Leukocytoclastic Vasculitis

Updated: Sep 21, 2022
Author: A Brooke W Eastham, MD; Chief Editor: Herbert S Diamond, MD 


Practice Essentials

Leukocytoclastic vasculitis (LCV), also known as hypersensitivity vasculitis and hypersensitivity angiitis, is a histopathologic term commonly used to denote a small-vessel vasculitis (see the image below).[1, 2] Histologically, LCV is characterized by leukocytoclasis, which refers to vascular damage caused by nuclear debris from infiltrating neutrophils. LCV classically presents as palpable purpura. Less common clinical findings include urticarial plaques, vesicles, bullae, and pustules.

Histopathology of leukocytoclastic vasculitis. Histopathology of leukocytoclastic vasculitis.

LCV may be secondary to medications, underlying infection, collagen-vascular disorders, or malignancy.[3] Cases of LCV have been reported following COVID-19 vaccination.[4, 5] However, approximately half of cases are idiopathic.[6, 7]

LCV may be localized to the skin or may be associated with systemic involvement.[8] Internal disease most often manifests in the joints, the gastrointestinal (GI) tract, and the kidneys.

In the absence of internal involvement, the prognosis is excellent, with the majority of cases resolving within weeks to months. Approximately 10% of patients will have chronic or recurrent disease.[9]

LCV may be acute or chronic. Patients with chronic disease may experience persistent lesions or intermittent recurrence. Cases that primarily involve the skin should be treated with nontoxic modalities whenever possible, avoiding the use of systemic corticosteroids and immunosuppressive agents.

Henoch-Schönlein purpura (HSP), a specific subtype of LCV warranting separate discussion, is characterized by predominant IgA-mediated vessel injury.[10] The classic clinical findings of palpable purpura in HSP are often preceded by viral respiratory illness. HSP is more common in children, but can also occur in adults. Children may develop systemic disease with GI, joint, and/or kidney involvement. In adults, arthritis and kidney disease occur more frequently.[11] HSP in adults, especially older men, may be associated with malignancy.[12]

For additional information on HSP, see Henoch-Schönlein purpura.

For additional information on cutaneous manifestations of leukocytoclastic vasculitis, see Hypersensitivity Vasculitis (Leukocytoclastic Vasculitis).


Immune complex deposition, with resultant neutrophil chemotaxis and release of proteolytic enzymes and free oxygen radicals, is a key component in the pathophysiology of LCV.[13, 14] In addition, other autoantibodies, such as antineutrophil cytoplasmic antibody (ANCA); inflammatory mediators, including tumor necrosis factor alpha; and enhanced expression of vascular adhesion molecules may play a role.[15] However, the exact mechanisms remain unknown.


Between one third and one half of LCV cases are idiopathic. The remainder have various identifiable causes, including drugs; infections; food or food additives; and collagen-vascular diseases, malignancies, and other diseases.

The most common drugs that cause LCV are antibiotics, particularly beta-lactam drugs, nonsteroidal anti-inflammatory drugs, and diuretics. However, almost all drugs are potential causes. Foreign proteins such as streptokinase, those found in vaccines,[16]  and those used in monoclonal antibody therapy can be associated with a serum sickness syndrome with LCV.

LCV has been reported in users of cocaine adulterated with levamisole, a veterinary anthelminthic drug that was withdrawn from human use because of adverse effects including vasculitis but is found in as much as 70% of cocaine in the United States.[17]  Although most cases of levamisole-induced LCV are associated with high titers of antineutrophil cytoplasmic antibodies (ANCA), ANCA-negative vasculitis also occurs in levamisole-adulterated cocaine.[18]  

Infections that may be associated with vasculitis include the following:

  • Upper respiratory tract infections, particularly with beta-hemolytic streptococci, and viral hepatitis are implicated most often
  • HIV infection is also associated with some cases of LCV; in addtion, LCV has been posited as an immune reconstitution inflammatory syndrome (IRIS) related to antiretroviral treatment for HIV infection [19]
  • Leukocytoclastic vasculitis may be seen with  bacterial endocarditis
  • Hepatitis C is a commonly recognized cause of LCV, likely through the presence of cryoglobulins. [20]

When LCV develops in a patient who has received pharmacologic treatment for an infection (eg, antibiotics for an upper respiratory tract infection), determining whether the infection or the drug is responsible for the LCV may be impossible.

Collagen-vascular diseases account for 10-15% of LCV cases. In particular, rheumatoid arthritis, Sjögren syndrome, and systemic lupus erythematosus may have an associated vasculitis. In many cases, the presence of vasculitis denotes active disease.

Inflammatory bowel disease, ulcerative colitis, and Crohn disease[21]  may be associated with LCV.

Leukocytoclastic vasculitis may be associated with underlying malignancy and may behave as a paraneoplastic syndrome.[22]  Lymphoproliferative diseases, such as monoclonal gammopathy of undetermined significance,[23]  multiple myeloma, and hairy cell leukemia, may be more common culprits. However, any type of tumor at any site may be related to LCV.

A study analyzing 421 adult cases of LCV found that 16 patients (3.8%) had an underlying malignancy, including nine hematologic malignancies and seven solid-organ malignancies. The most common presenting sign was palpable purpura, which preceded the diagnosis of malignancy by an average of 17 days. Paraneoplastic LCV was found more commonly in older patients with constitutional symptoms and in those with anemia and immature cells on peripheral smears.[9]

Effective treatment of the malignancy has led to an apparent cure of the vasculitis in some patients.

Cutaneous vasculitis may be part of a larger-vessel vasculitis such as the following[24] :



United States

The incidence of leukocytoclastic vasculitis is unknown, but the disorder is presumed to be uncommon.


Several studies on leukocytoclastic vasculitis have been conducted in Spain.[25, 26, 27] Hypersensitivity vasculitis (see first image below) occurs in 10-30 persons per million persons per year. Fourteen cases of Henoch-Schönlein purpura (see second image below) per million persons per year have been reported.

Hypersensitivity vasculitis. Hypersensitivity vasculitis.
Henoch-Schönlein purpura. Henoch-Schönlein purpura.

Race-, sex-, and age-related differences in incidence

Leukocytoclastic vasculitis is reported more often in whites than in other races.

Leukocytoclastic vasculitis affects men and women in approximately equal proportions. Some studies from Spain suggest that LCV may be slightly more common in men than in women.

Leukocytoclastic vasculitis may occur at any age. Henoch-Schönlein purpura is more common in children under 10 years of age.


The prognosis in patients with cutaneous vasculitis depends on the underlying syndrome or the presence of end-organ dysfunction.[28]  Patients with disease that primarily affects the skin, joints, or both have a good prognosis.[29]  If the kidneys, GI tract, lungs, heart, or central nervous system are involved, morbidity may increase and mortality can occur.

Patients with granulomatosis with polyangiitis (formerly known as Wegener granulomatosis), polyarteritis nodosa, eosinophilic granulomatosis with polyangiitis (formerly known as Churg-Strauss syndrome), or severe necrotizing vasculitis have potentially fatal disease. Treatment with corticosteroids and/or immunosuppressive or cytotoxic agents is often lifesaving.

Cutaneous lesions of LCV are often asymptomatic, but may be associated with pruritus or pain.

Bullous lesions, as well as chronic cutaneous disease, may involve ulceration or painful episodes of purpura, which may cause physical limitations.




Patients with leukocytoclastic vasculitis (LCV) may experience itching, burning, or pain, or they may have asymptomatic lesions. See the image below.

Erythema elevatum diutinum, a rare cutaneous vascu Erythema elevatum diutinum, a rare cutaneous vasculitis.

Leukoctyoclastic vasculitis may manifest as a cutaneous eruption only, or it may occur in conjunction with any of the following:

  • Collagen-vascular disorders
  • Paraproteinemia
  • Certain foods
  • Oral or parenteral medications
  • Infections
  • Malignancy

A thorough history with complete review of systems should be obtained, with specific evaluation for the following:

  • Preceding fever
  • Arthralgias
  • Arthritis
  • Myalgias
  • Abdominal pain
  • Diarrhea
  • Melena
  • Hematochezia
  • Cough
  • Hemoptysis
  • Sinusitis
  • Parasthesias
  • Weakness
  • Hematuria

Additional questions should be asked regarding new prescription, over-the-counter, and herbal medications, as well as dose changes in pre-existing medications. Consideration should also be given for an underlying disorder, such as collagen vascular disease, including rheumatoid arthritis, systemic and cutaneous lupus erythematosus, and Sjögren syndrome, hepatitis, inflammatory bowel disease, and history of blood transfusion. A thorough social history should be obtained regarding recent travel, new environmental exposures, and illicit drug use.


The most common manifestation of leukocytoclastic vasculitis (LCV) is palpable purpura, but other manifestations may develop. Features of palpable purpura in LCV are as follows:

  • Lesions are usually round and 1-3 mm
  • They may coalesce to form plaques; in some instances, they may form bullae and ulcerate
  • Palpable purpura is most common on dependent areas, such as the lower legs; areas of tight-fitting clothing; and areas of trauma (Koebner phenomenon [30] ); however, any surface can be involved
  • In some cases, the purpuric lesions are barely palpable

Urticarial lesions may develop in some patients with LCV. In rare cases, this type of lesion predates the purpuric lesions.

The urticarial lesions associated with LCV differ from those of classic urticaria. The following three characteristics of these lesions, although not always present in every patient, are typical of urticarial vasculitis:

  • Longer duration (often >24 h)
  • Residual pigmentation or ecchymosis after resolution (see the image below)
  • Patients experience more burning than itching


    Urticarial vasculitis. Lesions differ from routine Urticarial vasculitis. Lesions differ from routine urticaria (hives) in that they last longer (often >24 h), are less pruritic, and often resolve with a bruise or residual pigmentation.

To determine the duration of individual lesions, the examiner may encircle several lesions and ask the patient to periodically observe them and note when they resolve or move to another site.

Patients with hypocomplementemic urticarial vasculitis syndrome may develop arthritis, chronic obstructive pulmonary disease, uveitis, episcleritis, and glomerulonephritis. Consequently, careful examination of the joints, heart, lungs, eyes, and kidneys is warranted.

Other distinguishing features are as follows:

  • Livedo reticularis or racemosa are rarely manifestations of small-vessel vasculitis; these are more common in patients with occlusive or inflammatory disease of medium-sized vessels

  • Nodular lesions may develop in some patients with small-vessel vasculitis, although these are more common in patients with medium-vessel vasculitis

  • Ulceration is more common in vasculitis that affects larger vessels, but it may complicate intense LCV and is often referred to as bullous LCV

  • A careful physical examination is warranted in patients with vasculitis and should include specific observation of the cardiopulmonary, musculoskeletal, and gastrointestinal systems

  • Retiform purpura has been described by Piette and Stone and has been linked to immunoglobulin A (IgA)–associated disease[31]



Diagnostic Considerations

Other problems to consider in the differential diagnosis of leukocytoclastic vasculitis include the following:

  • Hypersensitivity vasculitis[32]

  • Hypocomplementemic urticarial vasculitis syndrome[33, 34]

  • Polyangiitis overlap syndrome

  • Thrombocytopenia

  • Urticarial vasculitis[35]

Differential Diagnoses



Laboratory Studies

The evaluation of a patient with leukocytoclastic vasculitis (LCV) serves two purposes. The first is determining the presence of systemic disease. The second is identifying an associated disorder, which can provide prognostic information.[36]

Although no standard protocol has been established, testing in all adult patients with LCV should include the following:

  • Complete blood cell count
  • Erythrocyte sedimentation rate or C-reactive protein level
  • Urinalysis
  • Blood chemistry panel, with careful assessment of kidney function

Serologic studies, such as antinuclear antibody, ANCA (cytoplasmic ANCA [cANCA], perinuclear ANCA [pANCA], atypical ANCA), and rheumatoid factor, should be obtained in patients without an obvious cause of their disease. One study has linked IgA-type antiphospholipid antibodies with Henoch-Schönlein purpura in adult patients.[37]

In patients with suspected systemic lupus erythematosus or urticarial vasculitis, complement levels should be obtained, including total hemolytic complement (CH100 or CH50), C3 levels, and C4 levels. Patients with hypocomplementemic urticarial vasculitis syndrome, and less commonly in those with systemic lupus erythematosus, often have circulating anti-C1q antibodies with concomitant low levels of C1q.[38]

In patients without an identified etiology, laboratory analysis should include serum protein electrophoresis with immunofixation to assess for paraproteinemia, cryoglobulins, and hepatitis C antibody. Hepatitis B was previously thought to be associated with LCV; however, the association appears to have occurred by virtue of coinfection with hepatitis C. Cryoglobulins may be present in patients with LCV, especially in association with infections (hepatitis C, bacterial endocarditis). Results for rheumatoid factor are often positive in patients with cryoglobulinemia. Immunofixation electrophoresis is useful to identify subtle paraproteinemia that has been reported in some patients with leukocytoclastic vasculitis.

The following studies may also be appropriate:

  • Patients with fever and/or a heart murmur should undergo cardiac ultrasonography and blood cultures to assess for endocarditis.
  • HIV testing should be performed in patients at high risk and in patients with an otherwise unidentifiable cause of LCV.
  • If the peripheral blood smear result is abnormal, obtaining bone marrow may be useful [39]

Whether patients with LCV need to be tested for malignancy is controversial. In general, the authors believe that such testing should be performed only in the presence of suggestive symptoms or findings.[40] However, in older adults with LCV who have not been screened for colorectal cancer, stool guaiac testing or fecal immunochemical testing (FIT) should be performed.

Imaging Studies

Chest radiography is part of the routine evaluation for LCV in patients with respiratory symptoms.

Visceral angiography may be indicated in patients with a history of abdominal pain, melena, hematochezia, hematuria, or kidney involvement.

Other Tests

Pulmonary function tests should be obtained in patients with hypocomplementemic urticarial vasculitis syndrome (HUVS) to assess for chronic obstructive pulmonary disease.

Ocular examination should be performed in patients with HUVS to assess for episcleritis and uveitis.


A skin biopsy of a relatively new lesion should be performed in most adult patients with suspected leukocytoclastic vasculitis (LCV). The diagnostic yield is higher when skin biopsy is performed in the first 24 to 48 hours after onset of LCV.[41] Children with suspected LCV are often not forced to endure biopsy for humanitarian reasons.

If the cause of LCV is relatively clear, such as a new medication exposure or recent infection, postponement of biopsy may  be considered. If the lesions resolve within several weeks, biopsy may not be necessary.

Muscle, nerve, or visceral organ biopsy may be warranted in patients with severe vasculitic syndromes; however, most patients with LCV of the skin do not require such tests.

If Henoch-Schönlein purpura is suspected, direct immunofluorescence (DIF) microscopy should be performed to assess for perivascular deposition of IgA. In confirming Henoch-Schönlein purpura by cutaneous biopsy, a kidney biopsy may be avoided in some patients. Biopsy for DIF should be performed within 24-48 hours of the appearance of a lesion.

Histologic Findings

Skin biopsy reveals the presence of vascular and perivascular infiltration of polymorphonuclear leukocytes with formation of nuclear dust (leukocytoclasis), extravasation of erythrocytes, and fibrinoid necrosis of the vessel walls (see image below). This process is dynamic, and biopsy of a lesion performed too early or too late in the evolution of LCV may not reveal these findings. The presence of eosinophils has been correlated with drug-associated disease. Neutrophilia has been associated with severe bacterial infections.[42]

Histopathology of leukocytoclastic vasculitis. Histopathology of leukocytoclastic vasculitis.

The picture of leukocytoclastic vasculitis is a pattern that can occur in any vasculitic syndrome but may also occur in nonvasculitic diseases such as neutrophilic dermatoses, at the base of an ulcer, or in some insect bite-reactions. Careful clinical-pathologic correlation is necessary.

Immunofluorescent staining may reveal immunoglobulins (eg, immunoglobulin G, immunoglobulin M) and complement components (eg, C3, C4) deposited on the skin basement membrane, suggesting immune complex deposition. In Henoch-Schönlein purpura, IgA-predominant deposits may be found.



Medical Care

Once a diagnosis of leukocytoclastic vasculitis (LCV) is established and the patient is fully evaluated, specific or nonspecific management options may be used, depending on the etiology and the extent of the disease. Possible interventions include the following[43, 44] :

  • LCV often affects dependent areas; thus, elevation of the legs or compression stockings may be useful
  • Patients with an identifiable cause should receive treatment for that cause. [45] Removal of a drug thought to be causing LCV may result in rapid clearing of the process in as little as 2 weeks
  • In patients with LCV, with or without joint manifestations, colchicine or dapsone may be helpful. [46, 47, 48]

Patients with urticarial lesions may be treated with antihistamines, including both sedating and less-sedating agents. However, these patients may fail to respond to antihistamines, and often a trial of colchicine or dapsone may be needed. In some cases, a combination of these agents is needed to control the disease manifestations. Some patients respond to nonsteroidal anti-inflammatory agents.

Patients with severe visceral involvement may require high doses of corticosteroids (1-2 mg/kg/d) with or without an immunosuppressive agent (eg, cyclophosphamide, azathioprine, methotrexate, mycophenolate mofetil, rituximab). Patients with bullous lesions may require a brief course of systemic corticosteroids in order to gain rapid control and minimize ulcer formation at the sites of bullae. Due to the possible adverse effects of prolonged corticosteroid use, other treatments should be considered if long-term treatment is needed.[49]

Treatment of patients with chronic LCV is a challenge. Patients may attempt a restrictive elimination diet, which rarely can allow for identification of the cause and control of the disease.[50]

Colchicine at 0.6 mg twice daily and/or dapsone at 100-200 mg/d may control the disease. The combination of those two agents seems to be complementary. In patients whose conditions do not respond or respond poorly, other agents may be administered, including immunosuppressive or cytotoxic agents, (eg methotrexate, mycophenolate mofetil, azathioprine). Patients with severe or debilitating disease might also be treated with biologic agents such as rituximab or intravenous immunoglobulin. Of note, these agents are rarely needed for cutaneous LCV.

In a multicenter, randomized, double-blind trial, Stone et al found that rituximab (375 mg/m2/wk for 4 wk) was more efficacious than cyclophosphamide (2 mg/kg/d) for inducing remission of relapsing ANCA-associated vasculitis. Prednisone was gradually tapered downward; 67% of the rituximab group compared with 42% of the cyclophosphamide group reached the primary end point, which was remission of disease without use of prednisone at 6 months (P = 0.01).[51]

Inpatient care is needed in patients who have severe systemic vasculitic syndromes and severe organ dysfunction. Most patients with cutaneous LCV are treated in an outpatient setting.


Surgical Care

Surgical care is rarely needed in patients with vasculitis. However, surgery may be appropriate in any of the following circumstances:

  • A tumor is identified as a cause of the process
  • A recalcitrant ulceration persists after the active disease has been controlled
  • An organ biopsy is needed


The following specialty consultations may be indicated:

  • Rheumatologist
  • Dermatologist
  • Nephrologist
  • Gastroenterologist or hepatologist
  • Immunologist or allergist
  • Pulmonologist

Diet and Activity

No specific diet is required in patients with leukocytoclastic vasculitis. A restrictive elimination diet may be considered for diagnostic and therapeutic purposes.[50]

No specific restrictions on activity are necessary in patients with leukocytoclastic vasculitis. However, leg elevation may be helpful.

Long-Term Monitoring

Transfer to a tertiary care facility should be considered in patients with severe visceral disease. Patients with chronic LCV are often referred to a tertiary care center for specialty care.

The design of a follow-up program depends on the vasculitic syndrome, its chronicity, and the organ systems affected.  Once the process is inactive in a patient with leukocytoclastic vasculitis (LCV), further follow-up care may be unnecessary.

Patients with Henoch-Schönlein purpura may develop impaired renal function or hypertension; therefore, regular follow-up care, even after complete clearing of their disease, is needed.




Medication Summary

No effective therapy has been established in all patients with leukocytoclastic vasculitis (LCV). The authors most frequently use colchicine or dapsone as first-line options in patients with cutaneous-predominant LCV, who may or may not have associated arthralgia. Agents used for LCV affecting internal organs, and for life-threatening LCV, include corticosteroids, cytotoxic/immunosuppressive agents (eg, cyclophosphamide), and rituximab.[51] Few therapies for LCV have been tested in controlled trials.

Anti-inflammatory Agents

Class Summary

These agents inhibit key events involved in the inflammatory process.


Has effects against neutrophils, which are involved in the pathogenesis of cutaneous vasculitis. Has been demonstrated to be steroid sparing in open-label studies. The only double-blind, placebo-controlled trial failed to demonstrate efficacy; however, the study had several methodological errors.


Class Summary

Some types of antimicrobials (eg, dapsone) have anti-inflammatory properties.

Dapsone (Avlosulfon)

Small, open-label studies or single case reports have suggested that dapsone is effective in some patients with cutaneous vasculitis.


Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Orasone, Meticorten)

Indicated for vasculitis affecting internal organs such as kidneys, lungs, or CNS. Skin involvement with bullous lesions may require corticosteroid therapy in order to prevent cutaneous ulceration and scarring.

Cytotoxic/Immunosuppressive Agents

Class Summary

These agents inhibit cell growth and proliferation, decreasing immune reactions.

Cyclophosphamide (Cytoxan, Neosar)

Useful in life-threatening cases of vasculitis. Patients with only skin disease generally should not be treated with this agent. Useful in patients with polyarteritis nodosa, granulomatosis with polyangiitis (formerly known as Wegener granulomatosis), and eosinophilic granulomatosis with polyangiitis (formerly known as Churg-Strauss syndrome). Alkylating agent that depresses T-cell and B-cell function.

Azathioprine (Imuran)

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Methotrexate (Rheumatrex, Folex PFS)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Adjust dose gradually to attain satisfactory response.

Mycophenolate mofetil (CellCept)

Inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, thereby inhibiting their proliferation. Inhibits antibody production.

Two formulations are available and are not interchangeable. The original formulation, mycophenolate mofetil (MMF, CellCept) is a prodrug that, once hydrolyzed in vivo, releases the active moiety mycophenolic acid. A newer formulation, mycophenolic acid (MPA, Myfortic) is an enteric-coated product that delivers the active moiety. The latter is often associated with less gastrointestinal disturbance.

Rituximab (Rituxan)

Antibody genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. Antibody is an IgG1-kappa immunoglobulin that contains murine light- and heavy-chain variable region sequences and human constant region sequences.


Questions & Answers


What is leukocytoclastic vasculitis (LCV)?

What is Henoch-Schönlein purpura (HSP)?

How frequently is leukocytoclastic vasculitis (LCV) idiopathic?

Where in the body does leukocytoclastic vasculitis (LCV) manifest?

What is the prognosis of leukocytoclastic vasculitis (LCV)?

What are the forms of leukocytoclastic vasculitis (LCV)?

What is the pathophysiology of leukocytoclastic vasculitis (LCV)?

What is the incidence of leukocytoclastic vasculitis (LCV) in the US?

What is the global incidence of leukocytoclastic vasculitis (LCV)?

What is the prognosis of leukocytoclastic vasculitis (LCV)?

What are the racial predilections of leukocytoclastic vasculitis (LCV)?

How does the prevalence of leukocytoclastic vasculitis (LCV) vary by sex?

How does the prevalence of leukocytoclastic vasculitis (LCV) vary by age?


What are the signs and symptoms of leukocytoclastic vasculitis (LCV)?

Which disorders may be comorbid with leukocytoclastic vasculitis (LCV)?

What should be the focus of the medical history in suspected leukocytoclastic vasculitis (LCV)?

Why is consideration of the underlying disorder required in the evaluation of leukocytoclastic vasculitis (LCV)?

What is the most common manifestation of leukocytoclastic vasculitis (LCV)?

Which types of lesions may develop in patients with leukocytoclastic vasculitis (LCV)?

How is urticarial vasculitis differentiated from leukocytoclastic vasculitis (LCV) during the physical exam?

How is the duration of individual leukocytoclastic vasculitis (LCV) lesions determined?

How is hypocomplementemic urticarial vasculitis differentiated from leukocytoclastic vasculitis (LCV) during physical exam?

What should be included in the physical exam of suspected leukocytoclastic vasculitis (LCV)?

What are the causes of leukocytoclastic vasculitis (LCV)?

What are the most common drugs that cause leukocytoclastic vasculitis (LCV)?

Which infections may cause leukocytoclastic vasculitis (LCV)?

How often is can an infectious etiology be differentiated for a drug-related cause of leukocytoclastic vasculitis (LCV)?

What is the prevalence of a collagen-vascular disease etiology of leukocytoclastic vasculitis (LCV)?

What are the GI causes of leukocytoclastic vasculitis (LCV)?

What is the role of malignancy in the etiology of leukocytoclastic vasculitis (LCV)?

What are the signs and symptoms of a malignant etiology for leukocytoclastic vasculitis (LCV)?

Which larger-vessel vasculitis conditions are associated with leukocytoclastic vasculitis (LCV)?


Which conditions should be included in the differential diagnoses of leukocytoclastic vasculitis (LCV)?

What are the differential diagnoses for Leukocytoclastic Vasculitis?


What are the goals of evaluation of a patient with leukocytoclastic vasculitis (LCV)?

What is the role of lab testing in the evaluation of leukocytoclastic vasculitis (LCV)?

When are serologic studies indicated for the evaluation of leukocytoclastic vasculitis (LCV)?

When should complement levels be obtained in the evaluation of leukocytoclastic vasculitis (LCV)?

Which lab studies are indicated in the evaluation of leukocytoclastic vasculitis (LCV) without an identified etiology?

Which additional studies may be useful in the diagnosis of leukocytoclastic vasculitis (LCV)?

When is testing for malignancy indicated in the evaluation of leukocytoclastic vasculitis (LCV)?

What is the role of imaging studies in the evaluation of leukocytoclastic vasculitis (LCV)?

What are some other tests used for the diagnosis of hypocomplementemic urticarial vasculitis syndrome (HUVS)

What is the purpose of direct immunofluorescence (DIF) microscopy in the diagnosis of leukocytoclastic vasculitis (LCV)?

What is the role of skin biopsy in the evaluation of leukocytoclastic vasculitis (LCV)?

What is the role of muscle, nerve, or visceral organ biopsy in the evaluation of leukocytoclastic vasculitis (LCV)?

Which biopsy findings are characteristic of leukocytoclastic vasculitis (LCV)?

Which histologic findings are characteristic of leukocytoclastic vasculitis (LCV)?

What does immunofluorescent staining reveal in patients with leukocytoclastic vasculitis (LCV)?


What are treatment options for leukocytoclastic vasculitis (LCV)?

How are the urticarial lesions of leukocytoclastic vasculitis (LCV) treated?

What are the treatment options for severe visceral involvement in leukocytoclastic vasculitis (LCV)?

What are the treatment options for chronic leukocytoclastic vasculitis (LCV)?

What are the treatment options for severe or debilitating leukocytoclastic vasculitis (LCV)?

What is the role of rituximab in the treatment of leukocytoclastic vasculitis (LCV)?

When is surgery indicated in the treatment of leukocytoclastic vasculitis (LCV)?

Which specialists should be consulted for the management of leukocytoclastic vasculitis (LCV)?

Which diet modifications helpful in the treatment of leukocytoclastic vasculitis (LCV)?


What is the role of medication in the treatment of leukocytoclastic vasculitis (LCV)?

Which medications in the drug class Cytotoxic/Immunosuppressive Agents are used in the treatment of Leukocytoclastic Vasculitis?

Which medications in the drug class Corticosteroids are used in the treatment of Leukocytoclastic Vasculitis?

Which medications in the drug class Antibiotics are used in the treatment of Leukocytoclastic Vasculitis?

Which medications in the drug class Anti-inflammatory Agents are used in the treatment of Leukocytoclastic Vasculitis?