Ocular Manifestations of Systemic Disease
The eye can provide clues in many systemic disease processes. Optometrists may be the first to identify systemic disease.
Release Date: April 2011
Expiration Date: April 30 2014
As primary care practitioners on the front line of health care, optometrists are increasingly helping patients get the assistance and treatment they need, not only for their ocular health but also for their systemic health. This course explains how to identify ocular manifestations of systemic diseases, and how treatment is rendered both for the eye and the body.
Carlo J. Pelino, O.D., and Joseph J. Pizzimenti, O.D.
COPE approval for 2 hours of CE credit is pending for this course. Check with your local state licensing board to see if this counts toward your CE requirement for relicensure.
This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.
Drs. Pelino and Pizzimenti have no relationships to disclose.
We see sick patients all the time. But it’s not just their eyes that are sick. As primary care practitioners on the front line of health care, optometrists are increasingly helping patients get the assistance and treatment they need. In some cases, we can be the first ones to suggest the diagnosis not just of ophthalmic disease but systemic diseases.
You know how this applies for systemic conditions, such as diabetes, in which the eye is a “prime player.” But what about other conditions—such as cardiovascular disease, breast cancer or sarcoidosis—in which ocular involvement might not be the foremost consideration?
Although the death rate from cardiovascular disease (CVD) has declined over the years, mortality data show that CVD accounted for more than one-third of all U.S. deaths in 2007.1 Coronary heart disease caused one of every six deaths in the U.S. in 2007. Each year, an estimated 785,000 Americans will have a new coronary attack, and about 470,000 will have a recurrent attack. Approximately every 25 seconds, an American will have a coronary event, and approximately every minute, someone will die of one.1
In other words, every American (not only every health care professional) should be concerned about heart disease. So, when you suspect cardiovascular disease, question the patient further. (See “Cardiovascular Review of Systems.”) Most often, vascular disease affects blood flow through arteries and/or veins by blocking or weakening the vessel, or by damaging the valves that are found in veins. As a result of decreased or blocked blood flow, organs and other body structures may be damaged by vascular disease.2,3
Cardiovascular Review of
- Leg pain in calf or thigh
- Chest pain (sharp, crushing or heaviness)
- Heart racing (palpitations)
- Fainting spells
- Sudden shortness of breath at night or
- Swelling of legs (edema)
- Smoking or drinking alcohol
- Diet high in salt, saturated fats
- Lack of exercise
- Family history of heart problems
- Visual changes
Atherosclerosis is the most frequent cause of morbidity from vascular disease. The highest incidence occurs in Finland, Great Britain, Canada and the United States.2,4 Atherosclerosis is defined as a fibrous plaque (atheroma) within the intima of an artery. Atheromas are frequently found in the coronary arteries (heart), the larger branches of the carotid arteries, the circle of Willis (brain), the large arteries of the lower extremities, and the renal and mesenteric arteries.2,4
The incidence of atherosclerosis increases with age. Other risk factors for the formation of atheromas are gender (more common in men in all age groups, but the incidence increases in postmenopausal women), hypercholesterolemia (especially high LDL levels), hypertension, diabetes mellitus, cigarette smoking, obesity, “type A” personality, physical inactivity and the use of oral contraceptive drugs.2,4
Atheromatous plaques have a central core consisting of cholesterol and cholesterol esters, lipid-laden macrophages, calcium and necrotic cellular debris.2,4
Ulceration, hemorrhage into the plaque or calcification of the plaque may occur. Systemic obstructive disease ensues if a thrombus develops at the site of the plaque or embolization occurs.5
A thrombus is a solid mass of platelets and/or fibrin (and other components of blood) that forms locally in a vessel.2,4,5 An embolus moves through the bloodstream until it lodges in a narrowed vessel and blocks circulation. Cardiogenic emboli are a recognized etiology of ischemic stroke and retinal vascular occlusive disease. The mitral and aortic valves are the most common sources of cardiac emboli. Amaurosis fugax (transient monocular vision loss) and cerebral transient ischemic attacks may also occur from cardiogenic emboli.2,4,5 Fibro-platelet and cholesterol emboli originating from the carotid arteries may also cause amaurosis fugax, transient ischemic attack or stroke.
Atherosclerosis may lead to ischemic heart disease and myocardial infarction (the most common cause of death in the United States). Other complications include stroke, ischemic bowel disease, peripheral vascular occlusive disease and renal arterial ischemia with secondary hypertension. Weakening of the blood vessel wall may also lead to aneurysm formation.2,4,6
Inflammation may also cause vascular disease. In general, inflammation of blood vessels is referred to as vasculitis. Inflammation may cause narrowing and/or blockage of vessels. Trauma or injury that involves a blood vessel may lead to inflammation or infection. This, in turn, may damage the vessel and lead to its narrowing and/or blockage.2,7
Ocular Manifestations of Cardiovascular Disease
Ocular ischemic syndrome (OIS) is a vision-threatening condition in which hypoperfusion leads to acute and chronic defects in ocular and orbital tissues. OIS can occur before cerebrovascular and cardiovascular complications, so optometrists may be the first provider to encounter these patients.
Ocular ischemic syndrome encompasses a spectrum of clinical findings that result from chronic ocular and orbital hypoperfusion. Venous dilation in association with mid-peripheral dot-and-blot hemorrhages, superficial flame-shaped hemorrhages and microaneurysms in patients with carotid artery obstruction had been termed venous stasis retinopathy, but is now referred to as hypoperfusion retinopathy.8
Ischemic oculopathy describes ischemic changes related to carotid artery occlusive disease not limited to the posterior segment, but also in the anterior segment. Both posterior and anterior segment involvement is referred to as OIS.9
Who Gets OIS?
OIS occurs at a mean age of 65 and is rare before age 50. Men are affected twice as often as women due to a higher incidence of atherosclerotic disease in men.10 No racial predilection exists. Bilateral involvement may occur in up to 22% of cases. The incidence of OIS is estimated at 7.5 cases per million people each year.11 The five-year mortality rate in patients with OIS is about 40%. The leading cause of death is cardiac disease, followed by stroke and cancer.10-12
Up to 29% of patients with a symptomatic carotid artery occlusion manifest retinal vascular changes that are usually asymptomatic, and 1.5% of them per year progress to symptomatic OIS.12
The most common etiology of OIS is severe unilateral or bilateral atherosclerotic disease of the internal carotid artery or marked stenosis at the bifurcation of the common carotid artery. Decreased vascular perfusion may result in tissue hypoxia and increased ocular ischemia, leading to neovascularization.13 Other causes of OIS include giant cell arteritis, carotid artery dissection, neurofibromatosis type I, scleroderma and radiation therapy.
OIS is probably under-reported because it may be misdiagnosed or even masked by other ocular vascular diseases, such as retinal vein occlusions and diabetic retinopathy. The most common symptoms are amaurosis fugax, gradual or sudden visual loss, and ocular, periocular or facial pain. About 20% of diabetes patients with unilateral retinopathy or marked asymmetry of retinopathy have significant carotid artery stenosis. The stenosis may be contralateral or ipsilateral to the eye with the more severe diabetic retinopathy.14 Also, consider OIS in elderly patients with asymmetric anterior uveitis, intraocular pressure or cataract. (See “Major Clinical Features of OIS.”)
In addition to a comprehensive ophthalmic workup, perform arm pulses and carotid auscultation. In patients with suspected giant cell arteritis, ESR and CRP levels must also be evaluated. Duplex carotid ultrasonography is the most commonly used non-invasive test to detect carotid occlusive disease.
Major Clinical Features of OIS
- Semi-dilated pupil or sluggish reaction
- Afferent pupillary defect
- Ectropion uveae
- Neovascularization of the iris or angle
- Anterior uveitis (usually mild)
- Asymmetric cataract
- Dilated (non-tortuous) retinal veins
- Narrow arteries
- Hemorrhages in mid-periphery
- Disc edema
- Cotton-wool infarct
- New vessels on the disk (NVD)
- New vessels elsewhere (NVE)
Treatment of OIS
Ocular treatment is directed toward controlling anterior segment inflammation, minimizing retinal ischemia, and preventing or treating neovascular glaucoma. Initial topical therapy may include steroids and cycloplegic agents to reduce inflammation and stabilize the blood-aqueous barrier.
Panretinal photocoagulation causes regression of iris neovascularization in 36% of the treated eyes with OIS.10 If neovascular glaucoma develops, incisional surgery or cycloablation are often needed.
Given the high rate of vascular death, these patients must be referred to a neurologist or to the patient’s primary care physician for full medical assessment and management. Therapeutic options include antiplatelet agents, pharmacotherapy of hypertension, diabetes, dyslipidemia or coronary artery disease, as well as cessation of smoking and weight reduction. Evidence suggests that aspirin 325mg p.o. q.d. be used as a first-line agent in OIS patients with atherosclerosis.15
The American Academy of Neurology and the American Heart Association/American Stroke Association recommend carotid endarterectomy (CEA) for symptomatic stenosis of 50% to 99% if the perioperative risk of stroke or death is less than 6%.16 In asymptomatic patients, CEA is recommended for a stenosis of 60% to 99% if the perioperative risk of stroke or death is less than 3%.16 CEA is most beneficial for the treatment of OIS if performed early, before neovascular glaucoma develops.
How is breast cancer related to the eye? By metastasis.
Malignant neoplasms are capable of spreading by invasion and metastasis. Metastasis may occur in several ways. It can result from spread into body cavities, which involves direct “seeding” of serous membranes. Another route of metastasis is by lymphogenous spread, in which cells travel through the lymphatic system to nearby or distant nodes. Metastasis may also occur by hematogenous spread, in which cells travel through the bloodstream.
Breast cancer is defined as a neoplasia that forms in tissues of the breast, usually the ducts and lobules (milk-producing glands). Malignant cancers of the breast arise through a series of molecular alterations at the cellular level, resulting in the uncontrolled outgrowth and spread of epithelial cells.
Breast cancer is the leading cause of cancer death among women worldwide. (Male breast cancer, though rare, can occur.) The American Cancer Society estimated nearly 1.4 million new cases of invasive breast cancer worldwide in 2008.17 In the United States, an estimated 207,090 women were diagnosed with breast cancer and 39,840 women died of it in 2010.17
Breast Cancer Risk Factors
Epidemiological studies have identified several factors that increase the chance of a woman developing breast cancer. Risk factors are identified based on their effect on the level and duration of exposure to endogenous estrogen.
- Age. The median age of diagnosis for breast cancer is about 61.18 The chance of getting breast cancer increases with advancing age.
- Personal health history. Having cancer in one breast increases the risk of cancer in the other breast.18
- Family health history. Risk is increased if a first-degree relative has breast cancer. The risk is even higher if the family member had breast cancer before age 50.18
- Genetic factors. Mutations in certain genes, such as BRCA1 or BRCA2, substantially increase the risk. Women who inherit a mutation in the BRCA1 or BRCA2 gene have an estimated 50% to 80% lifetime risk of developing breast cancer.18
- Radiation therapy to the chest. Women who have had radiation therapy to the chest (including the breasts) before age 30 are at an increased risk.18
- Reproductive and menstrual history. Women who never had children are at an increased risk. The older a woman is when she has her first child, the greater the chance of breast cancer. Women who had their first menstrual period before age 12 are at an increased risk. Those who went through menopause after age 55 are at an increased risk of breast cancer.
- Race. In the U.S., breast cancer is diagnosed more often in white women than in other races.18
- Breast density. Women whose mammogram shows a larger than normal area of dense tissue (compared to others in their age group) are at increased risk of breast cancer.18
- Hormone replacement therapy (HRT). Postmenopausal women on HRT are at greater risk for breast cancer incidence and mortality.18
- Excess weight. The chance of getting breast cancer after menopause is higher in women who are overweight, or obese.18
- Alcohol. Studies suggest that the more alcohol a woman drinks, the greater her risk of breast cancer.18
Breast Cancer and the Eye
Intraocular/orbital metastasis is the most common malignancy of the eye, but often goes undiagnosed.20 The frequency of intraocular metastasis in patients dying of cancer is approximately 12%. Breast carcinoma in women and lung carcinoma in men are the most common primary foci.20
The uveal tract, with its rich vascular network, is the site in the globe most often involved in metastatic disease. Less commonly, other ophthalmic structures—including the optic nerve, conjunctiva and lacrimal
gland—are the sites of metastatic
cancer. The overall survival time
(eight to 12 months on average) for
these patients is poor.20-22
Review of Systems for
|Change in bowel or bladder habits.
A sore that does not heal.
Unusual bleeding or discharge.
Thickening of lump in breast or else
Indigestion or difficulty swallowing.
Obvious change in wart or mole.
Nagging cough or hoarseness.
Treatment and Management
Management of intraocular/
orbital metastasis may include
observation, chemotherapy, photocoagulation, cryosurgery, surgical
resection, localized plaque therapy
and external beam radiation.20,22 The specific therapy chosen is an individualized process that must take
into account the clinical condition of
The choice of cancer therapy for
the primary site depends upon the
location and grade of the tumor(s),
the stage of the disease, and the
general status of the patient. Surgery
is considered primary treatment for
breast cancer, as many early-stage
patients are cured with surgery
Medical treatment may include
chemotherapeutic drugs. These
agents are divided into the following
groups: natural products, angiogenesis inhibitors and biologic therapy
(immunotherapy).23,24 Tamoxifen is
a selective estrogen receptor modulator (SERM) that binds to and inhibits estrogen receptor signaling in the
breast. Remember that tamoxifen
treatment might bring about ocular
side effects, including maculopathy.
Radiation therapy may be indicated as either a therapeutic or palliative measure. Monoclonal antibody
therapy and bone marrow transplant may also be effective.17,19,24
Treatment of choroidal metastasis
is not without potential complications and side effects, such as cataract, radiation retinopathy, optic
neuropathy, exposure keratopathy,
retinal detachment and epiretinal
Sarcoidosis (also called sarcoid) is
a granulomatous condition (i.e., one
that is characterized by an organized
collection of macrophages). It can
affect virtually every body system,
especially the respiratory and lymphatic systems.25 Pulmonary symptoms occur in up to one-half of all
sarcoidosis patients and most commonly include dyspnea, dry cough
and chest tightness or pain.25,26
When sarcoidosis affects the
pulmonary system, the lungs are
involved in more than 90% of
patients.25 Parenchymal infiltration
and irreversible pulmonary fibrosis
can occur if the disease progresses,
eventually leading to respiratory failure. Sarcoidosis also can affect the
lymphatic, ocular, nervous, hepatic,
renal, endocrine, musculoskeletal
and myocardial systems.25,26
In the U.S., sarcoidosis is slightly
more predominant in women than
in men.25-27 The annual incidence in
whites is 10 to 14 cases per 100,000
people. The annual incidence is much
higher in blacks, especially women,
at 36 to 64 cases per 100,000.27 The
condition usually presents between
20 and 29 years of age.25
Mortality from sarcoidosis is
about 5% in the U.S., most commonly due to respiratory failure
from pulmonary involvement.25-27
Ocular Manifestations of
The ocular manifestations of this
condition are well documented.
About one quarter of patients with
systemic sarcoidosis have ocular
involvement. Uveitis is the most
common of these, affecting 25%
percent of sarcoidosis patients.28 Anterior uveitis occurs in 20% to
70% patients, typically as an acute
iritis or iridocyclitis.29-31 Physical findings of acute anterior uveitis
indicative of sarcoidosis are muttonfat or granulomatous keratic precipitates.32
The posterior segment is affected
in about 20% of patients, usually
in the form of chorioretinitis. Ocular sarcoidosis can also affect the
adnexa and the orbit, typically the
lacrimal gland. Much less frequent
ocular manifestations include scleritis, glaucoma and cataracts.
Neurosarcoidosis has been called
the “the great mimicker” because
those affected with the disease can
present with non-specific and variable symptoms that can be seen with
many other pathologies. Although
sarcoidosis may present early, even
before a known diagnosis of systemic sarcoidosis is found. Neuro-ophthalmic sarcoidosis may affect the
afferent or efferent visual pathways,
along with the presentation of ocular motor, trochlear, abducens and
facial nerve palsies.33,34 While many
sarcoidosis patients with ocular
involvement experience severe pain
and photophobia, more than one
third have no ocular symptoms.35
Pathways to Diagnosis
The lack of a single diagnostic
test, as well as the diverse presentations, make the diagnosis challenging. Patients with sarcoidosis most
commonly present in winter and
early spring, suggesting an environmental trigger.26,36
For a definitive diagnosis, histologic proof of a noncaseating epithelioid granuloma, clinicoradiologic
features and exclusion of similar diseases are necessary.25,37,38 A complete blood count (CBC) with differential
and platelets, along with serum
calcium and 24-hour urine calcium
levels, should be performed if you
Sarcoid granulomas produce
both angiotensin-converting enzyme
(ACE) and lysozyme. Serum ACE
levels are significantly elevated in
patients with sarcoidosis. So serum
ACE levels should be tested to help
monitor both disease activity and
treatment response.26,37 However, this test has poor sensitivity because
it is found to be elevated in only
40% to 60% of sarcoid patients.39 Serum lysozyme should also be tested because it has been shown to be a
more sensitive marker of sarcoidosis
Because 90% of sarcoidosis
patients have radiographic involvement, a postero-anterior chest radiograph should be obtained to stage
the disease. The four stages:
- Stage I pulmonary sarcoid: bilateral hilar lymphadenopathy (BHL).
- Stage II: BHL plus pulmonary
- Stage III: pulmonary infiltrates
- Stage IV: pulmonary fibrosis.
Pulmonary function testing can
be ordered to identify defects in lung
diffusing capacity and vital capacity.26,37,38
Biopsy is required for diagnosis
in most cases. The skin is the most
easily accessible tissue for biopsy,
although conjunctival tissue has also
been used. A transbronchial lung
biopsy is the most accurate method
and will show the presence of noncaseating granulomas.25,26,37
Most cases of sarcoidosis are not
fatal, so the primary goals of treatment are to alleviate symptoms,
resolve inflammatory lesions that
interfere with organ function, and
prevent pulmonary fibrosis. There is
no curative treatment.25,26,38-41 Oral corticosteroids for a minimum of 12
months are the mainstay of treatment for pulmonary sarcoid.
Patients with Stage I disease do
not require treatment.25,42 Symptomatic patients with Stage II or III
disease usually show improved chest
radiograph findings during treatment. Patients with Stage IV disease
usually respond poorly or not at all
to systemic therapy; lung transplantation may be a viable option for
Multiple relapses may occur, and
patients may require long-term, lowdose corticosteroid therapy.42 Cytotoxic agents and immunomodulators
may be used in patients who do
not respond to corticosteroids or as
steroid-sparing agents. Rheumatrex
(methotrexate, STADS Pharmaceuticals) and Imuran (azathioprine,
GlaxoSmithKline) are preferred.
Antimalarials such as Plaquenil
(hydroxychloroquine, Sanofi Aventis) and Aralen (chloroquine, Sanofi
Aventis) can also be considered
in patients with pulmonary sarcoid.25,38,42,43
Consider referring any patient
who presents with evidence of
bilateral, granulomatous, recurrent
or chronic uveitis for systemic and
radiologic testing to rule out sarcoidosis. Optometrists can facilitate
early diagnosis and treatment of this
disease to enhance the patients quality of life.
Dr. Pizzimenti is an associate
professor at Nova Southeastern University College of Optometry. Dr.
Pelino is an assistant professor at
Pennsylvania College of Optometry
at Salus University. Both doctors
lecture extensively on oculosystemic
disease, and they co-author Review’s
“Review of Systems” column.
- Roger VL, Go AS, Lloyd-Jones DM, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart
disease and stroke statistics-2011 update: a report from the American Heart Association. Circulation. 2011 Feb 1;123(4):e18-e209.
- Schneider AS, Szanto PA. The Vascular System. In: Pathology,
2nd. ed. Philadelphia: Lippincott Williams & Wilkins; 2001:117-28.
- Whitaker RH. Anatomy of the Heart. Medicine. 2006 May 1;
- Libby P. Atherosclerosis. In: Fauci A, et al (eds.). Harrison’s
Principles of Internal Medicine. 14th ed. New York: McGraw-Hill;
- Dul M, Haskes C. Cardiogenic Emboli and Valvular Heart Disease.
In: Marks E, Adamczyk D, Thomann K. Primary Eyecare in Systemic
Disease. Norwalk, Conn.: Appleton & Lange; 1995:Ch. 4.
- Califf RM. Acute Myocardial Infarction and Other Acute Ischemic
Syndromes. In: Braunwald E, ed. Atlas of Heart Disease. 8th ed. St.
Louis, Mo: Mosby; 1996:1.1-15.13.
- Pearson TA, Mensah GA, Alexander RW, et al.; Centers for Disease
Control and Prevention; American Heart Association. Markers of
inflammation and cardiovascular disease: application to clinical and
public health practice: A statement for healthcare professionals from
the Centers for Disease Control and Prevention and the American
Heart Association. Circulation. 2003 Jan 28;107(3):499-511.
- TP Kearns, RW Hollenhorst. Venous stasis retinopathy of occlusive disease of the carotid artery. Proc Staff Meet Mayo Clin. 1963
- Young LH, Appen RE. Ischemic oculopathy. A manifestation of
carotid artery disease. Arch Neurol. 1981 Jun;38(6):358-61.
- Sivalingam A, Brown GC, Magargal LE. The ocular ischemic
syndrome. III. Visual prognosis and the effect of treatment. Int Ophthalmol. 1991 Jan;15(1):15-20.
- Sturrock GD, Mueller HR. Chronic ocular ischaemia. Br J Ophthalmol. 1984 Oct;68(10):716-23.
- Klijn CJ, Kappelle LJ, van Schooneveld MJ, et al. Venous stasis
retinopathy in symptomatic carotid artery occlusion: prevalence,
cause, and outcome. Stroke. 2002 Mar;33(3):695-701.
- Kahn M, Green WR, Knox DL, Miller NR. Ocular features of
carotid occlusive disease. Retina. 1986 Winter;6(4):239-52.
- Duker JS, Brown GC, Bosley TM, et al. Asymmetric proliferative
diabetic retinopathy and carotid artery disease. Ophthalmology. 1990
- Chen CS, Miller NR. Ocular ischemic syndrome: review of clinical presentations, etiology, investigation, and management. Compr
Ophthalmol Update. 2007 Jan-Feb;8(1):17-28.
- Hauch TL, Busuttil RW, Yoshizumi MO. A report of iris neovascularization: an indication for carotid endarterectomy. Surgery. 1984
- American Cancer Society. Breast Cancer Facts & Figures 2009. Available at: www.cancer.org/downloads/STT/
- American Cancer Society. Risk Factors for Breast Cancer. Available at: www.cancer.org/Cancer/BreastCancer/
- American Cancer Society. Cancer Facts & Figures
2009. Atlanta: American Cancer Society; 2009.
- Quillen DA, Blodi BA. Intraocular Tumors. In: Clinical
Retina. Chicago: American Medical Association Press;
- Wiegel T, Kreusel KM, Bornfeld N, et al. Frequency
of asymptomatic choroidal metastasis in patients with
disseminated breast cancer: results of a prospective screening programme. Br J Ophthalmol. 1998
- Shields CL, Shields JA, Gross NE, et al. Survey of
520 eyes with uveal metastases. Ophthalmology. 1997
- Weinberg RA. The Biology of Cancer. New York: Garland Science; 2006: ch.1-5.
- Visvanathan K, Chlebowski RT, Hurley P, et al. American society of clinical oncology clinical practice guideline
update on the use of pharmacologic interventions
including tamoxifen, raloxifene, and aromatase inhibition
for breast cancer risk reduction. J Clin Oncol. 2009 Jul
- Wu JJ, Schiff KR. Sarcoidosis. Am Fam Physician
2004 Jul 15;70(2):312-22.
- Gould KP, Callen JP. Dermatologic Manifestations of
Sarcoidosis. Available at: www.emedicine.com/DERM/
topic381.htm (accessed March 2011).
- Rybicki BA, Major M, Popovich J Jr, et al. Racial
differences in sarcoidosis incidence: a 5-year study in a
health maintenance organization. Am J Epidemiol 1997
- Evans M, Sharma O, LaBree L, et al. Differences in
clinical findings between Caucasians and African Americans with biopsy-proven sarcoidosis. Ophthalmology
- Bradley DA, Baughman RP, Raymond L, Kaufman AH.
Ocular manifestations of sarcoidosis. Semin Respir Crit
Care Med 2002;23:543-8.
- Jabs DA, Johns CJ. Ocular involvement in chronic
sarcoidosis. Am J Ophthalmol 1986;102:297-301.
- Silver MR, Messner LV. Sarcoidosis and its ocular
manifestations. J Am Optom Assoc 1994;65:321-7.
- Herbort CP, Rao NA, Mochizuki M; Members of
Scientific Committee of First International Workshop on
Ocular Sarcoidosis. International criteria for the diagnosis
of ocular sarcoidosis: results of the first International
Workshop On Ocular Sarcoidosis (IWOS). Ocul Immunol
- Ng D, Jacobs M, Mantil J. Combined C-11 methionine
and F-18 FDG PED imaging in a case of neurosarcoidosis.
Clin Nucl Med 2006; 31:373-375.
- Phillips YL, Eggenberger ER, Neuro-ophthalmic
sarcoidosis. Current Opinion in Ophthalmology 2010,
- Rothova A, Alberts C, Glasius E, et al. Risk factors for
ocular sarcoidosis. Doc Ophthalmol 1989;72:287-96
- Rossman MD, Kreider ME. Lesson learned from
ACCESS (A Case Controlled Etiologic Study of Sarcoidosis). Proc Am Thorac Soc 2007 Aug 15;4(5):453-6.
- Judson MA, Thompson BW, Rabin DL, et al.
The diagnostic pathway to sarcoidosis. Chest 2003
- Pietinalho A, Tukiainen P, Haahtela T, et al. Early treatment of stage II sarcoidosis improves 5-year pulmonary
function. Chest 2002 Jan;121(1):24-31.
- Phillips YL, Eggenberger ER. Neuro-ophthalmic sarcoidosis. Curr Opin Ophthalmol. 2010 Nov;21(6):423-9.
- Martin WJ 2nd, Iannuzzi MC, Gail DB, Peavy HH.
Future directions in sarcoidosis research: summary of an
NHLBI working group. Am J Respir Crit Care Med 2004
Sep 1; 170(5):567-71.
- Grutters JC, van den Bosch JM. Corticosteroid treatment in sarcoidosis. Eur Respir J 2006 Sep;28(3):627-36.
- Nunes H, Bouvry D, Soler P, Valeyre D. Sarcoidosis.
Orphanet J Rare Dis 2007 Nov 19;2:46.
- Hilton JM, Cooper DM, Henry RL. Hydoxychloroquine
therapy of diffuse pulmonary sarcoidosis in two Australian
male children. Respirology 1997 Mar;2(1):71-4.