Round 6 - A Case of Wegener's Granulomatosis - Arthritis Information

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Granulomatosis
Round 6: A Case of Wegeners

Granulomatosis
by John H. Stone, M.D., M.P.H.
Associate Professor, Division of Rheumatology
Johns Hopkins University School of Medicine.
Release Date: July 12, 2006

Expiration Date: July 12, 2008
Dr. Stone has no signi cant nancial interest or relationships to disclose.
For CME credit,TAKE POST-TEST & EVALUATION
In telling this patients story, Im going to take a page from the book of Quentin Tarantino (Director of the
movie Pulp Fiction) book and tell the story in a non-linear fashion. If youve seen Pulp Fiction, youll
recall that the movie started in the middle of the characters story line, proceeded through the end ot the
story line, then went back to the beginning, concluding in an unforgettable scene in which an attempted
robbery had just occurred in a restaurant full of people. The ploy was a very appealing storytelling device,
and also eased the blow of the fact that Vincent Vega, played by John Travolta, was killed in the coursed of
the movie. The moviegoer had an uplifted feeling at the end of the show because, through the non-linear
storytelling device, Vega (Travolta) still sauntered out of the restaurant at the end of the movie. With
https://www.hopkinsarthritis.org/physiciancorner/rheumatologyrounds/rounds6acaseofwegenersgranulomatosis/ 1/14
regard to this presentation today, I am not foreshadowing the death of the patient I am going to tell you
about, although as you will see he has had a couple of close brushes when I thought he might not make it.
Scene 1: Red Eyes

In May, 2003, the patient rst appeared in clinic. (Remember: this being a Pulp Fiction case presentation,
we begin in the middle of his medical story, some time after he had already been diagnosed with his
underlying illness.)
He presented that May with six days of sinus congestion, fever to 102oF, and complaints of aches and pain,
malaise, myalgia. This was de nitely a change from his baseline, as his underlying disease had been stable
then for many months. The patient had a diffuse, erythematous, maculopapular rash. He also had a
creatinine of 3.8 mg/dL, which was up from his baseline creatinine of 2.0 mg/dL. He was admitted promptly
to the hospital.
On hospital day 2, the patient had some nasal crusting on physical examination and his creatinine had risen
even higher, 4.5 mg/dL. He also was noted to have elevations of his hepatic transaminases; they ultimately
peaked several days into his hospitalization at >900 mg/dL. He was neutropenic and thrombocytopenic,
with white blood cell and platelet counts of 3.5 x 109/mm3and 169 x 109/mm3, respectively. Both of these
counts declined somewhat further during his hospitalization. On hospital day 2, he also developed
voluminous, non-bloody diarrhea.
On hospital day 4 there was still no answer to his acute illness. He became progressively short of breath; it
worsened throughout the day. An arterial blood gas showed pO2of 66 and a pCO2of 29. The patient
became tachypneic. A cardiac event of some type was suspected, and assays for cardiac enzymes revealed
a very high CK (1842 U/L; normal < 200 U/L) and a whoppingly high troponin I (>200 mg/mL; normal < 5
mg/mL). An electrocardiogram showed no pattern of acute myocardial injury, but an echocardiogram
performed just prior to transfer to the Cardiac Care Unit showed an ejection fraction of 15%.
Thus, Scene 1 ends, with the underlying diagnosis unrevealed, the cause of his acute presentation
unknown, the etiology of his rapid decompensation in the hospital unclear, and the patient in orid
congestive heart failure.
Scene 2: Holiday Party

The patient traced the start of his underlying illness to a holiday party several years earlier: December,
2001. In fact, the patient blamed the onset of his illness on the candles and perfume that were present at
the party. He had been seized at the party with intense nasal and sinus congestion entirely new for him
which persisted for weeks after the party. Ultimately, his primary care doctor referred him to an
otolaryngologist for evaluation of his persistent upper respiratory complaints. Upon examination of the
patient, the otolaryngologist found brown, bloody nasal crusts.
Slide 10
The otolaryngologist recommended that the patient undergo sinus surgery to correct the problem,
presumably diagnosed as chronic sinusitis of some sort. In preparation for the surgery, the otolaryngologist
ordered a routine pre-operative chest radiograph, which showed a mass. Following discovery of the lung
mass on chest X-ray, the patient underwent a computed tomography scan of the chest (below), leading to
other referrals.
In short, the patient was told that he probably had lung cancer, and that he was needed to have a needle
biopsy to secure the diagnosis and determine the cell type. He underwent a biopsy and, as you are probably
guessing by now, no cancer was revealed. Rather, the biopsy showed a large area of necrosis the
pathologist referred to as geographic necrosis. (shown below)
In the right setting, this nding suggests the diagnosis of Wegeners granulomatosis (WG). There were also
Langerhans giant cells in the tissue, typical of WG, and other parts of the biopsy revealed pulmonary
vasculitis.
Only a few days later, then, the patient had made his way to the Johns Hopkins Vasculitis Center, where we
evaluated him. The immediately striking feature of his appearance was the redness of his eyes
episcleritis.
The eyes were not painful or tender, but they were obviously red. His hands and joints, however, were
painful.
In fact, his joints were so painful that he could not even get up on the examining table without assistance
and once we had nally hoisted him onto the table, he could not get back off. His arthritis resembled that of
a patient with orid, untreated, polyarticular rheumatoid arthritis.
The tips of his ngers were cyanotic because of ischemia, and his ngernails manifested multiple splinter
hemorrhages. Perhaps his worst discomfort, however, was a tongue ulcer that was incredibly painful.
Although oral ulcers are part of the ACR classi cation criteria for WG, but in fact oral ulcers are not usually
a prominent part of the clinical presentation. Finally, the patient had one of my favorite physical
examination ndings in WG (shown below): nodules on the elbows that are not rheumatoid nodules, but
rather cutaneous extravascular necrotizing granulomas, known more commonly as Churg-Strauss
granulomas.
The presence of Churg-Strauss granulomas which may occur over any extensor surface and even within
internal organs (but which are found most often over the olecranon area, precisely where rheumatoid
nodules are found) often leads to the misdiagnosis of rheumatoid arthritis early on in the course of WG.
Even without laboratory data at that point, we realized immediately that the patient needed to be
hospitalized because of the diffuse nature of his condition. We sent directly to the Emergency Room for his
rst dose of methylprednisolone because there was no bed available in the hospital at that moment. In the
Emergency Room when we began to get the results of routine laboratory tests, we discovered that the
patient had 2+ proteinuria, 40-50 red blood cells per high-powered eld, and urinary red blood cell casts.
Fortunately, his serum creatinine was only 1.3 mg/dL. Ultimately, after two days in the hospital, an
immuno uorescence assay for anti-neutrophil cytoplasmic antibodies (ANCA) was found to be positive in a
cytoplasmic (C-ANCA) pattern, with an antibody speci ty for proteinase-3.
There was no question about the diagnosis: the patient had WG, characterized by many classical features
of that disease, positive for the autoantibody strongly correlated with that condition, and proven by lung
biopsy. The only question, given the general approach to therapy today, was whether to give him daily
cyclophosphamide (CYC) administered orally along with his glucocorticoids, or to administer the CYC in an
intermittent, intravenous fashion. On this debate in the medical literature, however, there is no clear
resolution. A trial has been completed in Europe known as CYCLOPS compared oral daily CYC to
intermittent CYC. The regimen of intermittent CYC employed in CYCLOPS was differs somewhat (i.e., is
more intensive) from the National Institutes of Health protocol for intravenous CYC in lupus. The
European investigators gave pulses of CYC every three weeks for six months: a total of 10 pulses during
that time. Preliminary results, still not published in a peer-reviewed manner, purport to indicate that the
intermittent administration of CYC, at least in the regiment employed in CYCLOPS, is more effective and
less toxic than daily CYC. If these results hold up under the scrutiny of peer review, then this study is
extremely important and certainly runs against the grain of accepted remission induction strategies for
WG in the United States, where daily CYC regimens remain the standard. Because the data are not yet all
in on the CYCLOPS study, Im reserving judgment and continue to use daily CYC therapy for the remission
induction in WG. Some evidence admittedly from underpowered studies indicates a higher likelihood of
sustained remission with daily regimens. Moreover, with the use of daily CYC the dose is titratable to the
white blood cell count and therefore conducive to avoiding profound neutropenia.
The patient was treated with pulse methylprednisolone and daily CYC. In addition, because of the very
limited ability of conventional medications to sustain remissions, he was enrolled in an ongoing trial, the
Wegeners Granulomatosis Etanercept Trial (WGET). I will discuss this trial in greater detail later. As it
turned out though we did not know this until the end of the trial the patient was in the etanercept
group. Therefore, his therapy consisted of CYC, glucocorticoids, and etanercept.
During the patients initial hospital stay, he received three doses of methylprednisolone. His serum
creatinine, 1.3 mg/dL on admission, was 1.4 mg/dL at discharge. He felt dramatically better almost
immediately after starting treatment, with essentially complete resolution of his arthritis. My sense was
that we had detected and treated his WG just in time. Five days later in clinic, however, his creatinine was
2.7 mg/dL. I remember telling his wife, It takes a while to turn the train around when it is steaming fast in
the wrong direction. I evaluated the patient again a few days later, by which time the serum creatinine had
risen to 5.1 mg/dL. Quite concerned now, I admitted him to the hospital again for three more doses of
methylprednisolone. Three weeks after his initial hospitalization, his serum creatinine continued to rise
inexorably, to 7.4 mg/dL.
Thus ends Scene 2, with the newly-diagnosed WG patient now in orid renal failure.
Scene 3: The Past Several Years

In this scene, I will take a step outside the story to review some of the recent evidence-based data that
have accumulated in the past few years with regard to the treatment of WG. The discussion will center
around the results of three major clinical trials: 1) CYCAZAREM [CYC versus Azathioprine for the
Maintenance of Remission]; 2) NORAM; and, 3) the Wegeners Granulomatosis Etanercept Trial [WGET].
If one were to take 100 WG patients with this or a similar presentation and treat them according to the
current standard of care, what would be the likelihood of getting them into remission? Among the rst
studies to present controlled data on this point was CYCAZAREM (Jayne et al. N Engl J Med 2003;
346(1):36-44). Although CYCAZAREM was not a blinded study, 143 of the 155 patients (93%) of the
patients in both groups achieved disease remission. All patients in the trial were treated initially with 2
mg/kg of CYC and high doses of glucocorticoids. Upon achievement of remission, the 143 patients were
randomized either to continue CYC for up to 1 year, or to switch to azathioprine (AZA) after 3 to 6 months.
All participants in the trial remained on not less than 10 mg/day of prednisone for the rst year, and then
7.5 mg/day. There was no difference between the two treatment arms in the number of patients who ared
during the period of follow-up, demonstrating that AZA is good as continued CYC for the maintenance of
remission.
The second informative study is known as NORAM (Groot et al. Arthritis & Rheumatism 2005; 52(8):2461-
2469). NORAM was a comparison of CYC with methotrexate (MTX) for early-generalized, ANCA-
associated vasculitis. Of the 95 patients enrolled, 89 had WG; 6 had microscopic polyangiitis. NORAM was
also not a blinded trial, but 90% of the patients in both treatment arms achieved disease remission. The
prednisolone was tapered a little bit faster in this trial than in CYCAZAREM, down to 7.5 mg/day by month
6, and then all after 1 year. In the MTX group, patients were treated with an identical prednisolone tapering
regimen, and both CYC and MTX were tapered off after 10 months.
We can compare these three trials for their steroid regimens and their are rates.
CYCAZAREM NORAM WGET

(n= 144) (n=100) (n=180)
Treatments CYC vs. AZA CYC vs. MTX Etanercept plus standard of care
Blinded No No Yes
Placebo-controlled No No Yes
90% MTX
Remission Rate 93% 91%
94% CYC
7.5 mg
Steroids 6 mos. >10 mg prednisolone Off
Prednisolone
7.5 mg
Steroids 12 mos. Off Off
Prednisolone
70% MTX
Flare Rate 15% 51%
47% CYC
As noted, CYCAZAREM patients stayed on 10 mg prednisolone for the entire rst year (not just 6 months
but the rst year), and then 7.5 mg after that. The are rate in that trial was only 15%. In NORAM, patients
had a faster prednisolone taper off prednisone by 1 year and had a dramatically higher are rate. In the
WGET trial (WGET Research Group, N Engl J Med 2005; 352(4):351-61.), a trial in which prednisone was
tapered to discontinuation after 6 months, 91% of the patients achieved disease remission. Thus, WGET,
which had the most aggressive tapered regimen of steroids, had a 51% are rate. One of the things I would
like you to take away from this talk is that we probably fail to appreciate the immense value of maintenance
glucocorticoids even low doses of prednisone for the maintenance of remission. We put a lot more faith
in steroid-sparing agents employed for the purpose of maintaining disease remissions, e.g., methotrexate
and AZA, than perhaps is warranted. Perhaps even low doses of glucocorticoids would maintain remissions
better.
Back to our patient.His creatinine is now 8.1 mg/dL, and rising on a daily basis. What do we do? Options
included:
Give him more steroids. (He had already gotten six pulses of methyprednisolone)
Give him more CYC. (He was already on a sizeable dose: 125 mg/day)
Perform a kidney biopsy (thinking that maybe he has anti-glomerular basement membrane disease).
Initiate a course of plasmapheresis.
An argument that we sometimes have on the ward is about whether or not plasmapheresis or plasma
exchange is indicated in these situations. There are little data regarding either one of these interventions.
Data from the MEPEX trial (methylprednisolone versus plasma exchange), completed several years ago,
have still not been published in a peer-reviewed format albeit some results have been presented at
subspecialty meetings. Inclusion criteria for MEPEX were a new diagnosis of ANCA-associated vasculitis
and advanced renal dysfunction (serum creatinine of >4 mg/dL). Patients were treated with oral CYC and
glucocorticoids in addition to either 7 plasma exchanges over 14 days, or pulse methylprednisolone, 1-3
doses. The data show no difference in survival between the two treatment arms. Only 52% of patients
were dialysis-free at 12 months perhaps not surprising because they had such advanced renal
dysfunction at the beginning. Between the two groups, 45% of the patients treated with
methylprednisolone were dialysis-free at 1 year compared with 59% of those in the plasma exchange group
at 1 year. Again, this is not statistically signi cant. These data, the most objective to date, do not indicate
any clear advantage to the addition of plasma exchange to standard therapies of CYC and prednisone.
For my patient, we actually decided tolowerthe dose of CYC despite his continued renal worsening, and to
hold off on any other treatments. We hoped that in due time his renal function would begin to improve, just
as the rest of his disease had (the arthritis, tongue ulcer, digital ischemia, for example, were gone, and the
lung lesion rapidly disappearing). The purpose of lowering his CYC dose was to avoid potentially lethal
complications of this treatment as his serum creatinine worsened and his ability to excrete CYC
metabolites declined. The daily CYC dose was lowered to 50 mg, and held there. Approximately six weeks
after starting treatment for his WG, the patient started dialysis on an elective basis.
One day about six weeks later, the patient mentioned to me that his serum creatinine that day at dialysis
had been 4.7 mg/dL. I noted to myself that this was lower than one would expect for a patient on chronic
hemodialysis, and thought perhaps we were seeing the rst sign of a renal recovery. Sure enough, over the
next few weeks the patients renal function improved suf ciently for him to discontinue hemodialysis. His
baseline creatinine settled out at 1.9 mg/dL. After 5 months of CYC, I switched him to AZA. But remember,
we are still in the middle of this course, and there is more to come. Before the next scene, though, I will
review the major results of the WGET.
In the WGET, 180 patients were enrolled, making it the largest prospective study conducted to date in this
disease. Patients were treated with standard of care therapies plus either etanercept or placebo in the
remission maintenance phase. The conventional therapy was tapered off as patients continued the
etanercept or placebo, with the primary outcome being to determine whether etanercept could sustain
remissions better than placebo. As noted, the WGET protocol called for the discontinuation of prednisone
by 6 months. Patients switched from CYC to either MTX or AZA after 3 to 6 months if they had achieved
remission. Patients with limited disease treated with MTX from the start of enrollment and began to taper
this medication after they had been in a sustained remission for 1 year. In both groups, 90% of the patients
achieved disease control or remission. Whether they were newly diagnosed or whether they had pre-
existing disease before trial entry, 90% of them achieved disease remission.
Could we keep them there (in remission) with etanercept? The group did pretty well: about 70% of them
with a 6-month period of no disease activity. Unfortunately, the control group actually did a little bit better,
at least numerically: 75% achieved sustained remissions. Another remarkable point was that, taking both
groups together, only 49% of the patients achieved remissions and maintained them throughout the trial.
There was no difference in are rates between the two groups (66 per 100 patient years vs. 74 for 100
patient years) or in the number of severe ares between the two groups. There were virtually no outcome
measures, in fact, that distinguished the two treatment groups. In terms of adverse events, during 22
months of patient follow-up, 56% of the patients in the etanercept group had an adverse event that was
severe, life-threatening, or fatal. The control group was no different: 57% of the patients in that group had
a severe or life-threatening event or died. Thus, the WGET data indicate that, even using CYC and the
other conventional medications in a more moderate way than the NIH longitudinal protocol did, the
adverse event rate associated with these conventional medications is still quite alarming.
Additional interesting data to emerge from the WGET trial involved venous thrombotic events (VTEs). We
demonstrated that WG patients actually have a much higher incidence of VTEs: deep-vein thromboses and
pulmonary emboli (Merkel, et al. N Engl J Med. 2005; 352(4):330-2). Most of these events in the WG
patients occurred rather early on after their inclusion in the trial, suggesting an association with active
disease. In addition, the VTEs occurred mostly in patients with severe (as opposed to limited) disease the
type of patients with a vasculitic kind of presentation rather than a granulomatous one. This may be
because the vasculitis associated with WG, unlike that of other forms of disease associated with vasculitis,
involves veins as well as arteries. The relative risk for VTE was 7 times higher among the WG patients than
among a comparable group of patients from the Johns Hopkins Lupus Center cohort, a group of patients
we know suffers from a hypercoagulable state. The relative risk in WG was also 23 times higher than that
of healthy Scandinavian males in a population-based study, and 23 times higher than rheumatoid arthritis
patients treated with etanercept. The incidence in WG was approximately equivalent to patients who had
already had one VTE, which predisposes them to others.
With regard to deaths in the WGET trial, there was no difference between groups. One important point,
however, is that not a single one of the 180 patients died of overwhelming WG. All deaths in WGET were
the result of causes not directly related to WG: complications of treatment and events that were perhaps
incidental (e.g., cardiac arrest), but mostly complications of treatment. With regard to malignancy, however,
there was another issue. Six solid malignancies developed in the etanercept group. All etanercept patients
who developed malignancies during the trial also received CYC. In contrast, no solid malignancies occurred
in the control group. There is some biological rationale for believing this might be a real nding, of course,
because the cytokine we targeted speci cally for inhibition in the trial wastumor necrosis factor. Perhaps
it should not be altogether surprising that patients on CYC and a TNF inhibitor might be more at risk for
solid malignancies.
We compared these ndings and the incidence of solid malignancy in the WGET group to the SEER
database. The numbers of events in the WGET were small, of course, but the standardized incidence ratio
for solid malignancy in the WGET group was 3.12 highly statistically signi cant (P = 0.01). We are
preparing to conduct a follow-up study of the WGET cohort now.
Returning to our patient:Three years after getting off dialysis, he was doing beautifully. He had served as
the Best Man in his sons wedding. He and his wife had recently been shopping for retirement properties on
the Eastern shore of Maryland. He had become ANCA negative.
Should ANCA negativity be reassuring for a WG patient in remission? The WGET trial has given us more
data on ANCA. In terms of making the diagnosis, ANCA can be extremely helpful. The presence of ANCA
actually obviates the need for biopsy in some patients now who present with classic disease
manifestations. In the WGET, 96% of the patients with severe disease were ANCA-positive; 83% of those
with limited disease were ANCA-positive.
In terms ofpredictingdisease ares, we now have data through the WGET indicating that ANCA are
useless for this purpose. At entry into the trial, 134 patients were PR3-ANCA-positive. (For the purposes of
this analysis, we excluded the 24 patients who were MPO-ANCA-positive and only evaluated the PR3-
ANCA-positive patients.) Of the 134 patients, 101 (75%) achieved sustained remission, a percentage quite
comparable to the rest of the cohort. And among the 101 who achieved sustained remission, 67 had no
increase in ANCA through the remainder of the trial, with serology checked every 3 months. Yet 30 of
those 67 patients eventually suffered disease relapses during the WGET. Furthermore, 34 of these 101
patients had increases in PR3-ANCA titers, but 18 of those did not relapse; 9 relapsed within 1 year of the
rise in ANCA titer. So, how does one interpret a are 11 months after a rise in ANCA titer? I think it is hard
to point to a true association there. Four relapsed in more than 1 year after the ANCA rise, and there were
3 who ared either right before or concurrently with the rise. Unfortunately, I think the data show that, in
terms of predicting imminent ares, ANCAs are not helpful.
Scene 4: Red Eyes Redux

We return now to the patient going to the CCU in 2003 for congestive heart failure.
He had 6 days of sinus congestion before this presentation, but it was rather mild; not the intense kind of
nasal and sinus problems he had had at the time of his original diagnosis. Then again, maybe we were just
catching him early this time. He did not have arthritis. He had myalgia and malaise. He did not have tongue
lesions or elbow nodules. Chest imaging showed no nodular or cavitary lesions or other types of in ltrate
(his heart failure developed after his hospitalization). He did not have active urine sediment, and his ANCA
was negative. He did have nasal crusting, however, which I concluded was probably due to the effect of dry
hospital air on damaged nasal mucosa rather than active nasal in ammation. He had a striking fever, to
104F. He had a skin rash that really looked more like a viral rash (diffuse, erythemaous, blanching,
maculopapular), and he did not have purpura. He had low platelets and elevated liver function tests. At this
point he was on etanercept and AZA, but he had not had any cytopenias or liver function test abnormalities
before, except at diagnosis (when his liver function tests were elevated). Then, as he became increasing
short of breath during his hospitalization, I became increasingly mysti ed.
The diagnostic serology returned from the lab after the patient had been transferred to the CCU. The
serology was not an ANCA (for the record, the patient was still ANCA negative during this hospitalization),
but rather a serological test for IgM antibodies toEhrlichia chaffeensis. During a trip to the Eastern Shore
to hunt for a retirement property, the patient had been bitten by a tick that transmitted the etiologic agent
of human monocytic ehrlichiosis, shown below.
Further history revealed that his wife had pulled a tick off of herself, but he obviously had missed the tick
that was on him. Outpatient presented in May 2003, exactly when most ehrlichiosis cases are reported
late spring, early summer owing to the life cycle of the tick. Doxycycline is remarkably effective in
treatingEhrlichiosis; one dose completely abolished his fever. Over the next 2 to 3 months, his
cardiomyopathy resolved completely; he had an ejection fraction of 15% to 55% three months later.
SUMMARY POINTS
The great majority of patients with WG achieve at least temporary disease control with currently
available immunosuppressive therapy.
Even the shorter courses of CYC now used for the induction of remission are associated with
substantial treatment-induced morbidity.
Disease relapses are common, whatever the remission used for remission induction. Discontinuation
of glucocorticoids appears to correlate well with disease relapses in many patients.
In the remission maintenance phase, AZA or MTX can generally be used safely as substitutes for the
more toxic CYC.
Etanercept is not effective for the maintenance of remission in patients with WG. Further
investigation of the potential association among TNF inhibition, CYC, and the induction of
malignancy is appropriate.
Although ehrlichiosis may or may not be regarded as an opportunistic infection in the true sense of
the term after all, the infection would not have occurred without a tick bite infection should
always be a leading concern when WG patients present with clinical decompensation.
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Updated: August 10, 2012
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DISEASE INFORMATION NEWS PATIENT CORNER ASK THE EXPERT

PHYSICIAN CORNER OUR RESEARCH ABOUT US

Round 6: A Case of Wegeners

Release Date: July 12, 2006

Dr. Stone has no signi cant nancial interest or relationships to disclose.

For CME credit,TAKE POST-TEST & EVALUATION

Scene 1: Red Eyes

Scene 2: Holiday Party

pathologist referred to as geographic necrosis. (shown below)

Scene 3: The Past Several Years

CYCAZAREM NORAM WGET

Scene 4: Red Eyes Redux

Updated: August 10, 2012

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