Conjunctival Dysplasia in Soldiers Exposed to Mustard Gas During the Iraq-Iran War

Safaei, Akbar; Saluti, Ramin; Kumar, Perikala V.

doi:10.1159/000328362

Cited by 19 publications

(8 citation statements)

References 9 publications

(5 reference statements)

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“…Javadi et al [2005] reported clinical signs of 48 severely injured eyes in SM victims, including changes in ocular surface, blepharitis and diminished tear meniscus (100%), limbal ischemia (81.3%), abnormalities in conjunctival vasculature (50.0%), corneal scar or opacity (87.5%), corneal neovascularization (70.8%), corneal thinning (58.3%), corneal lipid deposits (52.1%), corneal amyloid deposits (43.8%), and corneal epithelial defects or irregularities (31.3%). Safaei et al [2001] noted dryness, conjunctival scarring, decreased visual acuity, conjunctival dysplasia with mild inflammation, and squamous metaplasia as delayed ocular symptoms in SM-exposed victims.…”

Section: Delayed Ocular Complicationsmentioning

confidence: 84%

“…Different studies have been performed by Iranian scientists on Iranian veterans who had been injured by SM exposure [Safaei et al, ; Javadi et al, ; Etezad‐Razavi et al, ; Ghasemi Broumand et al, ; Javadi et al, ; Shohrati et al, ; Ghasemi et al, ,]. In a study by Etezad‐Razavi et al [] blurred vision (50%), itching (42.5%), burning sensation (37.5%), photophobia (30%), tearing (27.5%), reading difficulties (10%), red eye (10%), eye pain (2.5%), and foreign body sensation (2.5%) were reported as delayed ocular symptoms.…”

Section: Delayed Ocular Complicationsmentioning

confidence: 99%

See 1 more Smart Citation

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Panahi

Rajaee

Sahebkar

2017

J of Cellular Biochemistry

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Sulfur mustard (SM) is a strong blistering, highly reactive, lipophilic chemical war agent that causes injury in different organs including the skin, eyes, and respiratory tract. The Eyes are especially susceptible to the consequences of SM poisoning because of the aqueous and mucosal nature of conjunctiva and cornea. DNA alkylation and depletion of glutathione, are the most important mechanisms of SM action in the eye injuries. Acute clinical symptoms are including decrease in visual acuity, dryness, photophobia, blepharospasm, conjunctivitis, and complaints of foreign body sensation and soreness that gradually progress to severe ocular pain. Corneal abrasions, ulcerations, vesication, and perforations are common corneal consequences in SM injured victims. Appearance of chronic symptoms has been reported as chronic inflammation of the corneal and conjunctival vasculature, ischemia, lipid and cholesterol deposition, scarring in cornea, corneal thinning, opacification and perforation of the cornea, limbal stem cell deficiency (LSCD), and neovascularization. Different medical and surgical protocols have been documented in the management of SM-induced ocular injuries, including preservative-free artificial tears, topical steroids and antibiotic, mydriatic, antiglaucoma drops, therapeutic contact lenses, dark glasses and punctal plugs/cauterization, N-acetylcysteine, tarsorrhaphy, amniotic membrane transplantation, stem cell transplantation, and corneal transplantation. New drugs such as resolvin E1, topical form of essential fatty acids, thymosin β4, 43 amino-acid polypeptides, topical form of curcumin, newly formulated artificial tears, diquafosol, rebamipide, tretinoin, and oral uridineseems to be beneficial in the management of ocular lesion associated with sulfur mustard poisoning. Further studies are needed to approve these drugs in SM victims. J. Cell. Biochem. 118: 3549-3560, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Delayed Ocular Complicationsmentioning

confidence: 84%

Section: Delayed Ocular Complicationsmentioning

confidence: 99%

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Panahi

Rajaee

Sahebkar

2017

J of Cellular Biochemistry

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“…On the other hand, the severity of the initial exposure and duration of the ophthalmic symptoms is directly related to the likelihood of later keratopathy (Ghasemi et al ., 2009a). Although the underlying pathogenesis of this chronic phenomenon remains unknown, formation of free radicals (Aasted et al ., 1987), by‐product toxicity (Safaei et al ., 2001), necrotic changes (Pleyer et al ., 1999), destruction of the limbal vasculture (Maumenee and Scholz, 1948; Solberg et al ., 1997) and autoimmune reactions (Hughes, 1942; Solberg et al ., 1997; Javadi et al ., 2005) have been proposed as plausible core mechanisms. Moreover, direct limbal stem cell injury by MG is believed to account for the ocular pathology following MG exposure (Kehe and Szinicz, 2005; Rowell et al ., 2009).…”

Section: Eye Injurymentioning

confidence: 99%

Mustard gas toxicity: the acute and chronic pathological effects

Ghabili

Agutter²,

Ghanei

et al. 2010

J of Applied Toxicology

132

114

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Ever since it was first used in armed conflict, mustard gas (sulfur mustard, MG) has been known to cause a wide range of acute and chronic injuries to exposure victims. The earliest descriptions of these injuries were published during and in the immediate aftermath of the First World War, and a further series of accounts followed the Second World War. More recently, MG has been deployed in warfare in the Middle East and this resulted in large numbers of victims, whose conditions have been studied in detail at hospitals in the region. In this review, we bring together the older and more recent clinical studies on MG toxicity and summarize what is now known about the acute and chronic effects of the agent on the eyes, skin, respiratory tract and other physiological systems. In the majority of patients, the most clinically serious long-term consequences of MG poisoning are on the respiratory system, but the effects on the skin and other systems also have a significant impact on quality of life. Aspects of the management of these patients are discussed.

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“…Inhibition of respiratory enzymes resulting in the formation of free radicals has been suggested as the underlying pathomechanism affecting predominantly germinative epithelial cells in the ocular surface 20 . Byproducts toxicity, 21 necrotic changes after the initial injury, 22 destruction of the limbal vasculture, and degenerative processes 10,11 have also been proposed as causes of long‐term damage.…”

Section: Discussionmentioning

confidence: 99%