واسکولیت

Question 1

در دسته ی Small vessel vasculitis چه بیماری هایی داریم؟

Answer 1

ANCA- associated:
1-GPA
2-MPA
3-EGPA
Granulomatosis with polyangiitis (GPA; previously known as Wegener’s granulomatosis), microscopic polyangiitis (MPA), eosino- philic granulomatosis with polyangiitis (EGPA; previously known as Churg-Strauss syndrome), and renal-limited vasculitis (RLV) affect small and medium-sized blood vessels and may be associated with ANCA

Henoch- schonlein purpura

Question 2

اپیدمیولوژی سنی HSP ?

از لحاظ جنسیت؟

Answer 2

Henoch-Schönlein purpura (HSP) is a small vessel vasculitis that occurs most frequently in young children, with a peak age at onset of 4 to 6 years, but can also occur in adults.

Males are more commonly affected than females (approximately 2:1), and HSP occurs more frequently during the winter and spring months.

Question 3

شایع ترین واکسمولیت در بچه ها؟

Answer 3

HSP accounts for almost half of all cases of childhood vasculitis.

در درجه دوم : کاوازاکی

Question 4

در دسته ی medium vessel vasculitis چه بیماری هایی داریم؟

Answer 4

PAN

Kawasaki disease

Question 5

What is the characteristic feature of PAN?

Answer 5

Polyarteritis nodosa (PAN) is a medium vessel vasculitis that is characterized by arterial aneurysmal and stenotic lesions of muscular arteries, often located at segmental and branch points.

Question 6

فرق PAN و small vessel vasculitis, ؟

Answer 6

In contrast to small vessel vasculitis, renal involvement in PAN is not characterized by glomerulonephritis but rather by aneurysms and stenoses of renal arteries that may result in hypertension or renal dysfunction or both.

In addition, ANCAs are usually negative in PAN.

Question 7

اتیولوژی PAN?

Answer 7

PAN may occur either as a primary vasculitis

or secondary to viral infections, mainly hepatitis B or C, or human immunodeficiency virus (HIV).

Question 8

اپیدمیولوژی کاوزاکی؟

Answer 8

Kawasaki disease is a medium vessel vasculitis most often seen in boys younger than 5 years of age.

It is the second most common vasculitis in childhood after HSP, accounting for about 23% of all childhood vasculitis cases.

Question 9

در دسته ی large vessel vasculitis چه بیماری هایی داریم؟

Answer 9

Giant cell arteritis

Takayasu Or pulseless disease

Question 10

What is the most common form of vasculitis? in adults

در مردا بیشتره یا زنا

Answer 10

Giant cell arteritis (GCA), also known as temporal arteritis, is the most common form of vasculitis in adults.

It is a large vessel vasculitis that typically affects patients of Eastern European descent, with a mean age at onset of 70 to 75 years.

It affects women more commonly than men (3:1).

Question 11

اپیدمیولوژی تاکایاسو؟

در زنا بیشتره یا مردا؟

Answer 11

Takayasu’s arteritis (TAK), or “pulseless disease,” is a rare large ves- sel vasculitis that was initially identified in young women from East Asia but is now described worldwide.

In adults, the female-to-male ratio is about 8:1, with an average age at diagnosis in the mid-20s.

Question 12

کوموربیدیتی شایع در GCA?

Answer 12

About 40% of patients with GCA have the related condition, polymyalgia rheumatica (PMR), which is characterized by subacute onset of aching and stiffness in the muscles of the neck, shoulder girdle, and hip girdle.

However, only 10% to 25% of patients with PMR have or will develop GCA.

Question 13

پاتولوژی GPA & MPA

Answer 13

the pathology of GPA is typically characterized by necrotizing granulomatous inflammation of small blood vessels supplying the upper and lower respiratory tract.

In both GPA and MPA, renal pathology shows a pauci-immune necrotizing crescentic glomerulonephritis.

Question 14

پاتولوژی EPGA

Answer 14

In EGPA, there is a strong association with allergic and atopic disorders, including allergic rhinitis, nasal polyposis, and asthma. Approximately 70% of patients with EGPA have elevated lev- els of immunoglobulin E (IgE) and eosinophilia of peripheral blood and tissue.

Small vessel histopathology typically reveals transmural eosinophilic infiltrates with scattered plasma cells and lymphocytes and extravascular granulomas.

Question 15

پاتولوژی HSP

Answer 15

The pathology of HSP is characterized by a leukocytoclastic vascu- litis of small vessels with IgA deposition seen on immunofluorescence. Various infectious agents, including bacteria and viruses, have been reported as triggers for HSP.

Question 16

پاتولوژی GCA و TAK?

Answer 16

The pathology of GCA and TAK are very similar histologically.
In both, large vessels demonstrate a lymphoplasmacytic inflammatory infiltrate. Giant cells and granulomas may be seen in the media, and lumen-occlusive arteritis may occur from exuberant intimal hyperplasia.

Additional pathologic features include proliferation of vascular smooth muscle cells and fragmentation of the internal elastic lamina.

Question 17

چه علایمی در همه واسمولیت ها مشترکه؟

Answer 17

Fever, weight loss, malaise, anorexia, arthralgias, and myalgias may occur with all vasculitides.

Question 18

علایم شایع GPA؟

Answer 18

GPA most commonly affects the sinuses and upper airway, the lungs, and the kidneys, although almost any organ system may be affected.

Chronic refractory sinusitis, nasal crusting and ulcers, epistaxis, septal perforations, and otitis media are common presenting manifestations.

Chronic nasal cartilaginous inflammation and destruction may lead to the characteristic “saddle nose” deformity.

orbital pseudotumors can also occur from GPA, and they may cause optic nerve compression, proptosis, and/or extraocular muscle palsies.

Question 19

درگیری ریه در GPA و MPA باعث چی میشه؟

Answer 19

Lung involvement in GPA or MPA can include pulmonary nodules (often cavitary in GPA), infiltrates, or diffuse alveolar hemorrhage due to capillaritis. Importantly, life-threatening pulmonary hemorrhage may manifest simply as progressive acute dyspnea with hypoxia or respiratory failure, and not necessarily hemoptysis. Laryngotracheal disease may manifest as hoarseness or subglottic stenosis;

Question 20

درگیری کلیه در GPA MPA

Answer 20

The renal manifestations in GPA, MPA, or RLV are those of nephritic syndrome, including acute renal failure, hematuria, hypertension, and subnephrotic proteinuria.

Urine microscopy may reveal dysmorphic red blood cells.

Renal biopsy reveals pauci-immune necrotizing crescentic glomerulonephritis.

Additional organ manifestations that may occur in either GPA or MPA include neurologic, cutaneous, musculoskeletal, cardiovascular, and constitutional signs and symptoms.

Question 21

سندرم pulmonary renal چیه؟

Answer 21

Patients may have subacute symptoms (weeks to months of sinusitis, arthralgias, and fatigue)

or may exhibit acute “pulmonary-renal syndrome” with rapidly progressive glomerulo- nephritis and life-threatening alveolar hemorrhage with respiratory failure.
در GPA

Question 22

علایم بالینی EPGA?

تفاوت سینوزیتش با GPA?

Answer 22

In EGPA, the clinical features comprise severe asthma, eosino- philia (>1500 cells/mL), and vasculitis involving two or more organs.

Additional organ involvement in EGPA may include the nervous system, kidneys, skin, heart, and gastrointestinal tract.

Sinus involvement in EGPA is typically not destructive as in GPA, and pulmonary infil- trates may be fleeting.

Question 23

روش اصلی تشخیص AAVs,?

Answer 23

The diagnosis of any of the AAVs is most frequently established by tissue biopsy (e.g., kidney, lung, skin, sinus, nerve).

Question 24

چه زمبنی برای مریضی که شک داریم ب واسکولیت تست ANCA انجام میدیم؟ 2

Answer 24

ANCA testing plays an important diagnostic role in suspected small vessel vasculitis and is helpful in differentiating between GPA and MPA.

Almost 90% of patients with renal disease have positive ANCA on testing.

Most GPA patients have the cytoplasmic (cANCA) antiproteinase 3 (anti-PR3) type,

whereas most MPA patients have the perinuclear (pANCA) antimyeloperoxidase (anti-MPO) type.

Question 25

اختصاصیت مثبت شدن ANCA برای تشخیص ولکسمولیت ها چقدره؟

Answer 25

زیاد نیس چون در ایناهم مثبته :

The differential diagnosis for positive ANCA testing includes:
1- drug-induced effects,
2-infections,
3-and other autoimmune conditions.

Question 26

روش افتراق بین AAV & EGPA?

Answer 26

EGPA can be distinguished from other AAVs on the basis of a prior history of adult-onset asthma or allergic rhinitis and blood or tissue eosinophilia.

Question 27

Ddx of small vessel vasculitis? 6

Answer 27

The differential diagnosis for any small vessel vasculitis includes;
1- infection,
2-disorders of coagulation,
3-drug toxicity,
4-atherosclerotic and embolic disease,
5-malignancy,
6-and secondary vasculitides associated with other autoimmune diseases.

Question 28

علایم تیپیکال HSP? 4

سایع ترین علامت کلیوی؟

Answer 28

Patients with HSP have lower extremity purpura,
arthritis (typically of the large joints),
abdominal pain,
and renal disease at presentation

🔸In children, arthritis and abdominal pain affect about 75% of patients; the gastrointestinal manifestations may precede the purpura by up to 2 weeks and include hematochezia.

🔸 The most common renal manifestation is microscopic hematuria with or without proteinuria.

Question 29

روش تشخیص HSp?

Answer 29

The diagnosis of HSP is most often based on clinical and laboratory evidence, although skin or renal biopsy revealing IgA deposition may be helpful in solidifying the diagnosis.

By classification criteria from the EULAR,

Question 30

کرایتریای تشحیص HSP?

Answer 30

patients with HSP must have purpura or petechiae with lower limb predominance and at least one of the following:

1-arthritis or arthralgias
2-abdominal pain
3-histopathology demonstrating IgA deposition
4-and renal involvement

Question 31

Ddx of HSP?

Answer 31

The differential for HSP includes :

1-other causes of abdominal pain

2-other causes of purpura in childhood

3-and hypersensitivity vasculitis

Question 32

What is hypersensitivity vasculitis?
اتیولوژی؟
علایم تیپیکش؟
درمان؟

Answer 32

Hypersensitivity vasculitis is also a small vessel vasculitis that may occur in both children and adults and may be idiopathic or triggered by infections or drug exposures.

It typically manifests as an isolated cutaneous leukocytoclastic (neutrophils and neutrophil debris in small vessels) vasculitis that is self-limited with treatment of the underlying cause (e.g., treatment of infection, discontinuation of drug culprit).

Question 33

علایم شایع PAN?

کدوم سه ارگان به طوز شایع درگیر میشن؟

Answer 33

The most common organ systems affected in PAN are the gastroin- testinal, renal, and nervous systems.

🍋Mesenteric aneurysms or stenoses resulting in gut ischemia lead to symptoms of abdominal pain or “intestinal angina” (pain after eating).

🍋Renal artery aneurysms or stenoses result in hypertension or renal dysfunction, rather than glomerulonephritis as in MPA.

🍋Neurologic involvement may manifest as mononeuritis multiplex (painful asymmetrical sensory and motor peripheral neuropathy involving at least two separate nerve areas).

🍋Orchitis may be seen, manifesting as acute testicular pain.

🍋Anemia, elevated ESR or CRP or both, and hypertension (if renal artery involvement is present) are common.

🍋As in all vasculitides, constitutional symptoms may also be present.

Question 34

روش تشخیص PAN?

Answer 34

The diagnosis of PAN is made based on angiographic or biopsy findings in the appropriate clinical setting.

🍒ANCAs typically are absent in PAN.

🍒A work-up for infection, including tests for hepatitis B and C and HIV, is warranted, given their known associations with PAN.

Question 35

Ddx of PAN?

Answer 35

The differential diagnosis includes :

1-MPA

2-and mixed cryoglobulinemic vasculitis (defined by the presence of cryoglobulins in the blood).

The latter vasculitis shares many clinical features with PAN, including
peripheral neuropathy, arthralgias, myalgias, purpura, and association with hepatitis C.

Question 36

علایم کاوازاکی؟

Answer 36

The clinical presentation of Kawasaki disease includes :
1-fever lasting longer than 5 days,
2-conjunctival injection,
3-oropharyngeal changes (straw- berry tongue, mucous membrane desquamation),

4-peripheral extremity changes (cutaneous desquamation),

5-polymorphous rash,

6-and cervical lymphadenopathy.

Arthralgias, abdominal pain, hepatitis, aseptic meningitis, and uveitis have also been reported.

Question 37

کاوازاکی چه کامپلیکیشن های قلبی ای ایجاد میکنه؟
با چه فاصله ای بعد شروع بیماری ایجاد میشه؟
روش تشخیص؟

Answer 37

Coronary artery aneurysms, one of the most serious complications of this vasculitis, appear within the first 4 weeks after onset of disease and are often detectable with echocardiography.

Although areas of ectasia and small aneurysms may regress, larger aneurysms often persist and can result in coronary ischemia at any time after development, even into adulthood.

Question 38

۳ فاز بیماری کاواساکی؟

Answer 38

Kawasaki disease is a triphasic disease consisting of :

1-an acute febrile period lasting up to 14 days

2-a subacute phase of 2 to 4 weeks

3- and a convalescent phase that can last months to years.

In the acute phase, the fever is persistent and high (>38.5° C) and is minimally responsive to antipyretics.

Question 39

Ddx of kawasaki? 5

Answer 39

The differential diagnosis is wide and includes :

1-viral infections

2- toxin-mediated illnesses (e.g., toxic shock syndrome, scarlet fever)

3-systemic juvenile idiopathic arthritis

4-hypersensitivity reactions

5-and drug reactions (e.g., Stevens-Johnson syndrome).

Question 40

علایم GCA?

Answer 40

Giant Cell Arteritis or Temporal Arteritis
At presentation, patients with GCA most commonly have :
1-new continuous headache
2-jaw claudication
3-visual disturbances (e.g., amaurosis fugax, diplopia)
4-fatigue
5-and arthralgias

Disease onset may be insidious or acute. Blindness due to anterior ischemic optic neuropathy occurs in 10% to 15% of patients with GCA and can occur at disease onset.

Question 41

یافته های P/E در GCA?

Answer 41

They are usually older than 50 years of age, have :
1-tender or thickened temporal arteries
2-and have an elevated erythrocyte sedimentation rate (>50 mm/hr by the Westergren method).

Question 42

روش تشخیص GCA?

Answer 42

The diagnosis of GCA is often made by a biopsy of the superficial temporal artery.

It is important to obtain a sufficient length of tissue (2 to 3 cm) because the vasculitis can have “skip lesions.”

Question 43

تشخیص افترافی مهم GCA که نیاز بع مانیتورینگ ویژه داره چیه؟

Answer 43

Given the association between GCA and PMR, patients with PMR should be educated regarding signs and symptoms of GCA, and patients with GCA should be monitored for symptoms of PMR.

Question 44

علام تیپیکال TAK?

11

Answer 44

The typical clinical manifestations of TAK include a :
1-systolic blood pressure difference of greater than 10 mm Hg between the arms

2-decreased brachial or radial artery pulses,

3-bruits auscultated over the subclavian arteries or aorta,

4-claudication of extremities,

5-neck or jaw pain

6-headache
7-dizziness
8-hypertension
9-constitutional symptoms
10-arthralgias
11-and myalgias.

Question 45

روش تشخیص TAK?

Answer 45

The diagnosis of TAK is often based on vascular imaging studies that demonstrate long, tapering stenotic lesions or aneurysmal lesions in the aorta and primary branches.

Vascular imaging studies including computed tomographic angiography and magnetic resonance angiography are typically performed for both diagnosis and disease surveillance.

Question 46

Ddx of TAK? 5

Answer 46

The differential diagnosis includes:
1- syphilis
2-spondyloarthropathies
3- rheumatoid arthritis
4-inflammatory bowel disease
5-and connective tissue disorders.

Question 47

درمان دارویی ANCA asdociated vasculitis?

Answer 47

Glucocorticoids, often with other agents, are uniformly used to induce and maintain remission in AAV. They are typically initiated at a prednisone equivalent dose of 1 mg/kg/day with or without pulse methylprednisolone (1 g IV daily × 3 days), followed by a gradual taper over approximately 6 to 12 months.

In addition, the standard of care in both GPA and MPA has traditionally been cyclophosphamide, either oral or intravenous, for 3 to 6 months. This yields remission rates vary- ing from 30% to 93% in GPA and from 75% to 89% in MPA.

Rituximab, an anti-CD20 chimeric monoclonal antibody that depletes B cells, was shown to be noninferior to cyclophosphamide in remission induction for AAV in several randomized controlled trials (RITUXVAS and RAVE trials).

Question 48

اندیکاسیون پلاسما فرز در AAV?

Answer 48

Plasmapheresis, or plasma exchange therapy (PLEX), is often used in combination with remission induction therapy in patients with life-threatening disease such as

1- alveolar hemorrhage,

2- or rapidly progressive glomerulonephritis (pulmonary-renal syndrome)

Question 49

در درمان RPGN ناشی ار AAV ،پلاسما فرز موثر تره یا متیل پردنیزولون های دوز؟

Answer 49

PLEX was shown to be superior to methylprednisolone in reducing the number of patients remaining dependent on dialysis.

Question 50

درمان severe AAV?

Answer 50

adjunctive PLEX and two oral glucocorticoid regimens

Question 51

درمانGPA early and limited?

بعد از شروع درمان، برای جلوگیری از عود چی میدیم؟

Answer 51

For limited (early) GPA, such as disease confined to the upper respiratory tract, methotrexate may be used for remission induction, rather than cyclophosphamide; this conclusion was supported by evidence in the NORAM trial.

Trimethoprim-sulfamethoxazole was shown in two randomized controlled trials to be helpful in preventing relapses after remission induction in GPA.

Question 52

درمان EPGA?

Answer 52

For EGPA, mepolizumab, an anti–interleukin-5 monoclonal anti- body, has recently been shown in a multicenter double-blind place- bo-controlled trial to be superior to placebo in producing a higher proportion of patients in remission and longer duration of remission in those who were relapsing or refractory to standard therapy. Only 47% of those in the mepolizumab group relapsed, compared to 81% of those in the placebo group, over 52 weeks. Hence, mepolizumab is now being used as a steroid-sparing therapy in EGPA patients who are relapsing or refractory to standard therapy.

Question 53

What are maintenance therapy in AAV?

Answer 53

Remission maintenance therapies in AAV include :
1-methotrexate, 
2-azathioprine, 
3-mycophenolate mofetil, 
4-and rituximab (RTX).

Question 54

چرا از سیکلوفسفامبد در remission maintenance in AAV. استفاده نمیشه؟

Answer 54

Because there are known risks of bladder cancer, hemorrhagic cystitis, and bone marrow suppression with cumulative use of cyclophosphamide, it no longer has a role in remission maintenance in AAV.

Question 55

درمان HSP?
خفیف؟
خطرناک و همراه با رنال فیلر؟

Answer 55

In mild cases, the therapy for HSP is simply supportive care (i.e., hydration and analgesics).

However, glucocorticoids are commonly used to hasten the resolution of symptoms; early use of glucocorticoids has been associated with improved outcomes, especially when there is severe gastrointestinal involvement.

In life-threatening cases and in severe acute renal failure, additional immunosuppressive agents or plasmapheresis may be considered.

The prognosis of HSP is generally good, with fewer than 1% of patients developing end-stage renal disease.

Question 56

درمان PAN?
اگر شدید بود و عود میکردد؟
چه عواملی پروگنوز رو بد میکنن؟

Answer 56

Treatment of PAN includes

1-glucocorticoids
2-or nonsteroidal anti-inflammatory drugs (NSAIDs) or both.

🍕If disease is severe and persistent or relapsing, additional limmunosuppressive agents are used, such as cyclophosphamide (especially for gastrointestinal or cardiac involvement), methotrexate, colchicine, or intravenous immunoglobulin (IVIG).

🍕Prognosis is typically worse with more systemic complications such as renal or neurologic involvement.

Question 57

درمان PANای که همراه با هپاتیت بی یا سی؟

Answer 57

In cases of PAN associated with hepatitis B or C, antiviral therapy is required not only for attaining control of the viral infection but also for treatment of the associated vasculitis itself.

🍓Corticosteroids and cyclophosphamide have improved patient outcomes, and the 1-year survival rate is now 85%.

Question 58

درمان kawasaki?

Answer 58

Treatment of Kawasaki disease includes :
🍊high-dose aspirin (30 to 100 mg/kg/day) for the first 48 hours,
then 3 to 5 mg/kg/day.

🍊IVIG is standard therapy and has significantly decreased the incidence of coronary artery aneurysm complications in this disease. The initial IVIG dose is 2 g/kg within the first 10 days after presentation, with at least one repeat dose typically given if the first IVIG dose fails to improve the child’s condition.

Question 59

پروگنوز kawasaki?

Answer 59

The prognosis of Kawasaki disease, if promptly treated, is good; however, approximately 15% to 25% of patients develop coronary artery aneurysms that increase morbidity and mortality.

Question 60

درمان GCA?

Answer 60

Glucocorticoids are the cornerstone of therapy in GCA.

Most patients require a glucocorticoid treatment duration of 1 to 2 years, but it may be longer, especially in those with symptoms of PMR.
In PMR without GCA, lower doses of glucocorticoids (10 to 20 mg/day of prednisone equivalent) are effective and provide prompt clinical response.

Question 61

چجوری میشه ار کوری در GCA جلوگبری کرد؟

با چه دوزی؟

Answer 61

To prevent vision loss, treatment should be instituted immediately (within 24 hours) if clinical suspicion for GCA is high or if visual disturbances are present.

The initial dose of glucocorticoids is typically 1 mg/kg/day with a gradual taper.

Question 62

در بیماری با GCA ، بعد از تیپر کردن کورتون بیماری عود کرده. چه میکنیم؟ ۳

Answer 62

If patients experience relapse with glucocorticoid tapering, other immunosuppressive agents may be used.

🌸Methotrexate was shown in a meta-analysis of three randomized controlled trials to be a beneficial adjunctive agent in reducing risks of first and second relapses in GCA, with a significant decrease in the cumulative dose of glucocorticoids.

🌸Low-dose aspirin is an important adjunctive therapy in protecting against cranial ischemic events (level II evidence from two large retro- spective studies).

🌸 tocilizumab given subcutaneously weekly or every other week with a 26-week prednisone taper result in more sustained glucocorticoid-free remission compared to either 26-week or 52-week prednisone tapering courses plus placebo. Hence, tocilizumab is now being used as an effective steroid-sparing agent to maintain remission in GCA.

Question 63

درمان TAK?

دوز اولیه ؟

Answer 63

Glucocorticoids are also the
cornerstone of therapy for TAK;

they are typically initiated at a dose of 0.5 to 1 mg/kg/day.

Question 64

اگر TAk بعد ار تیپر کردن کورتون عود کرد چی میدیم؟

شباهت و تفاوت این مرحله با GCA?

Answer 64

Although most patients respond to the initial dose, relapses occur in more than 50% of patients during glucocorticoid tapering. Hence, steroid-sparing agents are often used to aid in maintaining disease remission.

🍀The most commonly used steroid-sparing agents are methotrexate and azathioprine.

🍀In TAK, unlike in GCA and PMR, the tumor necrosis factor (TNF) inhibitors have shown promise in treating refractory disease.

🍀As in GCA, low-dose aspirin is believed to play a beneficial adjunctive role in preventing ischemic complications.

Question 65

دربیماران تاکایاسو چه زمانی Revascularisation اندیکاسیون ذاره؟ 6

Answer 65

Revascularization interventions are often indicated in patients with TAK whose presenting symptoms include:
1- cerebrovascular disease,
2-coronary artery disease,
3-moderate to severe aortic regurgitation,
4-reno-vascular hypertension,
5-progressive limb claudication,
6-or progressive aneurysm enlargement.

Elective intervention should be performed when the disease is quiescent.

Question 66

پروگنوز و وضعیت عود در TAK & GCA?

Answer 66

🔥In both GCA and TAK, aortitis—a common manifestation of large vessel involvement—can lead to an increased risk of aortic aneurysm and subsequent dissection and rupture.

🔥In both GCA and TAK, disease flares occur in most patients, rendering them chronic, progressive, and relapsing conditions.

Question 67

در بیماری که براش کورتون گذاشتیم چه پروفیلاکسی هایی بزای عفونت باید بذاریم؟

Answer 67

Patients receiving combination therapy with moderate- to high-dose glucocorticoid (>20 mg/day of prednisone equivalents) and another immunosuppressive agent should also receive prophylaxis for Pneumocystis jirovecii pneumonia (previously known as PCP).

Question 68

در بیماری که براش کورتون گذاشتیم اگر دچاز عفونت شد چه‌ میکنیم؟

Answer 68

infections can often mimic or result in flares of systemic vasculitis.

🔺Glucocorticoid therapy should never be discontinued abruptly, even in the setting of infection, because of the risk of adrenal crisis or disease relapse or both.

In most cases, other immunosuppressive agents should be discontinued if infection is suspected or diagnosed.

Question 69

در بیماری که براش کورتون گذاشتیم برای پیشگیری از استئوپروزش چه میکنیم؟

Answer 69

Because significant bone loss can occur even within the first 6 months of therapy, calcium and vitamin D supplementation should be initiated, and a baseline bone density study should be obtained.

Question 70

به جز استیوپروز و عفونت کورتون چه عوارض دیگه ای دارند ک باید درنظر بگیریمشون؟

Answer 70

Consideration should be given to additional bone protection therapies (e.g., bisphosphonates). Methotrexate and cyclophosphamide are teratogenic, and cyclophosphamide may result in premature ovarian failure. These factors must be consid- ered when choosing therapies for women of child-bearing age. Immunosuppressive agents also can be associated with bone marrow suppression and with additional long-term risks such as malignancy.