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Essay: Case Report: Steroid-Induced Ocular Defects- Prednisolone Side Effects Discussed

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  • Published: 5 December 2019*
  • Last Modified: 22 July 2024
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 A CASE REPORT ON STEROID INDUCED OCCULAR DEFECTS

 ABSTRACT

Prednisolone (Wysolone) is a corticosteroid drug having high glucocorticoid and low mineralo corticoid activity, making it useful for the treatment of a wide range of inflammatory and auto-immune conditions. Common side effects include visual, auditory or tactile hallucinations ,fluid retention of face and acne. We report a case of a 38 year old female patient presented with multiple conditions after  started Prednisolone 60mg OD for rheumatoid arthritis. Now she is admitted in the emergency department of our hospital with signs and symptoms of seizures. Her past medication history includes leviterecetam 500mg BD for seizures and Prednisolone 60mg OD for rheumatoid arthritis. Thereafter she progressively complained about loss of vision .Her vitals were stable. Ophtalmology consultation revealed steroid induced cataract for which she was started with Carboxy methyl cellulose sodium eye drops (Refresh tear drops).Clinicians and Ophthalmologists should be aware of the occular side effects of steroids(1).  .Our case highlights the occurrence of adverse outcomes with Prednisolone  therapy  especially in autoimmune disorders.

Keywords: Glaucoma, Prednisolone, Steroid,  ophthalmology, adverse effects

Table of Contents

Introduction

Prednisolone is a steroid  which prevents the release of substances in the body that causes inflammation. The mechanism of action is that  the drug  irreversibly binds with glucocorticoid receptors ,alpha and beta for which they have a higher  affinity. Alpha receptors  and Beta receptors  are found in virtually all tissues with variable numbers / per cell, depending on the tissue involved. (2-3)Prednisolone can activate and influence biochemical behaviour of most cells. (4)The steroid/receptor complexes can  interact with cellular DNA in the nucleus, binding to steroid-response elements and modifying gene transcription. They induces the  synthesis of some proteins, and inhibit the synthesis of others.

CASE PRESENTATION

A 38 year old female patient who is a known case of  rheumatoid arthritis was brought to the Emergency department of our hospital with signs and symptoms of seizures . She was previously  hospitalized at the department of rheumatology  for  stiffness of legs.  During  the stay in Emergency department she complained about loss of vision so she was referred to Ophtalmology. She was on Prednisolone 60mg OD for arthritis. On examination her eyes revealed stromal edema and  was diagnosed to have steroid induced cataracts and was stabilized with Carboxy methyl cellulose sodium eye drops .The patient had  history of Hypertension and  Epilepsy(5-8)  Her family history was clear and she is a non smoker and non alcoholic. Furthermore she had no history of allergy or hypersensitivity to any other drugs or foods

Physical Examination:

She was conscious ,oriented,  cool, calm, and drowsy. Heart rate was :147/mt Respiratory rate R: 24/mt Blood Presurre :118/72 mmHg and S PO2:99 %,

Laboratory Investigations:

Hemoglobin- 11.5g/dl.; sodium- 127mEq/l.; potassium- 2.6mEq/l.; calcium- 68mg/dl.; Random Blood Sugar- 77mg/dl.; Blood Urea Nitrogen- 37mg/dl.; CRP 156.4,ESR 42

Medications received during hospital stay

The patient received prednisolone  60mg OD for rheumatoid arthritis and leveteracetam 500 mg BD for seizures , syp. Kcl was started for hypokalemia , eye drops carboxymethyl cellulose sodium  was prescribed for cataract .The patient experienced a partial  recovery after having treated for 10 days and was discharged.

DISCUSSION

Prednisolone is a synthetic glucocorticoid with weak mineralocorticoid properties. Its therapeutic effects results from inhibition of macrophage accumulation ,suppression of capillary wall permeability,and collagen deposition the drug is readily absorbed fom gastrointestinal tract . The drug is used for the treatment of wide range of diseases involving inflammation.The side effects depends on dosage and duration of therapy. However ,Occular side effects are common that includes cataracts, exophthalmus, eyelid edema, glaucoma, intraocular pressure increased, irritation. Other side effects includes endocrine, dermatological,CNS,etc. There have also been a few reports of serious adverse reaction however. In May 2005 a case of prednisolone induced gluacoma was reported .The intraocular pressure rise that can complicate the use of topical or systemic corticosteroid has been recognised for 50 years. More recently, following isolation of the myocilin gene (previously known as the trabecular meshwork inducible glucocorticoid response or TIGR gene), there has been renewed interest in this steroid-responsive phenomenon. In 1963, Becker and Mills demonstrated that patients who had glaucoma, or had been diagnosed as glaucoma suspects, had marked IOP rises in response to several weeks' exposure to topical corticosteroids.

CONCLUSION

Patients should be counseled with adequate information regarding the side effects of prednisolone and advised to report back to physician if any symptoms persist . Clinicians and Ophthalmologists should be aware of the occular defects in such patients.

ACKNOWLEDGEMENT

First and foremost, I thank god and my parents for giving   me the strength and

courage to aspire my aims., then  I would like to thank Dr. Midhun, Dept of  Rheumatology

, without whose guidance and support,reporting of this Adverse effect would not have been possible.

References

1)Howlett SA. glucoma associated with prednisolone therapy for arthrithis . SouthMed J. 1975; 68:504-506.

2)McLean JM. Use of ACTH and cortisone. Trans Am Ophthalmol Soc 1950; 48: 293'296.

3)Espildora J, Vicuna P, Diaz E. Cortisone-induced glaucoma: a report on 44 affected eyes (in French). J Fr Ophthalmol. 1981;4(6-7):503-508.

4) Herschler J. Intractable intraocular hypertension induced by repository triamcinolone acetonide. Am J Ophthalmol. 1972;74(3):501-504.

5) Ferry AP, Harris WP, Nelson MH. Histopathologic features of subconjunctivally injected corticosteroids. Am J Ophthalmol. 1987;103(5):716-718.

6)Becker B, Hahn KA. Topical corticosteroids and heredity in primary open-angle glaucoma. Am J Ophthalmol 1964;54:543-551.

7)10. Davies TG. Tonographic survey of the close relatives of patients with chronic simple glaucoma. Br J Ophthalmol. 1968;52:32-39.

8)11. Becker B. Diabetes mellitus and primary open-angle glaucoma. The xxvii Edwards Jackson memorial lecture. Am J Ophthalmol. 1971;1:1'16.

9)Bollinger KE, Smith SD. Prevalence and management of elevated intraocular pressure after placement of an intravitreal sustained-release steroid implant. Curr Opin Ophthalmol. 2009;20(2):99-103.

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