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Ocular Manifestations of Granulomatosis with Polyangiitis: a Review of the Literature

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Ocular Manifestations of Granulomatosis with Polyangiitis: a Review of the Literature Ophthalmol Ther https://doi.org/10.1007/s40123-019-0176-8 REVIEW Ocular Manifestations of Granulomatosis with Polyangiitis: A Review of the Literature Evdokia Sfiniadaki . Ioanna Tsiara . Panagiotis Theodossiadis . Irini Chatziralli Received: January 13, 2019 Ó The Author(s) 2019 ABSTRACT intervention is required to reduce the rates of relapse and morbidity in patients with GPA. Granulomatosis with polyangiitis (GPA) is a rare systemic autoimmune disease of unknown eti- ology that is characterized by granulomatous Keywords: Eye; Diagnosis; Ocular; Orbital; inflammation, tissue necrosis, and vasculitis in Treatment; Wegener’s small- and medium-sized vessels. Ocular and orbital manifestations are common in almost half of patients with GPA, affecting every INTRODUCTION structure of the eye, from the eyelid and orbit to the retina, the choroid, and the optic nerve, Granulomatosis with polyangiitis (GPA), for- with a wide range of severity. Since imaging merly known as Wegener’s granulomatosis findings are not always specific for the diagnosis (WG), is a rare systemic autoimmune disease of of GPA, biopsy is useful to confirm the diagno- unknown etiology that occurs predominantly sis. Regarding treatment, a localized pharma- in Caucasians and is extremely rare in black ceutical and surgical approach may be helpful populations [1]. The prevalence of GPA is esti- to achieve remission, while immunosuppressive mated to be 3 cases per 100,000 people, and the therapy, corticosteroids, and cyclosporine are annual incidence is approximately 8–10 cases also useful. In any case, multidisciplinary per million, but this varies depending on loca- tion [1]. The disease was first described in 1931 by Heintz Klinger, but was named in 1936 by a Evdokia Sfiniadaki and Ioanna Tsiara contributed German pathologist, Friedrich Wegener, who equally to this manuscript. defined the disorder and clearly distinguished it Enhanced Digital Features To view enhanced digital from other inflammatory diseases [2]. GPA is features for this article go to https://doi.org/10.6084/ characterized by granulomatous inflammation, m9.figshare.7798676. tissue necrosis, and variable degrees of vasculitis in small- and medium-sized blood vessels [2]. E. Sfiniadaki Á I. Tsiara Granulomatosis with polyangiitis has a wide Medical School, National and Kapodistrian spectrum of clinical manifestations with vari- University of Athens, Athens, Greece able severity. In order to facilitate the classifi- P. Theodossiadis Á I. Chatziralli (&) cation of patients, GPA may be broadly divided 2nd Department of Ophthalmology, National and into a limited form and a systemic form. The Kapodistrian University of Athens, Athens, Greece e-mail: [email protected] limited form is characterized by the absence of Ophthalmol Ther renal involvement and is isolated to the upper the disease process. Antineutrophil cytoplas- and lower respiratory tracts. The systemic form matic antibody (ANCA), either c-ANCA or may involve kidneys and other organs besides p-ANCA, is associated with the appearance of the respiratory tract. Thus, patients with the GPA. In particular, c-ANCA against proteinase 3 systemic form suffer a more severe course of the (PR3-ANCA) is present in over 90% of patients disease compared to those with the limited with the disease, while the p-ANCA pattern form [2–4]. There is no gender predilection for (typically caused by antibodies against the disease, although women are more likely to myeloperoxidase, MPO) occurs in approxi- have the limited form of the disease [3]. Patients mately 10% of patients. The presence of ANCA are typically in their fourth or fifth decade at the stimulates neutrophil degranulation, leading to time of diagnosis, and fewer than 15% of all the release of lytic enzymes and reactive oxygen cases involve those under 19 years old [2–4]. species, which damage the endothelium and Ocular and orbital manifestations are com- provoke vasculitis. B cells and T cells are also mon in almost half of patients with either the involved in the pathogenesis of vasculitis. There limited or the systemic form of GPA, and they is a strong association of granulomatous can be also present as initial features of the inflammation with T-cell response [5, 9]. disease [4]. In light of the above, the purpose of Environmental etiologic factors that have this review is to shed light into the ocular been associated with GPA include dust inhala- manifestations of GPA while also emphasizing tion, exposure to silica, pollution, smoking, its pathogenesis. metals, chemicals, and medicines such as This article is based on previously conducted hydralazine, phenytoin, sulfasalazine, antithy- studies and does not contain any studies with roid medication, and allopurinol. In addition, a human participants or animals performed by role of microbes in the pathogenesis of the any of the authors. disease is demonstrated by the fact that chronic nasal carriage of S. aureus is connected with relapses of GPA [5]. PATHOGENESIS Although the pathogenesis of GPA remains OCULAR MANIFESTATIONS unknown, attempts to identify its etiology have OF GRANULOMATOSIS been made and have focused on the roles of WITH POLYANGIITIS genetic, immunologic, and environmental fac- tors as well as microbial pathogens [5]. Ocular and orbital involvement can occur in The predominance of GPA in Caucasians patients with GPA, affecting every structure of may indicate that genetic factors contribute to the eye from the eyelid and orbit to the optic the pathogenesis of the disease. Moreover, GPA nerve, with a wide range of severity [4]. has been observed in siblings, and higher fre- quencies of certain HLA markers have been Orbit identified without presenting a consistent rela- tionship with the disease [5, 6]. Other respon- sible gene pathways include alpha-1 antitrypsin Orbital involvement is one of the most frequent deficiency and polymorphisms of CTLA-4 manifestations of GPA, occurring in almost (which is involved in T-cell activation) and Fcc 45–50% of patients. It may be the result of receptor IIIb on the surfaces of neutrophils and contiguous disease in adjacent paranasal sinu- monocytes/macrophages. Furthermore, the ses, or it may occur as a focal disease with presence of the PTPN22 R620W allele (associ- orbital granuloma formation or vasculitis [4]. ated with T-cell activation) and SERPINA1 gene Orbital manifestations concern the lacrimal variants has also been implicated in GPA [7, 8]. gland (dacryoadenitis), extraocular muscles The interaction between cellular and (orbital myositis), and soft tissues (orbital humoral immunity is believed to contribute to pseudotumor) [4, 10–13]. Ophthalmol Ther Common signs and symptoms of orbital GPA syndrome [4, 12, 15]. Nasolacrimal duct include proptosis, epiphora, diplopia, sudden obstruction is a late finding and can be either onset of pain, erythema, eyelid edema and secondary to inflammatory spread from adja- reduced vision. Proptosis is considered an cent sinonasal disease, or a direct result of focal important clinical sign in patients with sus- GPA inflammation. As a result of the naso- pected GPA, since in combination with upper or lacrimal blockage, dacryocystitis and epiphora lower airway disease or glomerulonephritis, it can occur. Florid xanthelasma (yellow lids) can implies a diagnosis of GPA. Proptosis and lid appear even in patients with normal metabo- destruction may provoke exposure keratopathy, lism, and is a result of orbital inflammation in which can lead to corneal ulceration, ocular GPA, which may cause lipid accumulation perforation, and blindness. Rarely, proptosis is [16, 17]. followed by enophthalmos, which is a late Conjunctival disease has been reported in up consequence of chronic orbital inflammation to 16% of patients with GPA. Early involvement due to fibrotic changes in the orbit. Epiphora is is presented with conjunctival hyperemia. another symptom of orbital involvement that is Granuloma ulceration and necrosis can be pre- often provoked by nasolacrimal duct obstruc- sent, leading to cicatrizing conjunctivitis. Pro- tion or by lacrimal sac mucocele. Diplopia arises gressive conjunctival cicatrization can cause as a result of inflammation of extraocular mus- symblepharon or the formation of fibrovascular cles (orbital muscles), vasculitis of the vasa tissue that spreads across the ocular surface to vasorum above, and compression of the optic the eyelid [4, 18, 19]. This results in entropion nerve by the orbital mass, which may lead to and trichiasis, with eyelashes turned against the optic nerve ischemia and even blindness. GPA globe. Conjunctival involvement can exhibit may infiltrate the orbital apex and thus the symptoms such as ocular redness, foreign body optic nerve, resulting in painless optic neu- sensation, blurred vision, and possibly bloody ropathy and edema of the optic nerve followed tears [4]. Tarsal conjunctivitis, which can be by atrophy. Further infiltration is responsible associated with nasolacrimal duct obstruction for painful ophthalmoplegia and blindness. and subglottic stenosis, has been also reported Extension of the orbital mass leads to destruc- in patients with GPA [20]. tion of neighboring bony structures or neo-os- sification. Note that orbital disease is associated Sclera with significant morbidity, including visual loss and facial deformity [10–13]. It is also worth Scleritis is an inflammation of the whole mentioning that in the few cases of GPA in thickness of the sclera, which can cause serious children, it initially presents with orbital man- ocular morbidity
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