Pediatric Henoch-Schonlein Purpura Workup

  • Author: Noah S Scheinfeld, MD, JD, FAAD; Chief Editor: Craig B Langman, MD   more...
 
Updated: Nov 23, 2010
 

Laboratory Studies

No specific diagnostic laboratory test is available to assess for markers of Henoch-Schoenlein purpura (HSP). Coppo et al reported that in patients in whom severe proteinuria, hypertension, or crescents are present at onset, the risk for Henoch-Schoenlein purpura progression is greater in adults and females and appears linked with increasing mean proteinuria levels during follow-up, even more so than in patients with decreased renal function at onset.[31] Factor XIII activity apparently correlates tightly with the severity of abdominal manifestations, and, thus, measuring factor XIII activity aids in identifying patients with severe GI manifestation who could benefit from substitution therapy.[32, 33]

General laboratory tests may reveal the following:

  • Antinuclear antibody and rheumatoid factor are absent.
  • The level of plasma coagulation factor XIII (F XIII) is reduced in about 50% of patients.
  • Urinalysis reveals hematuria. Proteinuria may also be found.
  • Antinuclear antibody and rheumatoid factor are absent.
  • The CBC count can show leukocytosis with eosinophilia and a left shift. Thrombocytosis is present in 67% of patients.
  • Platelet counts may be elevated. Low platelet levels suggest thrombocytopenic purpura. The erythrocyte sedimentation rate (ESR) is variably elevated. Some reports state that the ESR is mildly elevated in 75% of patients.
  • A stool guaiac test may reveal occult blood. BUN and creatinine levels may be elevated, indicating decreased renal function.
  • Plasma D-dimer concentrations can be substantially increased.
  • Plasma concentrations of TAT complex, PF-1, and PF-2 can be abnormal.
  • The prothrombin time (PT) and activated partial thromboplastin time (aPTT) can be reduced (eg, hypoprothrombinemia).
  • Serum IgA levels are increased in about 50% of patients during the acute phase of illness. Circulating IgA immune complexes may be present in some patients, though data supporting the presence of classic antigen-antibody complexes have been questioned.
  • Factor VIII levels are decreased in some patients.
  • The antistreptolysin O (ASO) titer is elevated in 30% of patients.
  • CH50 is decreased in 30% of patients.
  • C3 and C4 levels are occasionally low.
  • Immunocomplexes of IgG and IgA can be increased.
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Imaging Studies

Ultrasonography

Abdominal ultrasonography can be used if GI symptoms are present. Diagnosis of Henoch-Schoenlein purpura using sonography and radionuclear scanning in a child presenting with bilateral acute scrotum as the main symptom of Henoch-Schoenlein purpura has been reported. In children with GI involvement of Henoch-Schoenlein purpura, dedifferentiated wall thickening demonstrated by ultrasound reveals a poor clinical prognosis.[34]

Radiography

Plain radiography of the abdomen may help in diagnosing intestinal obstruction, and a barium enema study may be used to confirm and treat intussusception. Chest radiography may help in determining the presence and extent of pulmonary hemorrhage. Testicular ultrasonography may help in assessing the testes for hemorrhage or torsion.

Contrast-enhanced radiography of the small intestine demonstrates thickened mucosal folds or small barium flecks. Endoscopy may reveal multiple irregular ulcers, mucosal redness, and petechiae in the duodenum. The second part of the duodenum is sometimes predominantly affected. Ulcerating lesions accompanied by hematomalike protrusions can be detected in patients with histopathologically proven leukocytoclastic vasculitis.

MRI

Some suggest that MRI is useful to assess neurologic findings in Henoch-Schoenlein purpura.

In one case, a 6-year-old boy with Henoch-Schoenlein purpura presented with depression, generalized convulsions, and cortical blindness. Sequential MRI revealed bilateral cerebral ischemic lesions in the cortex and white matter of parieto-occipital lobes caused by vasculitis.

Summary of radiologic findings

Radiologic GI findings mainly include bowel ischemia with thumbprinting and bowel-wall edema, which is sometimes visible on abdominal radiographs.

Bowel ultrasonographic findings include thickening of the bowel wall, free fluid, and intussusception.

Hydrops of the gallbladder is rarely seen.

Renal involvement may result in no ultrasonographic features. If nephritis or nephrotic syndrome occurs, renal enlargement with loss of corticomedullary differentiation due to edema is observed.

If barium studies are performed, typical findings of ischemic colitis may be found, including a narrow colon with thickened mucosa and thumbprinting.

Some believe that imaging studies are indicated only if the diagnosis is uncertain.

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Procedures

In some cases, renal biopsy may be useful. Renal biopsy should be performed when the nephrotic syndrome persists (although other manifestations may have subsided) and when renal function deteriorates.

During the acute phase of the disease, renal biopsy may reveal glomerular crescents. The extent of the crescents is of prognostic importance.

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Histologic Findings

Henoch-Schoenlein purpura is a vasculitis that often involves the kidneys.

Histopathologic features of the skin lesions in infantile Henoch-Schoenlein purpura can range from a typical leukocytoclastic vasculitis with or without fibrinoid necrosis to the less specific findings of a lymphohistiocytic perivascular infiltrate with extravasation of erythrocytes.

Direct immunofluorescence (DIF) testing is a useful adjunct to histopathology; the yield of a positive test result is substantially higher when the test is performed within 48 hours of presentation. Immunofluorescence studies reveal perivascular IgA deposition in almost all patients; this finding is rare in infantile Henoch-Schoenlein purpura, in which C3 and IgM are most commonly found in the affected vessel walls.

The histology of the kidney in Henoch-Schoenlein purpura widely varies. In some cases, most glomeruli appear unaffected when assessed using light microscopy; only a few show mesangial proliferation. In instances of moderate renal involvement, focal and segmental intracapillary and extracapillary proliferation may be present with adhesions and small crescents. Severe cases are characterized by a diffuse proliferation with infiltration of neutrophils and circumferential crescents in most of the glomeruli. Tubular atrophy and interstitial infiltration with mononuclear cells may also be present.

Deposits of IgA in the mesangium and the walls of cutaneous capillaries are detected in most patients. The IgA deposited in the mesangium is mainly of the IgA1 subclass, although deposits of IgA2 are rarely noted. In addition to IgA, the deposits in mesangium and cutaneous capillaries frequently contain C3, IgG, and fibrin. The deposits of C3 are often accompanied by properdin, whereas C1Q and C4 are usually not present. This observation suggests that the complement components have been activated by means of the alternative pathway.

The specific renal pathology of Henoch-Schoenlein purpura includes the following:

  • Diffuse hypercellularity
  • Focal and segmental proliferation
  • Mesangial proliferation
  • Minimal change to severe crescentic glomerulonephritis
  • Segmental sclerosis fibrosis
  • Mononuclear cell infiltration
  • Mesangial, subendothelial, and subepithelial deposits
  • Diffuse glomerular deposits of IgA, C3, fibrin, IgG, properdin, and IgM
  • IgA deposits in the mesangium
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Contributor Information and Disclosures
Author

Noah S Scheinfeld, MD, JD, FAAD  Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice

Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Optigenex Consulting fee Independent contractor

Coauthor(s)

Elena L Jones, MD  Clinical Assistant Professor of Dermatology, College of Physicians and Surgeons of Columbia University; Clinic Chief, Department of Dermatology, St Luke's-Roosevelt Hospital Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard Neiberger, MD, PhD  Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group

Disclosure: The Osler Institute Honoraria Speaking and teaching

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Adrian Spitzer, MD  Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center

Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Howard Trachtman, MD  Program Director, Pediatrics Research, Schneider Children's Hospital, Department of Pediatrics, Division of Nephrology, Professor, Albert Einstein College of Medicine

Howard Trachtman, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD  The Isaac A Abt, MD, Professor of Kidney Diseases, Feinberg School of Medicine, Northwestern University; Division Head of Kidney Diseases, Children's Memorial Hospital, Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology

Disclosure: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

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Purpuric papules and plaques of the lower extremity characteristic of Henoch-Schönlein purpura.
Hemorrhagic macules, papules, and patches on the ankle and foot of a child with Henoch-Schönlein purpura.
 
 
 
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