |
| 6. | Beynel P, Guerin JC : Anaphylactic reactions to systemic corticosteroids. Review of the literature concerning 3 cases (In French). Rev Mal Respir1999; 16 : 529-537. |
| 7. | Reitamo S, Laurma AI, Forstrom L : Detection of contact hypersensitivity to topical corticosteroids with hydrocortisone-17-butyrate. Cont Dermat 1989; 21 : 159-165. |
| 8. | Lopez-Serrano MC, Moreno-Aneillo A, Contreras J et al : Two cases of specific adverse reactions to systemic corticosteroids. J Investig Allergol clin Imrnunol 1996; 6 : 324-327. |
| 9. | Romankiewicz JA, Franklin JE JR : Allergic reactions to corticosteroid therapy. Am Med Assoc 1976; 236 : 1939. |
| 10. | Von Maur K, Rocklin RE, Stevens MB : Corticosteroid allergy in a patient with systemic lupus erythmatosus. Jonhs Hopkins Med J 1974; 134 : 356-364. |
| 11. | Rasanen L, Hasan T : Allergy to systemic and intralesional corticosteroids. Br J Dermatol 1993; 128 : 407-411. |
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