Immunologic conjunctivitis, formerly known as allergic conjunctivitis, is a hypersensitive immune response of the conjunctiva to external allergens. The conjunctiva is often exposed to airborne allergens such as pollen, dust, animal feathers, etc. It is also susceptible to infection by bacteria or other microorganisms (whose proteins can be sensitized), and the use of medications can cause allergic reactions in the conjunctival tissue.
Humoral immune-mediated immune conjunctivitis has a rapid course and is clinically common in chytridiomycosis, atopic conjunctivitis and springtime keratoconjunctivitis; cell-mediated has a chronic course and is commonly seen in vesicular keratoconjunctivitis. Long-term medication of the eye can in turn lead to medically induced conjunctival contact or allergic conjunctivitis, both rapid and delayed. There is also an autoimmune disease that includes dry keratoconjunctivitis, conjunctival aspergillosis, Stevens-Johnson syndrome, etc.
I. Immunological mechanism of ocular surface allergy
Ocular surface allergic diseases, like dry eye, are one of the most common ocular surface diseases, and incomplete statistics show that 5% of the global population suffers from allergic eye disease every year. The number of patients will be even larger. Ocular surface allergy is triggered by contact with various allergens, including plant pollen, animal fur debris, air dust, dust mites, molds, cosmetics, drugs, etc. After the allergens contact the conjunctiva and undergo antigenic processing, the antigenic information is presented to immune effector cells, activating type I hypersensitivity reactions, and in some allergic conjunctivitis type IV hypersensitivity reactions are also involved.
Clinical characteristics and treatment principles of ocular surface allergy
Classification] The international trend is to classify acute ocular surface allergy according to the onset of the disease, including seasonal allergic conjunctivitis, perennial allergic conjunctivitis and contact conjunctivitis, and acute ocular surface allergy accounts for 80%-90% of ocular surface allergy. Another major category is chronic ocular surface allergy, including springtime keratoconjunctivitis, giant papillary conjunctivitis and atopic keratoconjunctivitis, which account for 10%-20% of ocular surface allergy.
Clinical manifestations] The common symptoms of ocular surface allergy patients include itchy eyelid skin and conjunctiva, tearing, burning sensation, pins and needles, photophobia, and aqueous discharge, etc. Among them, the proportion of eye itchiness appears to be 99%, foreign body sensation is 80.8%, and eye redness is 93.7%. Patients’ subjective symptoms can last throughout the allergy season, worsening in warm and dry weather and tending to resolve when the weather becomes colder or wetter. Common signs are mild to moderate conjunctival edema and congestion, with papillary hyperplasia in the upper lid present in 88.1% and follicular hyperplasia in 78.4%. In severe conjunctival edema, eyelid skin edema is also present, more pronounced in the lower lid due to gravity. In severe allergic reactions occasional corneal infiltrates, in the form of coins, are seen, located in the subepithelial and peripheral parts of the cornea.
Diagnosis] In addition to the patient’s symptoms and signs, the collection of medical history is also important in the diagnosis of ocular surface allergy. The focus of the inquiry includes whether there has been a similar course of illness in the past, the season of onset, whether there has been exposure to chemicals, drugs or plants or animals, whether there is a history of systemic allergy, and whether there is a family history.
Conjunctival scraping for eosinophils is an important laboratory diagnostic technique. Normal conjunctival scraping does not find eosinophils, so the finding of eosinophils or eosinophilic granules on conjunctival scraping supports the diagnosis of allergic conjunctivitis. After the occurrence of ocular surface allergy, the IgE content in the patient’s tears is significantly increased. Using nitrocellulose acetate filter paper, tears are aspirated from the inferior vault and quantified by radioimmunoassay for IgE analysis, which can help in the diagnosis as well as in evaluating the effectiveness of therapeutic drugs. Skin tests for antigens or in vitro antigen testing are mostly used for the diagnosis of seasonal and perennial conjunctivitis, but there are some false positives. Conjunctival impression cytology reveals degenerative epithelial cells as well as eosinophils also help in the clinical diagnosis. Conjunctival biopsy for mast cells, eosinophils, or T lymphocytes may be considered in some patients with atypical clinical signs, and needs to be done with caution because it is an invasive test. In addition, ocular excitation tests of antigens can be performed. The diagnosis can be made by using eye drops of suspected antigen suspension, and ocular surface allergy signs such as eye itching within 3-5 min and conjunctival congestion within 20 min, but it is difficult for patients to accept and the clinical application is limited.
【Treatment】 Unlike other ocular surface diseases, allergic conjunctivitis rarely leads to permanent vision loss and has a tendency to remit after removal of the allergenic factors. Therefore, the treatment of ocular surface allergy focuses on prevention of the initiation of allergic reactions and control of symptoms during acute attacks. Depending on the therapeutic target, there are seven major classes of antihistamines, mast cell membrane stabilizers, dual-action drugs (antihistamine + mast cell stabilization), glucocorticoids, nonsteroidal hormone anti-inflammatory drugs, immunosuppressants, and vasoconstrictors.
In the remission and intermittent phases, the main focus is on prevention, and mast cell stabilizers alone can be used along with ocular surface lubricants to increase ocular comfort. For mild allergy, dual-action drugs alone or antihistamine/antihistamine decongestant combination with mast cell stabilizers may be used. For moderate allergy, use a dual-action drug or antihistamine/mast cell stabilizer in combination with a nonsteroidal hormone. For severe allergy, use dual-action drugs in combination with glucocorticoids or immunosuppressive agents.
III. Spring keratoconjunctivitis
Vernal keratoconjunctivitis (VKC), also known as spring keratoconjunctivitis and seasonal conjunctivitis, is a recurrent bilateral chronic ocular surface disease that accounts for 0.5% of allergic eye diseases and has an environmental and racial predisposition. It mainly affects children and adolescents, and is more common in males under 20 years of age.
IgE-mediated hypersensitivity is the most basic pathogenesis of VKC, but type I hypersensitivity alone cannot fully explain the pathogenesis of VKC, and recent studies have found that there is a large number of monocytes infiltrating the conjunctival stroma of VKC patients, most of which belong to the type I hypersensitivity. The majority of these cells are Th2 cells. Therefore, VKC is a combination of type I hypersensitivity (rapid hypersensitivity) and type IV hypersensitivity (delayed hypersensitivity) with the participation of both humoral and cellular immunity.
Clinical manifestations] The main symptom of VKC is ocular itching. After stimulation or environmental triggers during the day, such as dust, dandruff, bright light, wind, sweat stains and rubbing, the symptoms worsen at night; other symptoms include pain, foreign body sensation, light shyness, burning sensation, tearing and increased mucous discharge. Depending on the ocular signs, springtime keratoconjunctivitis is clinically classified as lid-conjunctival type, keratoconjunctival margin type, and mixed type.
The lid-conjunctival type is characterized by a pinkish conjunctiva with giant papillae of the upper lid conjunctiva arranged in a paving stone pattern. The papillae are variable in shape, flat in appearance, and contain capillary plexuses. The papillae are seen under slit lamp to be between 0.1 and 0.8 mm in diameter and connected to each other. Fluorescein can stain the top of the papillae, and there is often a layer of mucousy milky secretion between the papillae and on their surface, forming a pseudomembrane (Figure 7-8). Diffuse small papillae may appear in the lower lid conjunctiva. Follicular reaction is generally not observed in the affected conjunctival area. Conjunctival papillae usually resolve completely without scarring after the inflammation has subsided, unless traumatic manipulations such as freezing, radiation therapy, and surgical removal of the papillae are performed.
The keratoconjunctival rim type is more commonly seen in black individuals. Small papillae appear on both the upper and lower lid conjunctiva. The important clinical manifestation is a yellowish-brown or reddish gelatinous growth at the corneal limbus, which is evident above the corneal limbus. Mixed lid conjunctiva and cornea appear simultaneously as seen on examination in both types.
All types of springtime keratoconjunctivitis can involve the cornea, and the literature reports that the incidence of corneal damage varies from 3% to 50%. The lid-conjunctival type is more common and is mainly caused by the release of inflammatory mediators from mast cells and eosinophils. Corneal damage is most often manifested as diffuse punctate epithelial keratitis, or even shield-shaped aseptic epithelial defects, mostly in the upper middle third of the cornea called “spring ulcers”. In some patients, white Horner-Trantas nodules may be seen at the corneal limbus in the acute phase. Conjunctival smears and biopsies of Trantas nodules with Giemsa staining show a large number of eosinophils and eosinophilic granules. Microvascular opacities may be present in the superior cornea, and rarely there is full circumferential corneal vascularization.
Some patients may also present with ptosis, which may be associated with increased eyelid weight secondary to papillary hypertrophy, and sometimes increased lower lid skin folds may be observed (Dennie’s line). the clinical course of VKC may last intermittently and repeatedly for 2 to 10 years, gradually disappearing in adulthood. in recent years, VKC has been suggested to be associated with the development of cone corneas and atopic cataracts.
[Diagnosis] Patients with severe VKC have typical signs: lid conjunctival papillary pavement stone like hyperplasia, corneal shield ulcers, Horner-Trantas nodules, etc. However, in mild cases, the diagnosis is more difficult to confirm and often requires the use of laboratory tests. The finding of eosinophils or eosinophilic granules in conjunctival scrapings suggests that a local allergic reaction is occurring. In addition, the patient has an increased number of eosinophils, neutrophils or lymphocytes in the tear fluid; IgE levels are higher than normal (7.90mg/ml±0.32mg/ml) and can reach 80.48mg/ml±3.35mg/ml.
Treatment】 Spring keratoconjunctivitis is a self-limiting disease. Short-term medication can reduce symptoms, while long-term medication has a damaging effect on ocular tissues. The choice of treatment depends on the patient’s symptoms and the severity of the ocular surface lesions. Physical therapy includes ice packs and an air-conditioned room to make the patient comfortable. Patients may be considered for relocation to colder areas when treatment is not effective.
Topical glucocorticoids are also effective in suppressing delayed hypersensitivity reactions. Patients in the acute phase can be treated with intermittent hormone therapy, starting with frequent topical (e.g., every 2 hours) application of hormones for 5 to 7 days, followed by rapid dose reduction. In cases of persistent lid conjunctival-type spring keratoconjunctivitis, 0.5 to 1.0 ml of a short-acting hormone such as dexamethasone sodium phosphate (4 mg/ml) or a long-acting hormone such as deferiprone ned (40 mg/ml) can be injected above the lid. However, it is important to note that long-term use can produce serious complications such as glaucoma and cataract.
NSAIDs can be used in both the acute and intermittent phases of an allergic attack and have shown some therapeutic effect in relieving ocular signs and symptoms such as itchy eyes, conjunctival congestion, and tearing.
Mast cell stabilizers such as disodium tinted glycolate and nedolomide, which are commonly used, are best used before exposure to allergens and are less effective in treating patients who have already had an attack. Currently, it is advocated to use cell membrane stabilizers 4 to 5 times a day during the spring season when keratoconjunctivitis is prone to occur, to prevent flare-ups or to maintain the therapeutic effect, and to use hormones for a short period of time for shock treatment only when inflammation strikes.
Antihistamines antagonize the biological activity of the released inflammatory mediators and reduce the patient’s symptoms, and are more effective in combination with mast cell stabilizers. It may reduce ocular discomfort.
In recalcitrant cases with intense photophobia to the point of inability to live normally despite a series of drug treatments (antihistamines, vasoconstrictors), topical application of 2% cyclosporine can quickly control local inflammation and reduce the amount of hormones used. 0.05% FK506 can inhibit IL-2 gene transcription and IgE synthesis signaling pathway, which has good therapeutic effect on intractable spring keratoconjunctivitis.
Artificial tears dilute inflammatory mediators released by mast cells and also improve ocular foreign body sensation caused by punctate defects in the corneal epithelium, provided a preservative-free formulation is used. The effectiveness of desensitization to pollen and other allergens is not yet certain. Staphylococcal blepharitis and conjunctivitis accompanying keratoconjunctivitis in spring should be treated accordingly.
Seasonal allergic conjunctivitis
Clinical manifestations], also known as hay fever conjunctivitis, is the most common type of ocular allergic disease, and its allergens are mainly plant pollen. The disease is characterized by seasonal episodes (usually in spring); it usually develops in both eyes, has a rapid onset, occurs when exposed to the allergen, and resolves or disappears quickly after removal from the allergen. The most common symptom is ocular itching, which can occur in almost all patients and varies in severity. Foreign body sensation, burning sensation, lacrimation, photophobia and mucus discharge may also be present, and the symptoms are aggravated in hot environments.
The main signs are conjunctival congestion and nonspecific lid conjunctival papillae, sometimes combined with conjunctival edema or eyelid edema, which is more likely to occur in children. It rarely affects the cornea, with occasional mild manifestations of punctate epithelial keratitis. Many patients have a history of allergic rhinitis and bronchial asthma.
Treatment]
General treatment includes removal of the allergen, cold compresses on the eyelids, and saline rinsing of the conjunctival sac.
The common medications include antihistamines, mast cell stabilizers, nonsteroidal anti-inflammatory drugs and vasoconstrictors. For patients with severe disease and ineffective treatment with other medications, short-term use of glucocorticoids can be considered. For patients with extraocular symptoms, systemic antihistamines, NSAIDs and glucocorticoids can be used.
Desensitization therapy can be considered if the allergen has been clearly identified. The results are relatively good for allergic conjunctivitis caused by plant pollen and weeds. However, for many other causes of allergic conjunctivitis, the treatment is often not satisfactory.
Prognosis] The prognosis is good, with no visual impairment and few complications.
Five, perennial allergic conjunctivitis (perennial allergic conjunctivitis)
The clinical manifestations are much less common than seasonal allergic conjunctivitis. Allergens are usually house dust, insect mites, animal fur, cotton and linen, and feathers. Clinical manifestations are similar to seasonal. Because the antigens are present year-round, their symptoms persist, with some patients experiencing seasonal exacerbations. Ocular symptoms are usually milder than those of seasonal allergic conjunctivitis. Examination often reveals conjunctival congestion, papillary conjunctivitis combined with a few follicles, and transient eyelid edema. Some patients may have no obvious positive signs.
Treatment] The treatment is basically the same as for seasonal allergic conjunctivitis. Because the allergen is present year-round, long-term medication is usually required. Antihistamines and mast cell stabilizers are commonly used. Glucocorticoids are only used when other treatments are ineffective and should not be used for long periods of time. The effect of desensitization therapy is often very unsatisfactory, so it is rarely used.
Prognosis] The prognosis is good, mostly without visual impairment and rarely with complications.
Six, giant papillary conjunctivitis
The disease is most often seen in those who wear corneal contact lenses (especially those who wear soft corneal contact lenses with inferior materials) or prosthetic eyes. Giant papillary conjunctivitis is closely related to antigen deposition and microtrauma, and is the result of a combination of mechanical stimulation and hypersensitivity, with immune damage based on IgE-mediated type I tachyphylaxis and cell-mediated type IV delayed hypersensitivity.
Clinical manifestations】Patients often first manifest contact lens intolerance and eye itch, but also can appear visual (due to contact lens deposits), foreign body sensation and secretions. The average time to develop macropapillary conjunctivitis is 8 months for those who continuously wear soft contact lenses, compared to 8 years for hard contact lenses.
Examination first shows mild papillary hyperplasia of the upper lid conjunctiva, which is later replaced by large papillae (>0.3 mm), eventually becoming giant papillae (>1 mm). Clinically, giant papillary conjunctivitis is divided into four stages according to the progression of the disease: stage 1, in which the patient has itchy eyes, mild lid conjunctival congestion, and tiny papillary hyperplasia. stage 2, with increased itchy eyes, more mucous discharge, upper lid conjunctival congestion, and irregular papillary hyperplasia. stage 3, with moderate-to-severe itchy eyes, more mucous discharge, upper lid conjunctival papillary hyperplasia with >1mm papillae, and upper lid congestion and edema. stage 4, with severe itchy eyes, large mucus discharge, hyperplasia of the upper lid conjunctival papillae greater than 1 mm, some mushroom-shaped with apical necrosis, and positive fluorescein staining (Figure 7-9). Macropapillary conjunctivitis rarely involves the cornea, but a few patients may present with superficial punctate keratopathy and Trantas’ spots.
[Treatment].
General treatment Replace contact lenses, choose highly permeable contact lenses or small-diameter rigid contact lenses, shorten contact lens wearing time; enhance contact lens care, avoid using care solutions containing preservatives and mercury with potential antigenic activity; it is best to stop wearing contact lenses during the period of worsening inflammation. Prosthetic eyes must be cleaned daily with soap, soaked in water, and placed in a dry place for backup. For those with sutures and silicone rubbing, they should be removed if the situation permits.
Pharmacologic treatment of giant papillary conjunctivitis focuses on reducing histamine release from mast cells and inhibiting local inflammation. Commonly used medications include mast cell stabilizers, antihistamines, glucocorticoids, and nonsteroidal anti-inflammatory drugs. Glucocorticoids should be avoided at all costs and should be limited to the acute phase of megaloblastic conjunctivitis to reduce lid plate congestion and inflammation, but their use can be relaxed in patients wearing prosthetic eyes.
Despite the slow regression of signs and symptoms during treatment, the prognosis is generally good and visual impairment rarely occurs.
Allergic conjunctivitis
It is an inflammation caused by a hypersensitivity reaction of the ocular tissues to an allergen. This section refers specifically to those conjunctivitis that are allergic due to exposure to drugs or other antigens. There are two types of allergic conjunctivitis: rapid and late. The allergens that cause rapid allergy are pollen, corneal contact lenses and their cleaning solutions, etc. Drugs generally cause delayed allergy, such as ciliary muscle paralysis drugs atropine and postmatropine, aminoglycoside antibiotics, antiviral drugs iodoside and trifluorothymidine nucleoside, antiseptic thimerosal and ethylenediaminetetraacetic acid and pupil reduction agents.
Clinical manifestations】 Type I hypersensitivity reactions occur rapidly after a few minutes of exposure to allergenic substances, with ocular pruritus, eyelid edema and swelling, conjunctival congestion and edema. Very few patients may show systemic allergic symptoms. Late onset type IV hypersensitivity reactions occur 24 to 72 hours after the administration of topical medication. This is manifested by acute eczema and leathery lesions of the eyelid skin. Lid conjunctival papillae proliferate, follicle formation, and in severe cases, conjunctival epithelial exfoliation. Speckled epithelial erosions are seen in the lower cornea. The sequelae of chronic contact blepharoconjunctivitis include hyperpigmentation, skin scarring, and lower lid ectropion.
The diagnosis is based on a history of more obvious allergen exposure and rapid resolution of symptoms after removal from exposure; eosinophilia is found on a smear of conjunctival sac secretions.
Treatment】 Find the allergen. Type I hypersensitivity reactions can be relieved by avoiding allergen exposure or by stopping the medication. Local glucocorticoid eye drops (such as 0.1% dexamethasone), vasoconstrictors (0.1% epinephrine or 1% ephedrine), with lid skin redness, papules, can be used 2-3% boric acid water wet compresses. In recent years, the development of several new drugs such as non-steroidal anti-inflammatory drugs 0.5% ketorolac aminotriol, antihistamines 0.05% emetine fumarate and cell membrane stabilizer nedolimus sodium dots, can significantly reduce the symptoms. In severe cases, systemic anti-allergic drugs, such as paracetamol, Xylazine, antihistamines or hormones, can be added.
Eight, vesicular keratoconjunctivitis
It is a delayed immune reaction disease caused by microbial proteins. Common pathogenic microorganisms include; Mycobacterium tuberculosis, Staphylococcus aureus, Candida albicans, Coccidioides spp. and L1, L2, L3 serotypes of Chlamydia trachomatis.
Pathology】Histological section staining showed diffuse polymorphonuclear granulocyte and monocyte infiltration in the epithelium with obvious epithelial edema, vesicles between the epithelium separating the epithelium from the stroma, visible necrotic tissue at the ulcer site, stromal edema, vasodilation, extravasation of erythrocytes, and scattered distribution of fibroblasts and proliferating vascular granulation tissue.
Clinical manifestations】Most commonly seen in women, adolescents and children, with good incidence in spring and summer. There is a mild foreign body sensation, and the symptoms are aggravated if the cornea is involved. Vesicular conjunctivitis is initially solid, with a small raised red lesion (1 to 3 mm) surrounded by a congested area. The lesion is triangular in shape at the corneal limbus, with the tip pointing toward the cornea and the tip easily ulcerating to form an ulcer that heals within 10 to 12 days without scarring. When the lesion occurs at the corneal limbus, there are single or multiple small grayish-white nodules, which are smaller than those in vesicular conjunctivitis, and the lesion is locally congested. After the symptoms of the initial vesicular conjunctivitis have subsided, recurrences may occur in the presence of triggers such as active blepharitis, acute bacterial conjunctivitis, and picky eating. Repeated episodes of herpes can lead to central invasion and the growth of new blood vessels, known as fascicular keratitis, leaving a thin band of opacities after healing and gradual atrophy of the vessels. In rare cases, herpes can occur in the cornea or lid conjunctiva.
Diagnosis] The diagnosis can be made correctly based on the typical symptoms of solid nodular vesicles at the corneal limbus or bulbar conjunctiva with surrounding congestion.
Treatment】Treat the underlying disease that triggered the disease. Topical glucocorticoid eye drops are ordered. Vesicular conjunctivitis caused by tuberculosis mycobacterial proteins is sensitive to hormone therapy, and the main symptoms are reduced within 24 hours of hormone use, and the lesions disappear within 24 hours of subsequent use. Bacterial infection with adjacent tissues should be given antibiotic treatment. Supplementation with various vitamins and attention to nutrition to enhance physical fitness. For patients with severe vision loss due to corneal scarring caused by recurrent fascicular keratitis, corneal transplantation can be considered for treatment.
Autoimmune conjunctivitis
Autoimmune conjunctivitis can cause damage to the epithelium of the eye surface and decrease in the stability of the tear film, leading to the occurrence of ocular surface tear disease, which can seriously affect vision. The main diseases are sjogren’s syndrome (SS), conjunctival aspergillosis, Stevens-Johnson syndrome, etc.
(A) sjogren’s syndrome
The syndrome includes dry eye, dry mouth, and connective tissue damage (arthritis). The diagnosis is made by the presence of two of the three symptoms. It is more prevalent in menopausal women. The lacrimal gland is infiltrated with lymphocytes and plasma cells, causing hyperplasia and structural and functional disruption.
[Clinical manifestations] SS causes dry eye symptoms. Conjunctival congestion and irritation in the lid area, mild conjunctival inflammation and mucous filiform secretions, punctate defects in the corneal epithelium, mostly in the lower cornea, filiform keratitis is not uncommon, and pain is characterized by lightness and severity. Loss of tear film, abnormal tear secretion test, positive conjunctival and corneal tiger red stain and lissamine green stain help clinical diagnosis.
Diagnosis】 Salivary gland tissue biopsy with lymphocyte and plasma cell infiltration, combined with clinical symptoms can confirm the diagnosis.
Treatment】 Mainly for symptomatic treatment, relieve symptoms, treatment measures should be targeted. Artificial tears, closed tear dots, wet room mirror and other measures can be used. For details, see the chapter on ocular surface diseases related to dry eye disease.
(B) Stevens-Johnson syndrome (Stevens-Johnson syndrome)
Etiology】 Stevens-Johnson syndrome is associated with the deposition of immune complexes in the dermis and conjunctival parenchyma. Some drugs such as aminophenazone, anticonvulsants, salicylates, penicillin, ampicillin and isoniazid; or herpes simplex virus, Staphylococcus aureus, adenovirus infection can induce this disease.
The disease is characterized by polymorphic erythema of the mucous membranes and skin, which occurs in young people and rarely develops after the age of 35. After exposure to sensitive drugs or compounds, patients may have prodromal symptoms such as fever, headache or upper respiratory tract infection before eye and skin damage occurs, and severe cases may be accompanied by high fever, muscle pain, nausea, vomiting, diarrhea and wandering arthralgia and pharyngitis. After several days, skin and mucous membrane damage occurs, and the typical course of the disease lasts 4 to 6 weeks.
Ocular manifestations are divided into two categories: acute and chronic. In the acute phase, patients complain of eye pain irritation, discharge and photophobia. The conjunctiva of both eyes is involved. The initial presentation is mucopurulent conjunctivitis and superficial sclerositis. Corneal ulceration is rare in the acute phase, and severe anterior uveitis can occur in some patients. The intense ocular surface inflammatory response leads to loss of conjunctival culet cells, resulting in mucin deficiency, decreased tear film stability, and destruction of conjunctival culet cells coupled with scarring obstruction of the lacrimal secretion ducts can result in severe dry eye. Conjunctival inflammation leads to chronic irritation of the cornea due to entropion, impingement and lid margin keratosis, resulting in persistent epithelial damage and scarring of the corneal vessels, which severely affects vision.
Treatment】 Systemic glucocorticoids can slow down the progression of the disease, while local hormone use is ineffective in treating ocular damage and may cause corneal melting and perforation. Artificial tears can reduce the discomfort after the conjunctivitis secretions are cleared. The presence of impingement and lid entropion should be surgically corrected.
(iii) Cicatricial pemphigoid
A nonspecific chronic conjunctivitis of unknown etiology and poor treatment outcome with oral, nasal, petrous and cutaneous lesions. The severity is higher in female patients than in males. There is a tendency for some of them to reduce on their own.
[Clinical manifestations] often present as recurrent moderate, nonspecific conjunctivitis with occasional mucopurulent changes. It is characterized by conjunctival lesions that form scarring and cause lid adhesions, especially in the lower lid, as well as lid entropion and impingement. Depending on the severity of the disease, it can be divided into stage I subconjunctival fibrosis, stage II narrowing of the dome, stage III lid adhesions, and stage IV extensive lid adhesions resulting in ocular motility disorders.
Recurrent episodes of conjunctival inflammation can damage cup cells and conjunctival scarring obstructs lacrimal gland duct secretion. The lack of aqueous humor and mucin in the tear fluid eventually leads to dry eye. In combination with lid entropion and impingement, corneal damage, corneal vascularization, aggravated scarring, ulceration, and squamous metaplasia of the ocular surface epithelium occur.
Diagnosis] Diagnosis can be made based on clinical manifestations, the presence of eosinophils on conjunctival biopsy, and the presence of immunofluorescence-positive substances (IgG, IgM, IgA) in the basement membrane. Anti-basement circulation antibodies can be detected in the serum of some patients with pemphigus vulgaris.
Treatment] Treatment should be started before scar formation to reduce the degree of tissue damage. Oral aminophenazone and the immunosuppressant cyclophosphamide are effective in some patients. Recent studies have suggested that intravenous immunoglobulin can treat autoimmune diseases including aspergillosis. Those with a long course of the disease tend to lose their vision due to severe complications such as corneal dryness and complete lid adhesions, and may undergo ocular surface reconstruction surgery as appropriate.