Uncovering the Complexities of Rheumatoid Arthritis with Dr. Alan Zalkowitz

Unmask the hidden complexities behind rheumatoid arthritis with renowned rheumatologist, Dr Alan Zalkowitz from the Kayal Orthopedic Center, in this thought-provoking conversation. We trace Dr Zalkowitz’s journey in the medical field, before diving into the depths of rheumatoid arthritis – a systemic, inflammatory condition that affects millions worldwide. From understanding its risk factors to discerning its symptoms, we leave no stone unturned.

As we journey further into uncharted territories, we explore the intricacies of diagnosing and assessing rheumatoid arthritis. Dr Zalkowitz guides us through the physical exams and the nuanced signs that often escape the untrained eye. We also delve into the world of imaging modalities and laboratory tests that are vital in confirming a diagnosis. The importance of early detection and treatment is emphasized, as we unveil how it can alter the course of this debilitating disease.

Finally, we navigate through the maze of treatment options and understand the significance of combination therapy. We compare the roles of rheumatologists and orthopedic surgeons, highlighting the value of their collaborative effort in managing chronic diseases. From understanding joint deformities to discussing the potential cure of rheumatoid arthritis, this episode is a goldmine of information. Join us as we embark on this enlightening journey with Dr Zalkowitz, whose expertise brings a wealth of knowledge to our multi-specialty practice.

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Episode Transcript

Robert A. Kayal, MD, FAAO (00:00):
Hello and welcome to another edition
of the Kale Ortho podcast.
Today, our special guest is ourvery own Dr Alan Zalkowitz, the
chief of rheumatology at theKale Orthopedic Center.
Welcome to the podcast, drZalkowitz.
Thank you so much.
It's such an honor andprivilege to have Dr Zalkowitz
with us today.
Dr Zalkowitz is a renownedrheumatologist and we're so

(00:22):
privileged to have him practicewith us at the Kale Orthopedic
Center, servicing the communityof patients in Northern New
Jersey and New York.
Before we get started, whydon't you tell us a little bit
about your education, trainingand your family life as well?

Alan Zalkowitz, MD (00:36):
Yes, hi, I'm Dr Alan Zalkowitz and I started
the rheumatology fellowshipprogram at Mounds-Sinai Medical
Center in New York City manyyears ago and helped run the
arthritis clinics atMounds-Sinai in autoimmune
disorders, rheumatoid arthritis,lupus.
When I came to Northern NewJersey I was the only

(01:00):
board-certified rheumatologistfrom the Delaware Water Gap to
the George Washington Bridge.
Needless to say, that was aherculean task to cover all of
the many, many patients whorefer to me, from physicians who
used to send in to New York orto Philadelphia.

(01:21):
I remember that the highlightof my becoming a rheumatologist
takes me back to my last year atYale, new Haven.
At that time an advertisementcame out in the New England
Journal of Medicine that therewas a new position, a new
fellowship that was beingstarted at Mounds-Sinai funded

(01:44):
by the National Institute ofHealth.
I went for the interview alongwith 200 others and met the
chief there, dr Harry Spira, andhe took me.
I was the sixth interview.
He took me down the hallway andshowed me a mail about 30 years
of age, bent over, and he saidto me Alan, make a diagnosis.

(02:08):
And I did and I said he hasankylosing spondylitis.
And he said you have theposition of the first fellow at
Mounds-Sinai.
I then entered a group of allMounds-Sinai doctors there was
one, I think, from AlbertEinstein.
We were all subspecialists andI divided my time mainly between

(02:33):
several hospitals and taught atthe medical center.
I would leave the office atabout 8 o'clock at night, having
started at 6.30 in the morning,and then go to other hospitals
to do consultations.
My wife, who has been with meover 50 years and helped put me

(02:54):
through medical school.
She brought up my three sonstill they all left for college
and I'm very appreciative of allthe work that she's done to do
that.

Robert A. Kayal, MD, FAAOS (03:07):
Wow, thank you so much for that
history.
I've had the privilege ofknowing you for probably close
to 30 to 40 years potentially.
I had the privilege of growingup with your three boys.
I graduated high school withHoward.
I was very, very good friendswith Howard during my childhood

(03:27):
years and high school years.
I have fantastic memories ofthat relationship with Howard.
In addition, I remember workingat a gym in Wyckoff and you and
your wife would very frequentlywork out in that gym in Wyckoff
called the gym, where I workedbehind the desk and as a trainer
, and I have very fond memoriesof those years.

(03:50):
In fact, like I've told you many, many times, forever be
indebted to you for your adviceand wisdom, guidance and
direction in helping me maybeget into medical school and
actually land my first hospitalprivileges at Valley Hospital in
Ridgewood, writing my lettersof recommendation from medical

(04:12):
school and programs that I wouldwish to matriculate in, and I'm
just forever indebted andgrateful for all of that and
feel so honored and privilegedto have you here with us today.
Your wisdom and expertise fundof knowledge and experience is
just indescribable and just sohappy to have you with us today

(04:34):
to talk to us all and educateour community of patients about
this very important conditioncalled rheumatoid arthritis.
Rheumatoid arthritis is verydifferent from other forms of
arthritis, and it's very, veryimportant to distinguish between
rheumatoid arthritis and otherforms of arthritis.

(04:55):
So, dr Zalcowicz, why don't youtell our community of listeners
and viewers why it's importantto distinguish between the
different types of arthritis,and then we'll get into focusing
on rheumatoid arthritis.

Alan Zalkowitz, MD (05:08):
Arthritis is an inflammation of a joint or
joints like the knees, the hips,the hands, the feet.
This leads to inflammation andstiffness and pain in those
joints.
It may be years before theactual inflammation and joint
pain developed.
Unfortunately, there are abouta hundred different types of

(05:31):
arthritis, from infectiousarthritis, of which most of you
heard about Lyme disease, todegenerative wear and tear
arthritis, which isunfortunately about 33 million
Americans have where caught lidsand bone breaks down and a lot

(05:52):
of orthopedists see the stagesof it where one may need to have
a joint replacement to theother.
Inflammatory arthritis isdifferent and the most common
symmetrical polyarthritis isrheumatoid arthritis that
affects approximately 1% of thepopulation.

(06:13):
That means about one and a halfmillion people in the United
States.
It's a progressive arthritisleft untreated that can cause
deformity and severe morbidity.

Robert A. Kayal, MD, FAAOS (06:30):
So, just to elaborate on what Dr
Zalcowicz was mentioning,there's different forms of
arthritis.
Obviously, the most common formis degenerative wear and tear
arthritis, but there are otherforms as well.
Dr Zalcowicz alluded to thefact that there could be
infectious arthritis, what wecall septic arthritis, where an
infection can get into the jointand destroy the joint as well.

(06:52):
There's another conditioncalled post-traumatic arthritis,
where trauma can destroy thejoints, but in today's podcast
we're going to focus ourattention on inflammatory
arthritis, where there'sinflammation in the joint which
can also destroy the joint.
And in the realm ofinflammatory arthritis there's
different forms of inflammatoryarthritis, but today's podcast

(07:14):
will focus on a specificautoimmune condition called
rheumatoid arthritis.

Alan Zalkowitz, MD (07:20):
So in rheumatoid arthritis this is
usually a newness of women,three to one over men, and it
usually happens at 30 to 60years of age is the major peak,
and one of the reasons may bethat you have a preponderance of

(07:43):
women is that in this conditionmale hormones can cause a
pro-inflammatory effect whichcauses there to be a larger
amount of rheumatoid disease inwomen and men.
We find that in rheumatoidarthritis that after 60, the

(08:07):
incidence of the disease isabout equal male and female,
because the hormone level inwomen decrease.
The causes of rheumatoidarthritis, which is really
caused by the white blood cellsthat normally secrete proteins

(08:30):
and enzymes and inflammatorycells that usually protect the
system from infection andinflammation, goes out of whack
and these inflammatory what wecall cytokines, cause an
inflammation on the joints or onthe muscles or on the tendons

(08:53):
or ligaments, causing systemicproblems that can affect not
only joints.
But in rheumatoid arthritis itcan affect the heart and
therefore in rheumatoidarthritis you have an increased
risk of heart disease and heartattacks and stroke.
And if you control therheumatoid arthritis you

(09:15):
eliminate that increased risk ofheart attacks and stroke.
It can affect the eyes, whereyou get dry eyes, uveitis, which
is inflammation of the eyes.
It can affect the lungs, inabout 10% of people, where they
get problems with breathing.
It can affect the skin whereyou get nodules, in about 15% of

(09:40):
patients by the elbows.
So rheumatoid arthritis isubiquitous in terms of affecting
most joints.
We want to suppress theinflammatory condition.
We want to suppress thecytokines, we want to suppress

(10:01):
certain cytokines that arecalled leukotrienes and
prostaglandins, and we can dothat with medication.
We can do that with certainchanges in our lifestyle.

Robert A. Kayal, MD, FAAOS (10:15):
So just to further elaborate on
what you just discussed, drZalkowicz, I think the take-home
message is that, unlikedegenerative wear and tear
arthritis, rheumatoid arthritisis a systemic disease.
It's important to remember thatrheumatoid arthritis is an
autoimmune disease that reallyaffects the entire body.
It can result in damage toorgans, like you mentioned the

(10:40):
heart, the lungs, and so it'simportant to distinguish between
other forms of arthritis, likepost-traumatic arthritis, septic
arthritis, degenerative wearand tear arthritis and, most
importantly, be able to identifythose patients that are
suffering from a systemicdisease like rheumatoid

(11:00):
arthritis, and get them in thehands of a board-certified
fellowship trainedrheumatologist like Dr Alan
Zalkowicz.
Let's take this opportunity tojust explain to our audience
what exactly is happening inthis condition called rheumatoid
arthritis.
We already discussed that thisis an autoimmune condition where
the patient's immune system isessentially attacking itself.

(11:22):
We've discussed that it canattack organs.
We discussed that it can attackeven systems like the
cardiovascular system and thepulmonary system and other
systems of the body.
But specific to the joints,what's happening inside that
joint?

Alan Zalkowitz, MD (11:38):
What's happening is that the
inflammatory condition causescertain enzymes and hormones and
cytokines to develop what wecall osteoclasts, and they eat
up the bone and the cartilageand therefore destroy the joint.

(11:58):
In addition, there's aninflammatory layer of tissue
that forms that is called panaceand that causes the bones again
to become inflamed and todeteriorate.

Robert A. Kayal, MD, FAAOS (12:13):
Yeah , so it's primarily affecting
the synovial lining of the jointcorrect.

Alan Zalkowitz, MD (12:17):
Yes, the synovial lining of the joint is
affected and then it goeseventually to cartilage and to
bone and erodes the bone andtherefore in a significant case
of rheumatoid arthritis onedevelops erosions.
When one sees erosions as arheumatologist and you see a

(12:39):
patient for the first time andthey have them, you know that we
have failed to prevent that.
It used to be that one of thehallmarks of rheumatoid
arthritis and making thedifferential diagnosis is
erosions.
But if you see erosions, we'venot been successful in
preventing them because thoseare very difficult to reverse,

(13:02):
if at all.

Robert A. Kayal, MD, FAAOS (13:03):
So, dr Zolkowitz, what are some of
the risk factors whenconsidering the diagnosis of
rheumatoid arthritis in ourpatients?
Are there some risk factorsthat put patients at increased
risk for getting diagnosed withrheumatoid arthritis?

Alan Zalkowitz, MD (13:18):
Yes, there are Myself and some of the other
rheumatologists that are partof Dr Kale's organization.
We often emphasize that onemust stop smoking.
Smoking causes inflammation toa great degree.
In addition to smoking, weoften make a great effort to

(13:41):
have someone get down to theirideal weight.
It's very interesting thatthere are certain inflammatory
markers in people overweightcalled leptins, and these
leptins are those cytokines thattravel in the blood system and
can land in a heart andtherefore lead you to more heart

(14:02):
disease, and heart attacks canlead to the joints and possibly
cause you to have more jointpain.
So the takeaway is to be lean,not smoke, and to exercise
regularly.
Exercise is a very importantthing.
Even in people who have wearand tear arthritis.

(14:24):
They should exercise under thephysician's guidance or someone
from physical therapy, becausethat's very helpful.

Robert A. Kayal, MD, FAAOS (14:31):
It's so interesting to hear all this
because when you're in medicalschool, they don't really teach
us at least not back when Iattended medical school that
autoimmune conditions likerheumatoid arthritis are
associated with smoking andobesity and even exercise.
So, dr Zolkowitz, how does thetypical patient present to your
office?
What is their chief complaintusually when they're being seen

(14:54):
and you ultimately diagnose themwith this condition called
rheumatoid arthritis?

Alan Zalkowitz, MD (14:58):
They usually present with polyarthritis,
joint pain, swelling of theirhands and feet.
You can have other jointsinvolved.
What's most important is incomparison to some degenerative
processes of the hands.
It affects the large knucklesand the medium-sized knuckles

(15:20):
and rarely ever affects thedistal knuckles, which is much
more common in osteoarthritis.
And they present with stiffness.
That's a key here stiffness agelation phenomenon that usually
is over an hour and sometimeseven longer than that.
It's hard for them to get outof bed.

(15:42):
The morning is the worst timefor them and as the day
progresses they get a little bit, a little bit better.
We normally use 15 to 30minutes as a mock-off to
determine inflammation.
More than 30 minutes to a fewhours.
Non-inflammation less than 30minutes.

(16:04):
Usually five to 15 minutes todetermine whether it's
inflammatory or not.
These patients can havesignificant fatigue.
Fatigue may be overwhelming andthat's a part of therapy that
only the most recent biologicshave addressed.

(16:24):
They often can have nodules bytheir elbow.
They may have their joints notbeing able to be straightened.

Robert A. Kayal, MD, FAAOS (16:36):
So yeah, I agree with you.
When I'm taking a history in myoffice and talking to patients,
I definitely inquire aboutmorning stiffness especially.
These patients are typically inthe prime of their life.
These are usually diagnosedmore in women than men in the
prime of their life.
When they start complainingabout morning stiffness that's

(16:57):
prolonged, like you'redescribing.
It's very concerning and that'swhen we'll often refer them to
you for a rheumatologicalevaluation.
In addition to that, because itis a systemic disease, an
autoimmune disease, very oftenthese patients will have
systemic symptoms.
Sometimes they'll have achesand chills fever, sometimes

(17:20):
they'll be lethargic.
They'll be tired a lot duringthe day as well.
Are these some of the thingsyou look for?

Alan Zalkowitz, MD (17:25):
Yes, we look for them In rheumatoid
arthritis to the adult.
If you have fever, that's alittle unusual.
It can happen and there is acondition called stills disease,
which is rheumatoid arthritisof the adult.
That's of a juvenile patternwhere the type of fever, whether

(17:48):
it's two or three times a day,gives away the diagnosis.
It's one of the pearls thatrheumatologists like myself use
to make that diagnosis.
But if we have fever we startto look towards infection and
other types of autoimmunedisorder, like lupus, like

(18:09):
vasculitis.
They often are lethargic andfatigued.
For a woman who has children,it may keep them in bed for such
a long time that they have realdifficulty taking care of their
children.
They have real difficultyholding a job and there's a
greater risk of those patientsgoing on disability because they

(18:33):
cannot do it, because thisoverwhelming systemic effect
affects every part of their body.

Robert A. Kayal, MD, FAAOS (18:41):
So, Dr Zalkowicz, I think it's very
important to note everything youjust described because it's
very different when patientspresent with the typical
degenerative wear and teararthritis.
A lot of the patients willcomplain of stiffness with
degenerative wear and teararthritis, but often that
stiffness is isolatedspecifically to the joint that's

(19:02):
being evaluated.
They'll say, Dr Kale, my kneeis stiff, my hip is stiff, my
shoulder is stiff.
But in rheumatoid arthritisthey'll very often complain of
diffuse stiffness in theirjoints and typically in a
symmetrical pattern and intypically the smaller joints of
the body right, Like the ankle,the elbows, the shoulders,

(19:24):
joints that aren't as ofteninvolved in the more ubiquitous
condition called degenerativewear and tear osteoarthritis.
Is that correct?

Alan Zalkowitz, MD (19:33):
That's certainly correct.
The thing that haunts theseyoung women again, they're three
times as likely than men istheir hands, wrists, feet, as
mentioned, have really stoppedthem from being able to function
in business and at home withswelling of their joints.

(19:55):
These joints become swollen,warm and hot.

Robert A. Kayal, MD, FAAOS (19:59):
So, yeah, everything you're
mentioning, dr Zalkowicz, a lotof these things are not present
in the typical orthopedicpatient complaining of a painful
joint.
They may complain of stiffness,but again, it's not a systemic
problem, it's typically notinvolving multiple joints and
it's typically not associatedwith other systemic complaints.

(20:20):
So now, dr Zalkowicz, you'vetaken an adequate history.
You've begun to establish adifferential diagnosis in your
own mind that perhaps thispatient is suffering from an
inflammatory arthritis, mayberheumatoid arthritis.
What's next?
What do you do on physicalexamination to try to really
hone in on that diagnosis andreally confirm that we're

(20:42):
dealing with a patient thatprobably has rheumatoid
arthritis?

Alan Zalkowitz, MD (20:46):
When we do the examination we look very
carefully at the skin.
Something that has become muchless frequent are nodules by the
elbows.
They're usually non-tender,they're usually mobile.
We used to see them in New Yorkat Mount Sinai, frequently,

(21:07):
because we saw only the worstpatients.
Now we don't see them veryfrequently because patients are
treated, even by their primarycare, with medications and
therefore those medicationsinterfere with inflammation.

Robert A. Kayal, MD, FAAOS (21:25):
So specifically in rheumatoid
arthritis.
Dr Zalkowicz, what do youtypically find when you're
focused on examining the jointsof these patients?

Alan Zalkowitz, MD (21:34):
So we're looking for inflammation,
swelling of the joints, warmthof the joints, difficulty,
inflection or extending thejoints.
And sometimes we find that someof the joints form some
abnormalities where they canlook like swans the joints.
They're called swan neckdeformities.

(21:56):
And then there are others thatare called boutonniere
deformities, that are specificfor rheumatoid disease.
We don't see that much as wedid 30 years ago because of a
lot of the medications forexample methotrexate, in my own
view has revolutionized thetreatment.
But we look for whetherpatients can straighten their

(22:19):
joints, whether there's anywarmth to the joints, whether
there's any tapering of thejoint, whether the patient feels
in the small joints thissymmetrical attack on their
joints of their hands and theirfeet.

Robert A. Kayal, MD (22:36):
Furthermore , a lot of these patients can
have physical deformities of thefingers, something we call like
a boutonniere deformity or aswan neck deformity, which we'll
see sometimes in the hand.
These are not common conditionsin the orthopedic community.
So you had mentioned, drZalkowicz, that when rheumatoid
arthritis affects the hands ittypically involves certain

(22:57):
joints in the hands.
Can you demonstrate for ourviewing audience at least what
part of the hands are typicallyinvolved, which joints are
involved typically withrheumatoid arthritis and which
joints are more commonlyinvolved with the typical
degenerative wear and tearosteoarthritis?

Alan Zalkowitz, MD (23:13):
In the hand, for example.
We look at these joints calledthe metacopal phalangeal joints
and we look at the proximalphalangeal joints.
The distal and phalangealjoints are usually not involved
and what we look for is swelling, tapering warmth, and we look
to see whether they can fullyflex and extend their joints.

Robert A. Kayal, MD, FAAOS (23:37):
So yeah, I agree with you
wholeheartedly, dr Zalkowicz.
When I see patients in theoffice and I see swelling around
this joint right here, thesejoints, the metacopal phalangeal
joints, I very much think of arheumatological condition.
Very often these patients willhave what's called an ulnar
deviation deformity at themetacopal phalangeal joints as
well, where those fingers willbe ulnarly deviated towards the

(23:59):
ulna bone.
So when we start to see acombination of these conditions
like the swelling, redness andwarmth in the metacopal
phalangeal joints, the ulnardrift in those joints, possibly
a boutonniere deformity or aswan neck deformity, our
antennas go up and that's whenwe really want to refer that
patient to Dr Zalkowicz and ourother physicians at the Kale

(24:21):
Rheumatology Center to make surewe're not dealing with an
autoimmune systemic disease suchas rheumatoid arthritis.
I think that's important whenwe're assessing patients.
When these patients arecomplaining of a symmetrical
nature of their joint pains andswelling, we definitely get
concerned about an inflammatoryautoimmune condition.
And in addition, theseconditions often affect the

(24:45):
smaller joints of the body right, the joints like the ankles,
the elbows, the shoulders, muchmore commonly than the typical
degenerative wear and tearosteoarthritis.
In our profession, inorthopedics, we see way more
patients suffering from kneearthritis and hip arthritis as
opposed to ankle arthritis, forinstance, or elbow arthritis or

(25:07):
even shoulder arthritis.
And so when we start seeing apatient with multiple joints
involved, with pain and bone onbone deformity in the smaller
joints especially, we very muchget concerned about inflammatory
arthritis and that this patientmay possibly be suffering from
an autoimmune condition and it'sreally very important that we

(25:29):
refer those patients forrheumatological evaluation.

Alan Zalkowitz, MD (25:33):
That's very true.
These patients have to bepicked up early.
If it's very early, there is apossibility within several weeks
of preventing the memory Tcells.
But the early you treat, beforeyou have further damage and
what we call panis, which is athickening of the tissue by a

(25:56):
joint, the more that you canreverse this and put patients
into remission.

Robert A. Kayal, MD, FAAOS (26:01):
So, dr Zalco, what else can you do
on physical examination to helpsupport the diagnosis of
rheumatoid arthritis?

Alan Zalkowitz, MD (26:09):
So we actually do a full examination,
the rheumatologist with the Kalegroup and we look in particular
at the lungs.
We're listening for what we calldry-course rals, to suggest
that the rheumatoid is one ofthe 10% of patients who may have
inflammation of their lungswhich require special therapy.

(26:32):
We look at their eyes to see ifthey have dry eyes, to see if
they have any inflammationcalled iritis or uveitis which
require a two minute-crossfactor.
That's different than othermedications to treat them,
whereas it also treats theireyes.
We listen to their heart to seeif they have any sign of any

(26:54):
cardiac involvement of the heart, in particular whether they
have something called pulmonaryhypertension that we can pick up
on auscultation of the heartand an echocardiogram.
We look to see if they have onabdominal examination and
enlarged spleen and that issomething that we see

(27:15):
infrequently but it can happen.
And, most importantly, we lookat the nervous system, the
nerves, and we do check forwhether these people have a
peripheral neuropathy, becauseif we catch a peripheral
neuropathy due to rheumatoiddisease and we are able to

(27:37):
confirm that with an EMG nerveconduction, then there is
medication to control that.
But it also signifies to us tolook for underlying inflammatory
disorder called vasculitis.

Robert A. Kayal, MD, FAAOS (27:52):
Wow, that was so helpful, dr Zalcow.
So at this point it sounds likeyou've taken an adequate
history.
The patient's chief complaint,their history of their present
illness, their physicalexamination are all pointing and
suggesting rheumatoid arthritisas a diagnosis.
What other objective tests canyou do to further support that

(28:15):
diagnosis?

Alan Zalkowitz, MD (28:17):
One of the things that we do are joint
films, specifically handinvolvement, wrist involvement,
but then again we're not likelyto find significant findings.
In today's age we rarely seeerosions Again.
If they're present, you have ageneral diagnosis and the

(28:39):
patient hasn't been treatedcorrectly.
What we look for is swelling ofthe joints.
What we look for is somethingwhere there's some inflammation
of the side of joints, calledperiostitis.
We often see on the proximatephyllo angio joints that I
showed in the metacopal phylloangio joints we may see some

(29:02):
signs of some osteopenia.
That means thinning of thejoints on either side of the
joint.

Robert A. Kayal, MD, (29:08):
Sometimes you can see a subluxation of
the joints as well, which cancontribute in the diagnosis
correct.

Alan Zalkowitz, MD (29:14):
Yes, we see them on occasion Again, not as
often as we did 20, 30 years ago.

Robert A. Kayal, MD, FA (29:21):
Because you're diagnosing and treating
them sooner With bettermedications.
As far as other imagingmodalities, what else can you
employ to assist in thediagnosis?

Alan Zalkowitz, MD (29:30):
Well, this is very key.
We want to treat early toprevent panis formation and
prevent erosions that we see ona regular film.
That's by ultrasound and MRI.
We try ultrasound first becauseit's very simple.
In a skilled person who doesultrasound they can pick up

(29:53):
tino-synovirus, inflammation ofthe tendons and the synovium of
the joint and possibly someearly erosions before they
appear on the x-ray.
More and more.
To me and to most remittages,the gold standard is the MRI.
Again, what we're looking foris edema.

(30:15):
Even something as simple asedema will lead to erosions.
If I see edema on an MRI, thatwould get me to use a biologic
on a patient.
If I saw tino-synovirus,certainly very aggressive.
If I saw erosions on an MRI,all guns would be used to try

(30:39):
and prevent further erosions andtry and see if we can get some
of those erosions to reverse,which happens on occasion.
Again, the key is regular x-rayultrasound MRI the key for a
rheumatologist.

Robert A. Kayal, MD, (30:57):
Absolutely .
It sounds like to me the keyhere is the early diagnosis and
treatment.
Really, nothing's better inearly diagnosis than MRI,
especially in this condition.
The MRIs are so sensitive.
It'll show that edema.
It'll show that early erosionsaround the joint inflammation
that we cannot appreciate onplain radiograph.

(31:17):
I think it's a very, veryimportant point that you've just
made.
Now that we've made thediagnosis, you've done the
history, physical examination,you've looked at some of these
imaging studies, are there anylabs that you can order to
support that diagnosis as well?

Alan Zalkowitz, MD (31:33):
Yes, laboratory work for a
rheumatologist is the bane ofpatients.
Of course it means we take alot of blood.
We take a lot of blood oftenwhen we follow the patients
because they need recurrentvisits to see how they're doing
and making adjustments in theirmedication.
The test that we use forinflammation in general is

(31:57):
called a sedrate and aseroactoprotein.
They're elevated ininflammatory arthritis but can
be elevated in infection as well, so we have to be very careful.
But in degenerativeosteoarthritis they're not
elevated or borderline.

Robert A. Kayal, MD, FAAOS (32:16):
What about the rheumatoid factor
serology test?

Alan Zalkowitz, MD (32:19):
So the rheumatoid factor testing is the
latex fixation and the CCPantibody.
One of the specificinflammatory markers in
rheumatoid disease is called aVectra D, which is rather more
specific for inflammation.
The testing that we do is wecan do a latex fixation for

(32:43):
rheumatoid arthritis that ispositive in about three quarters
of the patients with rheumatoidarthritis.
It's not as specific as wewould like because you can see
that in people who havehepatitis and arthritis,
tuberculosis and arthritis,sarcoidosis and arthritis, the
test that we use more is calledan ACP, an anti-citrullin

(33:11):
peptide antibody.
The anti-citrullin peptideantibody is found mainly in
rheumatoid arthritis.
It has a specificity ofanywhere from 95 to 97 percent.
So if you have someone wholooks they have rheumatoid
arthritis clinically and there'ssome edema on MRI or you see

(33:35):
some tinocephalitis on anultrasound and if you have a
positive CCP antibody, you'vemade the diagnosis of rheumatoid
arthritis.
Moreover, the CCP antibody isthose patients that develop the
more severe type of cripplingrheumatoid arthritis that you

(33:58):
want to be most aggressive with.
The small percentage ofrheumatoids that have CCP
negative rheumatoid arthritisyou treat the same.
They don't respond to biologicsquite as well but they have a
better prognosis.
The higher the level of the CCPantibody, the worse the

(34:19):
prognosis.
So if you have a CCP antibodythat's mildly elevated, that's
much better than so now as astrongly elevated CCP antibody.
Now I will do other blood work.
I will do a serum proteinelectrophoresis to see if these
patients have early signs ofwhat we call a monoclonal

(34:41):
gemopathy.
That can lead to an illnesscalled amyloidosis or multiple
myeloma, which rheumatoids aremore prone to develop.
I will do blood work for otherautoimmune disorders like lupus
and vasculitis, and I will doblood work if they have another
type of genetic disease calledHLAB27 arthritis, like psoriasis

(35:06):
or ankylosing spondylitis.
I might do parvoviral titersand if they have a high IgM
titer I will tell them that theyprobably have parvoviral
disease.
I will do a hepatitis level andprofile on them and I'll do a
test for tuberculosis because ifthey're going to go on

(35:31):
methotrexate or biologic theyhave to be TB negative.
If they have had TB you cantreat them, if they, with
biologics and methotrexate, iftheir TB is dormant and the
blood tests will tell you that.

Robert A. Kayal, MD, FAAOS (35:49):
Do all patients that have
rheumatoid factor always testpositive for the latex test and
or the anti-CCP test?

Alan Zalkowitz, MD (35:59):
So patients who have rheumatoid factor or
latex fixation don't necessarilyhave to have rheumatoid
arthritis.
As I mentioned, it's anon-specific test.
You can have it in hepatitis,you can have it in other
inflammatory disorders.
The CCP antibody test isspecific for rheumatoid disease.

(36:22):
What most people have tounderstand is they can have a
positive latex fixation orrheumatoid factor or a CCP for
years and not have rheumatoidarthritis develop.
It can take up to four and ahalf years for them to develop

(36:43):
the inflammation, the stiffness,the symmetrical polyarthritis
of the hands and feet and otherjoints.
But when we test for it, ifthat's positive, it would mean
we are going to be veryaggressive in treatment.

Robert A. Kayal, MD, FAAO (36:59):
Could it work the other way, where
they do have the diagnosis butdon't have positive latex tests
and or anti-CCP tests?

Alan Zalkowitz, MD (37:08):
Yeah, so latex is positive 75% of the
time.
So you can have a latexpositive and have hepatitis.
You can have it with viralarthritis, which, by the way, is
in a differential and usuallyis gone within six to eight
weeks, whereas rheumatoid lastslonger.

(37:31):
So latex is not specific.
Ccp antibody is rather specificfor rheumatoid disease,
especially if they have historycompatible with it, positive
vector positive C-reactiveprotein and sedrate, and if they

(37:52):
have on MRI edema or tinosinavitis on ultrasound.
The seronegative patient thathas negative CCP antibodies and
has a negative latex has a muchmilder disease and you can have
people have a latex fixationthat's negative and have

(38:14):
rheumatoid disease, or a latexfixation that's positive and not
have rheumatoid disease.
I think that with CCP antibodyif you have the test positive
you have rheumatoid arthritis.
If it's negative then thechance of having rheumatoid
arthritis is remote, possible,but only by a few percentages of

(38:38):
patients.

Robert A. Kayal, MD, FAAOS (38:39):
The common culprit in a lot of
medical conditions isinflammation these days.

Alan Zalkowitz, MD (38:43):
There are several other things that a lot
of my patients take that canaffect inflammation.
First are the turmeric andcurcumin that a lot of people
take on their own.
It is anti-inflammatory.
It has approximately the sameanti-inflammatory effect as some

(39:05):
of the non-steroidalanti-inflammatory drugs, like
Celebrex, for example.
I just want to spend one momenton Celebrex because it does not
affect the platelet andtherefore does not interfere
with coagulation like the otheranti-inflammatories ibuprofen,

(39:27):
aliv, naprison.
Therefore, it's one of themedications that one can use, if
one has to, in people who haveconditions where they're taking
a blood thinner.
But turmeric you have to becareful of, and over the counter

(39:47):
preparations you have to reallyGoogle the side effects.
For example, it can causeoxalate formation.
So if you've had a kidney stone, we don't recommend that you
take it.
If you have iron deficiencyanemia, we don't suggest that
you take it because it caninterfere with iron absorption.

(40:11):
If you're on a blood thinner,we don't recommend that you take
it.
Something else that's veryimportant are omega-3 fatty
acids.
Omega-3 fatty acids are veryanti-inflammatory and have been
used in the past in patients whohave heart disease to help with

(40:32):
their cholesterol profile.
We know that they'reanti-inflammatory, whereas
omega-6 and omega-9 fatty acidshave the opposite effect.
But again, if you're going togo to surgery to get a hip or a
knee replacement, you must stopthat, as well as any

(40:54):
non-steroidal or turmeric,before you're going to go to
surgery for about a week atleast, because it can cause some
bleeding.
Other things that people havetaken are conjoitan and
glucosamine that have abeneficial effect on cartilage,

(41:16):
whether it's in inflammatorydisorders or degenerative
disorders.
It too can have an effect on amedication, cumidin.
If you're taking it, mostpeople come in and they talk
about having ginger tea, whichhas an anti-inflammatory effect.
I do recommend that.

(41:38):
But in degenerative wear andtear arthritis, the
Scandinavians have shown clearlythat rose hip tea or by mouth
has a beneficial effect onarthritis of the knees and of
the hands.
In addition, in Shrewsbury,massachusetts, a large study

(42:00):
showed that if you take Jell-Oit will help the arthritis of
someone in their knees.
There are a lot of things thatyou can do, but most importantly
to reduce inflammation is watchyour weight, don't smoke and

(42:23):
get down to an ideal weight.
What is the best diet?
The best diet generally is aMediterranean diet.
In people who have aninflammatory disorder that's
very painful, called gout, whichis by a different mechanism of
elevated uric acid.
We usually have people on a lowpurine diet.

(42:45):
In terms of inflammation, wehave changed over the last 30
years the prognosis inrheumatoid arthritis and in most
of the inflammatory autoimmuneconditions by using
disease-modifyinganti-inflammatory drugs and what

(43:06):
we call biologics.
The biologics can affect thebasic cause of the disease.
In rheumatoid arthritis thereare three different mechanisms
that we attack.
One is called tumor necrosisfactor.

(43:28):
That is made in the system tofight and prevent tumors.
But we also note that inrheumatoid arthritis and in most
inflammatory disorders, likepsoriatic arthritis, which about
3 million people in the worldhave and is one of the

(43:51):
differential diagnoses fromrheumatoid disease and is a
non-symmetrical arthritis,whereas rheumatoid arthritis is
usually symmetrical, the majorthings that we attack are
different.
In rheumatoid arthritis we tryand attack tumor necrosis factor

(44:12):
.
We try and attack somethingcalled interleukin 6 and
interleukin 1.
So we have now medications thatwill specifically attack those
pathways and cause people to gointo remission.
Years ago we used aspirin and weused drug called penicillamine

(44:39):
and we used gold and we had verylittle benefit.
Now what I've noticed over mycareer is that we've made such a
great difference in rheumatoidarthritis that we rarely see now
someone who has cripplingdisease, and the reason for that

(45:01):
mainly is when the drugmethotrexate, which was used for
hundreds of years to treattumors and malignancy, was
utilized to treat rheumatoidarthritis once a week by mouth
and if you go into higher doses,subcutaneously by injection,

(45:22):
and that by itself, withoutanything else, has caused one in
three rheumatoids to go intoremission.
When that is not enough, wethen usually add other oral
agents, a drug calledhydroxychloroquine or plaque.
We know that's had a lot ofplay in the literature in COVID,

(45:46):
where it may not play a roleand may not be beneficial, but
in rheumatoid arthritis andespecially lupus, it is
life-saving and has changed thewhole lifestyle of patients with
systemic lupus, and theiraverage age would be up to 55.

(46:06):
Now I have patients with lupuswho are in their 70s 80s and
have had lupus for over 40 yearswith the use of plaque, venal
and methotrexate and otherdisease modifying biologics.
We sometimes use even a drugcalled a sulfidine or

(46:28):
sulfasalazine, which is used inpeople who have inflammatory
bowel disease and in people whohave bladder infections over the
course of years.
In fact, in Europe it was thedrug of choice for many years in
terms of treating rheumatoiddisease, until they too learned

(46:50):
from us here in America thatmethotrexate was the drug of
choice.
I would venture to say that allof our rheumatologists in the
Kale organization and we have alarge experience over 80 years
between the several who are inthe group will all start a

(47:11):
patient with rheumatoid diseaseand most inflammatory arthritis
with methotrexate.
We're not certain how it worksactually, but it may have an
effect on folic acid metabolismof inflammatory cells and
therefore we don't want patientsto become folate deficient,

(47:32):
which is a vitamin B like B12.
So we give them folic acidalong with the methotrexate.
When we have patients who donot respond well enough to
methotrexate, possibly usinghydroxychloroquino and sometimes

(47:57):
using azulfidine, which is atriple therapy which was used
now for about 25 years rathersuccessfully, then we go on to
use biologic.
There are some people, myselfincluded, who use a biologic

(48:21):
much earlier.
There's some evidence that ifyou use methotrexate or a
biologic within the first fewmonths, first 14 to 16 weeks of
rheumatoid arthritis, thatperhaps you stop the T cells.
Remember that we've learnedfrom COVID that there are B

(48:45):
cells.
The body makes two types oflymphocytes that help with
inflammation in a positivemanner and in inflammatory
disorders in a negative manner.
One are called B cells and theother are called T cells or
thymus derived the cells.

(49:06):
If you give medication early inrheumatoid arthritis, you can
prevent the T cell from formingmemory cells and memory
antibodies.
If you prevent the memory cellsfrom developing and you treat a
patient early enough, you maybe able to cure them in a long

(49:28):
run.
Other than that, you can onlyhope to put patients into
remission.
Now that's something that wasunheard of 20 to 30 years ago
when the first biologic came outand we first started using
methotrexate, often together.

(49:50):
The biologics that we use noware multiple, depending on
whether we think someone hastumor necrosis factor as the
primary cause of theirrheumatoid disease, or
interleukin six or interleukinone.
The tumor necrosis factorinhibitors that we know of and

(50:15):
use today the most common one isumira, which is now has
biosimilas, so it's made thecost much, much cheaper and it's
given subcutaneously every twoweeks.
One that I like a great deal iscalled remicade, which is an
intravenous and one of theoldest, so I have a long history

(50:40):
of the side effects of remicadeand umira as well, and you have
more play with that.
In umira you give the same doseto someone who's skinny or
someone who's heavy.
Again, you want to be not heavyIn remicade.
You have the ability to alterthe dose and alter the timeframe

(51:04):
that you give the medication.
This is now that affect theinterleukin six system are drugs
called ectemora and kevzara.
What I'd like to spend a momentand get off rheumatoid disease

(51:25):
is that at age 60, I mentionedthat men are as frequently
involved with rheumatoiddiseases as women because the
restrogen level decreases.
Age 60 and above we findanother condition that has

(51:46):
muscular and joint involvement,called polymyadromatica.
Perhaps we'll have a sessionjust on that, but over 60, it's
just as frequent as rheumatoidarthritis.
One of the things that therheumatologists at the Kale
centers have shown is that wecan now treat polymyadromatica

(52:10):
and we have biologics for that.
Those biologics are the onesthat inhibit interleukin 6.
So when you have someone overage 60, especially if it's a
female, you need to look forpolymyalgia as part of your

(52:32):
differential from rheumatoidarthritis.
It's treated very similarly butnot quite the same.
In addition, you have to makecertain that you're not missing
some other types of arthritisthat are very common.
One would be infectiousarthritis.

(52:55):
I mentioned Lyme disease earlyand we're in the time period
where you have Lyme disease,usually spring, summer and fall.
It's usually done by aspirochete that gives you a bite
that you can't see thespirochete.
It's usually under the armpit,by the groin, by the backside.

(53:18):
Then you get a certain type oferythema, this reddish rash that
clears in the center.
Then you get usually one joint,usually a knee, but it could be
an ankle or a wrist.
Rarely does it cause apolyarthritis like you get in
rheumatoid disease and doesn'tusually affect small joints,

(53:41):
hands and feet, as rheumatoidarthritis does.
But there's also Parvo virus.
Moms will know that andteachers will know that because
it's called fifth diseaseamongst children and it's very
common.
And in children you get a bigred rash on the face and they

(54:01):
can develop arthritis and fever.
In adults you don't get anyrash, you just develop a
polyarthritis and a certainpercentage of those patients go
on to form rheumatoid arthritisand lupus and are treated often
the same.
Why is it important to know andto test for Parvo virus?

(54:25):
Because often it will getbetter by itself with time and
that's very reassuring to apatient.

Robert A. Kayal, MD, FAAOS (54:33):
So I know, dr Zalkowicz, that you
mentioned some of the medicaltherapies for the treatment of
rheumatoid arthritis, but Ithink it's so important for our
viewing audience to understandthe difference between treating
symptoms and actually modifyingthe course of disease in this
medical condition.
Some of the medications thatyou mentioned are called DMARDS,

(54:55):
which are actually diseasemodifying anti-rheumatoid drugs
which actually positively affectthe ultimate outcome for these
patients.
They can actually cause thiscondition to stop progressing
and actually go into remissionand sometimes, as you've

(55:15):
indicated, actually be curativeif you can diagnose them and
treat them early enough.
But disease modifyinganti-rheumatoid drugs such as
methotrexate andhydroxychloroquine also the
biological disease modifyinganti-rheumatoid drugs that
you've mentioned, like Humera,actually have this effect on

(55:37):
these medical conditions, likerheumatoid arthritis and others
that you've mentioned.
There are other treatments forrheumatoid arthritis as well
which do help with the symptomsof arthritis.
We already discussed thatarthritis is associated with a
tremendous amount ofinflammation, and inflammation
is the main culprit here.
In this autoimmune disease, itis in fact our body's immune

(56:01):
system which is attackingourselves.
The immune system is attackingnot only the joints in
rheumatoid arthritis but, aswe've mentioned previously, it's
affecting our organs as wellthe heart, the lungs, the
vascular system and others.
Anti-inflammatory medicationsare very, very helpful in this
condition.

(56:21):
As we've mentioned, some aredisease modifying
anti-inflammatory medications,like the ones we've previously
mentioned, but there are othersthat treat the symptoms but do
not actually modify theprognosis and outcome.
What are some of those otheranti-inflammatories?
Some are over the counter andsome are prescription strength.

Alan Zalkowitz, MD (56:42):
So we do use non-steroidal
anti-inflammatories.
They've been around for manyyears.
Some are over the counter, likeibuprofen and Aleve.
Most of the ones that I use areby prescription.
Interestingly enough, the onethat I use most is a drug called

(57:03):
Celebrex.
It's a sulfur preparation, soyou have to be careful in those
people who are allergic tosulfur.
And the reason that I use that,as I mentioned, it does not
interfere with anyone who is ona blood thinner.
In addition, in a large studyin the Cleveland Clinic

(57:28):
comparing Celebrex to patientswho have heart disease with
ibuprofen and naprason, itshowed less morbidity and less
mortality.
So I use that as my go-to.
For other's.
Dichlofenac or Voltaren isprobably the strongest, although

(57:53):
most rheumatologists would saythat most of the
anti-inflammatory drugs areinterchangeable in terms of
their potency.
I should mention that bothorthopedists and rheumatologists
use a drug like Voltaren,dichlofenac, in a cream form or
anointment form that we apply toa knee, for example, or a joint

(58:18):
that's typically giving moredifficulty.
I would mention again that ifyou're on a blood thinner
especially, you should makecertain that your physician is
knowledgeable enough to knowthat not all nonsteroidals are
the same in terms of causing anincrease of bleeding problem,

(58:40):
and that I do recommend, ifyou're not allergic to sulfur,
that you talk to them aboutusing Celebrex.
We have used nonsteroidalanti-inflammatories for many
years.
They're both by prescriptionand over-the-counter.
I should caution that they'regreat drugs but they have
potential for side effects onkidney and the cardiovascular

(59:02):
system.
So it should be under the careof a physician and you should
have blood work monitored.
We also use steroids.
That's a form of prednisone ormedrol that we use often to
suppress inflammation, either ina pulse we give it for a short

(59:22):
period of time or a longerperiod of time if we need it.
Those are great medications.
They take away the inflammationin their hands and the feet and
the joints of patients withinflammatory disorders.
However, we're trying to getaway from steroidals because

(59:44):
steroidals have an effect inraising the blood pressure,
glaucoma, diabetes andosteoporosis.
Again, if you're oncorticosteroid, that needs to be
under the care of a physicianthat has a lot of experience
with it.

Robert A. Kayal, MD, FAAOS (01:00:02):
Yeah , absolutely.
In my field of orthopedics Idefinitely poo-poo the usage of
steroids as much as possiblebecause we are the ones that see
and appreciate and treat thedreaded complication of steroids
called avascunocrosis, wherethe AVN or avascunocrosis can
deleteriously lead to the deathof the bone in the joint,

(01:00:25):
leading to collapse, arthritisand the need for hip, knee,
shoulder or ankle replacement.
I think it's so important toemphasize once again that, now
that we're talking about joints,when we definitively treat
these patients and treat theirjoints that have been destroyed
by this inflammatory autoimmunecondition, we are not yet done

(01:00:46):
treating the patient.
As opposed to an osteoarthritis, degenerative wear and tear
arthritis, for instance wetalked about hip and knee
arthritis are so common.
When we replace those joints,we've cured essentially that
patient of that arthritis inthat hip or in that knee or in
that shoulder or in that ankle.
That is not the case withinflammatory autoimmune diseases

(01:01:09):
such as rheumatoid arthritis.
These patients may ultimatelystill require a hip replacement,
a knee replacement, a shoulderreplacement or an ankle
replacement, but we're not donetreating that patient.
That patient can still getarthritis or inflammation in
that joint due to the autoimmunecondition because the synovial

(01:01:29):
lining is still there.
If the patient suffers a flareup of their underlying
autoimmune condition, they canstill get inflammation, swelling
and pain in that joint.
Yes, we get rid of most of thepain from the bone-on-bone
erosions that occurred secondaryto the inflammatory arthritis
by doing the hip or knee orshoulder ankle replacement, but

(01:01:51):
we do not get rid of thesynovial lining or tissue and so
they can still get symptoms.
That's why it's incumbent uponus to distinguish between
typical degenerative osteo-wearand tear arthritis from an
autoimmune condition, becausethat patient will more than
likely require a lifelongtreatment by an expert such as

(01:02:13):
Dr Zalkowitz, so that we cancontinue to suppress the
autoimmune condition, so itdoesn't continue to affect other
joints of the body.
Do you agree with that, drZalkowitz?

Alan Zalkowitz, MD (01:02:25):
Yes, I certainly do.
Some of the information hassuggested that about 25% of
patients can get off themedication over a period of time
.
But of those 25%, about half ofthose flare within a year or
two and then when you reapplythe medication, unfortunately it

(01:02:49):
doesn't work as well.
What we try and do is getpatients off two minicross
factor inhibitors or otherinterleukin inhibitors and see
if they still do.
Well, get them off of amethotrexate if we can.
We certainly make an effort toget these patients off of

(01:03:11):
steroids because they're theones that have a long-term
effect, not only in vascularcrosis but in cardiovascular
problems and cataracts and inhealing.
In some patients who arefortunate and able to look like
they're in remission.
That means they have nostiffness, swelling, no joint

(01:03:36):
pain, they have full flexionextension and there's no active
inflammatory process going onclinically and their laboratory
work, namely their sedrate andtheir seroactoprotein, are
normal.
We try and wean these patientsdown or for medication.
We certainly start withcorticosteroids.

(01:03:59):
That means prednisone, medrol.
We try then wean them off ofthat slowly and progressively
and look to see if there's anysign clinically of them
worsening.
Next we try and wean them offtheir two men across his factor
inhibitor, or theirinterleukin-6 or interleukin-1

(01:04:22):
inhibitor, their biologic.
That may be by using a biologiclike umira that's used every
two weeks, going to every threeweeks or every four weeks or
even further, and then whenwe're satisfied there being able
to withstand being off thebiologic, then we will wean down

(01:04:44):
the methotrexate slowly.
This can take a year or so todo.
And when they're offmethotrexate then we try and see
if we can wean them down ormaybe keep them on just some
hydroxychloroquine, perhaps onea day or one every other day,

(01:05:05):
having their eyes looked atevery six months by an
ophthalmologist.
If we're fortunate and we'reable to get some patients off
probably about 25% over thecourse of time, about half of
those a few years later willhave a flare of activity and

(01:05:27):
that flare of activity can bejust as they presented
originally, with swelling oftheir small joints of their
hands and feet and their purpleother joints, and can be
accompanied by stiffness,swelling, pain and difficulty,

(01:05:48):
straightening joints, theirsedraton seroactive protein and
their blood goes up.
And those patients we put backon medication and unfortunately
only about half of those respond.
The other half will havesignificant difficulty and will
be difficult to treat thereafter.
So what a lot of us do is weanoff cortisone that's an absolute

(01:06:13):
and try and wean them offnonsteroidals or they can stay
on a nonsteroidal if theirkidney function is, and blood
pressure, reasonably normal.
We then try and wean them off abiologic.
Those are the.
That's the mainstay.
If we can get by withmethotrexate and possibly

(01:06:33):
hydroxychloroquine and thepatients doing well, we may be
satisfied with that.
If we can get the methotrexatedown to a low dose, so how do
you follow these patients?

Robert A. Kayal, MD, FAAOS (01:06:46):
Dr Zalkowicz, Once you've made the
diagnosis and you began medicaltherapy, what's the typical
follow up for these patients?

Alan Zalkowitz, MD (01:06:53):
So there is the use of prednisone, which I
told you.
We try and get patients off.
But we often use prednisone atthe beginning as what we call
bridge therapy, because it takesmethotrexate several weeks,
platinol several weeks andbiologics several weeks for them
to start to kick in.

(01:07:14):
The prednisone, in very smalldoses, will usually do the trick
.
The patient will feel better.
We'll usually start them onmethotrexate either that first
visit or quite soon, and thenwe'll follow them clinically by
the amount of stiffness theyhave in the morning, by looking
at their joints for swelling,for whether they have any

(01:07:36):
inflammation of the redness or,and we'll look to see what the
sedrate and seroacuprotin theyshould be coming down.
And then we will probably seethem every few weeks at the
beginning and then, when they'rein doing very well or possibly
in remission, probably everyeight to 12 weeks.

(01:07:58):
I have some patients that I nowbeen in remission for several
years that I see every sixmonths to a year and they come
to me from all over the countrybecause I put them into
remission.
So they, I think, feel that ifthey come to me they're going to
stay in remission Even thoughthey have a rheumatologist,

(01:08:19):
either it in Florida or in NorthCarolina or in Connecticut, or
even in South America.

Robert A. Kayal, MD, FAAOS (01:08:28):
And how often do you use combination
therapy?

Alan Zalkowitz, MD (01:08:31):
That's a great question.
I always use combinationtherapy, just like we do in high
blood pressure.
In fact, I think that thepeople who use combination
therapy and high blood pressurelearn from us, the
rheumatologists.
We always have patients onmethotrexate almost always.

(01:08:53):
We often have patients on anantimalarial hydroxychloricin or
plaque when we sometimes havethem on sulfazalazine, which is
a sulfa preparation, and we havethem often if they're CCP
positive or have on an MRI signsof edema or tinoceinavitis on

(01:09:17):
the biologic.
So there are on severalmedications.
Now some of those are on ananasteroidal as well if they're
not on prednisone.
I really ever use ananasteroidal with the prednisone
at the same time because itincreases the risk of an NSAID

(01:09:38):
gastropathy.
That means inflammation of thestomach that can lead to
bleeding and it's silent becauseif you bleed in the stomach the
nerve endings are dulled so itincreases the risk of bleeding
sevenfold.
So rarely ever will I useprednisone or an anasteroidal.
Sometimes I'll be able to getby with an anasteroidal as

(01:10:02):
bridge therapy instead ofprednisone In a mild patient.
Usually you're CCP negative andusually has just some demer or
juctar ticolasty process.

Robert A. Kayal, MD, FAAOS (01:10:16):
Very interesting.
Well, dr Zalkowitz, as you knowand I've mentioned many, many
times I chose to be anorthopedic surgeon because I
appreciate instant gratification, I like fixing things that are
broken and I get that instantreward for the most part.
Thank God there are doctors likeyou who deal regularly with

(01:10:36):
chronic disease, because this is, in fact, a chronic disease,
right, it's not likeosteoarthritis, like I mentioned
, that we can do a hipreplacement or knee replacement
or a meniscus tear and take careof that surgically, where I fix
the problem and the patientgets on with their life.
This patient is your patient forlife and the onus is on you to

(01:10:58):
quarterback the care of thatpatient, told that patient's
hand and manage that patientmedically to keep that patient
remission their entire livesonce that diagnosis has been
made, because this is a chronicdisease that we had already
mentioned is progressive and cango on literally to kill
patients, right?
So it's so important, becauseof the cardiovascular

(01:11:20):
involvement and the involvementof other organs, that this
condition can literally killpatients.
So it's so, so important forthe medical community to
understand this diagnosis, toidentify it and diagnose it
early with treatment and referthe patient to a rheumatologist
like Dr Zolkowitz, so that he orshe can hold their hands their

(01:11:43):
entire lives and keep theircondition at bay, to keep them
healthy and active and live along, vivacious life.
Do you agree with that, drZolkowitz?

Alan Zalkowitz, MD (01:11:52):
Yes, there are just a few caveats.
I'd like to add.
Number one unfortunately we'renot making enough
rheumatologists.
There's usually in most centersa six-month wait for a new
patient to be seen, andgenerally they're seen by a
physician's assistant or nursepractitioner who are

(01:12:13):
knowledgeable but don't have theexperience of well-trained
rheumatologists being inpractice.
Fortunately, when Dr Kale and Idiscussed about joining
rheumatology and orthopedist, heunderstood that these are
lifelong patients that need alot more time because they have

(01:12:34):
a lot more underlying pathologyand develop infection, heart
attacks, a lung involvement,kidney involvement, amyloidosis,
multiple myeloma.
So they're often followed byfive or six other doctors that
we as rheumatologists have tolook at their notes and see how

(01:12:55):
they're doing.
And what's so wonderful aboutbeing a rheumatologist in the
Kale group is we're allowed thetime to deal with these patients
, to help them and to help thedoctors that are treating them
in other fields to know how therheumatoid arthritis or other

(01:13:15):
autoimmune disorders is playinga role in their patient's heart
disease or lung disease orkidney disease or neurological
disease, because we know a lotabout it, probably more than
they do, because we see a lotmore of it in our particular
field.

Robert A. Kayal, MD, FAAOS (01:13:36):
And we're so blessed to have each
other in our practice.
It's a multi-specialty group,it's a collaborative effort with
experts in every field wherewe're caring for these patients,
and I must say this has been avery enlightening discussion.
I've learned so much from youonce again, dr Zalkowitz, and I
appreciate your knowledge,wisdom and expertise.

(01:13:58):
I hope that you have found thisto be very informative and
helpful in your evaluation andmanagement of your patients and
your conditions, and I just wantto take this opportunity to say
how thankful I am that you'repart of our practice caring for
our patients all these years.
It's just a blessing to haveyou, dr Zalkowitz, and I look

(01:14:18):
forward to having you come backin the future so we can talk
about other rheumatologicalconditions, and thank you so
much for your time and wisdomand expertise.

Alan Zalkowitz, MD (01:14:29):
Thank you so much.
And remember at tail, as itsays on the sign, we'll see you
soon.
So if you have arheumatological problem, you're
not going to wait six months orsix weeks.
It's a matter of days beforeone of the various
rheumatologists look at you.
We look at you ourselves.

Robert A. Kayal, MD, FAAOS (01:14:50):
Amen , thank you, thank you.