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Cystoid macular edema secondary to nab-paclitaxel therapy.

Patient 1 is a 65-year-old woman with a diagnosis of breast cancer metastatic to bone, pleura, pericardium, and lymph nodes. She received adjuvant chemotherapy with cyclophosphamide, methotrexate, and fluorouracil following her original diagnosis in 1990. In 1998, she progressed systemically and was treated with multiple lines of endocrine therapy. She subsequently received sequential single-agent chemotherapy with capecitabine, gemcitabine, vinorelbine, paclitaxel, and weekly anthracycline therapy with conventional doxorubicin. Her past medical history included hypertension, obesity, and stable chronic renal impairment with symptomatic fluid overload responding to diuretic therapy. In July 2008 she started weekly nanoparticle albumin bound (nab) –paclitaxel (Abraxane; Abraxis Bioscience, Bridgewater, NJ) and bevacizumab; the bevacizumab was discontinued after a single dose because of proteinuria. In October 2008, she complained of deterioration in her vision over a period of 6 weeks that prevented her from reading the newspaper. Visual acuity was 20/60 in both eyes and color vision was intact. Fundoscopy was normal. Two weeks later, her visual acuity had deteriorated to 20/80 on the right. Fundoscopic examination was suggestive of macular edema bilaterally. Ocular coherence tomography (OCT) showed cystic spaces in the retina, confirming cystoid macular edema (CME), with no leakage of dye evident on angiography. The nab-paclitaxel was discontinued and she was treated with topical steroids and nonsteroidal antiinflammatory drugs. She experienced rapid recovery of her visual function, such that she could read newspapers comfortably on review 3 weeks after stopping nab-paclitaxel. Her visual acuity had recovered to 20/60 on the right and 20/40 on the left at the time of this review. Patient 2 is a 58-year-old woman who was diagnosed with a T2N0 left breast cancer at the age of 38 years in 1988. She was treated with wide local excision and axillary lymph node dissection, followed by adjuvant radiotherapy. She did not receive adjuvant chemotherapy or endocrine therapy. She developed bone, liver, and pleural metastases 10 years after her original diagnosis. She was treated with sequential endocrine therapies from January 1999 to May 2006. At that time she was switched to the oral antimetabolite chemotherapy drug capecitabine, and bevacizumab was added in March 2007. She was switched to nab-paclitaxel plus bevacizumab in August 2007. In January 2008 she complained of increased tear production, which was relieved by lubricant eye drops. An eye examination by her local ophthalmologist showed no evidence of canalicular stenosis. She continued to receive nab-paclitaxel and bevacizumab, although the bevacizumab was held from August 2008, in anticipation of possible cataract surgery. She experienced deterioration of her vision despite discontinuation of bevacizumab. On examination in September 2008, 11 months after commencing nab-paclitaxel, her best corrected visual acuity was 20/70 in both eyes. On dilated fundus examination there was evidence of bilateral cystoid macular edema (Fig 1). OCT confirmed bilateral cystic retinal changes (Fig 2, white arrows). Fluorescein angiography showed no evidence of leakage. The nab-paclitaxel was discontinued. On review 2 months later, her visual acuity had improved to 20/50 on the right and 20/30 on the left. Follow-up OCT performed 3 months after discontinuation of nab-paclitaxel confirmed marked decrease in macular edema (Fig 3, white arrows). Paclitaxel is a member of the taxane family of microtubule stabilizing agents that has demonstrated clinical efficacy in multiple human malignancies. Because of its hydrophobic nature, paclitaxel is poorly soluble. The first licensed formulation of paclitaxel (CrEL-paclitaxel or Taxol, Bristol-Myers Squibb, Princeton, NJ) used polyethylated castor oil (Cremophor EL) and ethanol to emulsify paclitaxel. The CrEL formulation can cause hypersensitivity reactions, requiring a prolonged infusion time and premedication with steroids and antihistamines. In addition, special infusion tubing and inline filters must be used when administering CrEL-paclitaxel. A newer formulation of paclitaxel, nab-paclitaxel, uses albumin bound nanoparticles to enhance the solubility of the drug. This formulation has been shown in pharmacokinetic studies to result in a higher paclitaxel clearance and volume of distribution than the CrEL formulation. A pivotal phase III trial in patients with metastatic breast cancer randomly assigned 454 patients to the standard arm of CrEL-paclitaxel 175 mg/m versus nab-paclitaxel 260 mg/m, with both drugs given every 3 weeks. The nab formulation was superior in terms of overall response rate (33% v 19%; P .001) and time to progression (23.0 v 16.9 weeks; hazard ratio, 0.75; P .006). Macular edema is a condition characterized by abnormal thickening of the retina associated with the accumulation of excess fluid in the extracellular space of the neurosensory retina. It can occur in Fig 1. JOURNAL OF CLINICAL ONCOLOGY D I A G N O S I S I N O N C O L O G Y VOLUME 28 NUMBER 33 NOVEMBER 2