This process is thought to stabilise the IgA molecule and make it less prone to proteolysis. The first sugar is always N-acetyl-galactosamine (GalNAc), followed by other galactoses and sialic acid. In HSP and IgAN, these sugar chains appear to be deficient. The exact reason for these abnormalities is not known. Classification
Multiple standards exist for defining Henoch–Schönlein purpura, including the 1990 American College of Rheumatology (ACR) classification and the 1994 Chapel Hill Consensus Conference (CHCC). Some have reported the ACR criteria to be more sensitive than those of the CHCC.More recent classifications, the 2006 European League Against Rheumatism (EULAR) and Pediatric Rheumatology Society (PReS) classification, include palpable purpura as a mandatory criterion, together with at least one of the following findings: diffuse abdominal pain, predominant IgA deposition (confirmed on skin biopsy), acute arthritis in any joint, and renal involvement (as evidenced by the presence of blood and/or protein in the urine). Differential diagnosis
Henoch–Schönlein purpura may present with an atypical manifestation, which can be confused with papular urticaria, systemic lupus erythematosus, meningococcemia, dermatitis herpetiformis, and  acute hemorrhagic edema of infancy. Treatment
As of 2017, the optimal way to treat Henoch–Schönlein purpura remains controversial. Analgesics may be needed for the abdominal and joint pains. Wound care is warranted if the skin death and ulcerations occur. It is uncertain as to whether HSP needs treatment beyond controlling the symptoms. Most people do not receive therapy because of the high spontaneous recovery rate. Experts disagree on whether to routinely use corticosteroids as treatment for HSP.
Abdominal aortic aneurysm
Abdominal aortic aneurysms (AAAs) are more common than their thoracic counterpart. One reason for this is that elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the abdominal aorta as compared to the thoracic aorta. Another is that the abdominal aorta does not possess vasa vasorum, the nutrient-supplying blood vessels within the wall of the aorta. Most AAA are true aneurysms that involve all three layers (tunica intima, tunica media and tunica adventitia). The prevalence of AAAs increases with age, with an average age of 65–70 at the time of diagnosis. AAAs have been attributed to atherosclerosis, though other factors are involved in their formation. The risk of rupture of an AAA is related to its diameter; once the aneurysm reaches about 5 cm, the yearly risk of rupture may exceed the risks of surgical repair for an average-risk patient. Rupture risk is also related to shape; so-called "fusiform" (long) aneurysms are considered less rupture-prone than "saccular" (shorter, bulbous) aneurysms, the latter having more wall tension in a particular location in the aneurysm wall.Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus. A bruit may be heard from the turbulent flow in the aneurysm. Unfortunately, however, rupture may be the first hint of AAA. Once an aneurysm has ruptured, it presents with classic symptoms of abdominal pain which is severe, constant, and radiating to the back.The diagnosis of an abdominal aortic aneurysm can be confirmed at the bedside by the use of ultrasound.