Treatment with plasma exchange of a pregnant woman with anti-PP1Pk alloimmunization: A case report.

The histo-blood group antigens P, P1 and Pk are a closely related set of glycosphingolipid structures expressed by red blood cells and other tissues. None of these three characters is expressed on p cells, a null phenotype that arises in the context of homozygous mutation of the A4GALT gene. Subjects with p phenotype spontaneously develop a natural alloantibody named anti-PP1Pk, which is a mixture of IgG and IgM against P1, P and Pk. While anti-P1 is a weak cold antibody with poor clinical significance, anti-P and anti-Pk antibodies are potent haemolysins responsible for severe hemolytic transfusion reactions. The rare anti-PP1Pk alloantibodies are associated with recurrent spontaneous abortion in the first trimester of gestation. P and Pk antigens are expressed at high levels on the placenta and antibodies directed against both these structures are deleterious to placental trophoblasts. Here we describe the use of plasma exchange (PEX) in a nulliparous 39-year-old woman with anti-PP1Pk antibodies and a history of repeated spontaneous early abortions and hypofertility. The patient underwent apheresis starting from the third week throughout the pregnancy and a healthy child was delivered by cesarean section at 35 WG. The newborn required only phototherapy within a few days of life. We can state that an early treatment with the only PEX has proven to be effective and safe in the management of a fetomaternal P-incompatibility caused by a high anti-PP1Pk titer (256).

Hyperchloremic metabolic acidosis after plasma exchange in a patient with renal transplant rejection: A case report.

Therapeutic plasma exchange (TPE) is an effective treatment for several renal disorders, including renal transplant rejection. However, repeated plasma exchanges can result in various metabolic disturbances and complications. We present a 61-year old male with a medical history of type 2 diabetes, hypertension, successfully treated multiple myeloma, and a post-mortem kidney transplantation 7 months prior to presentation. The patient was hospitalized with an antibody-mediated transplant rejection for which treatment with methylprednisolone, TPE with a 40 g/L albumin solution as a replacement fluid, and intravenous immunoglobulins was initiated. After four TPE treatments, the patient developed gastrointestinal complaints and muscle weakness. Despite daily oral bicarbonate supplementation, laboratory tests revealed a hyperchloremic metabolic acidosis: bicarbonate 11.7 mmol/L, chloride 111 mmol/L, and sodium 138 mmol/L. Metabolic acidosis due to citrate accumulation was ruled out with a normal total-to-ionized calcium ratio. After treatment with intravenous bicarbonate supplementation, the symptoms disappeared. Analysis of the albumin solution showed a chloride concentration of 132 mmol/L. This is the first case that describes severe metabolic acidosis after multiple sessions of TPE with an albumin solution in a patient with impaired renal function. The hyperchloremic metabolic acidosis is the result of administration of large volumes of an albumin solution with high chloride concentrations. Special attention should be paid to the acid-base balance during TPE in patients with impaired renal function. Future research should investigate the incidence of hyperchloremic metabolic acidosis during TPE in patients with impaired renal function.

Dual-chambered venous access port as alternative access for extracorporeal apheresis therapy.

PURPOSE: To evaluate the use of a dual-chambered venous access port for extracorporeal apheresis therapy. METHODS: This was a single-center retrospective analysis of all patients who received a dual-chambered venous access port for apheresis therapy over a 36-month period. Clinical success was defined as successful completion of at least one round of apheresis via the venous access port. Major complications were defined as any event requiring elevation of patient care and/or venous access port removal or repositioning. Minor complications were defined as venous access port issues resolved with clinical intervention. RESULTS: Forty-four patients had a venous access port placed at the time of this study. Patients underwent red cell exchange (n = 33), therapeutic plasma exchange (n = 6) or extracorporeal photopheresis (n = 5). Forty (90%) patients had autoimmune diseases and four (10%) had neoplastic processes. Clinical success was achieved in 42 (95.5%) patients. Average venous access port dwell time was 632 days (range = 42-1191 days). All therapies through the venous access ports were well tolerated and no patients reported pain or discomfort. Major complications were seen in nine (20.5%) patients-the majority (n = 7) of which were due to venous access port malfunction-and resolved with catheter revision. One (2.27%) major complication involved an infected venous access port, and one involved a large hematoma at the venous access port site. Minor complications were seen in eight (18.2%) patients, where simple flushing of the catheter with saline or tissue plasminogen activator resolved the issue. CONCLUSION: The dual-chambered venous access port was successfully used for sustained blood flow in apheresis therapy with a moderate, yet correctable complication rate.

Role of therapeutic plasma exchange in acute liver failure due to yellow phosphorus poisoning.

BACKGROUND: Therapeutic plasma exchange (TPE) has been utilized in various liver disorders. There is limited data on the efficacy of TPE in patients with acute liver failure (ALF). METHODS: Study group consisted of patients who underwent TPE for ALF due to yellow phosphorous poisoning (YPP) between 2015 and 2019. Demographic data and biochemical parameters were recorded before and after TPE. Overall survival and transplant-free survival (based on King's College Hospital Criteria [KCHC]) were analyzed. RESULTS: Forty-three patients underwent TPE for ALF due to YPP. Most of them were young males. Overall survival was 34 (79.06%). In our study population, 20 patients fulfilled KCHC (Group A) and 23 did not fulfill KCHC (Group B). Both the groups showed significant improvement in alanine aminotransferase, aspartate aminotransferase, and international normalized ratio (INR) after TPE (p < 0.05). In Group B, there was significant improvement in ammonia after TPE (p < 0.05) and all 23 patients (100%) survived after TPE. In Group A, 4 underwent liver transplantation (LT), 7 survived without LT, and the remaining 9 died without LT. Mean survival after completing TPE was 41.2 ± 44.5 days in Group A and 90 days in Group B. This difference was statistically significant (p = 0.001). There was statistically significant difference in post-TPE values of INR (p = 0.012) and ammonia (p = 0.011) between non-survivors and survivors. Adverse events such as hypotension (11.62%) and minor allergic reaction (4.65%) were managed conservatively. CONCLUSION: TPE is an effective procedure in ALF due to YPP, not fulfilling KCHC for LT. In KCHC fulfilled group, though it shows LT-free survival benefit, there is requirement of prospective, large volume, multi-center study to assess its efficacy.

Continuous infusion of calcium gluconate in 5% albumin is safe and prevents most hypocalcemic reactions during therapeutic plasma exchange.

While therapeutic plasma exchanges (TPEs) performed with 5% albumin are considered safe, concerns regarding venous access and hypocalcemic toxicity remain. We reviewed the frequency of complications during TPEs performed with 5% albumin supplemented with calcium gluconate and potassium chloride for a 5 year period in our institution. Eighty-four adult patients (46 males and 38 females) underwent 581 plasma exchanges during the study period. The most common indications were myasthenia gravis (37%), acute inflammatory demyelinating polyradiculoneuropathy (31%), and chronic inflammatory demyelinating polyneuropathy (13%). All procedures used 2.2% ACD-A delivered at a calculated average rate of 0.26 mg/kg/min, which led to a mean dose of citrate per TPE of 2.18 +/- 0.48 g or 27.8 +/- 5.24 mg/kg of body weight. Venous access difficulties occurred in 85 procedures (14.6%), but most TPEs were completed successfully. Hypotension and citrate toxicity were seen in <5% of the TPEs and were mostly reversible. Only 17 exchanges (3%) had to be aborted because of the loss of venous access (n = 9), hypocalcemic toxicity (n = 3), hypotension (n = 2), panic attacks (n = 2), and one atypical reaction due to the interaction with an angiotensin converting enzyme inhibitor. Comparison between pre- and post-TPE potassium levels showed a statistically significant mean decrease of 7%, from 4.1 mequiv/l to 3.8 mequiv/l (P < 0.0001). We attribute the low rate of hypocalcemia to our practice of adding calcium and potassium to the replacement fluid and suggest that this method could become standard of care.

Virus inactivation by solvent/detergent treatment and the manufacture of SD-plasma.

Solvent/Detergent (SD) is an extraordinarily effective means for eliminating enveloped viruses from plasma and plasma products. The safety margin suggested by the rapid and complete kill of enveloped viruses observed in the laboratory has been confirmed repeatedly by groups worldwide and by thirteen years of routine clinical use encompassing an estimated 35 million doses of a wide variety of products. Throughout this time, there has not been a single documented case of enveloped virus transmission by an SD-treated product. This record of safety spawned the development of SD-treated plasma as a substitute for fresh frozen plasma (FFP) and has encouraged the adoption of SD for the treatment of non-blood products such as monoclonal antibodies and those derived from recombinant DNA procedures. This review summarizes the use of SD treatment, including its use in combination with other viral elimination procedures, and also summarizes Vitex's initial experience in the manufacture of SD-Plasma, recently licensed by the U.S. FDA.

Prevention of citrate reactions during therapeutic plasma exchange by constant infusion of calcium gluconate with the return fluid.

We have examined the effectiveness of intravenous calcium gluconate infusion in the prevention of citrate reactions during therapeutic plasma exchange. Over 3 years, 636 procedures were performed on 90 patients, mostly for treatment of neurological disorders. Return fluid consisted of 4-5% human serum albumin in 0.9% NaCl. Anticoagulant ACD-A was used at a starting ratio of 1:16. Whole blood flow rates were 70-80 ml/min. Treatments were divided into three groups for management of citrate reactions: Group A (360 treatments) were managed using simple measures only, including slowing the whole blood flow rate, altering the ACD:whole blood flow ratio, and oral calcium carbonate wafers; Group B (102 treatments) received small intravenous boluses of 10% calcium gluconate, us to 25 ml during the procedure; Group C (174 treatments) received constant infusion of calcium gluconate (10 ml/liter of return fluid) during the procedure. Citrate reactions occurred in 35.6% of Group A and 29.4% of Group B treatments (P = 0.3), but in only 8.6% of Group C treatments (P < 0.0001). Men with and without reactions were the same age (mean 63.3 vs. 61 years, P = 0.0823), but women with reactions were younger than women without reactions (mean 49.9 vs. 57.9 years, P < 0.0001). Supplementation of the return fluid with calcium gluconate is an effective, convenient, and well-tolerated method for prevention of citrate toxicity during therapeutic plasma exchange procedures using albumin-based return fluid.