Birdshot Retinochoroidopathy

 

An informational site about BSRC and Uveitis.

It has many names: birdshot retinochoroidopathy, birdshot choroidopathy, birdshot retinochoroiditis, birdshot choroidretinitis. If it is an eye disorder with birdshot in the name, this is the place for information.

Usually a patient is diagnosed with uveitis. This is the inflammation of the uvea in the eye and has over 100 causes ranging from AIDS to unknown. Typically the diagnosis of BSRC is made after seeing white and yellow spots in the eye and followed up with a battery tests ruling out other causes and testing positive for the presence of HLA-A29.

My birdshot group:

http://groups.msn.com/BSRC/_whatsnew.msnw

My other birdshot site:

http://home.comcast.net/~dagmara56/wsb/html/view.cgi-home.html-.html

 

 Eye Physiology

 Medical Links

Medical Citations

 Medication Explanations

 My Experience

 Contact Information

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Eye Physiology

This information is paraphrased from The Eye Book by Gary H. Cassel, MD; Mchael D. Billog, OD, and Harry G. Randall, MD

The eye is approximately the size of a ping pong ball. The inside of the eyeball is a jelly-like substance called the vitreous; in the front of the its held together with the sclera (white of the eye), in the back its the retina. I'm going to skip the details about the front of the eye and skip to just the part we are all interested it: the retina.

Holding the vitreous jelly together are different membranes: The layers are:

- vitreous

- internal limiting membrane

- blood vessels

- ganglion cells

- bipolar cells

- rod cells

- cone sells

- pigment epithelial cell

- Bruch's membrane

- choroid

The retina starts at the blood vessel layer and includes all the layers down to Bruch's membrane. The choroid is external to the retina. The uvea is a term for the iris, ciliary bodies and choroid (like this isn't confusing enough!). Uveitis is the general term for anything wrong with the uvea. itis means "inflammation of", -opathy means "disease of". Thus BSRC has so many names depending upon the MD's view of what has gone wrong, the retina or the choroid. Symptoms of uveitis may be redness, throbbing pain, difficulty with bright light or silent. Determining the cause of uveitis is difficult. There are over 100 causes from AIDS to unknown.

I hope you are all as throughly confused as I am!

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Medical Links

Uveitis by Dr. S. Foster, MEEI

MEEI Uveitis Home Page

AAIDA

Uveitis and Other Eye Conditions (includes a personal story)

Eye Resources on the Internet

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Medical Citations

Birdshot, Retinochoroidopathy by Dr. Michael Samson Excellent!

What to do When You See Spots

Birdshot Chorioretinopathy: Clinical Characteristics and Evolution

Choroidal Abnormalities In Birdshot Chorioretinopathy: An Indocycanine Green Angiography Study

Birdshot chorioretinopathy5

Retinal Function in Birdshot Retinochoroidopathy

Mintravenous immunoglobulin (IVIg) for the treatment of birdshot retinochoroidopathy

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Medication Explanations Meds

From The Casey Eye Institute, Department of Ophthalmology

Excellent source for a basic explanation of uveitis, the eye, and various medications to include oral and injected steroids, cyclosporin, and other treatments.  This site goes into the how, why, of each medication as well as the side effects.  I have copied only the sections on oral steroids and cyclosporin.

Oral Corticosteroids

Many patients with uveitis may be treated with a hormone known as corticosteroid. This is most commonly taken by mouth in the form of a pill known as prednisone. Normally the body produces the equivalent of about 7.5 mg of prednisone per day. Inflammation is treated with variable amounts of prednisone. The side effects of prednisone depend upon the individual, the dosage of therapy, and the duration of therapy. Some of the side effects associated with prednisone therapy are listed in the accompanying table. Prednisone has the advantage of working quickly to reduce the inflammatory response. It is one of the most potent anti inflammatory medications known. However, it must be used cautiously because of the numerous side effects. In addition, the benefits from prednisone may diminish with long standing use as the body seems to adjust to chronic dosage.

It is often recommended that prednisone be taken in the morning since the body tends to produce its own cortisone mostly in the early morning hour. Prednisone is normally taken with food as it can increase acid production and lead to heart burn or ulcers at higher dosages. The body can become dependent upon prednisone. Consequently patients who have been on prednisone for longer periods of time need to reduce prednisone dosage gradually. Patients on prednisone therapy should normally carry a card in one's wallet listing this medication. Patients who have surgery or who are in an emergency situation such as a serious motor vehicle accident will need to receive extra amounts of prednisone temporarily since the body normally responds to stress by producing its own cortisone and its ability to respond to stress disappears when one is taking prednisone by mouth.

Examples of corticosteroid side effects:

Weight gain

Facial puffiness

Fluid retention

Mood change

Sleep disturbance

Acne

Lowered resistance to infection

Diabetes

Easy bruising

Osteoporosis

Glaucoma

Cataracts

Adrenal suppression

Ulcers

Cyclosporine

Cyclosporine is an effective medication for the treatment of uveitis in many instances. Cyclosporine helps to suppress the function of cells in the immune system without killing those cells. This distinguishes cyclosporine from other medications such as imuran, methotrexate, or cytoxan. Cyclosporine is a very popular medication in the treatment of medications who have received organ transplants. Patients who receive a donated organ such as a kidney will experience their immune system trying to reject this donated tissue. Cyclosporine helps to suppress the immune system sufficiently such that organ rejection is prevented. Cyclosporine is generally taken as a capsule every 12 hours. The dosage is based upon one's weight. Cyclosporine therapy can be associated with side effects which include flu-like symptoms, muscle cramps, tingling, sore gums, and hair growth. The chronic use of cyclosporine can cause kidney damage. Cyclosporine often elevates the blood pressure and an elevated blood pressure (hypertension) is a relative contraindication to the use of cyclosporine. Periodic laboratory tests and blood pressure determinations are important for patients who are receiving cyclosporine therapy. Patients on cyclosporine therapy may be more likely to develop infections because the immune system is impaired. Patients with diabetes may experience a worsening of that disease because of cyclosporine. Nonsteroid antiinflammatory drugs such as ibuprofen, motrin, advil, aleve, naprosyn, aspirin, voltaren, or orudis should be minimized while taking cyclosporine because these increase the kidney side effects of cyclosporine. In addition, cyclosporine interacts with many different medications and one may need to check with a physician specifically about potential interactions. Other names for cyclosporine include sandimmune or neoral.

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Retinopathy, Birdshot BSRC

From: C. Michael Samson, M.D., Fellow, Ocular Immunology and Uveitis Service, Harvard Medical School, Massachusetts Eye and Ear Infirmary and C. Stephen Foster, Professor, Director of Ocular Immunology & Uveitis Service, Ocular Immunology & Uveitis Service, Massachusetts Eye & Ear Infirmary

This is THE BEST explanation I have found for BSRC. Because the information is copywrited by eMedicine, it is not possible to reproduce any of the article here, but I highly recommend using the link to read it. I was treated by both, Dr. Sampson and Dr. Foster at MEEI, and found them to both be unusually empathetic and knowledgable physicians.

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What To Do When You See Spots Review of Opthamology

From: Retinal Insider, Edited by Jay S. Duker, MD and Carl Regillo, MD

This disease usually affects middle-aged individuals. There is no gender predominance.

This may be an autoimmune disease. Almost 90 percent of patients demonstrate HLA-A29 antigen, the strongest association of all the HLA-associated immune eye diseases. Presenting symptoms include blurry vision, photopsias, floaters, and night blindness. Most patients have bilateral involvement.

Ophthalmoscopy reveals multiple white or yellow, medium to large lesions scattered like "birdshot" around the posterior pole (Fig. 3). These lesions appear to be at the level of the choroid and deep retina. Posterior vitreous cellular reaction is always present. Vascular sheathing, disc edema and CME may also appear. As the lesions mature, they may enlarge, resulting in RPE atrophy. In the late stages, RPE hyperpigmentation and retinal arteriolar narrowing can appear, and the disc may be pale. Some patients develop disc neovascularization and vitreous hemorrhage.

Angiography reveals marked disc and cystoid macular leakage. The lesions stain relatively poorly, or not at all. The ERG is usually abnormal in both rod and cone function.

Because of the vision-threatening nature of this disease, systemic steroids and sometimes steroid sparing medications such as cyclosporine are necessary. The response is usually good. Though the disease is chronic, most patients retain useful vision in at least one eye.

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Birdshot Chorioretinopathy: Clinical Characteristics and Evolution BJO

From Priem HA, Oosterhuis JA, Eye Clinic, University of Ghent, Belgium, British Journal of Ophthalmology, 1988, Vol 72, 646-659

During the period 1980-6 102 patients from 14 European eye clinics were diagnosed as having birdshot chorioretinopathy (BSCR). All were Caucasian, and the series consisted of 47 men and 55 women, with a mean age of 52.5 years. The major findings in this rare disorder concern the ocular fundus. Most marked are the patterned distribution of depigmented spots without hyperpigmentation, radiation from the optic disc in association with vitritis, retinal vasculopathy with frequent cystoid macular oedema, and involvement of the optic nerve head. The distribution and appearance of the lesions suggest that they are related to the major choroidal veins. Complications of the disease were epiretinal membranes, retinal neovascularisation, recurrent vitreous haemorrhage, subretinal neovascular membranes occurring both in the juxtapapillary and macular regions, and optic atrophy. The medical history was not contributary. HLA testing showed very strong disease association with HLA A29 (95.8%). The evidence suggests that it is a single disease entity rather than a group of disorders because of the remarkable similarity in the ophthalmological appearance and the clinical course, combined with the exceptionally high association with HLA A29.

(c) 1988 by the British Journal of Ophthalmology

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Choroidal abnormalities in birdshot chorioretinopathy: an indocyanine green angiography study.

From: Eye 1997;11, Howe LJ, Stanford MR, Graham EM, Marshall J ( Pt 4):554-9, Department of Ophthalmology, UMDS, London, UKReview of Opthamology

Birdshot chorioretinopathy is a rare inflammatory disorder with an insidious onset that can slowly progress to severe visual loss. The pathogenesis is unknown. This study used indocyanine green (ICG) angiography to investigate the degree of choroidal vascular involvement with progression of disease and to determine the nature of the birdshot lesions. Seven patients with birdshot chorioretinopathy had ICG angiography performed with a scanning laser ophthalmoscope at various stages of clinical disease. Results were compared with fluorescein fundal angiography (FFA). All large choroidal vessels appeared normal. The birdshot lesions were demonstrated with ICG but not with FFA and were represented by dark areas on ICG angiography. Typically these areas were bordered by large or medium-sized choroidal vessels and their appearance suggested small choroidal vessel hypoperfusion. In disease of recent onset, some lesions masked fluorescence from large underlying choroidal vessels possibly due to inflammatory choroidal infiltrates. In long-standing disease, the choroidal angioarchitecture was relatively normal within the birdshot lesions. This study of birdshot chorioretinopathy demonstrates abnormalities in the small choroidal vessels within the birdshot lesions. ICG angiography detects the birdshot lesions more readily than FFA and may be of benefit in assessing disease activity.

PMID: 9425423, UI: 98086560

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Birdshot chorioretinopathy.

From: Ryan SJ, Maumenee AE; American Journal of Opthamology, 1980 Jan ; 89(1): 31-45

Thirteen patients had a new syndrome and entity in intraocular inflammation called birdshot retinochoroidopathy, which was characterized by a white, painless eye with minimal anterior segment inflammation but particlate debris in the anterior and posterior vitreous. There was profuse retinal vascular leakage with resultant retinal macular, and disk edema, which are the primary causes of the decreased vision in this syndrome. Long-term follow-up (mean of ten years) revealed that only two patients seemed to respond to anti-inflammatory therapy (systemic coricosteroids) and five patients progressed to 6/60 (20/200) or less visual acuity in at least one eye.

PMID: 7346785, UI: 80106925

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Retinal Function in Birdshot Retinochoroidopathy.

From: Eye Research Institute, Harvard Medical School, Boston, MA; Acta Ophthalmol (Copenhagen), 1991 Jun; 69(3): 327-37

The electroretinograms (ERGs) of 15 patients with birdshot retinochoroidopathy varied from super-normal to non-recordable, depending upon the severity and the stage of the disease. The abnormal ERGs were characterized by a disproportionate decrease of the b-wave amplitude compared with the a-wave amplitude demonstrating the negative (-) type response. This distinct ERG pattern has not been observed in any other type of uveitis or chorioretinitis, and appears specific to birdshot retinochoroidopathy. ERG findings indicate that in birdshot retinochoroidopathy the neural layers of the retina are more diffusely and severly involved than the receptor-retinal pigment epithelium-choroid complex. In the most advanced stage, the patient becomes night blind with a non-recordable ERG, a situation that is essentially the same as retinitis pigmentosa, except that pigmentation is conspicuously absent in the fundus.

PMID: 1927315, UI: 92024929

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Intravenous immunoglobulin (IVIg) for the treatment of birdshot retinochoroidopathy Ocular Immunology and Inflammation

Phuc LeHoang1, Nathalie Cassoux1, Françoise George2, Nathalie Kullmann1 and Michel Kazatchkine2
1University Pierre et Marie Curie, Hôpital de la Pitié-Salpêtrière, Department of Ophthalmology, Paris, France
2University Pierre et Marie Curie, Hôpital Broussais, Department of Immunology, INSERM U430, Paris, France

Intravenous polyclonal immunoglobulin (IVIg) treatment has been successfully used in a number of autoimmune conditions. Birdshot retinochoroidopathy (BRC) is a bilateral autoimmune posterior uveitis which, in its progressive form, frequently requires immunosuppressive therapy. We report a clinical study aimed at determining the tolerance and efficiency of IVIg treatment in patients with active BRC. The study was conducted in an open manner. Eighteen patients were included. The initial visual acuity (VA) was ≤20/30 in 26 eyes, 20/25 in five eyes, and 20/20 in five eyes. IVIg was given as sole treatment at 1.6 g/kg every four weeks for six months, followed by injections of 1.2-1.6 g/kg at six to eight-week intervals. The mean follow-up was 39 months, ranging between 12 and 53 months. The results showed that the final VA of the 26 eyes with an initial VA of ≤20/30 was increased by two lines or more in 14 eyes (53.8%) and decreased in two (7.7%). Of the five eyes with an initial VA of 20/25, four had improved to 20/20 and one remained stable. Of the five eyes with an initial VA of 20/20, four remained stable and one deteriorated to 20/25. When present, macular edema was improved in half of the eyes on fluorescein angiography. Benign side effects were observed in 12 patients: moderate transient arterial hypertension (7), headache (6), eczematous lesions (6), and hyperthermia (4). The results suggest that IVIg may represent a safe alternative therapy for patients with BRC.

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My Experience

In 1991, when I was 34 years old, while driving home from work, I noticed some floaters in my right eye. Two days later, I noticed the same floaters were still in my right eye, as well as my left. I knew enough about biology to realize floaters didn't migrate from eye to the other, and spent the next day in search of an opthamologist. The opthamologist I went to told me he thought he knew what the problem was, and it was not serious, but since he had never seen an actual case, he referred me to a retinologist for confirmation. I didn't want to go to the retinologist, but my husband co-erced me.

I knew I was in trouble when the retinologist asked me into his office.  I sat down, I was by myself, because I was so sure it was “nothing”.  The retinologist told me I had uveitis, that I was going to go blind.  I asked him, what is the cause of uveitis?  He told me: number 1 cause was AIDS, #2, syphilis, #3 TB, #4/5; kidney/liver failure, 20% of the time it was idiopathic, no known cause. 

Think of uveitis as a rash; something else causes it, and it is up to your MD to find the source. Based on my experience with three different MDs at three different times, they tend to start with testing for AIDS, syphilis, lupus, arthritis, TB, liver and kidney malfunction. In my case, everything they tested for came back negative. If the cause is unknown it is referred to as ideopathic; ideopathic uveitis occurs in about 20% - 30% of uveitis cases.  That other 20 – 30% can be nearly 100 other conditions, so it takes quite a bit of knowledge on the part of the MD to determine what the cause is; this is why its great to see an expert, such as Dr.Stephen Foster, MERSI.  (http://www.uveitis.org/contact.html)

I remember sitting there, his mouth was opening and closing, and I went deaf.  I couldn’t hear a word he said, I saw his mouth moving, but no sound was coming out.  The next thing I knew, I was standing in my kitchen.  I know that I went to a clinic and an xray taken, who knows what else happened, but I have no recollection of this.  So, I was standing in the kitchen, with my husband and the phone, and I said to him, good news is, I’m going blind.  Bad news is, there is a 80% chance I have AIDs, syphilis, TB, kidney or liver failure.  I don’t remember what happened after that, but he came home with a bouquet of carnations and a box of chocolates and said, you’ll be okay.  I told him, I will never be okay, I’ll be freaking blind, and there are no jobs for blind software engineers.  He told me, okay, you had your cry and your pity party, now get off your butt and make some plans and some decisions.  I told him again, are you nuts?  There are NO FREAKING JOBS FOR BLIND DATABASE ADMINSTRATORS.  He said to me, (very patiently), you trained to be a software engineer, didn’t you?  Well, you are more than just a software engineer, and you can be retrained.  Now, go figure out what you can do if you go blind, and get some training in that.  I thought, okay, there are blind people out there working every day, if they could do it, so can I.  And so, I calmed down.

I had to quit my consulting practice, because I had to see the MD every other day.  My optic nerves were under a great deal of pressure, and my retinologist started me on a course of steroids. After the completion of the course, I was taken off steroids, and the uveitis came back. This continued for another cycle; after the third cycle the uveitis was quiet and I was declared "cured". My vision was 20/20, but with little gray dots in both eyes; this was annoying, but not life-changing.  I went back to work, and life was good.

I've always felt there was a reason for the 1991 episode, and that it would return. In 1999, I had a hemorrhage in the left eye requiring laser surgery to seal the tear.   My opthamologist assured me it was just a one-time occurrence not related to my previous episode of uveitis; I was not convinced.  My primary care physician, Dr. David Deems, of Irving, Texas, referred me to an excellent retinologist, Dr. Shashi Dharmi.  (If living in the Dallas area, I highly recommend both of these caring physicians; they are an integral part of my health care team and are amazingly open to questions, literature, etc.  I cannot say enough good things about these two.)   Dr. Dharma performed the laser surgery to seal the tear.  Two weeks after the laser surgery to seal the tear in my left eye, I had hemorrhages in the right eye. After running another set of tests, again, all returned negative. Dr. Dharma felt I needed to see Dr. Foster, and only Dr. Foster.  She fought like a tiger with my insurance company to cover the cost, but was unsuccessful.  However I went anyway, (what is savings for?), and was able to get me an appointment within a few weeks at the Massachusetts Ear and Eye Infirmary, (MEEI). After exhaustive testing at MEEI, I was diagnosed with BSRC after testing positive for the HLA-A29 antigen and having an indo-cyanine green angiography (also called indo-cyanine green florocene or IGF, although this test can be harmful, its necessary, see the medical citation below). I have also tested positive for HLA-B8 and HLA-B44.

For those of you who have this condition, it may not be as terrible as it initially seems. For me, there were three distinct phases: the initial bleeds, the dispersion of the blood clots, and the final "settling".

When the hemorrhages first occur, the blood clots appear to be large brown amoebas "swimming" about the eye. I refer to them as "tadpoles" because they are brown in color, and over time the clots developed a tail. It has some odd side effects. I drove my husband crazy swatting and stomping on imaginary insects; it turned out the things flying around my head or crawling around on the floor were merely my "tadpoles". Another problem I encountered was I became horribly seasick. The tadpoles were swimming from side-to-side, with a slight up-and-down motion. I was not able to read, do computer work, or drive for more than a few minutes at a time without feeling as though I was standing on the deck of a ship in the middle of an Atlantic storm. After a few weeks, I adapted and nausea was no longer a problem.

In the second phase, the clots thinned, but were distributed throughout the eye fluid, which appeared as though I was looking through muddy brown river water. This was more frightening to me than the initial hemorrhages as I lost more vision. Gravity and physics eventually play their part, and in the settling phase, the blood particles and small clots fell to the bottom of my eye. The larger clots have thinned so they appear to be greasy, opaque blobs that still "swim" around in the center of my vision. Oddly, we see opposite, so the streamers and debris appear to me to be at the top of the eye, like little brown lightening bolts. I found wearing dark tinted glasses help immensely with my increased sensitivity to light and it reduces the contrast between my eye debris and my visual field.

I've experienced few effects, none are greatly life changing. One loss is the ability to do "fine" work; I can not knit or embroider with itsy bitsy needles. Using tweezers or other such items is difficult, but I've found special supplies for the visually disabled with magnifiers help (check out http://www.lighthouse.org/). I can't read tiny print, or print with little contrast (and for some reason, my co-workers enjoy making powerpoint slides that are dark with lines so I can't read the print). To solve this, my husband gave me a beautiful gold magnifier that hangs on a chain; so I can wear it around my neck during work to magnify the print. I no longer drive at night or before daylight, since its difficult for me to see in the dark (I'm the opposite of a vampire, I can only come out during daylight hours).  I had difficulty in driving during twilight and storms; this was alleviated by a brainstorm my husband had, by using driving/shooting lenses.  These are amber/yellow lenses which intensive the light and sharpen things up.  Clip ons can be purchased at sporting goods stores for around $10, glasses can be purchase for around $20.  I have two pair of Fitovers; Fitover Shooting glasses, and Fitover Sunglasses; I highly recommend both; an example are at:

http://www.cabelas.com/cabelas/en/templates/product/standard-item.jsp;jsessionid=NAXMAGM1B2J0HTQSNOISCOOOCJVZIIWE?id=0020422711783a&navCount=0&cmCat=srchdx&cm_ven=srchdx&cm_ite=srchdx&CM_REF=http%3A%2F%2Fwww.google.com%2Fsearch%3Fq%3Dyellow%2Bshooter%2Bglasses%26hl%3Den%26lr%3D%26start%3D10%26sa%3DN&_requestid=20007

Two areas that did cause me some distress was I could not read or sit in front of a PC for long periods of time (challenging for someone who is a systems analyst). My retinologist told me to limit my computer work and/or reading to 45 - 50 consecutive minutes and rest my eyes for 10 - 15 minutes; no more than 8 - 9 hours per day. When I tried  to cheat, I experience excruciating pain in both of eyes as well as recurrence of flashing lights. It hurts enough that I adhered very strictly to her guidelines. For me, it feels as though someone has rubbed the back of my eyes with sandpaper, and as though I'm being stabbed through my eyes. It starts at the back and continues through the entire eyeball with such a force it literally makes me physically ill. So if your retinologist tells you to limit your reading, DO IT!

Additional restrictions may include no physical exertion, sleeping on three pillows, keeping my head propped up above my torso (don't forget to tell your dentist so they don't drop your head down too low!), and resting my eyes as much as possible. When I've tried to do moderate exercise, I have "flashing lights"; and Dr. Dharma has put fear in my heart that flashing lights are bad if you have BSRC. Therefore, if you have uveitis or BSRC, the presence of flashing lights should warrant a visit to your MD to ensure all is well. I was restricted from lifting more than 5 lbs, (which in my case required cleaning out my purse). After work, I go home, sit in my chair, and wear an eye shade. Ask your relatives and friends to buy audio books for you to keep from going crazy on the weekends.

I was treated originally consists of steroids and cyclosporin in varying doses. Cyclosporin is the same drug given to transplant patients to prevent organ rejection, it dampens the immune system. There are some unpleasant side effects from the cyclosporin: bleeding gums, tremors, growing hair where it shouldn't, losing hair where it should be; and damage to the liver and kidneys to name a few.

Taking immunosupprssants can increases one's probability of contracting lymphoma, so you don't want to stay on this treatment any longer than necessary.   However, please remember, that thousands, (millions?) of transplant patients are out there, walking around, living their life, and they are on much higher doses of immuno-suppressants than we take, for many more years than we take, and never get lymphoma. 

Taking prednisone over 5 mg/day makes me either ravenously hungry or horrendously nauseous.  I had hirsuitism,  growing facial hair, and looked like monkey woman.  A very, round-faced, monkey woman.   If you are a woman, I recommend waxing the face; it removes the unwanted hair, leaves your skin a glowing pink, and when you are off the drugs, the hair will stop growing, and you will never knew there was problem.  If you do not know how to wax, I highly recommend spending the $12 every 2 months to have a professional do it for you.  When I was looking in the mirror one day, complaining about my fat face, and that I would never see my checkbones again, my husband asked me, would you rather never see your fat face, or never see?  Point taken.  Fear not, if you work at it, the weight can be lost as well.

Staying away from crowds and sick people are recommended. So far I have been extraordinarily lucky in staying well. I attribute this to avoidance of stores (my husband does the grocery shopping these days and I purchase other stuff via catalogs or the Internet), no traveling. The few times I venture out to eat, I ensure I wash my hands before I eat; in fact, I wash my hands after I get to work or touch anything in a public place (at least the length of the time it takes to sing "Twinkle Twinkle Little Star" per Discovery Magazine and strict instruction from my good friend Heather White: after washing your hands use extra paper towels to close the water taps and open the door). If water is not available, I make generous use of antibacterial hand wash; I have some in my purse, my car, and my office. I still go to work at the office but try to avoid contact with others as much as possible.

For me, cyclosporin and steriods made me tire easily. Initially, I could barely make it through the work day, and when I came home I'd eat, lay down, and sleep for three or four hours before going to bed. I've found two herbs that work wonders: ashwaghandra, which is for energy; and shizandra, which flushes toxins out of the liver; (I found out about these from Prevention magazine). This is not a medical recommendation, merely a personal anecdote.

I am currently on Cellcept and prednisone, and to date, have not had any new flares. 

 BSRC may change your life, but it is not necessarily the total loss of vision you may believe it is. If you are living with someone with BSRC, try to be patient, because having "stuff" swimming around in your eyes and facing possible blindness is quite frightening and takes some adjustment. When I first had uveitis in 91, I was an emotional wreck because I was terrified I would lose my sight. Knowing I have BSRC actually had a calming effect, because I know what I'm up against, and what the odds are. In my case, I'm on the treatment to save my sight, but there are days when I wonder if the treatment is not worse than going blind; and then I look at my husband and I have my answer. I hate to go to sleep at night, because I always wonder if I'll be able to see in the morning. Each morning I wake up and I do see, I feel I've received a precious gift. No one knows what will happen in life, and we just have to adjust to whatever occurs. For those of you with uveitis or BSRC, it will take some emotional adjustment, and some counseling is not a bad idea. For those of you living with someone with this; try to be understanding; sometimes the patient needs to vent and be angry.

I have a support group, and recommend interested individuals to read the posts:

http://groups.msn.com/BSRC/_whatsnew.msnw

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Contacts

If you would like to participate in a community of those interested in or have BSRC, you are invited to join our group at:

http://groups.msn.com/BSRC/_whatsnew.msnw

My second web site:

http://home.comcast.net/~dagmara56/wsb/html/view.cgi-home.html-.html

If you have questions, concerns, etc. feel free to email me:
Dagmar Bogan

 

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Last updated: 07/22/06