CASE REPORT
Interventional Medicine & Applied Science, Vol. 5 (2), pp. 89–93 (2013)
A rare presentation of Henoch–Schönlein purpura and myocardial infarction at the 5th decade of life RAJESH RAJAN*, PETER K. JOSEPH, VIJAYARAGHAVAN GOVINDAN Department of Cardiology Kerala Institute of Medical Sciences (KIMS), Trivandrum, Kerala State, India *Corresponding author: Dr. Rajesh Rajan, MD; Department of Cardiology Kerala Institute of Medical Sciences (KIMS), Trivandrum, Kerala State, 695029 India; E-mail: [email protected] (Received: September 20, 2012; Revised manuscript submitted: April 16, 2013; Accepted: April 17, 2013) Abstract: Henoch–Schönlein purpura is an IgA-mediated, autoimmune, hypersensitivity vasculitis of childhood that results in a triad of symptoms, including a purpuric rash occurring on the lower extremities, abdominal pain or renal involvement, and arthritis. However, any of the triad may be absent, which often leads to a confusion in diagnosing the condition. Although the cause is unknown, Henoch–Schönlein purpura (HSP) is often associated with infectious agents, such as group A streptococci and mycoplasma. It has also been associated with food reactions, exposure to cold, insect bites, and drug allergies. The treatment is supportive and needs close followup of renal status. This report describes a rare presentation of Henoch–Schönlein purpura with coronary vasculitis which leads to myocardial infarction at the age of 53. Henoch–Schönlein purpura was diagnosed on the basis of no infection, accelerated ESR (35 mm/h), normal platelet count, positive skin biopsy, proteinuria, and negative searches for rheumatoid factor (RF), antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA), and anti-dsDNA. Keywords: Henoch–Schönlein purpura, myocardial infarction, coronary vasculitis
Introduction
of severe abdominal pain, chest discomfort, sweating, and radiating pain to left hand of 3-h duration. Patient was referred to us from a local hospital with marked ECG changes. He had marked red spots predominantly over lower extremities. Complaints started as red spots over the right foot then spread over the right knee and left foot later on Fig. 1. Few red spots were seen in the hands, too. Without consulting a doctor he traveled to
Henoch–Schönlein purpura (HSP) is characterized by vasculitic involvement of small sized vessels and results in multisystemic manifestations that are most probably caused by an abnormal response of the immune system (hypersensitive vasculitis). The exact definition of the clinical and laboratory symptoms are not yet stable, they are continuously changing. Originally, it had been described as a disease exclusively of children (Heberden, 1801), but newly there are published reports of this hypersensitive vasculitis with IgA deposition manifested in adults as well, and also attaining the cardiovascular system. Henoch–Schönlein purpura is a disease that involves purple spots on the skin, joint pain, gastrointestinal problems, and glomerulonephritis [1]. It is more common in boys than in girls. Many people with Henoch–Schönlein purpura suffered upper respiratory illness during early weeks.
Case Report A 55-year-old male patient was referred from a local hospital as a case of inferolateral myocardial infarction and Henoch–Schönlein purpura presented with complaints
DOI: 10.1556/IMAS.5.2013.2.7
Fig. 1.
89
Red spots were noted over the extremities
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
Rajan et al.
tory rate: 25/min, blood pressure: 180/100 mmHg, lower limb blood pressure: 190 systolic. Red spots were noted over the extremities. On cardiovascular examination first and second heart sound normal, JVP was not elevated, chest: clear, other systems: within normal limits.
nearby state and spent 2 days over there. On return, he had severe intermittent epigastric pain during the night. Family physician advised to visit a surgeon at the earliest. He was admitted and treated as acid peptic disease for 4 days. Reaching home from the hospital, he had severe chest discomfort, sweating, and radiating pain to left hand during the night. He was taken to the local hospital and found to have marked ECG changes and was referred to our center. On routine evaluation, he was diagnosed to have type 2 diabetes mellitus, systemic hypertension and prostatomegaly. His development miles stones were normal. He has no history of cyanosis, giddiness, dyspnea on exertion or pedal edema. He gives history of several episodes of loose stools 2 months back. He is a non-smoker and non-ethanolic. Mother had history of cerebral thrombosis. On initial evaluation, patient had no dyspnea at rest, normally built, nourished, weight: 65 kg, height: 170 cm, and body mass index: 22.4. He was conscious oriented, pulse rate: 100/min, respira-
Fig. 2.
Investigations Laboratory evaluation of urine analysis showed proteinuria, cardiac enzymes were markedly elevated CK-MB: 48.67 ng/mL, troponin T: 0.773 ng/ml, total leukocyte count were elevated TC-24,100 cells/cumm, platelet count: 599,000/cumm, erythrocyte sedimentation rate (ESR): 35 mm/h, C-reactive protein: 1.5 mg/L, 24 h, urine protein: 190 mg/day. Renal and liver function tests were normal. Vasculitis workup – ANA: 0.33, anti-dsDNA: 0.54, c-ANCA, and p-ANCA was negative, IgA level normal, rheumatoid factor: normal. Histopathology: consistent with purpuric lesion, no active vasculitis, resolving HSP (Fig. 2). ECG: Normal sinus rhythm, heart rate: 74/mt, PR interval: 120 ms, QRS: 80 ms, QRS: +110*, ST elevation: II, III, AVF, V2–V6 (Fig. 3). 2D-echocardiography: concentric left ventricular (LV) hypertrophy, normal valves, good LV systolic function, EF: 83%, distal IVS, apex and apicolateral wall akinetic, wall thickness preserved, no clots/effusion. Cath notes: precath diagnosis – acute coronary syndrome, inferolateral myocardial infarction, type 2 diabetes mellitus, systemic hypertension, coronary vasculitis, HSP. Hardware: 7F sheath, 6F JL 3.5, JR4, and PTCA hardware. Coronary angiogram: (right femoral access). Left main coronary artery (LMCA): normal left anterior descending LAD: there is a total mid segment thrombotic occlusion (Fig. 4), proximal left anterior descending (LAD) is normal, left circumflex (Lcx): is non-dominant, large obtuse marginal (OM) which bifurcates into two branches, has thrombosis occlusion in both branches (Fig. 5). Right coronary artery (RCA): dominant and free of disease. Angiography at other sites: normal LIMA. Intervention: left coronary artery (LCA) cannulated with 7F JL3.5 guiding catheter and galeo floppy wire placed across the thrombotic occlusion and the vessels were dottered with a 2 × 11 mmHg balloon. Suboptimal forward flow established no lesion identified repeat dottering did not considerably improve the flow. Final diagnosis of coronary angiogram: thrombotic occlusion of left anterior descending and left circumflex artery.
Histopathology report
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
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Interventional Medicine & Applied Science
HSP and MI a rare presentation
Fig. 3.
Fig. 4.
Acute infero lateral myocardial infarction with evolved anterior
Left anterior descending LAD has a total mid segment throm
Interventional Medicine & Applied Science
Fig. 5.
91
Thrombotic occlusion in both branches of OM
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
Rajan et al.
– Upper respiratory tract infection tract (URI) prodrome, – Mesangioproliferative glomerulonephritis with or without IgA deposition.
Treatment Inferolateral myocardial infarction was treated with GP IIb IIIa inhibitor (Eptifibatide) and unfractionated heparin was started soon after angiogram. During angiogram, dottering of occluded vessels were done. Aspirin, Clopidogrel and Atorvostatin were also administered. HSP treated with steroids and antihistamine. Type 2 diabetes treated with injection insulin. Systemic hypertension treated with metoprolol and amlodepine.
Michel et al. [3] proposed criteria to differentiate HSP from hypersensitivity vasculitis, requiring three or more of the following be present to diagnose HSP: – Palpable purpura, – Bowel angina, – GI bleeding, – Hematuria, – Patient age of onset younger than 20 years.
Discussion Henoch–Schönlein purpura (HSP or anaphylactoid purpura) is an immunoglobulin (Ig) A-mediated smallvessel vasculitis that predominantly affects children but also is seen in adults. HSP is a subset of necrotizing vasculitis characterized by fibrinoid destruction of blood vessels and leukocytoclasis. Clinical manifestations primarily include palpable purpura [4], arthralgia or arthritis, abdominal pain, gastrointestinal (GI) bleeding, and nephritis. The most serious long-term complication from Henoch–Schönlein purpura is progressive renal failure, which occurs in 1–2% of patients. Heberden first described the disease in 1801 in a 5-year-old child with abdominal pain, hematuria, hematochezia, and purpura of the legs. In 1837, Johann Schönlein described a syndrome of purpura associated with joint pain and urinary precipitates in children. Eduard Henoch, a student of Schönlein’s, further associated abdominal pain and renal involvement with the syndrome. Frank proposed the term “anaphylactoid purpura” in 1915. This followed from the reasoning that the pathogenesis likely involved a hypersensitivity reaction to an inciting agent. Two major classification systems are used to make a diagnosis of HSP. The first, from the American College of Rheumatology, requires two or more of the following to be present: – Patient age younger than 20 years, – Palpable purpura, – Abdominal pain or GI bleeding, – Extravascular or perivascular granulocytes on biopsy.
Complications of Henoch–Schönlein purpura [5]: 1. Hepatosplenomegaly 2. Myocardial infarction 3. Pulmonary hemorrhage 4. Pleural effusion 5. Unnecessary abdominal surgery 6. Intussusception 7. Hemorrhage 8. Shock 9. Gastrointestinal bleeding 10. Bowel infarction 11. Renal failure 12. Hematuria 13. Proteinuria 14. Seizure 15. Mononeuropathies In this patient, we found a massive thrombus load in LAD and LCx. Thrombolysis was not considered in this patient in view of hemorrhagic risk. Usually, HSP related MI may not require angioplasty or stenting. Simple dottering is enough with the cover of GPIIb IIIa inhibitors and heparin is sufficient, as we did in this patient.
Conclusions Henoch–Schönlein purpura (HSP) was diagnosed on the basis of no infection, elevated ESR (35 mm/h), normal platelet count, positive skin biopsy, proteinuria and negative searches for RF, ANA, ANCA, and antidsDNA. Henoch–Schönlein purpura with myocardial infarction is a rare situation. Age of presentation is unusual. Henoch–Schönlein purpura is usually seen in children. Here adult presentation at the age of 53 years. In such cases, myocardial infarction-like pattern is caused by thrombus occlusion in coronaries due to coronary vasculitis. In this case patient was taken for coronary angiogram and start on GP IIb IIIa inhibitor (eptifibatide) and unfractionated heparin. Repeat coronary angiogram showed no further thrombus formation. Other standard management of HSP continued.
The second classification system, from the Chapel Hill Consensus Group, primarily uses nonclinical criteria and requires only the presence of small-vessel vasculitis with IgA deposition. Two additional sets of criteria have been suggested for the diagnosis of HSP. Helander et al. [2] posed that three or more of the followings should be present: – Direct immunofluorescence (DIF) results consistent with vascular IgA deposition, – Patient age younger than 20 years, – GI involvement,
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
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Interventional Medicine & Applied Science
HSP and MI a rare presentation 3. Michel BA, Hunder GG, Bloch DA, Calabrese LH: Hypersensitivity vasculitis and Henoch–Schönlein purpura: a comparison between the 2 disorders. J Rheumatol 19, 721–728 (1992) 4. Bloch DA, Michel BA, Hunder GG, Bloch DA, Michel BA, Hunder GG, McShane DJ, Arend WP, Calabrese LH, Edworthy SM, Fauci AS, Fries JF, Leavitt RY et al.: The American College of Rheumatology 1990 Criteria for the Classification of Vasculitis Patients and Methods Arthritis Rheum 33, 1068 (1990) 5. Mills JA, Michel BA, Bloch DA et al.: The American College of Rheumatology criteria for the classification of Henoch–Schönlein purpura. Arthritis Rheum 33, 1114–1121 (1990)
References 1. Miller ML, Pachman LM (2007): Vasculitis syndromes. In: Nelson Textbook of Pediatrics, 18th ed., eds Kliegman RM, Behrman RE, Jenson HB, Stanton BF, Saunders Elsevier, Philadelphia, PA: chapter 166 2. Helander SD, De Castro FR, Gibson LE: Henoch–Schönlein purpura: clinicopathologic correlation of cutaneous vascular IgA deposits and the relationship to leukocytoclastic vasculitis. Acta Derm Venereol 75, 125–129 (1995)
Interventional Medicine & Applied Science
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ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
Interventional Medicine & Applied Science, Vol. 5 (2), pp. 89–93 (2013)
A rare presentation of Henoch–Schönlein purpura and myocardial infarction at the 5th decade of life RAJESH RAJAN*, PETER K. JOSEPH, VIJAYARAGHAVAN GOVINDAN Department of Cardiology Kerala Institute of Medical Sciences (KIMS), Trivandrum, Kerala State, India *Corresponding author: Dr. Rajesh Rajan, MD; Department of Cardiology Kerala Institute of Medical Sciences (KIMS), Trivandrum, Kerala State, 695029 India; E-mail: [email protected] (Received: September 20, 2012; Revised manuscript submitted: April 16, 2013; Accepted: April 17, 2013) Abstract: Henoch–Schönlein purpura is an IgA-mediated, autoimmune, hypersensitivity vasculitis of childhood that results in a triad of symptoms, including a purpuric rash occurring on the lower extremities, abdominal pain or renal involvement, and arthritis. However, any of the triad may be absent, which often leads to a confusion in diagnosing the condition. Although the cause is unknown, Henoch–Schönlein purpura (HSP) is often associated with infectious agents, such as group A streptococci and mycoplasma. It has also been associated with food reactions, exposure to cold, insect bites, and drug allergies. The treatment is supportive and needs close followup of renal status. This report describes a rare presentation of Henoch–Schönlein purpura with coronary vasculitis which leads to myocardial infarction at the age of 53. Henoch–Schönlein purpura was diagnosed on the basis of no infection, accelerated ESR (35 mm/h), normal platelet count, positive skin biopsy, proteinuria, and negative searches for rheumatoid factor (RF), antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA), and anti-dsDNA. Keywords: Henoch–Schönlein purpura, myocardial infarction, coronary vasculitis
Introduction
of severe abdominal pain, chest discomfort, sweating, and radiating pain to left hand of 3-h duration. Patient was referred to us from a local hospital with marked ECG changes. He had marked red spots predominantly over lower extremities. Complaints started as red spots over the right foot then spread over the right knee and left foot later on Fig. 1. Few red spots were seen in the hands, too. Without consulting a doctor he traveled to
Henoch–Schönlein purpura (HSP) is characterized by vasculitic involvement of small sized vessels and results in multisystemic manifestations that are most probably caused by an abnormal response of the immune system (hypersensitive vasculitis). The exact definition of the clinical and laboratory symptoms are not yet stable, they are continuously changing. Originally, it had been described as a disease exclusively of children (Heberden, 1801), but newly there are published reports of this hypersensitive vasculitis with IgA deposition manifested in adults as well, and also attaining the cardiovascular system. Henoch–Schönlein purpura is a disease that involves purple spots on the skin, joint pain, gastrointestinal problems, and glomerulonephritis [1]. It is more common in boys than in girls. Many people with Henoch–Schönlein purpura suffered upper respiratory illness during early weeks.
Case Report A 55-year-old male patient was referred from a local hospital as a case of inferolateral myocardial infarction and Henoch–Schönlein purpura presented with complaints
DOI: 10.1556/IMAS.5.2013.2.7
Fig. 1.
89
Red spots were noted over the extremities
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
Rajan et al.
tory rate: 25/min, blood pressure: 180/100 mmHg, lower limb blood pressure: 190 systolic. Red spots were noted over the extremities. On cardiovascular examination first and second heart sound normal, JVP was not elevated, chest: clear, other systems: within normal limits.
nearby state and spent 2 days over there. On return, he had severe intermittent epigastric pain during the night. Family physician advised to visit a surgeon at the earliest. He was admitted and treated as acid peptic disease for 4 days. Reaching home from the hospital, he had severe chest discomfort, sweating, and radiating pain to left hand during the night. He was taken to the local hospital and found to have marked ECG changes and was referred to our center. On routine evaluation, he was diagnosed to have type 2 diabetes mellitus, systemic hypertension and prostatomegaly. His development miles stones were normal. He has no history of cyanosis, giddiness, dyspnea on exertion or pedal edema. He gives history of several episodes of loose stools 2 months back. He is a non-smoker and non-ethanolic. Mother had history of cerebral thrombosis. On initial evaluation, patient had no dyspnea at rest, normally built, nourished, weight: 65 kg, height: 170 cm, and body mass index: 22.4. He was conscious oriented, pulse rate: 100/min, respira-
Fig. 2.
Investigations Laboratory evaluation of urine analysis showed proteinuria, cardiac enzymes were markedly elevated CK-MB: 48.67 ng/mL, troponin T: 0.773 ng/ml, total leukocyte count were elevated TC-24,100 cells/cumm, platelet count: 599,000/cumm, erythrocyte sedimentation rate (ESR): 35 mm/h, C-reactive protein: 1.5 mg/L, 24 h, urine protein: 190 mg/day. Renal and liver function tests were normal. Vasculitis workup – ANA: 0.33, anti-dsDNA: 0.54, c-ANCA, and p-ANCA was negative, IgA level normal, rheumatoid factor: normal. Histopathology: consistent with purpuric lesion, no active vasculitis, resolving HSP (Fig. 2). ECG: Normal sinus rhythm, heart rate: 74/mt, PR interval: 120 ms, QRS: 80 ms, QRS: +110*, ST elevation: II, III, AVF, V2–V6 (Fig. 3). 2D-echocardiography: concentric left ventricular (LV) hypertrophy, normal valves, good LV systolic function, EF: 83%, distal IVS, apex and apicolateral wall akinetic, wall thickness preserved, no clots/effusion. Cath notes: precath diagnosis – acute coronary syndrome, inferolateral myocardial infarction, type 2 diabetes mellitus, systemic hypertension, coronary vasculitis, HSP. Hardware: 7F sheath, 6F JL 3.5, JR4, and PTCA hardware. Coronary angiogram: (right femoral access). Left main coronary artery (LMCA): normal left anterior descending LAD: there is a total mid segment thrombotic occlusion (Fig. 4), proximal left anterior descending (LAD) is normal, left circumflex (Lcx): is non-dominant, large obtuse marginal (OM) which bifurcates into two branches, has thrombosis occlusion in both branches (Fig. 5). Right coronary artery (RCA): dominant and free of disease. Angiography at other sites: normal LIMA. Intervention: left coronary artery (LCA) cannulated with 7F JL3.5 guiding catheter and galeo floppy wire placed across the thrombotic occlusion and the vessels were dottered with a 2 × 11 mmHg balloon. Suboptimal forward flow established no lesion identified repeat dottering did not considerably improve the flow. Final diagnosis of coronary angiogram: thrombotic occlusion of left anterior descending and left circumflex artery.
Histopathology report
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
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Interventional Medicine & Applied Science
HSP and MI a rare presentation
Fig. 3.
Fig. 4.
Acute infero lateral myocardial infarction with evolved anterior
Left anterior descending LAD has a total mid segment throm
Interventional Medicine & Applied Science
Fig. 5.
91
Thrombotic occlusion in both branches of OM
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
Rajan et al.
– Upper respiratory tract infection tract (URI) prodrome, – Mesangioproliferative glomerulonephritis with or without IgA deposition.
Treatment Inferolateral myocardial infarction was treated with GP IIb IIIa inhibitor (Eptifibatide) and unfractionated heparin was started soon after angiogram. During angiogram, dottering of occluded vessels were done. Aspirin, Clopidogrel and Atorvostatin were also administered. HSP treated with steroids and antihistamine. Type 2 diabetes treated with injection insulin. Systemic hypertension treated with metoprolol and amlodepine.
Michel et al. [3] proposed criteria to differentiate HSP from hypersensitivity vasculitis, requiring three or more of the following be present to diagnose HSP: – Palpable purpura, – Bowel angina, – GI bleeding, – Hematuria, – Patient age of onset younger than 20 years.
Discussion Henoch–Schönlein purpura (HSP or anaphylactoid purpura) is an immunoglobulin (Ig) A-mediated smallvessel vasculitis that predominantly affects children but also is seen in adults. HSP is a subset of necrotizing vasculitis characterized by fibrinoid destruction of blood vessels and leukocytoclasis. Clinical manifestations primarily include palpable purpura [4], arthralgia or arthritis, abdominal pain, gastrointestinal (GI) bleeding, and nephritis. The most serious long-term complication from Henoch–Schönlein purpura is progressive renal failure, which occurs in 1–2% of patients. Heberden first described the disease in 1801 in a 5-year-old child with abdominal pain, hematuria, hematochezia, and purpura of the legs. In 1837, Johann Schönlein described a syndrome of purpura associated with joint pain and urinary precipitates in children. Eduard Henoch, a student of Schönlein’s, further associated abdominal pain and renal involvement with the syndrome. Frank proposed the term “anaphylactoid purpura” in 1915. This followed from the reasoning that the pathogenesis likely involved a hypersensitivity reaction to an inciting agent. Two major classification systems are used to make a diagnosis of HSP. The first, from the American College of Rheumatology, requires two or more of the following to be present: – Patient age younger than 20 years, – Palpable purpura, – Abdominal pain or GI bleeding, – Extravascular or perivascular granulocytes on biopsy.
Complications of Henoch–Schönlein purpura [5]: 1. Hepatosplenomegaly 2. Myocardial infarction 3. Pulmonary hemorrhage 4. Pleural effusion 5. Unnecessary abdominal surgery 6. Intussusception 7. Hemorrhage 8. Shock 9. Gastrointestinal bleeding 10. Bowel infarction 11. Renal failure 12. Hematuria 13. Proteinuria 14. Seizure 15. Mononeuropathies In this patient, we found a massive thrombus load in LAD and LCx. Thrombolysis was not considered in this patient in view of hemorrhagic risk. Usually, HSP related MI may not require angioplasty or stenting. Simple dottering is enough with the cover of GPIIb IIIa inhibitors and heparin is sufficient, as we did in this patient.
Conclusions Henoch–Schönlein purpura (HSP) was diagnosed on the basis of no infection, elevated ESR (35 mm/h), normal platelet count, positive skin biopsy, proteinuria and negative searches for RF, ANA, ANCA, and antidsDNA. Henoch–Schönlein purpura with myocardial infarction is a rare situation. Age of presentation is unusual. Henoch–Schönlein purpura is usually seen in children. Here adult presentation at the age of 53 years. In such cases, myocardial infarction-like pattern is caused by thrombus occlusion in coronaries due to coronary vasculitis. In this case patient was taken for coronary angiogram and start on GP IIb IIIa inhibitor (eptifibatide) and unfractionated heparin. Repeat coronary angiogram showed no further thrombus formation. Other standard management of HSP continued.
The second classification system, from the Chapel Hill Consensus Group, primarily uses nonclinical criteria and requires only the presence of small-vessel vasculitis with IgA deposition. Two additional sets of criteria have been suggested for the diagnosis of HSP. Helander et al. [2] posed that three or more of the followings should be present: – Direct immunofluorescence (DIF) results consistent with vascular IgA deposition, – Patient age younger than 20 years, – GI involvement,
ISSN 2061-1617 © 2013 Akadémiai Kiadó, Budapest
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Interventional Medicine & Applied Science
HSP and MI a rare presentation 3. Michel BA, Hunder GG, Bloch DA, Calabrese LH: Hypersensitivity vasculitis and Henoch–Schönlein purpura: a comparison between the 2 disorders. J Rheumatol 19, 721–728 (1992) 4. Bloch DA, Michel BA, Hunder GG, Bloch DA, Michel BA, Hunder GG, McShane DJ, Arend WP, Calabrese LH, Edworthy SM, Fauci AS, Fries JF, Leavitt RY et al.: The American College of Rheumatology 1990 Criteria for the Classification of Vasculitis Patients and Methods Arthritis Rheum 33, 1068 (1990) 5. Mills JA, Michel BA, Bloch DA et al.: The American College of Rheumatology criteria for the classification of Henoch–Schönlein purpura. Arthritis Rheum 33, 1114–1121 (1990)
References 1. Miller ML, Pachman LM (2007): Vasculitis syndromes. In: Nelson Textbook of Pediatrics, 18th ed., eds Kliegman RM, Behrman RE, Jenson HB, Stanton BF, Saunders Elsevier, Philadelphia, PA: chapter 166 2. Helander SD, De Castro FR, Gibson LE: Henoch–Schönlein purpura: clinicopathologic correlation of cutaneous vascular IgA deposits and the relationship to leukocytoclastic vasculitis. Acta Derm Venereol 75, 125–129 (1995)
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