GULF WAR VETERANS 90-91 ASK FOR HELP WITH VISUAL PROBLEMS

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GULF WAR VETERANS HAVE VISUAL PROBLEMS IMPACTING SAFETY AND QUALITY OF LIFE

For 19 years the Gulf War Veterans have suffered.  Back in the 1990s during the time of the Comprehensive Clinical Examination Evaluation Program(CCEEP) Eye Examinations were being done!  But since then despite pleas to consider the visual problems of veterans of Operation Desert Storm, little has been done.  In the late 90s an article did appear in one Opthalmology Journal concerning Gulf War Veterans/Illness after this writer contacted them.  The system has some initial data from the CCEEP program that could be pulled up by the VA and DOD. 

The veterans that get 100% can get into the VA Eye Clinic and may have so that is another source of data.  There needs to be a way for veterans of the gulf war 90-91 to at least be seen in the VA eye clinics for at least an assessment!  A large number of veterans have spoken on this problem.  They get prescription glasses and still have problems.  Many Gulf War Veterans due to financial situation have taken to using the drug story to buy multiple, different strength magnification cheater glasses! 

Many of the Gulf War Veterans, particularly those that exited the military and went to commercial truck driving, have experienced particular problems in relationship to night driving and vision problems.  THIS IS A DEFINITE SAFETY AND QUALITY OF LIFE ITEM THAT NEEDS URGENT VA ATTENTION.

We recommend at least one VA research study be initiated on vision problems in relationship to Gulf War Illness.

The Mustard Gas Veterans of World War I and the Iran-Iraq War of the 80s should provide a great deal of research reference articles to initate at least a Research Review Article on Opthalmology in Mustard Gas Exposures and past war veterans.

Below are the 6 research articles I found with very little searching to get you started!  The writer encourages gulf war veterans to make comments to this article on their vision problems.
Clin Experiment Ophthalmol. 2006 May-Jun;34(4):342-6.

Delayed ocular complications of mustard gas poisoning and the relationship with respiratory and cutaneous complications.

http://www.ncbi.nlm.nih.gov/pubmed/16961503

http://www.ncbi.nlm.nih.gov/sites/entrez
Etezad-Razavi M, Mahmoudi M, Hefazi M, Balali-Mood M.

Ophthalmology Department, Khatamolanbia Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.

BACKGROUND: This study was aimed to determine the correlation between ocular complications and respiratory or cutaneous complications in a group of 40 Iranian veterans with late complications of sulphur mustard (SM) poisoning.

METHODS: Thorough ophthalmologic examination was performed on all severely SM-poisoned veterans in the province of Khorasan, Iran. Spirometric evaluation of pulmonary function, as well as estimation of the burned skin area, was performed for all the patients. The severities of ocular, respiratory and cutaneous complications were classified into four grades in each patient and were compared with each other, using Spearman’s rank correlation test.

RESULTS: Forty male patients (aged 43.8 +/- 9.8 years) with confirmed SM poisoning were studied 16-20 years after their initial exposure. Common symptoms were recorded as itching (42.5%), burning sensation (37.5%), photophobia (30%) and tearing (27.5%). Abnormal conjunctival and limbal findings were chronic conjunctivitis (17.5%), perilimbal hyperpigmentation (17.5%), vascular tortuosity (15%) and limbal ischaemia (12.5%). Abnormal corneal findings were subepithelial opacity (15%), corneal thinning (15%), diffuse corneal opacity (10%), neovascularization (7.5%) and epithelial defects (5%). A significant positive correlation was found between the severity of ocular and respiratory complications (r = 0.322, P = 0.043). Cutaneous complications revealed no significant correlation with either ocular or respiratory complications.

CONCLUSIONS: SM causes delayed destructive lesions in the ocular surface and cornea, leading to progressive visual deterioration and ocular irritation. Late complications of SM poisoning in the eyes, respiratory system and skin are mainly due to SM’s local irritant effects.

PMID: 16764654 [PubMed – indexed for MEDLINE]

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Ophthalmology. 2010 Feb;117(2):246-52. Epub 2009 Dec 16.
http://www.ncbi.nlm.nih.gov/pubmed/20018379

Limbal stem cell deficiency in chronic and delayed-onset mustard gas keratopathy.
Baradaran-Rafii A, Javadi MA, Rezaei Kanavi M, Eslani M, Jamali H, Karimian F.

Labbafinejad Medical Center, Shahid Beheshti University, Tehran, Iran.

PURPOSE: To evaluate limbal stem cell deficiency (LSCD) using impression cytology in patients with chronic and delayed-onset mustard gas keratopathy (MGK). DESIGN: Prospective observational case series.

PARTICIPANTS: Thirty-five eyes of 18 patients (all male) with MGK were included.

METHODS: A consecutive series of patients with MGK underwent impression cytology. Finding of goblet cells on the corneal side of specimens was considered as LSCD. Severity of corneal clinical manifestation was graded as mild, moderate, and severe in each quadrant. Relation between impression cytology findings and clinical grading was evaluated. MAIN OUTCOME MEASURES: Impression cytology findings and clinical grading.

RESULTS: There was LSCD in at least 1 quadrant of cornea in all 35 eyes (100% of cases). No differences were found between impression cytology findings (positive vs. negative for corneal goblet cells) among different quadrants (P = 0.378). Clinical grading was the same between nasal and temporal quadrants (P = 0.266) and between superior and inferior quadrants (P = 0.263). By combining superior and inferior quadrants (vertical zone) and nasal and temporal quadrants (horizontal zone), corneal clinical grading was more severe in horizontal versus vertical zones (P<0.001). There was no relation between LSCD and corneal clinical severity (P = 0.893).

CONCLUSIONS: A varying degree of LSCD was demonstrated in all patients with chronic or delayed-onset MGK using impression cytology. Corneal clinical manifestations are more severe in nasal and temporal quadrants. There was no relation between impression cytology findings (positive vs. negative for goblet cells) and corneal clinical grading. Other factors, such as perilimbal conjunctival ischemia, may play a role. Copyright (c) 2010 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.

PMID: 20018379 [PubMed – indexed for MEDLINE]

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Toxicology. 2009 Sep 1;263(1):59-69. Epub 2008 Nov 17.

Ocular injuries following sulfur mustard exposure–pathological mechanism and potential therapy.
Kadar T, Dachir S, Cohen L, Sahar R, Fishbine E, Cohen M, Turetz J, Gutman H, Buch H, Brandeis R, Horwitz V, Solomon A, Amir A.

Department of Pharmacology, Israel Institute for Biological Research, Ness-Ziona 74100, Israel.
http://www.ncbi.nlm.nih.gov/pubmed/19061933

Sulfur mustard (SM) is a potent vesicant, known for its ability to cause incapacitation and prolonged injuries to the eyes, skin and respiratory system. The toxic ocular events following sulfur mustard exposure are characterized by several stages: photophobia starting a few hours after exposure, an acute injury phase characterized by inflammation of the anterior segment and corneal erosions and a delayed phase appearing following a clinically silent period (years in human). The late injury appeared in part of the exposed eyes, expressed by epithelial defects and corneal neovascularization (NV), that lead to vision deficits and even blindness. During the last years we have characterized the temporal development of ocular lesions following SM vapor exposure in rabbits and have shown the existence of two sub-populations of corneas, those exhibiting delayed ocular lesions (clinically impaired) and those exhibiting only minor injuries if at all (clinically non-impaired). The aim of the present study was to investigate the pathological mechanism underlying the delayed injury by focusing on the unique characteristics of each sub-population and to test the efficacy of potential treatments. Clinically impaired corneas were characterized by chronic inflammation, increased matrix metalloproteinase (MMP) activity, poor innervation and limbal damage. Moreover, using impression cytology and histology, we identified the delayed lesions as typical for an ocular surface disorder under the category of limbal epithelial stem cell deficiency (LSCD). These results point to therapeutic directions, using anti-inflammatory drugs, MMPs inhibitors, neurotrophic factors and amniotic membrane transplantation. Topical anti-inflammatory drugs, either steroid (Dexamycin, DEX) or non-steroidal anti-infllammatory drug (NSAID, Voltaren Ophtha) were found to be beneficial in ameliorating the initial inflammatory response and in postponing the development of corneal NV, when given during the first week after exposure. When DEX was administered as a symptomatic treatment against NV, a significant regression in the angiogenic process was observed, however, the effect was temporal and blood vessels reappeared after therapy ceased. Chronic administration (8 weeks) of the MMP inhibitor Doxycycline was also effective in attenuation of the acute and delayed injury. Preliminary results, using amniotic membrane transplantation revealed some decrease of corneal edema with no effect on corneal NV. It is suggested that the chronic inflammation and prolonged impairment of corneal innervation are playing a role in the pathogenesis of the delayed LSCD following SM exposure by creating a pathological microenvironment to limbal epithelial stem cells, thus, leading to their slow death and to a second cascade of pathological events eventually resulting in severe long-term injuries. As of today, only topical anti-inflammatory drugs reached the criteria of an applicable efficient post-exposure ocular treatment for SM injuries. Further studies are required to investigate the effects of SM on epithelial stem cells and their involvement in the pathogenesis of the long-term injuries.

PMID: 19061933 [PubMed – indexed for MEDLINE]

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Cornea. 2009 Jan;28(1):51-7.

Living-related conjunctival-limbal allograft for chronic or delayed-onset mustard gas keratopathy.

http://www.ncbi.nlm.nih.gov/pubmed/19092406
Javadi MA, Baradaran-Rafii A.

Department of Ophthalmology and Ophthalmic Research Center, Labbafinejad Medical Center, Shaheed Beheshti Medical University, Tehran, Iran.

PURPOSE: To determine the long-term outcomes of living-related stem cell transplantation in patients with delayed or chronic mustard gas keratopathy (MGK).

MATERIALS AND METHODS: In this noncomparative interventional case series, 21 consecutive patients with advanced delayed or chronic MGK received living-related conjunctival-limbal allograft and were followed up for at least 1 year. All subjects received immunosuppression with systemic cyclosporine. Main outcome measures were reduction of subjective complaints, corneal epithelial healing, and regression of corneal neovascularization adjacent to the transplant area.

RESULTS: Twenty-five eyes of 21 patients (all male), including 4 patients who received bilateral grafts, were operated. Mean age at the time of surgery was 35.8 +/- 3.8 years, mean interval between mustard gas exposure and surgery was 12.2 +/- 3.5 years, and mean follow-up was 37.2 +/- 18.5 months. Average size of the donor lenticule was 71.16 +/- 17.34 degrees. Simultaneous penetrating and lamellar keratoplasty were performed in 5 and 2 eyes, respectively. All patients consistently reported marked subjective improvement. Mean time for epithelial healing was 7.76 +/- 3.2 days. Visual acuity was 1.35 +/- 0.81 LogMAR before surgery, which improved to 0.59 +/- 0.34 LogMAR 3 months after the procedure (P < 0.001). Mean visual acuity at final examination was 0.82 +/- 0.49 LogMAR (P = 0.001). Acute stem cell rejection was observed in 10 (40%) eyes, which improved by increasing the dose of topical and systemic steroids. Chronic stem cell rejection was diagnosed in 8 (32%) eyes, which led to failure in 5 (20%) eyes.

CONCLUSIONS: Living-related conjunctival-limbal allograft is effective in stabilizing the ocular surface in patients with delayed or chronic MGK.

PMID: 19092406 [PubMed – indexed for MEDLINE]

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Ophthalmology. 2005 Apr;112(4):617-25.

Chronic and delayed-onset mustard gas keratitis: report of 48 patients and review of literature.

http://www.ncbi.nlm.nih.gov/pubmed/15808253
Javadi MA, Yazdani S, Sajjadi H, Jadidi K, Karimian F, Einollahi B, Ja’farinasab MR, Zare M.

Ophthalmic Research Center and Ophthalmology Department, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

PURPOSE: To report the clinical features of 93 eyes of 48 patients with chronic and delayed-onset mustard gas keratitis. Clinicopathologic correlation in 5 eyes and a review of related literature are presented. DESIGN: Retrospective, noncomparative case series.

PARTICIPANTS: Forty-eight Iranian survivors of Iraqi chemical warfare with chronic or delayed-onset mustard gas keratitis.

METHODS: We reviewed the symptoms, clinical findings, course, and treatment of our patients and reviewed the literature. In 5 patients, histopathologic features of corneal and conjunctival specimens were evaluated. MAIN OUTCOME MEASURES: Ocular findings, clinical course, treatment measures, and histopathologic studies.

RESULTS: Of 48 patients, 31 (64.6%) had chronic symptomatology, whereas 17 (35.4%) experienced delayed-onset lesions. Visual acuity at referral ranged from hand motions to 20/20. Ocular surface changes included chronic blepharitis and decreased tear meniscus in all patients, limbal ischemia (81.3%), and conjunctival vascular abnormalities (50%). Corneal signs in order of frequency were: scar or opacity (87.5%), neovascularization (70.8%), thinning (58.3%), lipoid deposits (52.1%), amyloid deposits (43.8%), and epithelial defects and irregularity (31.3%). Many patients received conservative treatment; others underwent allograft stem cell transplantation (20 eyes of 17 patients), penetrating keratoplasty (12 eyes of 12 patients), and lamellar keratoplasty (4 eyes of 3 patients). Conjunctival specimens were evaluated by light microscopy. Decreased goblet cell density, attenuated or thickened epithelium, scarring in the substantia propria associated with plasmacytic and lymphocytic infiltration, and dilated lymphatic vessels were noted. Excised corneal buttons disclosed absence of epithelium and Bowman’s layer, fibrovascular pannus, stromal scarring, and vascularization.

CONCLUSIONS: Mustard gas causes chronic and delayed destructive lesions in the ocular surface and cornea, leading to progressive visual deterioration and ocular irritation. The pathophysiologic features of these changes are not clearly identified. Excised conjunctival and corneal specimens revealed a mixed inflammatory response without any specific features. Based on the clinical appearance of the lesions and the histopathologic findings, an immune-mediated component seems possible. This article contains additional online-only material available at.

PMID: 15808253 [PubMed – indexed for MEDLINE]

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Ophthalmology. 2010 Feb;117(2):246-52. Epub 2009 Dec 16.

http://www.ncbi.nlm.nih.gov/pubmed/20018379

Limbal stem cell deficiency in chronic and delayed-onset mustard gas keratopathy.
Baradaran-Rafii A, Javadi MA, Rezaei Kanavi M, Eslani M, Jamali H, Karimian F.

Labbafinejad Medical Center, Shahid Beheshti University, Tehran, Iran.

PURPOSE: To evaluate limbal stem cell deficiency (LSCD) using impression cytology in patients with chronic and delayed-onset mustard gas keratopathy (MGK). DESIGN: Prospective observational case series.

 PARTICIPANTS: Thirty-five eyes of 18 patients (all male) with MGK were included.

METHODS: A consecutive series of patients with MGK underwent impression cytology. Finding of goblet cells on the corneal side of specimens was considered as LSCD. Severity of corneal clinical manifestation was graded as mild, moderate, and severe in each quadrant. Relation between impression cytology findings and clinical grading was evaluated. MAIN OUTCOME MEASURES: Impression cytology findings and clinical grading.

RESULTS: There was LSCD in at least 1 quadrant of cornea in all 35 eyes (100% of cases). No differences were found between impression cytology findings (positive vs. negative for corneal goblet cells) among different quadrants (P = 0.378). Clinical grading was the same between nasal and temporal quadrants (P = 0.266) and between superior and inferior quadrants (P = 0.263). By combining superior and inferior quadrants (vertical zone) and nasal and temporal quadrants (horizontal zone), corneal clinical grading was more severe in horizontal versus vertical zones (P<0.001). There was no relation between LSCD and corneal clinical severity (P = 0.893).

CONCLUSIONS: A varying degree of LSCD was demonstrated in all patients with chronic or delayed-onset MGK using impression cytology. Corneal clinical manifestations are more severe in nasal and temporal quadrants. There was no relation between impression cytology findings (positive vs. negative for goblet cells) and corneal clinical grading. Other factors, such as perilimbal conjunctival ischemia, may play a role. Copyright (c) 2010 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.

PMID: 20018379 [PubMed – indexed for MEDLINE]

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