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BK virus retinitis: Authors’ reply
Ophthalmology Volume 106, Number 12, December 1999 effects related to a possible postischemic reperfusion injury cascade. We support Dr. Marmor’s suggestion to further evaluate therapeutic options in retinal arterial occlusion, such as treatment with steroids. To our knowledge, there are no controlled studies in the scientific literature, but a case series in which the circulation promoting effect of a high dose steroid bolus was documented angiographically.3 GISBERT RICHARD, MD Hamburg, Germany
In contrast, our patient featured grayish, subtle lesions with focal depigmentation surrounded by a zone of retinal edema.3 Also, patients with ocular toxoplasmosis will usually have raised antibody titers for Toxoplasma gondii,1,2 a finding not present in our patient. Finally, when tissue for histopathologic examination is available, the features encountered in BK virus retinitis1 are distinctly different from those found in ocular toxoplasmosis.1,4 STEFAN SEREGARD, MD, PHD Stockholm, Sweden
References
References
1. Hayreh SS. Retinal arterial occlusion with LIF using rTPA. Ophthalmology 1999;106:1236 –9. 2. Augsburger JJ, Magargal LE. Visual prognosis following treatment of acute central retinal artery obstruction. Br J Ophthalmol 1980;64:913–7. 3. Hausmann N, Richard G. Effect of high dose steroid bolus on occlusion of ocular central artery: angiographic study. BMJ 1991;303:1445– 6.
BK Virus Retinitis Dear Editor: In their case of BK virus retinitis in a patient with the acquired immune deficiency syndrome (AIDS), Hedquist et al1 observed “no signs of perivasculitis or vitritis.” The lesions in their patient could have been mistaken for toxoplasmic vitreoretinitis, but the absence of vitreous inflammatory cells made toxoplasmosis unlikely. Cytomegalovirus retinitis is always associated with the presence of tiny, white, usually linear, vitreous cells that can be seen only with careful biomicroscopic examination. We reported a case of bilateral bacterial retinitis in an AIDS patient, in which there was marked vitreous inflammation.2 The presence or absence of vitritis is a very helpful clue as to the pathogenesis of infectious retinitis. DAVID M. BACHMAN, MD Washington, DC References 1. Hedquist BG, Bratt G, Hammarin AL, et al. Identification of BK virus in a patient with acquired immune deficiency syndrome and bilateral atypical retinitis. Ophthalmology 1999; 106:129 –32. 2. Davis JL, Nussenblatt RB, Bachman DM, et al. Endogenous bacterial retinitis in AIDS. Am J Ophthalmol 1989;107:613– 23.
Authors’ reply Dear Editor: Indeed, as pointed out by Dr. Bachman, the presence of vitritis (absent in our patient) is very helpful when making a clinical diagnosis of ocular toxoplasmosis in patients with the acquired immune deficiency syndrome (AIDS).1,2 However, most patients with AIDS and ocular toxoplasmosis will also show more conspicuous lesions of the retina than the discrete multifocal lesions recognized in our patient. Such readily apparent homogenous, yellow-white lesions may show fluffy borders and adjacent vascular sheathing.1,2
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1. Holland GN, Engstrom RE Jr, Glasgow BJ, et al. Ocular toxoplasmosis in patients with the acquired immunodeficiency syndrome. Am J Ophthalmol 1988;106:653– 67. 2. Cochereau-Massin I, LeHoang P, Lautier-Frau M, et al. Ocular toxoplasmosis in human immunodeficiency virus–infected patients. Am J Ophthalmol 1992;114:130 –5. 3. Hedquist BG, Bratt G, Hammarin A, et al. Identification of BK virus in a patient with acquired immune deficiency syndrome and bilateral atypical retinitis. Ophthalmology 1999;106:129 – 32. 4. Seregard S. Retinochoroiditis in the acquired immune deficiency syndrome. Findings in consecutive post-mortem examinations. Acta Ophthalmol (Copenh) 1994;72:223– 8.
Weight Loss in Idiopathic Intracranial Hypertension Dear Editor: Johnson et al1 have made an important observation regarding the treatment of idiopathic intracranial hypertension. However, significant weight loss can be expected to occur secondary to the ingestion of oral diuretics.2 It is not necessarily the effect of diet alone. We wondered whether they had considered the possibility that the acetazolamide had contributed to, if not caused, the weight loss in the patients who had evidenced improvement in their papilledema. It may be that those patients who lost weight were highly motivated and were therefore the ones who were compliant with their acetazolamide regimen. It is therefore possible that the weight loss was an independent phenomenon and that the effect of acetazolamide on papilledema was related to a more direct effect on cerebrospinal fluid dynamics. We realize that one patient had complete resolution of papilledema without the use of acetazolomide but would suggest that for the remainder, the effects of weight loss per se cannot be distinguished from other possible effects of acetazolomide on the basis of this study. GAWN MCILWAINE, FRCS, FRCOPHTH CHRISTIAN LUECK, FRCPE, PHD Edinburgh, Scotland References 1. Johnson LN, Krohel GB, Madsen RW, March GA Jr. The role of weight loss and acetazolamide in the treatment of idiopathic intracranial hypertension (pseudotumour cerebri). Ophthalmology 1998;105:2313–7. 2. Patterson JH, Adams KF Jr, Applefield MM, et al. Oral torsemide in patients with chronic congestive heart failure: effects on body weight, edema, and electrolyte excretion.
In contrast, our patient featured grayish, subtle lesions with focal depigmentation surrounded by a zone of retinal edema.3 Also, patients with ocular toxoplasmosis will usually have raised antibody titers for Toxoplasma gondii,1,2 a finding not present in our patient. Finally, when tissue for histopathologic examination is available, the features encountered in BK virus retinitis1 are distinctly different from those found in ocular toxoplasmosis.1,4 STEFAN SEREGARD, MD, PHD Stockholm, Sweden
References
References
1. Hayreh SS. Retinal arterial occlusion with LIF using rTPA. Ophthalmology 1999;106:1236 –9. 2. Augsburger JJ, Magargal LE. Visual prognosis following treatment of acute central retinal artery obstruction. Br J Ophthalmol 1980;64:913–7. 3. Hausmann N, Richard G. Effect of high dose steroid bolus on occlusion of ocular central artery: angiographic study. BMJ 1991;303:1445– 6.
BK Virus Retinitis Dear Editor: In their case of BK virus retinitis in a patient with the acquired immune deficiency syndrome (AIDS), Hedquist et al1 observed “no signs of perivasculitis or vitritis.” The lesions in their patient could have been mistaken for toxoplasmic vitreoretinitis, but the absence of vitreous inflammatory cells made toxoplasmosis unlikely. Cytomegalovirus retinitis is always associated with the presence of tiny, white, usually linear, vitreous cells that can be seen only with careful biomicroscopic examination. We reported a case of bilateral bacterial retinitis in an AIDS patient, in which there was marked vitreous inflammation.2 The presence or absence of vitritis is a very helpful clue as to the pathogenesis of infectious retinitis. DAVID M. BACHMAN, MD Washington, DC References 1. Hedquist BG, Bratt G, Hammarin AL, et al. Identification of BK virus in a patient with acquired immune deficiency syndrome and bilateral atypical retinitis. Ophthalmology 1999; 106:129 –32. 2. Davis JL, Nussenblatt RB, Bachman DM, et al. Endogenous bacterial retinitis in AIDS. Am J Ophthalmol 1989;107:613– 23.
Authors’ reply Dear Editor: Indeed, as pointed out by Dr. Bachman, the presence of vitritis (absent in our patient) is very helpful when making a clinical diagnosis of ocular toxoplasmosis in patients with the acquired immune deficiency syndrome (AIDS).1,2 However, most patients with AIDS and ocular toxoplasmosis will also show more conspicuous lesions of the retina than the discrete multifocal lesions recognized in our patient. Such readily apparent homogenous, yellow-white lesions may show fluffy borders and adjacent vascular sheathing.1,2
2232
1. Holland GN, Engstrom RE Jr, Glasgow BJ, et al. Ocular toxoplasmosis in patients with the acquired immunodeficiency syndrome. Am J Ophthalmol 1988;106:653– 67. 2. Cochereau-Massin I, LeHoang P, Lautier-Frau M, et al. Ocular toxoplasmosis in human immunodeficiency virus–infected patients. Am J Ophthalmol 1992;114:130 –5. 3. Hedquist BG, Bratt G, Hammarin A, et al. Identification of BK virus in a patient with acquired immune deficiency syndrome and bilateral atypical retinitis. Ophthalmology 1999;106:129 – 32. 4. Seregard S. Retinochoroiditis in the acquired immune deficiency syndrome. Findings in consecutive post-mortem examinations. Acta Ophthalmol (Copenh) 1994;72:223– 8.
Weight Loss in Idiopathic Intracranial Hypertension Dear Editor: Johnson et al1 have made an important observation regarding the treatment of idiopathic intracranial hypertension. However, significant weight loss can be expected to occur secondary to the ingestion of oral diuretics.2 It is not necessarily the effect of diet alone. We wondered whether they had considered the possibility that the acetazolamide had contributed to, if not caused, the weight loss in the patients who had evidenced improvement in their papilledema. It may be that those patients who lost weight were highly motivated and were therefore the ones who were compliant with their acetazolamide regimen. It is therefore possible that the weight loss was an independent phenomenon and that the effect of acetazolamide on papilledema was related to a more direct effect on cerebrospinal fluid dynamics. We realize that one patient had complete resolution of papilledema without the use of acetazolomide but would suggest that for the remainder, the effects of weight loss per se cannot be distinguished from other possible effects of acetazolomide on the basis of this study. GAWN MCILWAINE, FRCS, FRCOPHTH CHRISTIAN LUECK, FRCPE, PHD Edinburgh, Scotland References 1. Johnson LN, Krohel GB, Madsen RW, March GA Jr. The role of weight loss and acetazolamide in the treatment of idiopathic intracranial hypertension (pseudotumour cerebri). Ophthalmology 1998;105:2313–7. 2. Patterson JH, Adams KF Jr, Applefield MM, et al. Oral torsemide in patients with chronic congestive heart failure: effects on body weight, edema, and electrolyte excretion.