Comparison of Features: Idiopathic Thrombocytopenic Purpura and Henoch-Sch_nlein Purpura
ITP HSP
~ 5 cases per 100,000 children annually
Epidemiology Peak incidence at 2-5 years (range 2-10 years)
Boys and girls are affected equally.
Anti-platelet antibody binds to the platelet surface, leading to
removal and destruction of platelets in the spleen and liver.
Causes/
Mechanisms/
Triggers
Most cases of ITP follow a non-specific viral illness.
As in other bleeding disorders affecting platelets, children with
ITP usually present with superficial bleeding into the skin
(petechiae and bruising.) Some have evidence of mucosal
bleeding. Other symptoms and physical findings are generally
absent.
Children with ITP should not have hepatomegaly or
splenomegaly on exam; the presence of either should prompt
evaluation for other conditions.
Clinical
features
Lab findings in ITP include thrombocytopenia (usually with
platelet counts < 20K) with a normal WBC and Hgb.
Abnormalities in either leukocyte or red cell counts require
additional evaluation.
Laboratory
Despite their low platelet counts, most children with ITP do not
Natural have significant bleeding. ~ 3% have severe epistaxis or other
history/ mucous membrane hemorrhage. The most concerning
Complications complication of ITP is intracranial hemorrhage, which occurs
rarely (0.1-0.5% of cases).
~ 10 cases per 100,000 children annually
Peak incidence at 4-6 years (range 2-17 years)
Boys are affected twice as often as girls.
Underlying mechanism is unknown; HSP is suspected to
represent an IgA-dominated immune response to infection or
other triggers. Biopsy of affected organs reveals
leukocytoclastic vasculitis and deposition of IgA.
50% of cases of HSP follow viral or bacterial upper respiratory
infections.
Skin lesions may begin as erythematous macules or urticarial
wheals that evolve to petechiae and palpable purpura. Rash is
symmetrically distributed in gravity-dependent or pressure-
sensitive areas (e.g. lower extremities, elbows). Younger
patients are more likely to have involvement of the face or
upper extremities.
Other common features of HSP:
• Colicky diffuse or periumbilical abdominal pain
(50%-75% of patients)
• Arthritis or arthralgia (40-75%)
• Renal disease (20-50%)
All children with HSP eventually develop skin findings. The
presence and timing of other disease manifestations are
unpredictable. Abdominal pain and joint involvement may
precede the rash, making it difficult to arrive quickly at a
diagnosis of HSP.
Laboratory findings are often normal and non-specific. Platelet
count should be normal. Coagulation studies may be helpful if
coagulation abnormalities cannot be excluded by history and
exam. Urinalysis is essential to determine the presence and
extent of renal involvement. Hematuria or proteinuria should
prompt assessment of BUN and serum creatinine. Stool guaiac
may provide useful information in the setting of abdominal
pain or other gastrointestinal symptoms.
 Options include observation, oral corticosteroids, IVIg, and
anti-D immunoglobulin (Rhogam). IVIg and anti-D Ig tend to
produce a more rapid rise in platelet count than the other
options, though a clinical benefit (i.e. ability to prevent
Treatment intracranial hemorrhage or other significant bleeding) has not
been clearly shown. Some pediatric hematologists use platelet
counts as a threshold for treatment (e.g. treating until the
platelet count is >20K); others base decision-making on
presence and severity of bleeding.