The O‐methyl phosphoramidate (MeOPN) motif is a non‐stoichiometric modification of capsular polysaccharides (CPS) in ≈70 % of all Campylobacter jejuni strains. Infections by C. jejuni lead to food‐borne illnesses and the CPS they produce are key virulence factors. The MeOPN phosphorus atom in these CPS is stereogenic and is found as a single stereoisomer. However, to date, the absolute stereochemistry at this atom has been undefined. We report the synthesis of the three repeating units found in C. jejuni 81‐176 CPS; one of these possesses a MeOPN group. In the course of these studies we established that the stereochemistry of the phosphorus atom in this MeOPN group is R. These studies represent the first unequivocal proof of stereochemistry of this group in any C. jejuni CPS. The compounds produced are anticipated to be useful tools in investigations targeting the function and biosynthesis of this structurally‐interesting modification, which so far has only been identified in campylobacter.

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Synthesis of β-C-d-galactosyl d- and l-alanines is carried out via a highly stereoselective Grignard reaction of glycosyl iodides, Sharpless dihydroxylation and SN2 displacement of the corresponding mesylate or tosylate. Alternatively, attempted triflation of the intermediate alcohols triggers a stereoselective debenzylative cyclization leading to interesting bicyclic trans-fused compounds.

Post-transfusion purpura (PTP) is a rare disease characterized by life-threatening thrombocytopenia after transfusion of any platelet-containing blood products, such as platelets(PLT) or packed red blood cells (PRBCs). We report an interesting case of PTP in a young lady after receiving multiple blood products. CASE PRESENTATION:A 36-year-old female with a past medical history of diabetes mellitus and left-sided below-knee amputation (BKA) was admitted to the Intensive Care Unit (ICU) for emphysematous osteomyelitis with intraosseous gas in the calcaneus, cuboid, and fifth metatarsal base of the right lower extremity. She underwent right-sided BKA, requiring multiple PRBC transfusions due to a combination of blood loss during surgery and chronic anemia. The initial platelet count was normal at 329,000/uL. Five days after the PRBC transfusion, it trended down to 17,000/uL and there was concurrent development of a purpuric rash over both arms. Bloodwork was notable for elevated prothrombin time and activated partial thromboplastin time. Hemolysis workup and Coombs test were negative. Fibrinogen was elevated, ruling out disseminated intravascular coagulation. PTP was suspected based on the clinical presentation and exclusion of other etiologies. Anti-human platelet antigen-1a (HPA-1a) antibodies were obtained. Empiric treatment with intravenous immunoglobulin (IVIG) and steroids was promptly initiated. Platelet count improved to 157,000/uL after four doses of IVIG. The patient tested positive for HPA-1a. However, due to the urgent need for treatment, the test sample for the anti-platelet antibodies was drawn after the initiation of IVIG. The development of thrombocytopenia in the classic time frame with the characteristic rash and improvement after receiving IVIG make PTP the most likely diagnosis. She was recommended to receive only washed PRBCs in the future to prevent a recurrence. DISCUSSION: PTP is a rare, underdiagnosed, and potentially fatal reaction, with the development of severe thrombocytopenia 2-14 days after transfusion of platelet-containing blood products. It is considered to be caused by alloimmunization against platelet antigens, with HPA-1a being the most common antibody1. Some cases of HPA-1b mediated PTP have been reported as well2. Diagnosis is often subtle and challenging, therefore a strong clinical suspicion is needed. A history of blood product transfusion a few days before the development of thrombocytopenia should make the physician think about the possibility of PTP. Treatment includes IVIG, steroids, or plasmapheresis3, and initiation of treatment should not wait for diagnostic confirmation.CONCLUSIONS: Clinicians should have high clinical suspicion for PTP in patients with acute, severe thrombocytopenia which develops after blood transfusions, and treatment should be initiated early to favorably alter the course of the disease.

A commonly seen phenomenon in the hospital and critical care setting is anaphylaxis. This acute systemic inflammatory reaction can lead to anaphylactic shock in severe cases and potentially be fatal. The role of platelets in anaphylactic reactions is not well established; however, platelets, among other mediators such as platelet-activating factor, have been shown to promote a prothrombotic state shortly after an acute hypersensitivity reaction. In addition, the aggregation of platelets promoted by platelet-activating factor and other mediators can also lead to thrombocytopenia. We present a case of a 57-year-old woman who developed severe anaphylaxis while receiving chemotherapy with paclitaxel suspended in Cremophor, a well-known allergen. She was profoundly thrombocytopenic following the reaction and was treated with therapeutic anticoagulation, with no thrombus formation.