New to group

August 14, 2001

Tonya,

If I can stress only one thing it is to see a pediatric rheumatologist. It

has made a world of difference for our daughter. Meds and dosing have been

handled in a much different way. . .for the better. Most notably prednisone

dose prescription and reduction. Our daughter Abbie is doing much better.

Christy

August 14, 2001

Ah, how hard it is when the children are affected. My story, husband

got diagnosed with stills, Then not. They don't know what it is.

But my Granddaughter was born with four major heart defects. Tetrology

of phallow (spelling?) Had open heart surgery at eight months and on a

vent for two weeks. She is speech delayed at 3 1/2 but, what a delight.

She looks at me with hands on hips and says " Gama " . Oh she is a tough

little troll.

Hang in there. I can relate. I refuse to dye my grays as I feel I

earned every last one.

Also Makaila wants to be a nurse like Gama, and work for Capt. Kirk.

Warp nine she says.

Steph

August 14, 2001

Suzie,

Thank you for your words of encouragement many days I feel sorry

for myself and think I am all alone.

Terah and myself spent most of the day in Galveston at UTMB

she had a check up with her pediatric immunologist, a chest xray

and then physical therapy. Tomorrow we go to Texas Childrens

hospital to see our new Pediatric Rheumotolgist Dr who

was recommended by our immunologist for a second opinion.

Our immunologist is Dr Schmalstieg and he has been wonderful and

Terah responds so well to him. He is trying to be conservative

with all her meds but mentioned starting her on Enbrel but wants

us to consult with the rhuemy first. Her sed rate has consistently

been around 120 for the last six weeks despite 3 straight days of

IV Methylprednisone in the hospital and another one day dose at

the infusion clinic. She has been pn MTX for almost 6 weeks so we

are hoping that will kick in soon. I have many questions but need

to get them all straight before asking. I know I have found the

right place for all my questions.

When was Chrissy diagnosed? Corpus Christi is not far from Lake

so let me know when you move.

Many Thanks..........Tonya

----- new to group

>

>> Hi! My name is Tonya and my daughter Terah(5) was just

>> diagnosed with systemic JRA in June 2001. we live in Lake

>> , Texas which is approx 1 hour south of Houston.

>> This is Terah's story.

>> In May she became ill her first symptoms were a sore throat,

>> very red conjuntive eyes and a rash on the insides of her

>> arms and legs that almost looked like polka dots. I took

>> her to a doctor that was filling in for our normal

pediatrician

>> and he diagnosed her with a throat infection and gave her

>> a prescription of Augmenten and some eye drops. The next

evening

>> she was very ill running a temp of approx 103 and was acting

>> strange so I immediately took her to the emergency room.

>> After waiting in the waiting room for almost 3 hours they

finally ran

>> some blood work and diagnosed her with a urinary tract

infection. I

>> knew this could not possibly be right but at 2AM did not feel

like

>> arguing so we went home with a prescription of Bactrum. SInce

this

>> was the Memorial Day weekend there was not much we could do but

stay

>> home and watch her carefully and she seemed to be doing

better.

>> By Tuesday she had taken a turn for the worse, she could barely

walk

>> and was not eating a thing so we took her to her regular doctor

who

>> diagnosed her with a Viral infection and sent us home with

yet

>> another prescription. The next day she could not get out of bed

and

>> her fever was once again 103 so we went back to her doctor and

he

>> admitted her into the hospital. They ran several tests and at

this

>> point did not know what was wrong with her. Her WBC was 35,000

so

>> they immediately started her on IV antibiotics which over a

course of

>> 2 days did not help her. Her doctor came to us and said he

thought

>> she had Kawasaki syndrome and said he was going to transfer us

to

>> UTMB childrens hospital in Galveston. Once there the team of

doctors

>> ran several more test and she was clinically diagnosed with

>> Kawasakis. She was given IV Gammaglobulin and aspirin but after

two

>> doses they had to finally give her steroids to make her feel

better.

>> After 7 days we went home with a prescription for 40MG of

steroids

>> and 2 childrens aspirins a day. For 4 weeks she seemed to be

better

>> but as we began decreasing her Prednisone and we got down to

20MG in

>> the morning only she took another turn with fevers as high as

105.2

>> and we were back at the

>> hospital. This is when the diagnosis changed to Systemic JRA.

She is

>> now on MTX 7.5MG a week and she is still on Prednisone 20MG in

Am and

>> 15MG in PM. She is still very ill and was unable to begin

>> kindergarten this year. Her biggest problem is her fingers and

her

>> feet and legs she is unable to play or sit on the floor so we

read

>> quite a few books and watch alot of Rugrats. She has a

wonderful

>> immunologist and she will begin seeing a rheumy this week.

>> The hardest part of this is watching your child go from a

healthy

>> happy child to a sick child who does not even look the same

because

>> of the steroids. I still cry every day and pray that this is

all a

>> big mistake and she will get better. We also have a 7 year

old

>> daughter who does not quite understand all the attention

her

>> sister is getting. At this point we are just hoping to get

the

>> disease under control and get some normalcy back in our lives!

Thank

>> you for letting us join your group I know I will learn alot!

>> Sincerely,

>> Tonya

>>

>>

August 14, 2001

Tonya,

Chrissy has had it since the age of 7, but did not recieve the correct

diagnosis until l998. She also has endured the iv pulses. I think she had

them five times earlier this year, when she was at her worst. We used

methotrexate for chrissys second flare and it worked wonderfully. This one

however we got up to a 50 mg dose by injection and decided to switch to the

arava, as we are on the enbrel waiting list. I know how hard it is to watch

your little one go through this, just know that we are here for you. I have

had many days of feeling sorry for myself too. And have vented my

frustrations, sadness, everything to this group. They are so understanding

and supportive. You will feel at home here.

Suzie

new to group

> >

> >> Hi! My name is Tonya and my daughter Terah(5) was just

> >> diagnosed with systemic JRA in June 2001. we live in Lake

> >> , Texas which is approx 1 hour south of Houston.

> >> This is Terah's story.

> >> In May she became ill her first symptoms were a sore throat,

> >> very red conjuntive eyes and a rash on the insides of her

> >> arms and legs that almost looked like polka dots. I took

> >> her to a doctor that was filling in for our normal

> pediatrician

> >> and he diagnosed her with a throat infection and gave her

> >> a prescription of Augmenten and some eye drops. The next

> evening

> >> she was very ill running a temp of approx 103 and was acting

> >> strange so I immediately took her to the emergency room.

> >> After waiting in the waiting room for almost 3 hours they

> finally ran

> >> some blood work and diagnosed her with a urinary tract

> infection. I

> >> knew this could not possibly be right but at 2AM did not feel

> like

> >> arguing so we went home with a prescription of Bactrum. SInce

> this

> >> was the Memorial Day weekend there was not much we could do but

> stay

> >> home and watch her carefully and she seemed to be doing

> better.

> >> By Tuesday she had taken a turn for the worse, she could barely

> walk

> >> and was not eating a thing so we took her to her regular doctor

> who

> >> diagnosed her with a Viral infection and sent us home with

> yet

> >> another prescription. The next day she could not get out of bed

> and

> >> her fever was once again 103 so we went back to her doctor and

> he

> >> admitted her into the hospital. They ran several tests and at

> this

> >> point did not know what was wrong with her. Her WBC was 35,000

> so

> >> they immediately started her on IV antibiotics which over a

> course of

> >> 2 days did not help her. Her doctor came to us and said he

> thought

> >> she had Kawasaki syndrome and said he was going to transfer us

> to

> >> UTMB childrens hospital in Galveston. Once there the team of

> doctors

> >> ran several more test and she was clinically diagnosed with

> >> Kawasakis. She was given IV Gammaglobulin and aspirin but after

> two

> >> doses they had to finally give her steroids to make her feel

> better.

> >> After 7 days we went home with a prescription for 40MG of

> steroids

> >> and 2 childrens aspirins a day. For 4 weeks she seemed to be

> better

> >> but as we began decreasing her Prednisone and we got down to

> 20MG in

> >> the morning only she took another turn with fevers as high as

> 105.2

> >> and we were back at the

> >> hospital. This is when the diagnosis changed to Systemic JRA.

> She is

> >> now on MTX 7.5MG a week and she is still on Prednisone 20MG in

> Am and

> >> 15MG in PM. She is still very ill and was unable to begin

> >> kindergarten this year. Her biggest problem is her fingers and

> her

> >> feet and legs she is unable to play or sit on the floor so we

> read

> >> quite a few books and watch alot of Rugrats. She has a

> wonderful

> >> immunologist and she will begin seeing a rheumy this week.

> >> The hardest part of this is watching your child go from a

> healthy

> >> happy child to a sick child who does not even look the same

> because

> >> of the steroids. I still cry every day and pray that this is

> all a

> >> big mistake and she will get better. We also have a 7 year

> old

> >> daughter who does not quite understand all the attention

> her

> >> sister is getting. At this point we are just hoping to get

> the

> >> disease under control and get some normalcy back in our lives!

> Thank

> >> you for letting us join your group I know I will learn alot!

> >> Sincerely,

> >> Tonya

> >>

> >>

August 14, 2001

Hi, Tonya,

Welcome to the group. My son Marc is 11 and has had Stills since just

before his third birthday. Although he is not doing at all well right now,

he has had long periods (up to 2 years) of being in great health several

times since his diagnosis. Look forward to those times, for certainly they

will come.

Like Suzie, your process in getting Stills diagnosed sounded familiar to me.

We went through a round of antibiotics for " ear infection " before our astute

family doctor sent us to a pediatric rheumatologist. And like Suzie, I have

found myself in the position of educating doctors about Stills more than

once.

Take it easy on yourself. There's a lot to learn, but your most important

job right now is supporting your daughter.

My brother and his family live in Lake , so perhaps we'll meet some

day. Best wishes to you as you go through this difficult time.

Another note to other parents of JRA kids -- Marc went to JRA camp in

Pennsylvania this summer and it was a wonderful experience for him. We'd

highly recommend it for others. This particular camp was for kids 6 to 16,

with older kids acting as " counsellors in training. "

Peace to you all,

Marilyn Mc.

_______________________________________________________

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August 15, 2001

Welcome Tonya and Terah;

Sorry to here from you this way but then it is so good to have this

many people to help us all.

I to was a sick kid 4th b day in the hospital they said I had

rheumatic fever but afew years later after we moved to Calif. the

family Doc. said no poss. scarlet fever I have been sick on and off as

long as I can remember but we put most of it at the time to just being a

person that got everything easy now at 43 and live in with still's

diagnosed for one year I can tell you when she has her good days look

out as some off us try to fit all we can in those day and some time we

just over do it I know as a kid I still got into trouble all the time

and when I felt good boy did I run around and drive everyone mad

including my sisters and brothers but they did have a hard time when I

got all the attention so all I can say to you is keep it as normal as

you can and let her be her self do not try and protect her to much and

also take time out for the others in your house kids and spouse as some

time sit is relay easy to forget them when we are focused on the one who

is ill like this week I sent my daughter and wife to calif. to visit so

thAT WAY they are not seeing me and what I go threw every day and

Grandma gets to spoiled them like they try to do to me so good luke pray

for remission that last and look for the good days and some times hours

LOL Marty Gilbertson

August 25, 2001

STUDIES HAVE PROVEN ANTIBIOTICS SAFE AND EFFECTIVE

Hi Angie,Thank you for the vote of confidence. Below are some studies I found

on the internet. Yes I do feel that the antibiotics are working for me. I have

been on them now for two weeks, and my wife cannot believe how much better I am

doing. I am actually going out and working with my landscape crews, and helping

around the house with things I haven’t been able to do for almost a year. I

also had an accidental experience with them 4 years ago when this first started.

After 3 weeks I was sent into remission for 3 years. I think this was too

coincidental. I was experimenting with Tetracycline before I knew anyone was

actually recommending this sort of therapy. So yes, some of what is fueling my

inspiration in this belief is feelings and speculation, but I have also read

study after study that proves that this therapy does just as much help as a lot

of the drugs that most of the Stilligans are on. So please forgive me for such

a long email, but I feel it is necessar!

y from the bottom of my heart to share this with anyone on this site who might

be interested.

P.s. I am sorry I haven’t had anything else to say except this theory. I hope

over time I will be able to share something else with all of you besides this.

I really do get a lot of help knowing others are out there going through this

disease.

Many treatments are available for arthritis. The literature is full of marginal

results with these various treatments, and no one knows better than the patients

that " many still face a future of chronic pain, progressive disability, and

limited prospects. " (WG Benson, et al, J of Rheumatology) June 1997). Treatment

with minocycline is medically and clinically tested and is scientifically proven

to be safe and effective. Since 1990, nine studies have tested this antibiotic

for rheumatoid arthritis and scleroderma; all nine have found it to be safe AND

effective validating the work of Dr. McP. Brown, begun decades ago.

The Netherlands 1st study: " At the end of the study all variables were

significantly changed compared with their pretreatment values. " FC Breedveld, et

al, Minocycline Treatment for Rheumatoid Arthritis: An Open Dose Finding Study,

J of Rheum, 1990; 17:1, pg 43-46. United States Univ. of Nebraska 1st

Follow-up: 15 patients who responded to the minocycline treatment in the

original study were followed for an average of 3 more years. 44% of those

patients continued to have dramatic benefit after 3 years with 5 in complete

remission. JR O'Dell, et al, Minocycline Therapy for Early Rheumatoid Arthritis:

Continued Efficacy at Three Years, (abstract) Am Col Rheum, 1997.

Israeli study: " Statistically significant improvement was noted in almost all

variables of disease activity. . . Of the 12 patients completing the study, 25%

had complete remission, 25% had more than a 50% improvement and the other 50%

had moderate improvement (>25%). " P Langevitz, et al, Treatment of Resistant

Rheumatoid Arthritis with Minocycline: An Open Study, J of Rhu, 1992, 19:10, pg

1502-1504. Chinese Minocycline Study: In a study of RA patients who had

failed standard DMARD treatment, less adverse side effects and a higher response

rate associated with minocycline treatment were found in Chinese RA patients. "

Lai Ning-Sheng, Treatment of DMARDs- Resistant Rheumatoid Arthritis with

Minocycline - A Local Experience Among the Chinese, abstract, 5th Asian Congress

of Rheumatology, Manilla, January 1998

The Netherlands 2nd study: " The trial was performed on patients with advanced,

evenintractable RA. Side effects may be considered mild in relation to other

established DMARDs Minocycline appears tohave beneficial properties in RA,

especially when laboratory parameters of disease activity are considered. "

MKloppenburg, FCBreedveld, et al Minocycline in Active Rheumatoid Arthritis,

Arth & Rheum,1994, 37:5, pg. 629-636. Nebraska 2nd Followup: After 4 years

of minocycline, 40% of minocycline patients were in remission without the use of

any DMARDs or steroids, while only 6% of placebo patients had achieved a

remission. JR O'Dell et al, Treatment of Early Seropositive Rheumatoid arthritis

with Minocycline, Arth & Rheum, 1999; 42:8, pgs. 1691-1695.

United States MIRA study: " Benefit became evident after 12 weeks of therapy, and

the proportion of patients treated with minocycline showing improvement

continued to increase through week 48 of the study. . . We observed significant

differences favoring minocycline over placebo in the primary outcome measures. "

BC Tilley, GS Alarcon, et al, Minocycline in Rheumatoid Arthritis: a 48 Week,

Double-Blind, Placebo-Controlled Trial, Ann Int Med, 1995;; 122:2, pg 81 -89.

Scleroderma Minocycline Study: 6 out of 11 patients with early, but severe

diffuse scleroderma finished 1 year of minocycline. At the end of 1 year, 4 of

the 6 had complete resolution of their skin disease and 3 of the 4 had normal

patient and physician assessments. These results are significantly superior to

those normally seen in drug studies for scleroderma patients. C Le, A Morales,

DE Trentham, Minocycline in Early Diffuse Scleroderma, Lancet, 1998, 352:9142,

pgs. 1755-1756.

United States 1st Univ. of Nebraska study: " 18 of the 46 patients who were

enrolled met 50% improvement criteria at 3 months, and maintained at least 50%

improvement for 6 months with no significant drug toxicity. (Fig.3 shows 5 out

of 18 in remission after 1 yr. of minocycline therapy) . . We believe our

results are even more remarkable because our study design almost certainly

decreased the chances of finding a positive effect. . . Data from our study and

others suggest that maximum benefit of minocycline does not occur until after 1

year of therapy. " JR O'Dell, et al, Treatment of Early Rheumatoid Arthritis with

Minocycline or Placebo: Results of a Randomized, DoubleBlind, Placebo-

Controlled Trial, Arth & Rheum, 1997, 40:5,, pg 842-848.

ANTIBIOTIC THERAPY OF RHEUMATOID ARTHRITIS: AN OBSERVATIONAL COHORT STUDY OF 98

PATIENTS WITH 451 PATIENT-YEARS OF FOLLOW-UP

Congress of Rheumatology. 1985:S85

ANTIBIOTIC THERAPY OF RHEUMATOID ARTHRITIS:

AN OBSERVATIONAL COHORT STUDY OF 98 PATIENTS

WITH 451 PATIENT-YEARS OF FOLLOW-UP

McP. Brown, M.D. *. W. Novak, M.S **; Marc C Hochberg, M.D.,

M.P.H.***; Anne S. Lindblad; M.S.**; A. Novak, M.S.N.**; Norma Morin,

Ph.D.*** and Harold W. , Ph.D.*

from

*The Arthritis Institute of the National Hospital, Arlington, VA

**The EMMES Corporation, Potomac, MD

***The s Hopkins Medical Institutions, Baltimore, MD

ABSTRACT

This is a retrospective observational study of 98 patients with definite or

classical RA who began treatment with antibiotic therapy during the five-year

period 1978-1982. The report details patient characteristics, patterns of

treatment with antibiotics, NSAIDs, steroids, and SAARDs where applicable.

Outcomes to treatment, including toxicity, symptomatic relief, activity level,

and duration of treatment are described. The probability of remaining on

antibiotic therapy, failure-free, at five years is 70%, based on 451 patient

years of follow-up. Symptomatic improvement is reported. Treatment-related

complications with long-term antibiotic therapy were acceptable.

Current concepts regarding the management of rheumatoid arthritis (RA) emphasize

medical therapy, physical and occupational therapy, and patient education. The

first-line agents used for medical therapy are the non-steroidal

anti-inflammatory drugs (NSAIDs). Patients who are not adequately controlled by

NSAIDs are usually treated with one or another of the slow-acting anti-rheumatic

drugs (SAARDs) such as hydroxychloroqulne, gold, or penicillamine. These drugs

are thought to modify the course of RA--as evidenced by a decrease in the signs

and symptoms of inflammatory synovitis, a decrease in rheumatoid factor titers,

and a decrease in the rate of formation and/or progression of radiographic joint

erosions.1,2 Unfortunately, the efficacy of the SAARDs is not uniform and

termination of treatment due to toxicity is common--with the result that many

patients continue to demonstrate progressive, deforming and disabling disease

requiring reconstructive orthopedic surgery.

Patients who fail on SAARDs and/or who develop toxicity to these compounds

become candidates for treatment with cytotoxic agents such as azathioprine,

methotrexate, and cyclophosphamide. Unfortunately, those alternatives also place

the patient at unusual risk of severe and even life-threatening complications

including leukopenia, thrombocytopenia, opportunistic infections, and long-term

oncogenesis.1,3,4 Clearly, other therapeutic regimens are needed which are

capable of producing long-term disease control without the undue risk of serious

treatment-related morbidity.

Recent studies in both the pathogenesis of RA and in the treatment of a variety

of arthritic disorders provide some basis for considering the use of antibiotic

therapy in the treatment of RA. Consider the model of pathogenesis suggested by

: the genetically predisposed host develops a complex cellular and humoral

immune response to an unknown antigenic stimulus which localizes in the joints,

where it leads to the development of proliferative synovitis and joint

destruction.5 The nature of the genetic predisposition appears, at least in most

individuals with seropositive RA, to be related to the major histocompatibility

gene products HLA-DR4, MB3, and MT3.6,7 While the nature of the antigenic

stimulus remains undefined, an exogenous infectious agent(s) has been

suspected'for many years. , in reviewing the role of infectious agents as

etiologic factors in RA, has noted " ...that a whole variety of organisms and/or

their products may be responsible for initiating... " !

rheumatoid arthritis and, furthermore, that " when the scope of processes that

can be associated with infection and arthritis is realized, one becomes aware of

the extraordinary difficulties involved in evaluating the possible etiology of

rheumatoid arthritis from this standpoint. " 8

One class of infectious organisms in particular, mycoplasma, has long been

suspected of having a role in the etiology of RA12. These organisms have been

associated with arthritis in numerous animal species including the pig,13

turkey,14 rat,15 mouse,115 and gorilla.16 Furthermore, they have been shown to

initiate an arthritic process of long duration that is typified by a chronic,

progressive course. However, because it has been difficult to isolate the

organisms from joints, except during the early phases of the disease,13,17,18

acceptance of the mycoplasma theory of etiology has been limited.

Clinical applications of the microbial theories of pathogenesis to the treatment

of a variety of arthritic conditions likewise have received attention. Recent

reports by Steere and colleagues on the efficacy of antibiotic therapy in

treating a chronic Lyme arthritis--which demonstrates an articular course

similar to that seen in RA including pannus formation, and cartilage and bone

destruction,19,20--lend support to the idea of treating arthritis

-2-

with antibiotics. Another disorder in which a bacterial infection has been

related to an arthritis that is similar pathophyslologically to RA is bypass

arthritis,21 wherein some patients who have undergone jejuno-ileal bypass for

morbid obesity develop an immune-complex-mediated polyarthritis that clinically

resembles RA. Utsinger has shown that circulating immune complexes containing

bacterial antigens, antibodies and complement are present in the sera of almost

all of those patients and can be identified in cryoprecipitates from synovial

fluid specimens.22 Invariably, these patients have responded to treatment with

Tetracycline used in conjunction with anti-inflammatory agents.21

Tetracycline and its derivatives have also been used for over 35 years by Brown,

of the Arthritis Institute, National Hospital (AINH), to treat patients with

RA.19 The scientific underpinning of Brown's work is rooted in a theory of

causation which involves infection by inycoplasma.9-11 The only randomized,

controlled clinical trial of Tetracycline in RA (Skinner et al) concluded that

there was " ... no significant benefit from long-term Tetracycline therapy in

patients with classic and definite rheumatoid arthritls. " 24 However, given its

small sample size (n = 30) and the relatively brief observational period (1

year), Skinner's study provides weak support for what must be considered a

far-reaching conclusion.

The purpose of this study was to provide an assessment of antibiotic therapy in

recently treated patients with RA; more specifically, the study sought to

characterize the course, duration and complications of antibiotic therapy used

by Dr. McP. Brown in patients with RA--and to assess available patient

outcomes such as symptomatic improvement and ability to tolerate and continue

therapy. Toward that end, a retrospective assessment of all of Brown's patients

with RA who began antibiotic treatment in the five-year period January 1,

1978-December 31, 1982, was undertaken.

MATERIALS AND METHODS

The study was requested by Brown and funded by the AINH; it was designed and

carried out by an independent statistical organization, The EMMES Corporation,

located in Potomac, land. The fim was solely responsible for the study

design, the abstraction of primary medical records and the summarization and

analysis of patient data reported in this manuscript. J.N, the firm's president,

served as project director and statistician; N.H., Associate Professor of

Medicine (rheumatology) and Epidemiology at the s Hopkins Medical

Institutions, served as an independent clinical and epidemiologic consultant.

A three-phase study plan was executed. During the first phase, the series of

patients to be evaluated was identified. In the second phase, hospital and

clinic records for those patients were abstracted; and information pertaining to

selected patient characteristics, course of treatment, current treatment status,

and response to treatment were captured. A third phase was introduced after

study commencement to obtain more current patient information than was available

from the charts reviewed.

Phase I. Hospital and clinic records for all patients hospitalized by Dr. Brown

between January 1, 1978 and December 31, 1982, at the National Hospital were

reviewed. The abstractor/reviewers were registered nurses with a minimum of one

year of experience in rheumatology. All abstractors attended a training session

which covered study objectives, search procedures and the proper use of precoded

forms which had been prepared for the study by The EMMES Corporation. The

trainer and data coordinator (C.N.) is a nurse specialist in rheumatology and is

a member of the Arthritis Health Professions Association section of the

Arthritis Foundation.

To have been eligible for inclusion in the study series, patients must have

begun antibiotic therapy during the designated period and, based on available

information, must have been classifiable as a definite or classical case of RA

per the revised criteria of the American Rheumatism Association (ARA).21

Patients who met fewer than five of the ARA criteria were excluded from this

study. In addition, patients who had a history or current evidence of

inflammatory rheumatic disease other than RA, or who were less than 16 years of

age at the time of disease onset were disqualified from study.

Of the 539 cases reviewed in Phase 1, 441 were disqualified from study: of

those, 169 were found to have begun treatment before January 1, 1978; available

records for 267 failed to indicate that the patient met five or more of the ARA

criteria; and five additional patients were found to have a disqualifying

coexistent disease: Reiter's disease (3), systemic lupus (1), juvenile RA (1).

Ninety-eight patients met all criteria for inclusion in the study; they form the

basis of this report. (See Table I.)

Phase II. All available hospital and clinic records were abstracted for the 98

patients included in the study. Patient characteristics and the course of all

medical treatment received during the study period were noted. Special attention

was given to the administration of antibiotics, NSAIOs, steroids, and SAARDs.

All complications of treatment were recorded, as were available baseline and

follow-up measures of disease status. Of particular interest were

patient-reported counts of the number of tender joints, the number of painful

joints, and the duration of morning stiffness. Also included were patient

reports of amount of weakness, fatigue, endurance, feeling of well being, mental

acuity, and periodic depression which had been collected by Dr. Brown using the

familiar zero-to-four scale.

Phase III. In order to obtain current information concerning treatment and and

disease status, attempts were made to contact all 98 patients by questionnaire.

At that time, all patients were also asked to complete and return the Stanford

Health Assessment Questionnaire (HAQ).22 Forty-eight of the 98 patients returned

the two questionnaires within four weeks of solicitation; 43 of the remaining 50

patients were contacted by phone and interviewed. Follow-up on six patients who

died during the study period and one patient who resided in a nursing home was

not pursued. For those seven patients, information obtained at the last recorded

visit was compared to baseline measures to obtain outcome values. All telephone

interviews were performed by Dr. N. Morin, an epidemiologist with experience in

rheumatology and in the use of the HAQ.

Criteria. The outcomes of particular interest in this study were treatment

failure, time to treatment failure, patient reports of symptomatic relief, and

toxicity. Patients were considered to be treatment " failures " for the following

reasons: (a) the termination of antibiotic treatment due to lack of efficacy,

toxicity or for unknown reasons, ( the addition of SARDs to the treatment

regimen, or © any increase in the dose of steroids because of worsening

disease. Treatinent duration was calculated from date of treatment start to the

last known date of treatment with antibiotics without the use of SAARDs or

increased use of steroids.

Patients reporting a 50% decrease in the number of tender joints, painful

joints, or duration of morning stiffness were considered to have demonstrated a

meaningful improvement in clinical status.23 Similarly, patients who

demonstrated at least a two-grade improvement on a four-point scale in the

amount of weakness, fatigue, endurance, feelings of well being, mental accuity

or periodic depression were considered to have exhibited a clinically meaningful

improvement in those parameters.

Statistical Methods

All data were double-keyed and stored in an IBM mainframe. Tailored computer

edit routines were used to assure data consistency. Kaplan-Meier estimates of

the time to treatment failure were calculated and a chi-square statistic was

used to evaluate time trends in response to treatment.24 The proportional

hazards methods of , as implemented by SAS, were used to evaluate the

significance of prognostic variables.25 Patients who died of unrelated causes or

who terminated treatment because of remission of symptoms or unavailability of

drug supply were censored in the analysis.

RESULTS

Patient Characteristics. Characteristics of the 98 study patients are summarized

in Tables 2 and 3. Mean age of the patients at commencement of antibiotic

therapy was 52 years; only 3% of patients were 70 years or older at the time

antibiotic therapy began. Sixty-two percent of patients were female, and 86%

were married at the time antibiotic therapy began. Almost all patients were

white; most had been diagnosed as having RA for five or more years prior to

beginning antibiotic therapy.

Eighty-seven of the 98 patients studied (88%) began their antibiotic therapy

during the first three years of the five-year study period. The sharp decline

observed in the number of patients beginning treatment during 1981 and 1982 has

been attributed to Dr. Brown's full schedule during that time. Two-thirds of the

patients studied were classified as having definite RA; while one-third were

classified as having classical RA. Morning stiffness, joint pain and swelling

had been experienced by 94% of the patients, respectively; all three symptoms

were reported for more than 90% of the group. The frequency with which other ARA

criteria and symptoms were found in the study group are summarized in Tables 3

and 4. Forty percent of patients had no previous therapy with SAAROs, e.g.,

gold, penicillamine, and antimalarials; no patient had received cytotoxic agents

prior beginning antibiotic therapy. Fifty-five of the patients (56%) had

received gold before beginning antibiotic therapy; 4!

1 patients (42%) were receiving corticosteroid therapy with 12 of those

receiving more than 10 mg per day.

Patterns of Treatment. During the course of treatment, a variety of antibiotics,

doses, schedules, and routes of administration were utilized. (See Table 5.)

Patterns of treatment varied widely among patients as well as within patients.

Almost all (98%) received both oral and intravenous (IV) antibiotics. During the

course of their therapy, 71% of patients received three or more agents orally

and 53% received three or more agents via the intravenous route. Vibramycin

(61%), Minocin (67%), and Ampicillin (55%) were used most commonly for oral

administration, while Lincocin (80%), Cleocin (60%) and Vibramycin (55%) were

most commonly used for IV administration. Erythromycin, Tetracycline and

Amoxicillin were also used with notable frequency.

While specific regimens used may have varied, the general pattern of treatment

tended to be consistent. Patients were generally given intravenous Tetracycline

(or one of its derivatives) daily for 10 days and this was repeated at six-month

intervals; most patients also received small doses of oral antibiotics such as

Vibramycin 50 mg or Minocin 100 mg three times per week between IV

administrations. Logistics (distance from hospital and clinic) and disease

activity were found to influence schedule, dose, and and drug selection. During

periods of extreme disease activity, the frequency of intravenous treatments or

dose of oral antibiotics was increased; and, prescription of an alternate

Tetracycline derivative or modification of dose was used to manage side effects

such as diarrhea or vaginitis, resistance to the antibiotic or poor absorption

of drug. Intramuscular injections were occasionally substituted for intravenous

treatments. Thirty-nine percent of patients also received!

intraarticular antibiotic therapy, which was given in conjunction with steroids

to 33 of the 38 patients.

No patient was treated with antibiotics alone; one or more NSAIDs were used in

all patients at some time in the course of their treatment with antibiotics.

Eighty-four percent of patients received one or another of the non-salicylate

NSAIDS, 51% received aspirin, and 69% received some other medication for pain,

usually acetominophene or propoxyphene.

Of the 41 patients who were using steroids at the commencement of antibiotic

therapy, 17 were able to end or decrease by 50% the amount of steroids used, and

were continuing antibiotic therapy as of last contact. Two patients, initially

on steroids, increased their steroid dosage without a later dose reduction; and

six patients not originally on steroids commenced their use after beginning

antibiotic therapy. Of the eight patients who increased their use of steroids,

five experienced a worsening in their disease status while on antibiotics, two

experienced a worsening of their disease after they were unable to obtain

further treatment with antibiotics, and one patient began taking steroids to

control allergies.

Complications of Treatment. The antibiotic therapy administered was generally

tolerated quite well. Thirty-eight percent of patients complained of one or

another complication of treatment: nausea 14%, diarrhea 13%, rash 9%, and

vaginitis 7%. Multiple complications, in either time or kind, were uncommon.

While severity of these complications could not be meaningfully graded from the

available records, there was no indication that they were particularly serious.

Four patients indicated that they terminated treatment because of adverse

reactions and have been counted as treatment failures: diarrhea (1), stomach

upsets (1), nausea (1), and severe headaches (1). It is noteworthy that all four

of those patients were advised to terminate antibiotic treatment by a physician

other than Dr. Brown. Neither hematologic complications nor proteinuria were

noted.

Treatment Outcomes. Twenty-seven of the 98 patients (28%) who began antibiotic

therapy are considered to have failed treatment. (See Table 6.) Nineteen of

those patients terminated antibiotic treatment because of complications (4),

lack of treatment efficacy (13), or for unknown reasons (2). The remaining eight

patients, though they were last known to be continuing antibiotic therapy, are

considered to be treatment failures because of: increased use of steroids (4) or

initiation of adjunctive treatment with SAARDs (penicillamine (2) and

antimalarials (2)). The duration of therapy for the 27 treatment failures ranged

from 9 days to 4 years; the median time to treatment failure for those patients

is estimated to be 16 months.

Results of a life table analysis of times to treatment failure for the 98 study

patients are summarized in Table 7, and they are graphically presented in Figure

1. As can be seen, our best estimate of the chance that a similar group of

patients would remain on antibiotic therapy failure free for one year is 90%;

for two years It is 84%; for three, four and five years it is 77%, 71% and 70%

respectively. Taking sampling error into account, we are 95% confident that >

59% of patients would be continuing antibiotic therapy failure free as defined

above after four years of observation. Time to treatment failure was not found

to be statistically related to sex, duration of disease, ARA classification (viz

classical or definite RA) or prior treatment with gold or steroids (p > .1)

Symptomatic Relief. Patient reports of symptomatic relief were reviewed and

summaries are provided in Tables 8 and 9. Eighty-four percent of patients for

whom baseline and follow-up information were available reported a 50% or greater

decrease in the number of tender joints, the number of painful joints, or the

duration of morning stiffness. Forty-nine percent of such patients experienced >

50% improvement in at least two of the three symptoms and 31% of evaluable

patients reported > 50% Improvement in all three symptoms. A trend analysis of

the data indicates a statistically significant association between year in which

therapy was initiated and response to treatment (p = .001). Symptomatic

improvement with respect to weakness, fatigue, endurance, feelings of

well-being, mental accuity, or depression was observed in three quarters of all

patients; improvement on multiple criteria was common. Here again, rate of

improvement on these criteria was associated with year of treatme!

nt start (p = .05).

Stanford Health Assessment Questionnaire (HAQ). Mean values were calculated for

the three parameters measured by the HAQ (viz pain, global assessment of disease

activity, and ability to function), as were bounds for the 95% confidence

intervals around the three means (Table 10). Similar calculations are presented

for two subgroups: (a) treatment failures and ( patients who cannot be

considered as failures at least at this time. Patients who have been identified

as failures consistently demonstrated scores suggesting increased levels of

pain, worsened global assessment of disease activity, and reduced ability to

function independently; there is no overlap among any of the three sets of 95%

confidence intervals.

DISCUSSION

Ultimately, the efficacy of any treatment can only be established through

well-designed and well-executed controlled clinical trials. The findings of this

uncontrolled retrospective study, however, do suggest that antibiotic therapy,

e.g., Tetracycline and its derivatives, has been of value in managing these 98

patients with classical or definite rheumatoid arthritis--60% of whom had

received one or another of the slow-acting anti-rheumatic drugs prior to

starting on antibiotic therapy, three-quarters of whom were seropositive for

rheumatoid factor, and all of whom had clinically active disease.

Antibiotic therapy was generally well tolerated; although 38% of patients

reported an adverse reaction, only four patients discontinued antibiotic therapy

for toxicity. Treatment failure, which was defined here as (a) the termination

of antibiotic therapy for lack of efficacy, toxicity or unknown reasons, ( the

increased use of adjuvant therapy with steroids, and/or © the initiation of

adjunctive therapy with any of the slow-acting antirheumatic drugs was seen in

only 27 patients (28%) after a total of 451 patient-years of observation. Life

table analyses indicate that the probability of remaining on treatment and free

of failure as defined for five years is 70%. In addition, the majority of

patients studied reported meaningful improvement in the number of painful and

tender joints and in the duration of morning stiffness; meaningful improvement

was also reported on all of the subjective symptoms evaluated, viz weakness,

fatigue, endurance, feelings of well-being, mental a!

ccuity, and depression. And, while the positive association observed between

time on treatment and the extent of symptomatic relief may be explained in a

variety of ways, clearly one possibility is that longer periods of therapy lead

to greater therapeutic benefit. Thus, antibiotic therapy appears to be

associated with an ability to maintain a majority of patients with RA in either

a stable or improved clinical state over a long period of time with a low degree

of toxicity and no serious life-threatening adverse effects.

As with all retrospective and/or observational studies, these findings must be

evaluated with great caution; and, interpretations must take into account the

risk of bias associated with patient selection and evaluation. In the current

study, efforts were made to minimize some of the more obvious sources of bias

that might have influenced study findings: an independent statistical center and

rheumatologist were used to design and carry out the study; to the extent

possible in a retrospective study, the patients form a series--all of whom met

ARA criteria for definite and classical RA; follow-up for almost all patients

was successfully pursued; and criteria for treatment failure and clinical

improvement were set forth before the study effort began and not afterward. It

is noteworthy that data gathered using the Stanford Health Activity

Questionnaire support the idea that the criteria used to determine " treatment

fallure " were clinically meaningful.

Alternate Therapies. The findings reported here also compare favorably to the

historical experience of other investigators who used either placebo or SAARDs

although given the lack of standardization in reporting methods26 and the

possibility that significant differences existed in patient populations, drug

regimens and outcome measures, such comparisons must be

-13-

interpreted with great caution. As noted above, the data reported here show that

Brown maintained 84% of patients on antibiotic therapy, failure-free, at two

years; in comparison, Sigler, using gold, was able to maintain 13 of 16 patients

(81%).on therapy for 24 months.27 However, the findings of several prospective

observational studies which reported on the long-term efficacy of gold therapy

do not compare well to Brown's experience of 71% and 70% treatment survival at

four and five years, respectively. In particular, Rothermich and colleagues

reported that 40 of 97 patients (41%) with definite or classical RA were

improved and still on therapy after one year of gold therapy--but that only 15%

of those patients were receiving gold at four years.28 In another report by

Rothermich et al, 91 of 171 patients (53%) who received gold therapy had

terminated treatment because of lack of response or toxicity by 12 months; and

that at the end of four years of observation, only 11% of !

patients remained on therapy.29 Kean and Anastassiades30 and Sharp and

colleagues similarly noted the lack of sustained benefit from

chrysotherapy.31,32

Long-term results with hydroxychloroquine are hardly better. Runge reported on a

life-table analysis of treatment failure for 101 patients with RA treated

between 1970 and 197733 indicating that median time to treatment failure was 13

months--and that the major cause of termination was lack of efficacy. In that

study, only 14 patients (14%) were still receiving hydrochloroquine and under

observation at 50 months--at which time the rate of treatment failure had

reached 70% with over 45% of failures due to lack of efficacy.

While only a few long-term observational cohort studies of penicillamine therapy

in RA have been reported,34-36 these reports, too, are not favorable.

Hill34 has noted that about 15% of patients discontinued therapy during the

first six months and that an additional third of the patients studied

discontinued during the second six months. Munthe and Kass,35 reporting on 266

patients with definite or classical RA treated with penicillamine over an

eight-year period have indicated that 40% of patients discontinued therapy with

penicillamine because of adverse effects or lack of response; and Runge,

reporting on 40 patients who received penicillamine indicated that the treatment

termination rate was 50% at 18 months.33 Thus, antibiotic therapy, as received

by the patient cohort reported herein, appears to compare favorably with the

reported experience with currently prescribed SAARDs--particularly in terms of

complications and treatment duration.

Several recent studies which used placebo-treated control groups also offer

interesting reference points for assessing antibiotic therapy. In a study which

was both too small and too short to be informative, Skinner et al found that at

one year 14 of 16 (88%) patients were still on placebo therapy, while 13 of 14

(92%) were still being treated with Tetracycline.20 In contrast, Ward et al

reported that 86% of patients assigned to a placebo group remained on therapy at

21 weeks,23 and Wenger and associates noted that only 54% of patients assigned

to a placebo control group remained on therapy at 6 months.37 While none of the

three studies unequivocally establishes the short-tern failure rate for placebo

therapy in patients with definite or classical RA, the Ward and Wenger reports

are certainly more in keeping with the common clinical experience than that

reported by Skinner et al. And, while the ability to maintain patients with

definite and classical RA on placebo therapy for !

four and five years remains completely unevaluated, the common experience once

again suggests that it would not be close to the 50-70% rate being reported here

for patients who received antibiotic therapy.

An Hypothesis. If antibiotic therapy is effective in RA, as is suggested by

these data, the mechanism of action may be similar to that observed in the

treatment of Lyme disease38 with antibiotics or of Tetracycline in the treatment

of bypass arthrltis.39 That is, if mycoplasmas are an inciting agent in RA, then

either or both of the mechanisms hypothesized by may be operative:

Last Update: 27-08-97

> <Stillsdisease > " Angie " Date: Fri, 25

Aug 2000 13:37:56 -0500

>Reply-To: Stillsdisease

> Re: new to group

>I was dx'd at 12 too, but I only experienced aspirin therapy. I think that

>if I was dx'd now that they would probably treat it more aggressively. I

>don't know if that would be a good thing. I was very sick for a long time,

>but eventually went into remission which lasted (mostly) through my 30's.

>

>I developed an allergy to NSAIDs, so aspirin is out for me now. I think that

>the antibiotic therapy might work too. When I would start to run my FUO's in

>my 20's, the docs would usually prescribe antibiotics as a routine measure.

>

>When they did, I would stop flaring. Looking back, I still don't know if it

>was the antibiotics helping, or my body regaining it's control over my body.

>The last time though, I was on antibiotics for months, and eventually

>slipped into one of those flares that almost kills us.

>

>So, if the antibiotics were working for me, they aren't any more. And I

>don't feel like they will work for me. But I also think that if feels

>like that's the right treatment for him, it very well could be. Medicine is

>as much art as it is science, and I am a very strong believer in gut

>feelings.

>

>Angie

>

> new to group

>>

>> > Hi! My name is Tonya and my daughter Terah(5) was just

>> > diagnosed with systemic JRA in June 2001. we live in Lake

>> > , Texas which is approx 1 hour south of Houston.

>> > This is Terah's story.

>> > In May she became ill her first symptoms were a sore throat,

>> > very red conjuntive eyes and a rash on the insides of her

>> > arms and legs that almost looked like polka dots. I took

>> > her to a doctor that was filling in for our normal pediatrician

>> > and he diagnosed her with a throat infection and gave her

>> > a prescription of Augmenten and some eye drops. The next evening

>> > she was very ill running a temp of approx 103 and was acting

>> > strange so I immediately took her to the emergency room.

>> > After waiting in the waiting room for almost 3 hours they finally ran

>> > some blood work and diagnosed her with a urinary tract infection. I

>> > knew this could not possibly be right but at 2AM did not feel like

>> > arguing so we went home with a prescription of Bactrum. SInce this

>> > was the Memorial Day weekend there was not much we could do but stay

>> > home and watch her carefully and she seemed to be doing better.

>> > By Tuesday she had taken a turn for the worse, she could barely walk

>> > and was not eating a thing so we took her to her regular doctor who

>> > diagnosed her with a Viral infection and sent us home with yet

>> > another prescription. The next day she could not get out of bed and

>> > her fever was once again 103 so we went back to her doctor and he

>> > admitted her into the hospital. They ran several tests and at this

>> > point did not know what was wrong with her. Her WBC was 35,000 so

>> > they immediately started her on IV antibiotics which over a course of

>> > 2 days did not help her. Her doctor came to us and said he thought

>> > she had Kawasaki syndrome and said he was going to transfer us to

>> > UTMB childrens hospital in Galveston. Once there the team of doctors

>> > ran several more test and she was clinically diagnosed with

>> > Kawasakis. She was given IV Gammaglobulin and aspirin but after two

>> > doses they had to finally give her steroids to make her feel better.

>> > After 7 days we went home with a prescription for 40MG of steroids

>> > and 2 childrens aspirins a day. For 4 weeks she seemed to be better

>> > but as we began decreasing her Prednisone and we got down to 20MG in

>> > the morning only she took another turn with fevers as high as 105.2

>> > and we were back at the

>> > hospital. This is when the diagnosis changed to Systemic JRA. She is

>> > now on MTX 7.5MG a week and she is still on Prednisone 20MG in Am and

>> > 15MG in PM. She is still very ill and was unable to begin

>> > kindergarten this year. Her biggest problem is her fingers and her

>> > feet and legs she is unable to play or sit on the floor so we read

>> > quite a few books and watch alot of Rugrats. She has a wonderful

>> > immunologist and she will begin seeing a rheumy this week.

>> > The hardest part of this is watching your child go from a healthy

>> > happy child to a sick child who does not even look the same because

>> > of the steroids. I still cry every day and pray that this is all a

>> > big mistake and she will get better. We also have a 7 year old

>> > daughter who does not quite understand all the attention her

>> > sister is getting. At this point we are just hoping to get the

>> > disease under control and get some normalcy back in our lives! Thank

>> > you for letting us join your group I know I will learn alot!

>> > Sincerely,

>> > Tonya

>> >

March 4, 2009

Hi my name is April, and my son Tommy has scoliosis. He is 4 years old and just

got his first cast. I noticed on this site that almost everyone here is talking

about plaster casts, and my son has a fiberglass Risser cast. Does anyone know

anything about this type of cast? Is it very different from the EDF casts

everyone here seems to know about? We took the watch and wait approach. He was

first diagnosed when he was 7 months old and was braced from 1 1/2 to 4 yrs.

When that was no longer working I decided to go ahead with the casting as there

seemed to be no other option. His dr. said that if i didnt do the casting he

would need growing rods within a year, but with the casting we could put off the

rods until he is 10 or older. I am praying for a miracle that he wont need the

rods ever, but I guess we will see... Any insight you have will be appreciated

thank you in advance, April

March 4, 2009

Hi April. Welcome! I'm new too. My name is Elly. I may be wrong, but I think they are the same. My daughter's cast is fiberglass on the outside and plaster inside. I think they all are. There are many on here with more knowledge than me though! If it is different I'll learn something too! Sent from my iPhone

Hi my name is April, and my son Tommy has scoliosis. He is 4 years old and just got his first cast. I noticed on this site that almost everyone here is talking about plaster casts, and my son has a fiberglass Risser cast. Does anyone know anything about this type of cast? Is it very different from the EDF casts everyone here seems to know about? We took the watch and wait approach. He was first diagnosed when he was 7 months old and was braced from 1 1/2 to 4 yrs. When that was no longer working I decided to go ahead with the casting as there seemed to be no other option. His dr. said that if i didnt do the casting he would need growing rods within a year, but with the casting we could put off the rods until he is 10 or older. I am praying for a miracle that he wont need the rods ever, but I guess we will see... Any insight you have will be appreciated thank you in advance, April

March 4, 2009

They are not the same.............EDF and a Risser cast. I will not even attempt to explain as well as would so I'll do the next best thing.......copy and paste one of her emails.And I am sure(and hope)she will chime in soon.See below:**************************************Welcome to CAST! May I recommend that you learn the differences betweenRisser casting and EDF (elongation, derotation, flexion) casting.

Scoliosis is a 3-dimensional problem that should be corrected on

all 3 planes. The EDF casting method has the ability to elongate the

spine through traction, derotate the spine/pelvis, and to improve lordosis and over all body shape/alignment.EDF

differs from Risser casting. EDF casts are over the shoulder, with a

large mushroom opening on the front to allow for proper chest

expansion. On the back, there is a small cutout on the concavity of the

curve, not going past the midline. It was found that the spine became

more aligned with this cutout than without and that it helped correct

rotation.

Early treatment w/ EDF is generally over a period of 9-12 months

depending on age and childs specific situation. When the child's Cobb

angle is under 10 deg, they are removed from their series of EDF

plaster casts and placed into a removable brace. Early treatment EDF does not alternate with bracing as Risser plaster casting can. It is a solid block of casts to decrease the childs curvature(s) , gently, slowly & permanently. The

biggest difference is the aim of treatment- which is cure,opposed to

containment. Dr's Cotrel & Morel developed the EDF technique years

ago in France and found that using one of these techniques in isolation

has it's own drawbacks, yet using all three simultaneously

potentialises the advantages of each.(Elongation, Derotation, Flexion).

Please read related articles in the Files section of this group and feel free to ask this group any

questions that you may have.

******************************Hope this helps you understand it better. Where is your son going for treatment?BTW-my son's cast were plaster and fiberglass over that.Let us know if you have any other questions.Welcome to the group!TashaMommy of twin boys- and 3 1/2 years oldFort Worth, Texas is currently in a brace at night.Casting 14 months.

Hi my name is April, and my son Tommy has scoliosis. He is 4 years old and just got his first cast. I noticed on this site that almost everyone here is talking about plaster casts, and my son has a fiberglass Risser cast. Does anyone know anything about this type of cast? Is it very different from the EDF casts everyone here seems to know about? We took the watch and wait approach. He was first diagnosed when he was 7 months old and was braced from 1 1/2 to 4 yrs. When that was no longer working I decided to go ahead with the casting as there seemed to be no other option. His dr. said that if i didnt do the casting he would need growing rods within a year, but with the casting we could put off the rods until he is 10 or older. I am praying for a miracle that he wont need the rods ever, but I guess we will see... Any insight you have will be appreciated thank you in advance, April

March 4, 2009

Wow, I had no idea! Thanks for new info for me! Shows how much I have to learn. I should probably just let you guys who have been at this longer answer. Thanks Tasha. Sorry April.Sent from my iPhone