Chronic Anterior Uveitis is the most common Uveitis and is usually treated with eye drops. Uveitis is an (inflammation in the internal layers of the eye) Intraocular Inflammatory condition resulting from an Infection or Autoimmune response in the body and is characterized by the presence of severe oxidative stress and inflammation in the local tissue. Chronic uveitis and unchecked inflammation can cause damage to eye tissue and reduce vision, and even severe vision loss.

Uveitis is the 3rd leading cause of blindness worldwide; a statistic that indicates a need for swift and thorough therapy to eradicate inflammation before it can damage the eye beyond repair.

The term “uveitis” is used because the disease often affects a part of the eye called the uvea. The uvea is located between the sclera (the eye’s white outer coat) and the inner layer of the eye (the retina). The uvea consists of the iris, ciliary body, and choroid.

Because the Uvea provides most of the blood supply to the intraocular structures; it acts as a conduit for immune cells, particularly lymphocytes, to enter the eye. Consequently, the uveal tract is represented in many intraocular inflammatory processes, irrespective of which tissue or cell is the original target of the immune process.

Uveitis is sometimes not limited to the uvea, however. It can affect the lens, retina, optic nerve, and vitreous, producing reduced vision or blindness.

Uveitis may be caused by problems or diseases occurring in the eye or it can be part of an inflammatory disease affecting other parts of the body and can happen to people of all ages.

Uveitis can last for a short (acute) or a long (chronic) time. The severest forms of uveitis reoccur many times.

Uveitis is usually classified by where it occurs in the eye.

Anterior Uveitis, Intermediate, Posterior, and Panuveitis are the most severe and highly recurrent forms of uveitis. They often cause blindness if left untreated.

Classification of Uveitis

What is anterior uveitis?

Anterior uveitis is the most common form of uveitis, and it occurs in the front (chamber) of the eye. It is the most common form of uveitis, predominantly occurring in young and middle-aged people. Many cases occur in healthy people and mainly occurs in one eye. Some are associated with Rheumatologic, skin, gastrointestinal, lung and infectious diseases.

Uveitis can affect one or both eyes. Symptoms may develop rapidly and can include:

  • Blurred vision
  • Dark, floating spots in the vision (floaters)
  • Eye pain
  • Redness of the eye
  • Sensitivity to light (photophobia)
Anterior Uveitis Image

What is intermediate uveitis?

Intermediate uveitis is commonly seen in young adults. The centre of the inflammation often appears in the vitreous (see diagram above). It has been linked to several disorders including: Sarcoidosis and Multiple Sclerosis.

What is posterior uveitis?

Posterior uveitis is the least common form of uveitis. It primarily occurs in the back of the eye, often involving both the retina and the choroid (thin pigmented vascular coat of the eye). It is often called Choroiditis or Chorioretinitis. There are many infectious and non-infectious causes to posterior uveitis.

What is panuveitis?

Panuveitis is a term used when all three major parts of the eye are affected by inflammation. Behcet’s disease is one of the most well-known forms of panuveitis and it causes severe damage to the retina.


Uveitis may be caused by:

  • An attack from the body’s own immune system (autoimmune diseases)
  • Infections or tumours occurring in the eye or in other parts of the body
  • Injury to the eye
  • Toxins that may penetrate the eye

The disease will cause symptoms, such as decreased vision, pain, light sensitivity, and increased floaters. In many cases the cause is unknown (idiopathic).

What diseases are associated with uveitis?

The Role of Autoimmune Diseases
The presence of Autoimmune diseases, which are chronic inflammatory diseases, increase the risk of ocular inflammation. The immune system which routinely helps protect us from germs or infectious agents, can become dysregulated leading to an autoimmune attack on a part of our own body.

The eye is made up primarily of collagen, as are ligaments, tendons, and tissue within joint spaces.

It is, perhaps, primarily because of this similarity in composition that the eye is often affected by many of the same diseases which affect joints. Additionally, the type of vasculature that is present in the eye has special characteristics that produce an extraordinarily sensitive “barometer” or “sentinel canary” in the eye for potentially lethal vasculitis.

Despite the fact that a patient’s Rheumatoid Arthritis may be “burned out” as far as active inflammation of the joints concerned, the eye is a potent indicator of subclinical and potentially lethal vasculitis.

In some cases the eye may be the specific and only target affected by certain autoimmune diseases. Such diseases include ocular cicatricial pemphigoid (45, 46), and Mooren’s corneal ulcer [1-3].

Uveitis Caused By Viral Infections
Uveitis can be caused by a viral infection:
– (like, cytomegalovirus, as seen in patients with AIDS) [4, 5] ,

Uveitis Caused By Fungal Infections
A fungal infection may cause Uveitis, such as, histoplasmosis. [6 – 9],

Uveitis Caused By Bacterial Infections
Uveitis is most commonly caused by bacterial infections (such as caused by Helicobacter [1012], Yersinia [13 – 17], Salmonella [18, 19], Shigella [20], and Chlamydia [21 – 26].

Uveitis Caused By Parasitic Infections
Uveitis can sometimes be ascribed to an infection caused by a parasite, like toxoplasmosis and may even cause a newborn to develop uveitis, if the mother was exposed to toxoplasmosis during pregnancy) [27 – 29]

Uveitis May Be Ideopathic
Numerous clinical cases have been described in which no cause could be determined and are unknown. Some researchers suggest that approximately 50% of cases are considered idiopathic.

Uveitis and Novel Infections
Recently, novel infections have been shown to be implicated in the development of uveitis, which suggest increased threat to the vision [27].These include: Rickettsioses, West Nile virus infection, Rift Valley Fever, Dengue Fever, and Chikungunya,

Smoking and Uveitis
Patients who smoke or have a smoking history have more Uveitis activity, which does not bode well for loss of vision. Often stopping smoking could be the turning-point in regaining control of the infection.

Diet and Uveitis
Simple Carbohydrates, such as, pies, pastries, cakes and deserts are simply deleterious to Uveitis suppression.


Although the initial events leading to uveitis are not always clear, the eventual loss of vision has always been ascribed to the ocular tissue damage caused by the amplification of the inflammatory processes. [3032]

Topical steroids are often the first-line as inhibitory agents in the treatment of uveitis.

Uveitis treatments primarily try to eliminate inflammation, alleviate pain, prevent further tissue damage, and reduce vision loss.

Treatments depend on the type of uveitis a patient displays.

Anterior uveitis treatments

Anterior Uveitis can be Chronic:

Regardless of the presentation, the treatment is with Uveitis eye drops are mostly in the form of steroid therapy as the first option for treating patients with non-infectious uveitis because it can suppress the hallmark inflammation.

Many doctors agree that treating the eye aggressively and early can help avoid complications and vison loss. Treating hourly with Pred Forte or every 2 hours with Durezol (difluprednate).

Intermediate, posterior, and panuveitis treatments

Dr Glenn Jaffe at Duke University starts with the anterior uveitis and says: “I treat aggressively in the beginning, it makes it easier for me to get the patient off the drops, as opposed to treating less aggressively and prolonging the treatment duration. I begin to taper the treatment once the anterior chamber is quiet.”

Local therapy options include a posterior sub-Tenon’s steroid injection or intravitreal steroids. However, I usually start with a posterior sub-Tenon’s injection. I can always go to an intravitreal injection later, if needed. As retinal specialists, we are almost programmed to treat people with intravitreal injections, but with a uveitis patient you can often achieve the treatment you need with a periocular steroid injection, which has the advantages of less risk for endophthalmitis and/or an increase in intraocular pressure. Having said that, though, if the inflammation is severe, or if the patient doesn’t respond to a periocular steroid injection, I’d use an intravitreal steroid.” For the intravitreal steroid route, Dr. Glenn Jaffe says that, at this point in the therapy, he prefers either an intravitreal injection of triamcinolone acetonide (1 mg in 0.1 ml) or a short-acting sustained drug delivery system such as Ozurdex (dexamethasone implant), which lasts six weeks to three months.

At a certain point, however, steroids will have to be ceased, and continued inflammation suppression is achieved by steroid-sparing therapy.

Some practice guidelines suggest that immunosuppressive therapy may be appropriate as the first therapeutic option in some cases of uveitis, including sympathetic ophthalmia, Vogt-Koyanagi-Harada disease and Behçet’s disease with retinal vasculitis, and in some rheumatologic disorders, such as Wegener’s granulomatosis, Behçet’s disease or polyarteritis nodosa, which affects the posterior segment.

However, immunosuppressive therapy requires close and careful follow-up, and there are systemic concerns that general ophthalmologists may not be aware of. For that reason, referral to a uveitis specialist may be warranted.

Referral may also be called for if the disease course is particularly violent, if it affects the retina, or if uveitis recurs every time the steroid is tapered down or eliminated. Dr. C. Stephen Foster (a leading specialist) suggested referral after 6 months of steroid use and that the timing of the referral can be of critical importance.

“Delayed referral is too common, and a change in practice patterns is going to be necessary if we are going to have any significant hope of reducing the prevalence of blindness secondary to uveitis,” Dr. Foster said. “Too often, the uveitis specialist gets the referral, gets the case, after sufficient damage has been done that precludes the patient ever seeing well again.”


Long-term steroid use for Chronic Uveitis may produce side effects such as stomach ulcers, osteoporosis (bone thinning), diabetes, cataracts, glaucoma, cardiovascular disease, weight gain, fluid retention, and Cushing’s syndrome.

Usually other agents like systemic NSAIDS are started if it appears that patients need moderate or high doses of oral steroids for more than 3 months.

Other immunosuppressive agents that are commonly used include medications such as methotrexate, mycophenolate, azathioprine, and cyclosporine. These treatments require regular blood tests to monitor for possible side effects. In some cases, biologic response modifiers (BRM), or biologics, such as, adalimumab, infliximab, daclizumab, abatacept, and rituximab are used. These drugs target specific elements of the immune system. Some of these drugs may increase the risk of getting cancer.


There are four important side-effects of corticosteroids Chronic Uveitis eye drop use:

  1. steroid-induced glaucoma,
  2. cataract formation,
  3. delayed wound healing, and increased susceptibility to infection.



Figure 1: A fundus photo of the optic nerve showing increased cupping, a risk factor for glaucoma.

Glaucoma is a condition in which there is damage to the optic nerve, often related to elevated intraocular pressure (IOP).

The result of this damage is a progressive, permanent vision loss.

The risk of steroid-induced glaucoma depends on the duration of use and potency of the steroids themselves as well as the individual’s baseline risk for glaucoma.6-8 

It is impossible to evaluate IOP changes constantly, and therefore avoid the moment at which this will occur and therefore the subsequent damage to the eye.


Posterior subcapsular cataract

Figure 2. Example of a posterior subcapsular cataract, the type of cataract that often forms from chronic steroid use. Photographer: James Gilman, CRA, FOPS, Moran Eye Center11

Long-term steroid Chronic Uveitis eye drop use is associated with an accelerated development of cataracts, andreduced vision. While the mechanism of cataract development in this setting is not well understood, it is thought to involve steroid-induced changes in gene transcription within lens epithelial cells.10

Classically, the type of cataract associated with steroid use is called a posterior subcapsular cataract, which forms in the back of the lens (Figure 1).11


Fluorescein staining of a dendritic ulcer

Figure 3: Fluorescein staining of a dendritic ulcer, pathognomonic for herpetic keratitis.  This is a type of corneal ulcer where steroids are absolutely contraindicated due to the risk of worsening the infection.

Steroids are often used in conjunction with topical antibiotics in ocular infections such as corneal ulcers. However research has identified that steroids inhibit growth factors critical in wound healing.12 Therefore local ocular infections treated with steroids may become worse, especially viral infections such as herpetic keratitis.12

While local steroid therapy is valuable in infections of the eye, owing to their ability to reduce inflammation and scarring, these benefits must be weighed against the risk of recurrent infection and poor wound healing and require the close monitoring of an eye specialist.


Ophthalmologists are often NOT familiar with the steroid-sparing agents available for the management of ocular inflammation and depend primarily on the use of corticosteroids- regardless of severe side-effects.

There is accumulating evidence that strongly supports the association between uveitis complications and inflammation. More specifically a recent study, points to macular oedema, as the most common cause of irreversible visual impairment in patients with uveitis- but it is considered a treatable entity. [30–33]. We at Bettamed believe that its clinical relevance, due to its relationship with chronic inflammatory activity – confirms its importance and treatment.

Multiple studies have shown that ROS and oxidative stress are significant components of such pathological conditions. Oxidative stress is critical to ocular inflammation of varied origin. The excessive ROS generation also weakens the tissue’s own antioxidant defense system.

With the reduced potency of the antioxidant system, the ROS mediated damage continues, which perpetuates the progression of inflammation and the disease process.

We regard these variables as truly significant in the composite treatment strategy that is developed.


Bettamed Eye Wash OcuSolve 15ml
  • Anti-inflammatory
  • Anti-microbial
  • Biocompatible
  • Helps Reduce Macular Oedema
  • Helps Maintain Visual Accuity
  • Helps Reduce Uveitis Complications
  • Improves Quality of Life
  • Safe for Long-term use

Macular oedema is the most common cause of irreversible visual impairment in patients with Chronic Uveitis, which we believe is a treatable entity. The relationship with chronic inflammatory activity and the ease with which this can be treated, confirms the importance of a safe and effective anti-inflammatory Bettamed™ Ocusolve’s inclusion in any treatment regime.

Bettamed OcuSolve Eye Drops are a life-altering advance in Uveitis Care. Our patented ECA Technology, mimics the same Oxychlorine composition as that manufactured by neutrophils in the body’s immune system.

Bettamed Ocusolve (with Hypochlorous Acid) is naturally produced by our white blood cells and is an essential part of our immune system. This process is called phagocytosis and is one of nature’s symbiotic actions- with no evidence of induced microbe resistance.5

Bettamed OcuSolve™ with (HOCl) exhibits potent broad-spectrum antimicrobial activity, including antibiotic-resistant strains of bacteria (including MRSA and VRE), viruses, fungi and spores- as demonstrated in numerous studies1,2,5,6,8,12,13, while reducing inflammation and increasing Oxygen (O2) in treated tissue.

There are no concerns about ocular toxicity with HOCL, in fact it has been found to be non-irritating and non-sensitising in various animal safety models.5

Bettamed OcuSolve™ is bio-compatible, non-toxic and non-sensitizing, making it safe for regular use.


As part of the immune response to microbial proliferation, mast cells flood the infection site, contributing to inflammation.

A significant portion of HOCl’s potency is derived from its anti-inflammatory effects, as a result of its modulating effect controlling mast cell response.

A study by Medina-Tamayo et al43 suggests a neutral PF Superoxidised Solution (SOS), acts like a mast cell membrane stabilizing inhibitor, inhibiting the cell machinery for granule secretion, without altering the signal transduction pathways. Additionally, many studies, including Sakarya et al44 demonstrate that HOCl induces significant healing, as well as a substantial reduction in signs of inflammation.

In 2013, Pelgrift et al45 proposed that HOCL is both antimicrobial and anti-inflammatory, which accounts for the reduction in pruritis in dermatology.

A study by Bongiovanni46 investigated the micro-circulatory integrity (oxygenation) of patients with venous leg ulcers and its effect on time to wound healing. Exposure of the Venous leg ulcers to HOCl elevated TcPO2 levels for up to 72 hours after exposure, which increased time to wound healing between 2-180 days.

The added advantage is that the dissolved Oxygen (O2) in Bettamed Ocusolve eye drops, improves Oxygen balance for infection control, creating a reversal of the tissue damage and possible vision loss caused by uncontrolled inflammatory processes.47,48,49


  1. Chen J, Xie H, Wang Z, Yang B, Liu Z, Chen L, Gong X, Lin Y. Mooren’s ulcer in China: a study of clinical characteristics and treatment. Br. J. Ophthalmol. 2000;84:1244–1249. [PMC free article][PubMed] [Google Scholar]
  2. Srinivasan M, Zegans ME, Zelefsky JR, Kundu A, Lietman T, Whitcher JP, Cunningham ET., Jr Clinical characteristics of Mooren’s ulcer in South India. Br. J. Ophthalmol. 2007;91:570–575. [PMC free article][PubMed] [Google Scholar]
  3. 3. Zegans ME, Srinivasan M. Mooren’s Ulcer.  Clin. Ophthalmol. 1996;36:81–88. [Google Scholar]
  4. Markomichelakis NN, Canakis C, Zafirakis P, Marakis T, Mallias I, Theodossiadis G. Cytomegalovirus as a cause of anterior uveitis with sectoral iris atrophy. Ophthalmology. 2002;109:879–882. [PubMed] [Google Scholar]
  5. Yoser SL, Forster DJ, Rao NA. Systemic Viral Infections and their retinal and choroidal manifestations. Surv. Ophthalmol. 1993;37:313–352. [PubMed] [Google Scholar]
  6. Craig EL, Suie T. Histoplasma Capsulatum in Human Ocular Tissue. Arch. Ophthalmol. 1971;91:285–289. [PubMed] [Google Scholar]
  7. Gonzales CA, Scott IU, Chaudhry NA, Luu KM, Miller D, Murray TG, Davis JL. Endogenous endophthalmitis caused by Histoplasma capsulatum var. capsulatum: a case report and literature review. Ophthalmology. 2000;107:725–729. [PubMed] [Google Scholar]
  8. Hawkins BS, Alexander J, Schachat AP. In: Ocular histoplasmosis.Ryan SJ, editor. St. Louis: Retina Mosby; 1994. pp. 1661–1675. [Google Scholar]
  9. Scholz R, Green WR, Kutys R, Sutherland J, Richards RD. Histoplasma capsulatum in the eye. Ophthalmology. 1984;91:1100–1104. [PubMed] [Google Scholar]
  10. Bakunowicz-Lazarczyk A, Maciorkowska E, Antosiuk R, Kaczmarski M. Helicobacter pylori as supposed factor of uveitis in children: a case report. Klin. Oczna. 1999;101:463–465. [PubMed] [Google Scholar]
  11. Otasevic L, Walduck A, Meyer TF, Aebischer T, Hartmann C, Orlic N, Pleyer U. Helicobacter pylori infection in anterior uveitis. Infection. 2005;33:82–85. [PubMed] [Google Scholar]
  12. Otasevic L, Zlatanovic G, Stanojevic-Paovic A, Miljkovic-Selimovic B, Dinic M, Djordjevic-Jocic J, Stankovic A. Helicobacter pylori: an underestimated factor in acute anterior uveitis and spondyloarthropathies? Ophthalmologica. 2007;221:6–13. [PubMed] [Google Scholar]
  13. Cancino-Diaz JC, Vargas-Rodríguez L, Grinberg-Zylberbaum N, Reyes-López MA, Domínguez-López ML, Pablo-Velazquez A, Cancino-Diaz ME. High levels of IgG class antibodies to recombinant HSP60 kDa of Yersinia enterocolitica in sera of patients with uveitis. Br. J. Ophthalmol. 2004;88:247–250. [PMC free article][PubMed] [Google Scholar]
  14. Careless DJ, Chiu B, Rabinovitch T, Wade J, Inman RD. Immunogenetic and microbial factors in acute anterior uveitis. J. Rheumatol. 1997;24:102–108. [PubMed] [Google Scholar]
  15. Huhtinen M, Laasila K, Granfors K, Puolakkainen M, Seppälä I, Laasonen L, Repo H, Karma A, Leirisalo-Repo M. Infectious background of patients with a history of acute anterior uveitis. Ann. Rheum. Dis. 2002;61:1012–1016. [PMC free article][PubMed] [Google Scholar]
  16. Larkin F. Yersinia infection in acute anterior uveitis. Arch. Ophthalmol. 1990;108:1515–1516. [PubMed] [Google Scholar]
  17. Osusky R, Kain HL. Uveitis after Yersinia enterocolitica infection. Klin. Monbl. Augenheilkd. 1991;198:451–452. [PubMed] [Google Scholar]
  18. Arora R, Das S, Chauhan D, Daraius S, Narula R, Sachdev R. Bilateral endogenous panophthalmitis caused by Salmonella typhi: first case report. Orbit. 2008;27:115–117. [PubMed] [Google Scholar]
  19. Yodprom R, Pathanapitoon K, Kunavisarut P, Ausayakhun S, Wattananikorn S, Rothova A. Endogenous endophthalmitis due to Salmonella choleraesuis in an HIV-positive patient. Ocul. Immunol. Inflamm. 2007;15:135–138. [PubMed] [Google Scholar]
  20. Sprenkels SH, Van Kregten E, Feltkamp TE. IgA antibodies against Klebsiella and other Gram-negative bacteria in ankylosing spondylitis and acute anterior uveitis. Clin. Rheumatol. 1996;S1:48–51. [PubMed] [Google Scholar]
  21. Altiparmak UE, Ozer PA, Ozkuyumcu C, Us AD, Aslan BS, Duman S. Postoperative endophthalmitis caused by Bacillus cereus and Chlamydia trachomatis. J. Cataract Refract. Surg. 2007;33:1284–1287. [PubMed] [Google Scholar]
  22. Garg SP, Bajaj MS, Jaffery NF, Mahajan VM. Chlamydial serology in uveitis. Rev. Int. Trach. Pathol. Ocul. Trop. Subtrop. 1989;66:7–20. [PubMed] [Google Scholar]
  23. Haller-Schober EM, El-Shabrawi Y. Chlamydial conjunctivitis (in adults), uveitis, and reactive arthritis, including SARA. Sexually acquired reactive arthritis. Best Pract. Res. Clin. Obstet. Gynaecol. 2002;16:815–828. [PubMed] [Google Scholar]
  24. Huhtinen M, Puolakkainen M, Laasila K, Sarvas M, Karma A, Leirisalo-Repo M. Chlamydial antibodies in patients with previous acute anterior uveitis. Invest. Ophthalmol.Vis. Sci. 2001;42:1816–1819. [PubMed] [Google Scholar]
  25. Krichevskaia GI, Vakhova ES, Maĭchuk F, Davydova GA. Implication of Chlamydia trachomatis in the etiopathogenesis of anterior uveitis. Vestn Oftalmol. 2008;124:48–51. [PubMed] [Google Scholar]
  26. Numazaki K, Chiba S, Aoki K, Suzuki K, Ohno S. Detection of serum antibodies to Chlamydia pneumoniae in patients with endogenous uveitis and acute conjunctivitis. Clin. Infect. Dis. 1997;25:928–929. [PubMed] [Google Scholar]
  27. Khairallah M, Chee SP, Rathinam SR, Attia S, Nadella V. Novel infectious agents causing uveitis. Int. Ophthalmol. 2010;32:465–483. [PubMed] [Google Scholar]
  28. Klaeger AJ, Herbort CP. Acute acquired toxoplasmic retinochoroiditis in a patient with anterior uveitis, amplified by immunosuppressive therapy. Int. Ophthalmol. 2009;29:191–193. [PubMed] [Google Scholar]
  29. Melamed J, Eckert GU, Spadoni VS, Lago EG, Uberti F. Ocular manifestations of congenital toxoplasmosis. Eye. 2010;24:528–534. [PubMed] [Google Scholar]
  30. Curi A, Matos K, Pavesio C. Acute anterior uveitis. Clin. Evid. 2005;14:739–743. [PubMed] [Google Scholar]
  31. Read RW. Uveitis: advances in understanding of pathogenesis. Curr. Rheumatol. Rep. 2006;8:260–266. [PubMed] [Google Scholar]
  32. Rathinam SR, Cunningham ET., Jr Infectious causes of uveitis in the developing world. Int. Ophthalmol. Clin. 2000;40:137–152. [PubMed] [Google Scholar]
  33. Wallis S, Macierewicz J, Shrestha BM. Behcet’s Disease: report of a case and review of the literature. J. Nepal Med. Assoc. 2006;45:362–365. [PubMed] [Google Scholar]
  34. Alebiosu CO, Raimi TH, Badru AI, Amore OO, Ogunkoya JO, Odusan O. Reiter’s syndrome–a case report and review of literature. Afr. Health Sci. 2004;4:136–138. [PMC free article][PubMed] [Google Scholar]
  35. Amor B. Reiter’s syndrome. Diagnosis and clinical features. Rheum. Dis. Clin. North Am. 1998;24:677–695. [PubMed] [Google Scholar]
  36. Cuttica RJ, Scheines EJ, Garay SM, Romanelli MC, Maldonado CJA. Juvenile onset Reiter’s syndrome. A retrospective study of 26 patients. Clin. Exp. Rheumatol. 1992;10:285–288. [PubMed] [Google Scholar]
  37. Francois J. Cortisone et tension oculaire. Ann D’Oculist 1954; 187: 805.
  38. Cantrill HL, Palmberg, Zink HA, Waltman SR, Podos SM, Becker B. Comparison of in vitro potency of corticosteroids with ability to raise intraocular pressure. Am J Ophthalmol 1975; 79: 1012–1017.
  39. Francois J. Corticosteroid glaucoma. Ann Ophthalmol 1977; 9: 1075–1080.
  40. James ER. The etiology of steroid cataract. J Ocul Pharmacol Ther 2007;23:403–20.

41.Moran CORE | Cataracts. (accessed 28 Jul 2018)

42.Srinivasan M, Mascarenhas J, Rajaraman R, et al. The Steroids for Corneal Ulcers Trial. Arch Ophthalmol 2012;130.

  1. Medina-Tamayo J, Sanchez-Miranda E, Balleza-Tapia H, et al. Super-oxidized solution inhibits IgE-antigen-induced degranulation and cytokine release in mast cells. Int Immunopharmacol. 2007;7(8):1013-1024.
  2. Sakarya S, Gunay N, Karakulak M, Ozturk B, Ertugrul B. Hypochlorous acid: an ideal wound care agent with powerful microbicidal, antibiofilm, and wound healing potency. Wounds. 2014;26(12): 342-350.
  3. Pelgrift R, Friedman AJ. Topical hypochlorous acid (HOCl) as a potential treatment of pruritus. Curr Derm Rep. 2013;2:181-190.
  4. Bongiovanni CM. Effects of hypochlorous acid solutions on venous leg ulcers (VLU): experience With 1249 VLUs in 897 patients. J Am Coll Clin Wound Spec. 2014;6(3):32-37
  5. Gottrup F. Oxygen in wound healing and infection. World J Surg 2004; 28(3):312–315.
  6. Sen CK. Wound healing essentials: let there be oxygen. Wound Repair Regen 2009; 17(1):1–18.