After using H&E, hematoxylin and eosin, to stain the samples, the researchers only found some inflammatory cells like neutrophils, monocytes, lymphocytes, and eosinophils. In four of the samples, immunofluorescence microscopy, where fluorescent antibodies bind to a protein of interest and the expression levels are observed through microscopy, was used but there were no signs of immunoglobulins such as IgG, IgM, IgA or C3 found. Since the first description of this condition, there were very few case reports after, indicating the infrequency of pruritic folliculitis. This was also shown by a prospective study that was conducted in 1994 by Roger et al. that concluded with one individual out of 3,192 pregnant mothers (0.03%) had symptoms which were consistent with the diagnosis of pruritic folliculitis. Pathophysiology
Folliculitis, by itself, is a common inflammation process of hair follicles in response to infection or damage to the hair follicles. This inflammatory response can be caused by bacteria, fungi, viruses, or simply ingrown hair. However, pruritic folliculitis of pregnancy is different in that it only occurs in pregnant individuals and during the second or third trimester of pregnancy. There is no clear mechanism in how pruritic folliculitis of pregnancy develops. Because this is a rare condition, there is still currently not enough research to study the cause of it. Some research suggest that this condition may be due to hormone level imbalance during pregnancy .
As the teratogenic effects of warfarin are well known, the medication is rarely prescribed to pregnant women. However, for some patients, the risks associated with discontinuing warfarin use may outweigh the risk of embryopathy. Patients with prosthetic heart valves carry a particularly high risk of thrombus formation due to the inorganic surface and turbulent blood flow generated by a mechanical prosthesis. The risk of blood clotting is further increased by generalized hypercoagulability as concentrations of clotting factors rise during pregnancy. This increased chance of blood clots leads to an increased risk of potentially fatal pulmonary or systemic emboli cutting off blood flow and oxygen to critical organs. Thus, some patients may continue taking warfarin throughout the pregnancy despite the risks to the developing child. Mechanism
Warfarins ability to cause fetal warfarin syndrome in utero stems from its ability to limit vitamin K activation. Warfarin binds to and blocks the enzyme Vitamin K epoxide reductase which is usually responsible for activating vitamin K during vitamin K recycling. Vitamin K, once activated, is able to add a carboxylic acid group to glutamate residues of certain proteins which assists in correct protein folding. Without active vitamin K, a fetus exposed to warfarin is unable to produce large quantities of clotting and bone growth factors. Without vitamin K, clotting factors II, VII, IX and X are unable to be produced. Without these vital parts of the coagulation cascade a durable fibrin plug cannot form to block fluid escaping from damaged or permeable vasculature.