NFD

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

Leukocytoclastic vasculitis may be secondary to medications, underlying infection, collagenvascular disorders, or malignancy. However, approximately half of cases are idiopathic. [2, 3]
Leukocytoclastic vasculitis may be localized to the skin or may be associated with systemic
involvement.[4] 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.[5]
Leukocytoclastic vasculitis 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-Schnlein purpura (HSP), a specific subtype of LCV warranting separate discussion,
is characterized by predominant IgA-mediated vessel injury. 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.[6] HSP in adults, especially older men, may be associated with malignancy. [7]
Once a diagnosis of leukocytoclastic vasculitis (LCV) is established and the patient is fully
evaluated, specific or nonspecific management options may be used.[27, 28]

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.[29]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
administered.[30, 31, 32]
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 colchicines or dapsone may be needed.
o In some cases, a combination of these agents is needed to control the disease
manifestations.
o 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.
Patients with chronic LCV may attempt a restrictive elimination diet, which rarely can allow
for identification of the cause and control of the disease.[33]
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.
o 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).[34]