Spring Fever Archetypes

Overview:

Henoch-Schonlein Purpura (HSP) is an inflammatory disorder, more commonly known as Spring Fever. It coined this nickname from the high occurrence in the beginning of spring, triggered by respiratory illnesses from winter. HSP was first noted in 1801 by Dr. William Heberden, a london physician, who made case notes on a young boy aged five that was displaying, what we know to now be, typical HSP symptoms.

HSP is a type of vasculitis, or inflammation of the blood vessels, that targets mainly children between two and thirteen years old. The disorder itself is rare, and recurrence even more rare, with adults showing much more severe symptoms than children on average. If untreated HSP can be fatal due to kidney and intestinal complications.

This leads to the inflammation and potential damaging of the kidneys and eventual kidney disease unless treated. HSP causes an extreme and severe form of IgAN. There are two forms of IgA, IgA1 and IgA2. IgA1 is the only form involved with HSP. “IgA with diminished hinge-region glycosylation are prone to aggregate into macromolecular complexes. These complexes activate the alternative pathway of complement, and then deposit into the renal mesangium” (Saulsbury). The bodies immune response gets triggered by an upper respiratory illness, and produces IgA antibodies. If these IgA antibodies have hinge regions that are not fully developed correctly then they go haywire; producing more and more and clumping together to form complexes that deposit themselves into the kidneys. These malfunctioning IgA1 antibodies also deposit themselves into blood vessel walls, causing them to rupture and blood to pool at the surface of the skin, the cause of the characteristic purple purpura rash (Saulsbury). Individuals who suffer from HSP do not always produce these malfunctioning IgA antibodies, and many researchers are puzzled by and still researching the “come and go” effect of IgAN affliction in correspondence to