Sex: F
Vaccine: HEPA, TTOX, UNK
Symptoms: Fluorescence angiogram abnormal, Full blood count normal, Fundoscopy abnormal, HLA marker study positive, Headache
Clinical narrative: left eye central vision loss; Acute Posterior Multifocal Placoid Pigment Epitheliopathy; extensive swelling of her macula on the left side; Severe Headache; Scotoma; clusters of lesions/large area of subretinal fluid with hypopigmented placoid lesions of the macula; Visual acuity reduced; This case was reported in a literature article and described the occurrence of central vision loss in a 25-year-old female patient who received Hepatitis A vaccine for prophylaxis.    Co-suspect products included POLIO VACCINE for prophylaxis and TETANUS VACCINE for prophylaxis.   The patient's past medical history included papular rash (3 months earlier).   On an unknown date, the patient received Hepatitis A vaccine at an unknown dose, POLIO VACCINE at an unknown dose and TETANUS VACCINE at an unknown dose. On an unknown date, 3 weeks after receiving Hepatitis A vaccine, the patient experienced central vision loss (serious criteria GSK medically significant), headache, acute posterior multifocal placoid pigment epitheliopathy (serious criteria GSK medically significant), scotoma, macular swelling (serious criteria GSK medically significant), eye disorder and visual acuity decreased. The patient was treated with ibuprofen and prednisolone acetate. On an unknown date, the outcome of the central vision loss, headache, acute posterior multifocal placoid pigment epitheliopathy, scotoma, macular swelling and eye disorder were unknown and the outcome of the visual acuity decreased was recovered/resolved.   The reporter considered the central vision loss, headache, acute posterior multifocal placoid pigment epitheliopathy, scotoma, macular swelling, eye disorder and visual acuity decreased to be possibly related to Hepatitis A vaccine.  Additional details were provided as follows: This case was reported in a literature article and described the occurrence of vision loss; severe headache; acute posterior multifocal placoid pigment epitheliopathy (APMPPE) in a 25-year-old female patient who was vaccinated with unspecified hepatitis A vaccine; unspecified polio vaccine, unspecified tetanus vaccines and unspecified meningococcal vaccine (manufacturer unknown) for prophylaxis.  Previously the patient health was good. There was no history of adverse event to immunizations (unknown). Other than a papular rash involving her hands, forearms, feet, and back 3 months earlier. No information on patient's family history was reported. On unspecified date, the patient had received unspecified hepatitis A vaccine; unspecified polio vaccine, unspecified tetanus vaccines and unspecified meningococcal vaccine (administration route and site unspecified, dosage unknown; batch number not provided). The age of vaccination was not provided. On an unspecified date, unknown period after vaccination and previous to vision loss, the patient experienced headaches in increasing severity over the course of four days, not relieved with 800 mg of ibuprofen daily.  On an unspecified date, 3 weeks after vaccination, the patient presented with left eye central vision loss in addition to scotoma and a severe headache. Ophthalmology evaluation included vision, intraocular pressure, slit-lamp, and dilated fundus examination. Examination showed extensive swelling of her macula on the left side with contiguous areas of hyperpigmentation near the superior arcade and hypopigmentation in the posterior pole of the right eye along the superior arcade. Fluorescein angiography in the venous phase showed a large blocking defect with punctate surrounding blocking defects in the left eye and clusters of lesions causing blocking defects in the right eye. Fundus photography showed a large area of subretinal fluid with hypopigmented placoid lesions of the macula without any optic nerve swelling in the left eye and faint hypopigmented placoid lesions along the superior arcuate and near the disk inferiorly without any swelling of optic nerve in the right eye. Indocyanine green angiography demonstrating a prominent large blocking defect with surrounding areas of coalescing punctate blocking defects in the left eye compared with clusters of lesions causing blocking defects in the right eye. The macula optical coherence tomography demonstrated marked subretinal and intraretinal fluid in her left eye. The fluorescein angiography and ICG demonstrated small areas of hypofluorescence in her right eye and placoid lesions with large blocking defect with areas of late leakage and pooling in her left eye. Acute posterior multifocal placoid pigment epitheliopathy was diagnosed based on ophthalmological findings. Neurologic conditions associated with headache were excluded with negative magnetic resonance imaging, computed tomography, lumbar puncture, and X-Ray.  Comprehensive viral and bacterial assays, complete blood count, metabolic panels, cardiolipin, and inflammatory markers were negative except for a mildly elevated C-reactive protein (CRP) of 1.26 (0.5) and coxsackie A immunoglobulin g (IgG) of 1:400 (1:100). Through human leukocyte antigen (HLA) typing, the patient was found to possess the HLA-B 40 and HLA-DB1 15 alleles. She was treated with topical prednisolone acetate 1 percent, which was tapered after three weeks. She was monitored for several months, and visual acuity returned to normal. The author commented, "After investigating other possible causes, immunization was the only identifiable event preceding our patient's APMPPE. Other than temporality, review of published case reports reveals no distinguishing epidemiologic (trigger association, interval, etc.) or demographic (age, gender, etc.) features among the APMPPE cases associated with vaccines. Authors have suggested that molecular mimicry, excessive lymphocyte activation, immune complex formation, or cytokine expression may play a role in the pathogenesis of APMPPE. Our patient possesses the HLA-DR2 antigen (DRB1 15 allele). The only other vaccine associated case of APMPPE in which HLA typing was performed was also HLA-DR2 positive.8 HLA antigens associated with infection-associated APMPPE or APMPPE-like presentations include HLA-B7, HLAB27, and HLA-A3 andC7. Our finding lends support to Wolf's speculation that the HLA-DR2 receptor may act in concert with infectious or vaccine epitopes to produce the characteristic chorioretinal lesions. Therefore, this case report both adds to the body of immunopathology knowledge surrounding APMPPE in association with immunizations and adds polio and tetanus to the growing list of vaccines potentially triggering the disease." The author concluded, "This case report adds to the body of knowledge regarding possible atypical interplay between vaccines and specific T-cell receptors of the host immune system and adds Polio and Tetanus to the growing list of vaccines potentially triggering acute posterior multifocal placoid pigment epitheliopathy. Increased awareness of the presentation of acute posterior multifocal placoid pigment epitheliopathy and that it may arise after immunization may also improve evaluation of acute changes in visual acuity."      Lab Comments: Lab test done on an unknown date. Ophthalmology evaluation included vision, intraocular pressure, slit-lamp, and dilated fundus examination. Examination showed extensive swelling of her macula on the left side with contiguous areas of hyperpigmentation near the superior arcade and hypopigmentation in the posterior pole of the right eye along the superior arcade. Fluorescein angiography in the venous phase showed a large blocking defect with punctate surrounding blocking defects in the left eye and clusters of lesions causing blocking defects in the right eye. Fundus photography showed a large area of subretinal fluid with hypopigmented placoid lesions of the macula without any optic nerve swelling in the left eye and faint hypopigmented placoid lesions along the superior arcuate and near the disk inferiorly without any swelling of optic nerve in the right eye. Indocyanine green angiography demonstrating a prominent large blocking defect with surrounding areas of coalescing punctate blocking defects in the left eye compared with clusters of lesions causing blocking defects in the right eye. The macula optical coherence tomography demonstrated marked subretinal and intraretinal fluid in her left eye. The fluorescein angiography and ICG demonstrated small areas of hypofluorescence in her right eye and placoid lesions with large blocking defect with areas of late leakage and pooling in her left eye. Neurologic conditions associated with headache were excluded with negative magnetic resonance imaging, computed tomography, lumbar puncture, and X-Ray. Comprehensive viral and bacterial assays, complete blood count, metabolic panels, cardiolipin, and inflammatory markers were negative. Through human leukocyte antigen (HLA) typing, the patient was found to possess the HLA-B 40 and HLA-DB1 15 alleles