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BLOG: How and why does asteroid hyalosis form?
The process by which asteroid hyalosis forms is a complicated one, but it’s an interesting one and one that’s worth knowing.
When I was a resident, I was taught that asteroid bodies (ABs) are soaps that precipitate out of solution. Not really remembering my chemistry, I probably just smiled and nodded. But it’s always been interesting to me whenever I see it, and I’ve always wondered why it’s so unilateral. So let’s dig into this thing we call asteroid hyalosis (AH).
A Google search of the word “hyalosis” reveals only links related to AH. As far as I can tell, the only situation where the word hyalosis is used is when referring to AH. The original term for AH used to be “asteroid hyalitis” but it was changed in the 1960s due to the absence of inflammatory changes. Both terms refer to the word “hyaloid” (from the Greek for “glassy” or “transparent”), which we use for the membrane encasing the vitreous. Thus, AH is “asteroid-like particles in the vitreous.”
In the 1920s, Verhoeff (he of the Verhoeff’s membrane fame) first postulated ABs were calcium soaps. The process of saponification requires us to remember some chemistry, so let’s pause here for a reminder.
Soaps occur when a fat is mixed with a strong base. People used to make bars of soap by boiling beef fat mixed with lye (sodium hydroxide). Remember that, organically, the structure of fat has chains of fatty acids with carboxyl groups on the ends. And recall that carboxyl groups are carbon atoms with one oxygen attached with a strong double bond, another oxygen atom with a single bond and a hydrogen atom more weakly attached. When mixed with a base, the carbon and hydrogen atoms are pulled off, which creates a negative charge and allows for the base (like sodium, which is Na+ or calcium, which is Ca2+) to bond to the fatty acid. Thus, a soap is formed: a fatty acid with a base on the end.
By the way, this happens all the time in the tear film. When we see a foamy, frothy tear film we are looking at soapy tears. When bacteria get into the tear film (from anterior blepharitis) they have a lipolytic effect on the meibum secreted from the meibomian glands. Chemically, meibum is composed of chains of fatty acids. And there are plenty of basic atoms (like sodium and calcium) in the tear film naturally. Typically, this combination doesn’t create saponification because there is no catalyst to start the reaction (like the heat in boiling beef fat). But when bacteria are added to the tear film, enzymes like lipase start to break down the carboxyl groups, allowing bases to bond.
The reason this is such a problem in the tear film is because soap has a detergent effect (obviously), which can wreak havoc on the ocular surface in the form of punctate epithelial erosions and inflammation.
Many studies over the years have confirmed that ABs are made primarily of calcium and phospholipids, which would make sense for a soap etiology. But its behavior is not consistent with soap because the ABs did not dissolve in acetic acid; also there didn’t seem to be much of a catalyst for the reaction. This left researchers looking for more clues about how AH is formed.
In the 1980s, Streeten wrote that the typical vitreous body is “unlikely to have sufficient phospholipids to create asteroid hyalosis bodies” and postulated that the lipids come from an outside source, like a brief inflammation in the vitreous/retina or a vitreous hemorrhage. This also might serve to explain its unilaterality.
In the early 2000s, Komatsu found that throughout the calcium and phosphate in ABs is a substance called hydroxylapatite (HOA). HOA is naturally found throughout the body, mostly in teeth and bones, and is used today in surgical implants. Komatsu found that as we age, the collagen in vitreous fibrils starts to degenerate, which causes the fibrils to clump together (syneresis) and develop a negative charge. These negative ions allow HOA formation by binding to calcium. This process is most consistent with lithiasis, or the formation of stone concretions like kidney stones. (Conjunctival concretions, by the way, do not have surface crystallization on electron microscopy as do ABs and kidney stones and are not considered a lithiasis).
So have we answered the question of how and why AH forms? Probably not. We know that medicine no longer considers AH a soap, and it is now thought to be a lithiasis. But many questions still exist, like why is it so unilateral?
Its unilaterality is thought to be between 75% and 90% based on many studies, including the Beaver Dam and the Blue Mountain Eye Studies. Those same studies put the prevalence at 1% to 1.6% of the overall population, but 0% under the age of 55 years and 2% over the age of 75 years. Most studies, like the high sample-sized ones mentioned, find no correlation with heart disease, diabetes or smoking. But other studies do find links to diabetes and obesity, including one that fed beagle puppies a diet of 30% galactose and caused every one of them to develop AH after 3 or 4 years.
What is the trigger that causes the lithiasis to happen? Does the phospholipid come from inside the vitreous, or is there an external source? Why do some people have such dense AH? Perhaps because more phospholipid entered into their vitreous? Why so unilateral? It seems like there are still a lot of questions left to be answered about AH. But I still think it’s a fascinating condition to contemplate.
References:
Bergren RL, et al. Am J Ophthalmol. 1991;111(3):289-293.
Kador PF, et al. Eye. 2008;22:1278-1285. doi:10.1038/eye.2008.35.
Kador PF, et al. Arch Ophthalmol Vis Sci. 2002;43(6):1916-1921.
Komatsu H, et al. Med Electron Microsc. 2003;36:112-119.
Mitchell P, et al. Am J Ophthalmol. 2001;132(1):70-75. doi:
Streeten BW. Arch Ophthalmol. 1982;100:969-975.
Topilow HW, et al. Arch Ophthalmol. 1982;100(6):964-968. doi:10.1001/archopht.1982.01030030972015.