Acute atherosis not in preeclampsia.
I had a case today, and periodically have had other cases, of the unexpected finding of acute atherosis in the spiral arteries in the placental membranes. This was a case of preterm premature rupture of membranes, and the infant was borderline small but there was no evidence of preeclampsia in the electronic medical record. I am puzzled as to what this finding means if anything to the future of the child or mother.
What is acute atherosis?
The lesion is most often found in pre-eclampsia but has been reported in unexplained intrauterine growth retardation and in a case of SLE. Acute atherosis appears to be a lesion of insudation of serum proteins including lipoproteins (hence foam cells) into the spiral artery media. Some have likened the lesion to that caused by angiotensin There are high concentrations of molecules in the renin angiotensin system in the decidua. However, injury to and serum leakage through the endothelium is perhaps a more plausible mechanism given the wide spread endothelial injury in pre-eclampsia. An understanding of the lesion should answer two critical questions: 1) why does the lesion occur only in spiral arteries, and 2) why is the lesion present in only some cases of preeclampsia?
Even large studies of maternal arteries have not found acute atherosis in other organs. It is not for lack of looking, e.g. 677 maternal autopsies reported by Sheehan and Lynch1. Perhaps it has something to do with the hormonal responsiveness of these vessels that constrict with menstruation, as elegantly demonstrated in endometrial transplants into the anterior chamber of monkey eyes. At the least, the arteries are unusual in that they shed with each menstruation and are surrounded in pregnancy by decidual cells.
Acute atherosis is present in only a minority of patients with preeclampsia. This is unlikely to be a sampling error, although not all membrane samples contain many or even any spiral arteries. I presented an abstract at our MAPS meeting showing little gain in diagnosis with 4 samples compared to one sample of membrane. Subsequently Yasser Morgan and I demonstrated that we could identify acute atherosis using a dissecting scope of the membranes stretched over a white card. Even with this technique spiral artery lesions may not be present. While a single sample of membranes may miss some cases of acute atherosis, the evidence suggests that in most cases the lesion is not really present. Perhaps acute atherosis is a marker for yet another preeclampsia associated angiopathic protein, like sFlt1 and endoglin.
Note to pathologists: A colleague tells me he never sees it! I suggest to novice pathologists that they should scan the entire membrane slide at low power for vascular lesions as part of the routine approach to placental slides. With experience acute atherosis will stick out like a pink highlighted text. I make the diagnosis if the bright pink fibrinoid of the media is present, and do not require foam cells. The diagnosis is more difficult in the basal decidua because most spiral arteries have been destroyed by trophoblastic invasion and are only fibrin lined shells lined with trophoblast. However, distinct acute atherosis does occur in the basal decidua, likely in vessels not invaded by tropphoblast.
1. Sheehan HL, Lynch JB. Pathology of Toxaemia of Pregnancy. Baltimore: The William and Wilkins Company; 1973.
I had a case today, and periodically have had other cases, of the unexpected finding of acute atherosis in the spiral arteries in the placental membranes. This was a case of preterm premature rupture of membranes, and the infant was borderline small but there was no evidence of preeclampsia in the electronic medical record. I am puzzled as to what this finding means if anything to the future of the child or mother.
What is acute atherosis?
The lesion is most often found in pre-eclampsia but has been reported in unexplained intrauterine growth retardation and in a case of SLE. Acute atherosis appears to be a lesion of insudation of serum proteins including lipoproteins (hence foam cells) into the spiral artery media. Some have likened the lesion to that caused by angiotensin There are high concentrations of molecules in the renin angiotensin system in the decidua. However, injury to and serum leakage through the endothelium is perhaps a more plausible mechanism given the wide spread endothelial injury in pre-eclampsia. An understanding of the lesion should answer two critical questions: 1) why does the lesion occur only in spiral arteries, and 2) why is the lesion present in only some cases of preeclampsia?
Even large studies of maternal arteries have not found acute atherosis in other organs. It is not for lack of looking, e.g. 677 maternal autopsies reported by Sheehan and Lynch1. Perhaps it has something to do with the hormonal responsiveness of these vessels that constrict with menstruation, as elegantly demonstrated in endometrial transplants into the anterior chamber of monkey eyes. At the least, the arteries are unusual in that they shed with each menstruation and are surrounded in pregnancy by decidual cells.
Acute atherosis is present in only a minority of patients with preeclampsia. This is unlikely to be a sampling error, although not all membrane samples contain many or even any spiral arteries. I presented an abstract at our MAPS meeting showing little gain in diagnosis with 4 samples compared to one sample of membrane. Subsequently Yasser Morgan and I demonstrated that we could identify acute atherosis using a dissecting scope of the membranes stretched over a white card. Even with this technique spiral artery lesions may not be present. While a single sample of membranes may miss some cases of acute atherosis, the evidence suggests that in most cases the lesion is not really present. Perhaps acute atherosis is a marker for yet another preeclampsia associated angiopathic protein, like sFlt1 and endoglin.
Note to pathologists: A colleague tells me he never sees it! I suggest to novice pathologists that they should scan the entire membrane slide at low power for vascular lesions as part of the routine approach to placental slides. With experience acute atherosis will stick out like a pink highlighted text. I make the diagnosis if the bright pink fibrinoid of the media is present, and do not require foam cells. The diagnosis is more difficult in the basal decidua because most spiral arteries have been destroyed by trophoblastic invasion and are only fibrin lined shells lined with trophoblast. However, distinct acute atherosis does occur in the basal decidua, likely in vessels not invaded by tropphoblast.
1. Sheehan HL, Lynch JB. Pathology of Toxaemia of Pregnancy. Baltimore: The William and Wilkins Company; 1973.
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