A number of phospholipids were found to be uniquely present in control but absent in glaucomatous TM and vice versa. Compared to a previous study of control and POAG blood, a number of these phospholipids are absent locally (TM), as well as systemically (in blood).

To compare phospholipid (phosphatidylcholine, phosphatidylserine, phosphatidylethanolamine and phosphatidylinositol) profiles of human control and glaucomatous aqueous humor (AQH). AQH samples were procured during surgery from human POAG and control subjects (n=15 each). Samples were used following institutional review board approved protocols and adhering to the tenets of the Declaration of Helsinki. Lipid extraction was performed using a modification of the Bligh and Dyer method, protein concentrations were determined using the Bradford’s method, and select samples were confirmed with Densitometry of PHAST gels. Lipids were identified and subjected to ratiometric quantification using a TSQ Quantum Access Max triple quadrupole mass spectrometer utilizing precursor ion scan (PIS) or neutral ion loss scan (NLS) using appropriate class specific lipid standards in a two step quantification process. The comparative profiles of phosphatidylcholines, phosphatidylserines, phosphatidylethanolamines and phosphatidylinositols between control and glaucomatous AQH showed several species common between them. A number of unique lipids in all four phospholipid classes were also identified in control eyes that were absent in glaucomatous eyes and vice versa. A number of phospholipids were found to be uniquely present in control, but absent in glaucomatous AQH and vice versa. Compared with a previous study of control and POAG red blood cells, a number of these phospholipids are absent locally (AQH).

A high percentage of cholesterol and glycosphingolipid species was found to be common between control and POAG AQH and TM. Several cholesterol and glycosphingolipid species was found to be unique in a subset of POAG or controls. Glaucomatous aqueous humor and TM showed relatively higher levels of zymosterol (an intermediate precursor of cholesterol) and decreased glycoceramide levels, respectively.

Purpose To identify the sphingolipid and ceramide species and their quantitative differences between normotensive and hypertensive intraocular pressure states in DBA/2J mouse aqueous humor (AH). Methods Normotensive and hypertensive AH was sampled from mice by paracentesis. Lipid extraction was performed using modifications of the Bligh and Dyer method. Protein concentration was estimated using the Bradford colorimetric assay. Sphingolipids and ceramides were identified and subjected to ratiometric quantification using appropriate class specific lipid standards on a TSQ Quantum Access Max triple quadrupole mass spectrometer. Results The comparative profiles of normotensive and hypertensive DBA/2J mouse AH showed several species of sphingomyelin, sphingoid base, sphingoid base-1-phosphate (S1P) and ceramides common between them. A number of unique lipids in each of the above lipid classes were also identified in normotensive AH that were absent in hypertensive AH and vice versa. Conclusion A number of sphingolipid and ceramide species were found to be uniquely present in normotensive, but absent in hypertensive AH and vice versa. Further pursuit of these findings is likely to contribute towards expanding our understanding of the molecular changes associated with increased intraocular pressure (IOP) and glaucoma.

Immune thrombocytopenic purpura (ITP) is an acquired thrombocytopenia where autoantibodies are generated against platelet antigens. Primary ITP is often idiopathic, whereas secondary ITP has many potential causes, including drug induced, infection related (human immunodeficiency virus, hepatitis C), leukemias, or autoimmune such as systemic lupus erythematosus. ITP is a common cause of thrombocytopenia in asymptomatic individuals, where evidence of bleeding may be minor or absent. Chronic silent bleeding leading to extreme anemia in patients with ITP is rare, and evidence of multiorgan damage is even rarer; hence the relevance of this case report. Here we describe a case of primary ITP with severe chronic blood loss leading to profound anemia causing renal failure and a type II non-ST elevation myocardial infarction. Our patient underwent extensive workup for the etiology of both thrombocytopenia and anemia and was eventually treated with packed red blood cell and platelet transfusions, along with intravenous steroids and immunoglobulin therapy.