Beneficial Effects of Corticosteroids on Ocular Myasthenia Gravis

Kupersmith, Mark J.; Moster, Mark L.; Bhuiyan, Sam; Warren, Floyd A.; Weinberg, H.

doi:10.1001/archneur.1996.00550080128020

Cited by 97 publications

(58 citation statements)

References 15 publications

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“…Our results confirm the findings of a previous study 9 that moderate dose (50-60 mg) daily prednisone, reduced over 6 weeks, followed by 10 mg or less daily, resolves diplopia in primary and downward gaze more frequently than with pyridostigmine alone. This treatment regimen also reduces the amount of PCT measured ocular deviation in primary and downward gaze.…”

Section: Discussionsupporting

confidence: 92%

“…3 In contrast, oral prednisone (up to 100 mg on alternate days) improved ocular motor function in seven of eight patients in one study 8 and alleviated diplopia for 2 years in 66% of 32 OMG patients with lower doses. 9 Using lower doses of prednisone and a more uniform treatment protocol than the previous study, 9 we evaluated the effect of prednisone and pyridostigmine in reducing diplopia and ocular motor dysfunction in 89 OMG patients. The development of GMG in this group has been described recently.…”

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confidence: 99%

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Ocular motor dysfunction and ptosis in ocular myasthenia gravis: effects of treatment

Kupersmith

2005

British Journal of Ophthalmology

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Aim: The optimal treatment of ocular myasthenia gravis (OMG) remains unknown. The authors evaluated the efficacy of prednisone and pyridostigmine in reducing diplopia, ocular motor dysfunction, and ptosis in patients with OMG. Methods: Review of records from a clinical database from one neuro-ophthalmology service of patients presenting with OMG between 1990 and 2002, excluding those who developed generalised MG within the first month after diagnosis. Institutional review board approval was obtained for this study. Participants/interventions: Non-randomised, unmasked, therapy was given. 55 patients with diplopia in primary or downward gaze and clinically demonstrable extraocular muscle dysfunction received prednisone. 34 patients who had contraindications to steroids or who refused treatment with prednisone received pyridostigmine only. Over 5 days the daily prednisone dose was increased to 50-60 mg and then gradually reduced to 10 mg, followed by further reduction as tolerated. The pyridostigmine dose was begun at 180 mg daily and increased as tolerated. Main outcome measures: Follow up evaluations, performed at 1, 3-6, 12, and 24 months, detailed the frequency of ptosis and diplopia and the amount of ocular motor deviation in primary and downward gaze. Results: The prednisone and pyridostigmine groups were similar for age, sex, acetylcholine receptor antibody level, prism cover test results for primary and downward gaze, diplopia in primary and downward gaze, and unilateral ptosis. Bilateral ptosis was present in 32.4% of the pyridostigmine group and 10.9% of the prednisone group (p = 0.02). The prednisone group showed resolution in primary gaze diplopia, downgaze diplopia, unilateral ptosis, and bilateral ptosis in 73.5%, 75.5%, 85.7%, and 98%, respectively at 1 month. The benefit persisted at 3-6, 12, and 24 months except for the bilateral ptosis. The pyridostigmine group showed resolution in primary gaze diplopia, downgaze diplopia, unilateral ptosis, and bilateral ptosis in 6.9%, 17.2%, 50%, and 76.7% of patients after 1 month of treatment. The prism cover results improved (p = 0.003) in the prednisone group only. In the prednisone group, four patients had no response to therapy. Among the 51 prednisone responsive patients, there were 33 recurrences in 26 patients. 12 patients, all prednisone treated, had remissions. Except for three patients who developed diabetes, no patient developed a clinically significant systemic corticosteroid complication. Conclusion: These results suggest that 50-60 mg daily prednisone followed by lower doses (10 mg or less) has the benefit of resolving ptosis and diplopia that lasts for at least 2 years in approximately 70% of patients.

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Section: Discussionsupporting

confidence: 92%

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confidence: 99%

Ocular motor dysfunction and ptosis in ocular myasthenia gravis: effects of treatment

Kupersmith

2005

British Journal of Ophthalmology

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“…If larger dosages are used for a short time, few major adverse effects should result, even if lower doses are continued for many months. Kupersmith et al 4 reported that a moderate dose, reduced during a 6-week course and followed by low-dose daily or alternate-day corticosteroid therapy, reduced the conversion rate to generalized myasthenia gravis to 9% in a small cohort of 32 patients. The development of systemic hypertension, diabetes mellitus, osteoporosis, gastrointestinal tract disorders, or infectious illness that typically occur with moderate-to high-dose daily or alternate-day therapy 7 should be minimized with long-term dosages of no greater than 10 mg/d, use of cointerventions to control blood pressure and hyperglycemia, 8,9 and use of prophylactic cointerventions for gastrointestinal tract and bone dysfunction.…”

Section: Resultsmentioning

confidence: 99%

Development of Generalized Disease at 2 Years in Patients With Ocular Myasthenia Gravis

Kupersmith¹,

Latkany²,

Homel³

2003

Arch Neurol

227

159

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“…If larger doses of prednisone are used for a short period of time, there should be few major side effects, even if lower doses are continued over many months. Three observational studies describe that the use of moderatedose followed by low-dose corticosteroids reduces the conversion rate to generalized myasthenia gravis to 4-11% at 2 years [4][5][6]. Two observational studies reported that a similar corticosteroid regimen restored binocular vision that persisted at 2 years in approximately 70% of patients [5,7].…”

Section: Introductionmentioning

confidence: 99%

Ocular myasthenia gravis: treatment successes and failures in patients with long-term follow-up

Kupersmith

2009

J Neurol

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We previously reported that prednisone reduced the frequency of generalized myasthenia (GMG) and controlled diplopia without major adverse effects at 2 years in patients with ocular myasthenia gravis (OMG). Questions remain as to whether study subjects had long-standing disease, biasing results towards a steroid benefit, and if prednisone merely delayed GMG onset. Here, we performed a record review of a referral neuro-ophthalmology service OMG database for patients who were followed-up for > or =4 years or until GMG developed. We studied the effect of prednisone on GMG incidence and control of ocular symptoms. Generally, patients with diplopia were recommended for prednisone therapy. Most remained on daily 2.5-10 mg for diplopia control. We compared the results for prednisone-treated and "untreated" (pyridostigmine only) patients. Of 87 patients, 55 were in the prednisone-treated and 32 were in the untreated groups. GMG developed in 7 (13%) of the prednisone-treated (OR 0.41; 95% CI 0.22-0.76) and in 16 (50%) of the untreated (OR 2.78; 95% CI 1.68-4.60) patients. After OMG onset, GMG developed at a mean 5.8 and 0.22 years in prednisone and untreated groups. Diplopia was present at the last exam in 27% of the prednisone-treated (mean 7.2 years) and in 57% of the untreated (mean 4.6 years) OMG patients. For 48 prednisone-treated patients who did not develop GMG, OMG treatment failure occurred in 13. Thus, prednisone delays the onset of GMG and has sustained benefit in reducing the incidence of GMG and controlling diplopia. Without prednisone, GMG develops in 50% of OMG patients, typically within 1 year.

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Beneficial Effects of Corticosteroids on Ocular Myasthenia Gravis

Cited by 97 publications

References 15 publications

Ocular motor dysfunction and ptosis in ocular myasthenia gravis: effects of treatment

Ocular motor dysfunction and ptosis in ocular myasthenia gravis: effects of treatment

Development of Generalized Disease at 2 Years in Patients With Ocular Myasthenia Gravis

Ocular myasthenia gravis: treatment successes and failures in patients with long-term follow-up

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