eMedicine Specialties > Pediatrics: General Medicine > Nephrology

Henoch-Schonlein Purpura

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
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
Contributor Information and Disclosures

Updated: Sep 28, 2009

Introduction

Background

Willan and Heberden appeared to have first noted Henoch-Schoenlein (or Henoch-Schönlein) purpura (HSP) in the early 1800s. However, Schönlein first described the combination of acute purpura and arthritis in children in 1837, and Henoch reported the manifestations of abdominal pain and nephritis in 1874.1

Henoch-Schoenlein purpura is an acute immunoglobulin A (IgA)–mediated leukocytoclastic vasculitis that primarily affects children. The dominant clinical features of Henoch-Schoenlein purpura include cutaneous purpura, arthritis, abdominal pain, GI bleeding, orchitis, and nephritis.

The prevalence of Henoch-Schoenlein purpura peaks in children aged 3-10 years. In the Northern hemisphere, the disease occurs mostly from November to January. The male-to-female ratio is 1.5-2:1. In one half to two thirds of children, an upper respiratory tract infection precedes the clinical onset of Henoch-Schoenlein purpura by 1-3 weeks. In general, patients with Henoch-Schoenlein purpura appear mildly ill. They often have a fever, with a temperature usually not higher than 38°C (100.4°F). Henoch-Schoenlein purpura is typically an acute, self-limited illness; however, one third of patients have one or more recurrences.

Purpuric papules and plaques of the lower extremi...

Purpuric papules and plaques of the lower extremity characteristic of Henoch-Schönlein purpura.

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Purpuric papules and plaques of the lower extremi...

Purpuric papules and plaques of the lower extremity characteristic of Henoch-Schönlein purpura.


Hemorrhagic macules, papules, and patches on the ...

Hemorrhagic macules, papules, and patches on the ankle and foot of a child with Henoch-Schönlein purpura.

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Hemorrhagic macules, papules, and patches on the ...

Hemorrhagic macules, papules, and patches on the ankle and foot of a child with Henoch-Schönlein purpura.


Pathophysiology

Etiology of Henoch-Schoenlein purpura

The etiology of Henoch-Schoenlein purpura remains unknown. However, IgA clearly plays a critical role in the immunopathogenesis of Henoch-Schoenlein purpura, as evidenced by increased serum IgA concentrations, IgA-containing circulating immune complexes, and IgA deposition in vessel walls and renal mesangium. Henoch-Schoenlein purpura is almost exclusively associated with abnormalities involving IgA1, rather than IgA2.

The predominance of IgA1 in Henoch-Schoenlein purpura may be a consequence of abnormal glycosylation of O-linked oligosaccharides unique to the hinge region of IgA1 molecules. Although several lines of evidence suggest a genetic susceptibility to Henoch-Schoenlein purpura, the fundamental basis for this abnormality remains unclear.

IgA aggregates or IgA complexes with complement deposited in target organs, resulting in elaboration of inflammatory mediators, including vascular prostaglandins such as prostacyclin, may play a central role in the pathogenesis of Henoch-Schoenlein purpura vasculitis.

A subpopulation of human lymphocytes bears surface Fc and/or C3 receptors (complement receptor lymphocytes), which can bind circulating immune complexes or C3 generated by activation of the alternative complement pathway. Such immune complexes appear in Henoch-Schoenlein purpura and may be part of the pathogenetic mechanism.

Some have speculated that an antigen stimulates the production of IgA, which, in turn, causes the vasculitis. Allergens, such as foods, horse serum, insect bites, exposure to cold, and drugs (eg, ampicillin, erythromycin, penicillin, quinidine, quinine), may precipitate the illness. Infectious causes include bacteria (eg, Haemophilus, Parainfluenzae, Mycoplasma, Legionella, Yersinia, Shigella, or Salmonella species) and viruses (eg, adenoviruses, Epstein-Barr virus [EBV], parvoviruses, varicella). Vaccines such as those against cholera, measles, paratyphoid A and B, typhoid, and yellow fever have also been implicated. Evidence supporting a direct role of herpesvirus, retrovirus, or parvovirus infection in Henoch-Schoenlein purpura is lacking.

Alterations in the production of interleukins (ILs) and growth factors may also have a role in the pathogenesis of Henoch-Schoenlein purpura. Tumor necrosis factor (TNF), IL-1, and IL-6 may mediate the inflammatory process present in Henoch-Schoenlein purpura. Transforming growth factor–beta (TGF-beta), is a recognized stimulant of IgA production. The elevated levels of hepatocyte growth factor present during the acute phase of Henoch-Schoenlein purpura may reflect endothelial-cell damage or dysfunction. Increased levels of vascular endothelial growth factor may at least partly induce these changes.

Cytokines have been implicated in the pathogenesis of Henoch-Schoenlein purpura, and endothelins (ETs), which are vasoconstrictor hormones produced by endothelial cells, may also have a role. Levels of ET-1 are substantially higher during the acute phase of the disease than during remission or in a control group of children. However, ET-1 levels do not appear to be correlated with morbidity, severity of disease, or acute-phase reactant response.

A functional correlation of the IL1RN-2 allele and IL-1ra production in patients with IgA nephropathy and Henoch-Schoenlein purpura nephritis (HSPN) has been described. Therefore, gene polymorphism may contribute to the diversity of clinical responses to inflammatory stimulation.

Emerging data

Results support a role of human leukocyte antigen (HLA)–B35 in the susceptibility to nephritis in unselected patients with Henoch-Schoenlein purpura.

Researchers are currently investigating the importance of nitric oxide (NO) production in disease activity. Inducible NO synthase polymorphism is associated with susceptibility to Henoch-Schoenlein purpura in northwestern Spain.

The prevalence of the human parvovirus B19 component NS1 gene in patients with Henoch-Schoenlein purpura and hypersensitivity vasculitis is increased.

Henoch-Schoenlein purpura that is likely due to montelukast has been noted in patients who present with subacute intestinal obstruction.

Other factors

Yilmaz et al examined 28 children with Henoch-Schoenlein purpura and 79 healthy children to evaluate activities of protein C, free-protein S, and antithrombin; resistance to activated protein C; and levels of fibrinogen.2 D-dimer, thrombin-antithrombin (TAT) complex, prothrombin fragments (PFs) 1 and 2, and von Willebrand factor antigen (vWAg) and its activity (RiCof) were also investigated.

Among patients with Henoch-Schoenlein purpura, fibrinogen, D-dimer, TAT complex, PF-1, PF-2, vWAg, and RiCof levels were significantly higher during the acute phase were than during recovery phase and were significantly higher than those of control subjects. The severity of disease was significantly correlated with TAT, PF-1, PF-2, vWAg, and D-dimer levels.

Aliyazicioglu et al has suggested that leptin and NO may play a role in the immunoinflammatory process of Henoch-Schoenlein purpura, especially in the acute phase.3

Frequency

United States

In the United States, the prevalence is approximately 14-15 cases per 100,000 population.

International

In the United Kingdom, the estimated annual incidence of Henoch-Schoenlein purpura is 20.4 cases per 100,000 population.4 In a Norwegian community hospital, the prevalence of Henoch-Schoenlein purpura was 3.3 cases per 100,000 inhabitants.5

In a study that examined the renal biopsy results of 65 children younger than 18 years obtained by the Clinical Hospital in the Croatian region of Dalmatia over a 10-year period (1995-2005), 10.8% of glomerulonephritis cases were due to Henoch-Schoenlein purpura.6  

Nong et al reviewed the records of 107 Taiwanese pediatric patients diagnosed with Henoch-Schoenlein purpura between 1991 and 2005 who had a mean age of 6.2 ± 2.5 years (range, 2-13 y); the male-to-female ratio was 1:0.7.7 The primary symptoms included the following:

  • Skin rashes (95.3%)
  • GI symptoms (72.0%)
  • Joint involvement (46.7%)
  • Kidney involvement (28.0%)

The most common first manifestations were as follows:

  • Skin rashes (56.1%)
  • GI symptoms (35.5%)
  • Joint involvement (12.1%)

From January 1983 to June 2004, Suehiro et al followed 4,502 patients at the Pediatric Rheumatology clinic in Brazil.8 A diagnosis of Henoch-Schoenlein purpura was made in 203 cases (4.5%); 5 patients (0.1%) had acute hemorrhagic edema of infancy (AHEI). All patients with AHEI were male, and the mean age at onset was 18 months (range, 8-21 mo).

Mortality/Morbidity

Henoch-Schoenlein purpura is only fatal in the rarest of cases. Initial attacks of Henoch-Schoenlein purpura can last several months, and relapses are possible. Kidney damage related to Henoch-Schoenlein purpura is the primary cause of morbidity and mortality. Overall, an estimated 2% of cases of Henoch-Schoenlein purpura progress to renal failure; as many as 20% of children who have Henoch-Schoenlein purpura and are treated in specialized centers require hemodialysis. The renal prognosis appears to be worse in adults than in children.

Race

Whites are affected more often than blacks.

In one study in Thailand, the most common age at presentation was 3-5 years.9 The frequency peaked from December to February. Organs involved included the skin (100%), GI tract (74.5%), and kidneys (46.8%). Joints were also affected (42.6%). Renal involvement was detected within the first 2 months in 16 patients (72.7%); however, it was delayed until 6 months after diagnosis in 6 patients. No risk factors for renal involvement could be identified. Mean follow-up was 2.6 years (range, 1-5 y). Residual renal disease occurred in 6 (38%) of 16 patients, but none were had end-stage disease.

In a study in China, a male predominance was observed in children but not in adults.10 Preceding infection was noted in 40.5% of children and 31.6% of adults; 8.3% of children and 13.2% of adults were receiving medication at the onset of the disease. Abdominal pain was more common in children than adults (70.2% vs 28.9%), but renal involvement was more common and severe in adults than in children; this involvement manifested as frequent hypertension and heavy proteinuria. During acute attacks, leukocytosis, thrombocytosis, and elevated serum C-reactive protein levels were most frequently observed in children, whereas elevated serum IgA and cryoglobulin levels were most common in adults.

Sex

Henoch-Schoenlein purpura occurs more often in boys than in girls; the male-to-female ratio is 1.5-2:1.

Age

In the United States, the prevalence peaks in children aged 5 years. Approximately 75% of cases occur in children aged 2-11 years. Henoch-Schoenlein purpura is rare in infants and young children. A related milder condition called AHEI occurs in infants younger than 2 years.11

Clinical

History

  • Prais et al studied 267 children (56.7% males) who were hospitalized secondary to Henoch-Schoenlein purpura (HSP); 7 of the children (2.7%) had Henoch-Schoenlein purpura that resulted in hospitalization 2 or more times.12 No specific risk factor for recurrence was determined. The mean age for the first recurrence in that subgroup was 3 years and 8 months (range, 10 mo to 7.4 y), and the mean age for the second recurrence was 5.03 years (2.2-10 y), with a mean lag time of 13.5 months ± 2.8 months (range, 2-26 mo). The duration of the recurrent clinical symptoms was 9-30 days. Resolution took more than 2 weeks in 72% of patients.
  • Associated conditions that precede Henoch-Schoenlein purpura include those listed in Causes.
  • Scrotal involvement is not uncommon in Henoch-Schoenlein purpura and may mimic testicular torsion, which must be excluded. Male patients may have associated inflammation and hemorrhage of the testes, appendix testes, spermatic cord, epididymis, or scrotal wall. True torsion is rare. Ha and Lee reported that neurologic symptoms, localized edema, and high serum C3 levels have a significant relationship with scrotal involvement in male patients with Henoch-Schoenlein purpura.13
  • GI symptoms can accompany the onset of Henoch-Schoenlein purpura or may develop later in the course of disease. Abdominal pain occurs in 35-85% of patients and is the third most common presenting symptom in Henoch-Schoenlein purpura. GI problems usually follow the onset of rash and joint pain. Multiple and recurrent intestinal perforations are an unusual complication of Henoch-Schoenlein purpura. In addition to abdominal pain, GI findings can include the following:
    • Nausea
    • Vomiting
    • Diarrhea with gross or occult blood
    • Hematemesis
    • Intussusception: This occurs in 2-3% of patients, and the lead point can be a submucosal hematoma.
    • Bowel infarction with or without perforation
    • Ileal stricture
    • Ileus with massive GI bleed
  • Arthralgias occur in 60-84% of patients with Henoch-Schoenlein purpura and most commonly affect the knees, ankles, and, less frequently, the wrists and fingers. True arthritis does not occur, and joint effusions are rare. Henoch-Schoenlein purpura leaves no permanent joint deformities.
  • In women, gynecologic symptoms can include painful menstruation.
  • Henoch-Schoenlein purpura can be accompanied by neurologic manifestations, particularly headaches. Ozkaya et al reported cerebral vasculitis in a child with Henoch-Schoenlein purpura and familial Mediterranean fever.14
    • In rare cases, Henoch-Schoenlein purpura can be associated with seizures, paresis, or coma.
    • Other manifestations include altered mental status, apathy, hyperactivity, irritability, mood lability, somnolence, seizures (partial, complex partial, generalized, status epilepticus), and focal deficits (eg, aphasia, ataxia, chorea, cortical blindness, hemiparesis, paraparesis, quadriparesis).
    • Polyradiculoneuropathies (eg, brachial plexus neuropathy, Guillain-Barré syndrome) and mononeuropathies (eg, facial nerve, femoral nerve, peroneal nerve, sciatic nerve, ulnar nerve) may also occur.
  • The liver and gallbladder can be involved in Henoch-Schoenlein purpura.
    • Hepatomegaly, hydrops of the gallbladder, and cholecystitis may ensue. These may contribute to a patient's abdominal pain.
    • Acute appendicitis has been noted in patients with Henoch-Schoenlein purpura.
  • Skin involvement is usually purpura. Chan et al noted a case of Henoch-Schoenlein purpura presented as painful bullae on both legs.15
  • Acute hemorrhagic edema of infancy (AHEI) usually occurs in infants aged 4-24 months.
    • AHEI often occurs after drug ingestion or infection. The onset of AHEI is dramatic, with acute palpable purpura, ecchymoses, and tender edema of the limbs and face. Fever, if present, remains mild. Infants remain hemodynamically stable.
    • Dermatologic findings are notable for a cockade (medallionlike), rosette-shaped pattern of macular-papular-hemorrhagic lesions on the face, auricles, and extremities. The lesions usually appear in successive crops. The cockades display variable stages of evolution at any given time.
    • Subcutaneous edema is most common in infants. Urticaria, petechiae, and ear lobe necrosis are additional rare skin manifestations of AHEI. Visceral involvement is rare.
  • Renal pathology is the most important cause of morbidity and mortality in patients with Henoch-Schoenlein purpura.
    • Renal involvement may precede skin manifestations (1-4% of patients) but is usually evident during the acute phase of the disease.
    • In most cases, the severity of nephritis is not related to the extent of other Henoch-Schoenlein purpura manifestations.
    • Hematuria, usually microscopic, can be accompanied by mild-to-moderate proteinuria (<2 g/d). Oliguria, hypertension, and azotemia are rarely present. Nephrotic syndrome (urinary protein excretion >40 mg/m2/h) can also occur.
    • In most cases, histologic examination of the kidneys reveals mesangial proliferation that can be diffuse or focal and segmental. Resolution of the renal involvement is the focus in these patients.
    • Patients who present with hematuria and persistent proteinuria have an approximate 15% risk of developing renal failure. The risk may increase to 50% in patients with a nephrotic-nephritic syndrome.
  • Urinary complications include bladder-wall hematoma, calcified ureter, hydronephrosis, and urethritis.
  • Hemoptysis and hemarthroses can develop in patients who have bleeding abnormalities such as coagulopathy, factor VIII deficiency, vitamin K deficiency, or hypoprothrombinemia. They also probably include factor V Leiden, protein C deficiency, and protein S deficiency, but this has not been documented.

Physical

Purpura of the skin is the most prominent physical finding in Henoch-Schoenlein purpura, but renal, GI, and joint manifestations are commonly present. Other manifestations have also been reported.

Henoch-Schoenlein purpura begins with a symmetrical erythematous macular rash on the lower extremities that quickly evolves into purpura. The rash may initially be confined to malleolar skin but usually extends to the dorsal surface of the legs, the buttocks, and the ulnar side of the arms. Within 12-24 hours, the macules evolve into purpuric lesions that are dusky red and have a diameter of 0.5-2 cm. The lesions may coalesce into larger plaques that resemble ecchymoses. Several cases of Henoch-Schoenlein purpura have been observed after varicella infections.

In children younger than 2 years, the clinical picture may be dominated by edema of the scalp, periorbital area, hands, and feet. This presentation is termed AHEI. The severity of edema is correlated with the severity of the vasculitis and not with the degree of proteinuria. However, the edema has been attributed to the enteric loss of protein. 

Overview of renal findings
The most serious complication of Henoch-Schoenlein purpura is renal involvement, which occurs in 50% of older children but is serious in only approximately 10% of patients. In 80% of patients, renal involvement becomes apparent within the first 4 weeks of illness. Overall, 2-5% of patients progress to end-stage renal failure (ESRF). In one series, acute glomerular lesions, including mesangial hypercellularity, endocapillary proliferation, necrosis, cellular crescents, and leukocyte infiltration, were observed in 41%, 12%, 50%, 29%, and 32% of patients, respectively.16 Only glomerular necrotizing lesions and cellular crescents correlated with the renal survival rate and were associated with clinically significant proteinuria and development of hypertension.

The relationship of Henoch-Schoenlein purpura and IgA nephropathy requires further definition. Whether they are the same or distinct entities remains unclear. Evidence of both their commonality and distinctiveness is presented herein.

Evidence that they are the same entity includes the following:

  • The occurrence of extrarenal manifestations in IgA nephropathy is similar to those observed in Henoch-Schoenlein purpura.
  • IgA nephropathy has developed in patients with a history of Henoch-Schoenlein purpura. Henoch-Schoenlein purpura and IgA nephropathy have occurred in the same families.
  • In a survey of 40 families in which 2 or more members had IgA nephropathy, 5 presented with Henoch-Schoenlein purpura.17
  • Patients with Henoch-Schoenlein purpura who undergo renal transplantation develop IgA deposits in the graft.
  • The prevalence of both conditions is high in certain geographic areas.
  • Similar changes in the IgA system (ie, high IgA, IgA-1C, IgA1-IC, IgA-fibronectin aggregates, aberrantly glycosylated IgA in the circulation) occur in both diseases.18,19,20
However, data indicate that Henoch-Schoenlein purpura and IgA nephropathy are distinct diseases. Zhou et al examined 31 children aged 3-15 years with IgA nephropathy and 120 children aged 4-15 years with Henoch-Schoenlein purpura, noting their clinical manifestations, blood biochemistries, serum immunology, and follow-up data.21 Renal pathologic findings on light microscopy, immunofluorescence study, and electron microscopy were analyzed and compared between 31 children with IgA nephropathy and 32 children with Henoch-Schoenlein purpura.

The age of onset was more than 12 years in 25.8% of the children with IgA nephropathy. However, the age of onset was more than 12 years in only 10% of those with Henoch-Schoenlein purpura. Clinical patterns of IgA nephropathy and Henoch-Schoenlein purpura were similar, but extrarenal manifestations were observed most often in patients with Henoch-Schoenlein purpura. All patients with Henoch-Schoenlein purpura had skin purpura, 59% of patients had GI symptoms, and 47% of patients had arthralgia. Abdominal pain occurred in only 3.2% of children with IgA nephropathy. In patients with IgA nephrology and in patients with Henoch-Schoenlein purpura, renal pathology revealed global sclerosis in 35.5% and 3.1%, mesangial sclerosis in 41.9% and 6.3%, endothelial proliferation in 29% and 65.6%, and thin basement-membrane nephropathy in 6.5% and 0%, respectively.

Electronically dense deposits in Henoch-Schoenlein purpura were sparse, loose, and widely spread in the glomerular mesangium, in the subendothelial area, and even in the intrabasement membranes, whereas the deposits were dense, lumpy, and mostly limited in mesangium and paramesangium in IgA nephropathy. Immunoglobulin G (IgG) was found in glomerular immune deposits in 71.9% of patients with Henoch-Schoenlein purpura but in only 19.4% of patients with IgA nephropathy. No IgG deposit was observed in 81.6% of those with IgA nephropathy; most had IgA and immunoglobulin M (IgM) and/or C3 deposit. Predominant IgG deposits were found in 12.5% of patients Henoch-Schoenlein purpura, with relatively weak IgA deposits. Moreover, 6.3% of patients with Henoch-Schoenlein purpura had linear IgG deposits in the glomerular capillary wall, which was not found in IgA nephropathy.

The follow-up data at an average of 20 months showed complete remission in 72.5% of patients with Henoch-Schoenlein purpura; the rate was 19.4% of those with IgA nephropathy after 34 months follow-up. Moreover, 64.5% of patients with IgA nephropathy had consistent hematuria and proteinuria, and 16.1% had active nephritides. Therefore, the difference was significant (P <.05).

Zhou et al found important clinicopathologic differences between Henoch-Schoenlein purpura and IgA nephropathy, which does not support the one-disease hypothesis.

Overview of GI findings
Abdominal pain and bloody diarrhea may precede the typical purpuric rash of Henoch-Schoenlein purpura in 14-36% of patients, complicating the initial diagnosis and even resulting in unnecessary laparotomy. GI manifestations occur in about 50% of cases and usually consist of colicky abdominal pain, melena, or bloody diarrhea. Hematemesis occurs less frequently. Intussusception should be suspected in patients Henoch-Schoenlein purpura with abdominal pain and/or melena. Barium enema is frequently therapeutic.

Overview of joint findings

Arthralgias occur in 60-84% of patients with Henoch-Schoenlein purpura. The pain most commonly affects the knees and ankles and less frequently the wrists and fingers. Frank arthritis does not occur, and joint effusions are rare. Henoch-Schoenlein purpura leaves no permanent joint deformities.
  • Skin manifestations
    • Palpable purpura usually occurs first on the lower limbs and then spreads to the buttocks. Purpura is usually most prominent over the buttocks, the posterior aspects of the lower legs, and the elbows.
    • Palpable purpura can also be present on the forearms and pinna. Scalp edema can occur. Hemorrhagic vesicles and bullae are rare. In most patients, the skin lesions are the first sign of Henoch-Schoenlein purpura.
    • Hives, angioedema, and target lesions can also occur. Vesicular eruptions and swelling and tenderness of an entire limb have been noted. Erythema multiforme–like lesions can be present.
    • Henoch-Schoenlein purpura with hemorrhagic bullae in children has been noted.
    • In AHEI, dermatologic findings are notable for a cockade (medallionlike), rosette-shaped pattern on the face, auricles, and extremities. The lesions usually appear in successive crops. The cockades display variable stages of evolution at any given time and look different from the normal purpura of Henoch-Schoenlein purpura.
    • The subcutaneous edema of AHEI is more common in infants. Urticaria, petechiae, and necrosis of the ear lobe are additional, rare skin manifestations of AHEI. AHEI is rarely associated with visceral involvement.
  • Renal manifestations
    • Possible renal manifestations include microscopic hematuria, proteinuria, nephrotic syndrome, progressive glomerulonephritis, ESRF (rarely), and intestinal perforation.
    • The relationship of Henoch-Schoenlein purpura and IgA nephropathy requires further definition. Whether they are the same or distinct entities remains unclear. Evidence of both their commonality and distinctiveness is presented in Overview of renal findings above.
    • If serial urine samples are obtained in patients with Henoch-Schoenlein purpura, microscopic hematuria is usually found and is probably present in 100% of the patients. However, frank nephritis appears in only 20-30% of unselected children. The entire clinical spectrum of glomerulonephritis may occur in Henoch-Schoenlein purpura. The most common renal manifestations are hematuria with mild-to-moderate proteinuria.
  • GI manifestations
    • The duodenum and small intestine are the most frequently involved segments of the GI tract.
    • Duodenal ulcers also occur.
    • Massive GI bleeding has been reported in Henoch-Schoenlein purpura.22
    • Ileal vasculitis has also been reported.
  • Joint manifestations
    • Arthritis and/or arthralgia affects 60-75% of patients and is the presenting feature in 25%.
    • Joints may be swollen, tender, and painful. The knees and ankles are most commonly affected. On rare occasions, symptoms involve the fingers and wrists.
    • Findings are transient but can occur again during active disease. The joints are not permanently deformed.
  • Cardiac manifestations: Vasculitis involving the myocardia can occur.
  • Pulmonary manifestations: Vasculitis can involve the lungs, resulting in pulmonary hemorrhage or severe bilateral pulmonary hemorrhage.
  • Urinary manifestations: Vasculitis may cause stenosing ureteritis, priapism, penile edema, or orchitis. Ha and Lee reported that neurologic symptoms, localized edema, and high serum C3 levels show a significant relation with scrotal involvement in male patients with Henoch-Schoenlein purpura.13
  • CNS manifestations: Vasculitis involving the CNS and intracranial hemorrhage has been reported.
  • Eye manifestations: Bilateral subperiosteal orbital hematomas have been noted.
  • Adrenal manifestations: Adrenal hematomas have occurred.
  • Pancreatic manifestations: In rare patients, acute pancreatitis is the sole presenting feature of Henoch-Schoenlein purpura.23

Causes

The following conditions may precede Henoch-Schoenlein purpura:

More on Henoch-Schonlein Purpura

Overview: Henoch-Schonlein Purpura
Differential Diagnoses & Workup: Henoch-Schonlein Purpura
Treatment & Medication: Henoch-Schonlein Purpura
Follow-up: Henoch-Schonlein Purpura
Multimedia: Henoch-Schonlein Purpura
References
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References

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  15. Chan KH, Tang WY, Lo KK. Bullous lesions in Henoch-Schonlein purpura. Pediatr Dermatol. May-Jun 2007;24(3):325-6. [Medline].

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Further Reading

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Keywords

Henoch Schönlein purpura, Henoch-Schönlein purpura, Henoch Schonlein purpura, Henoch-Schonlein purpura, Henoch Schoenlein purpura, Henoch-Schoenlein purpura, HSP, allergic purpura, Henoch's purpura, Schönlein purpura, Schönlein's purpura, Schönlein disease, Schönlein's disease, Henoch-Schönlein purpura, Henoch-Schönlein syndrome, Schönlein-Henoch syndrome, vascular purpura, acute vascular purpura, anaphylactoid purpura, hemorrhagic exudative erythema, purpura nervosa, purpura rheumatica, rheumatocelis, purpura fulminans, purpura hemorrhagica, nonthrombocytopenic purpura, rheumatoid purpura, allergic purpura

hemorrhagic capillary toxicosis, nonthrombocytopenic idiopathic purpura, peliosis rheumatica, rheumatic purpura, acute hemorrhagic edema of infancy, AHEI, postinfectious cockade purpura, Finkelstein disease, Finkelstein's disease, Seidelmayer syndrome, Seidelmayer's syndrome, infantile postinfectious irislike purpura and edema, vasculitis, arthritis, cutaneous purpura, orchitis, nephritis, species, adenoviruses, Epstein-Barr virus, EBV, parvoviruses, varicella, hypertension, proteinuria, mononucleosis, group A streptococcal infection, hepatitis, varicella-zoster infection

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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.

Medical Editor

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

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

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: Amgen Grant/research funds None; Altus Pharmaceuticals Grant/research funds None; Genzyme Grant/research funds None; Merck Grant/research funds None; NIH Grant/research funds None

 
 
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