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Parvovirus
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Avoidance of contact with infected children—or, if possible, children in general—is the best prevention. This is not always feasible. No specific antiviral therapy or vaccine is available for parvovirus B19 infection. Frequent hand washing is effective in preventing disease transmission [2]. Intravenous immunoglobulin (IVIG) prophylaxis is reasonable to consider for documented exposures in immunocompromised patients, although it is not currently recommended for prophylaxis in pregnancy.
Muscle Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Kourosh Rezania, Peter Pytel, Betty Soliven
Intravenous immunoglobulin (IVIG):14 starting dose is 2 g/kg divided over 4–5 days, every month for the first 2–3 months. This can be tapered to 0.5–1 g/kg every month depending on the individual response. IVIG is generally reserved for more severe and refractory cases and patients with significant adverse effects to steroids and other immunosuppressants.
Invasive Group A Streptococcal Infections
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Treatment consists of intravenous benzylpenicillin. All GAS strains isolated from invasive infections produce toxins, and antibiotic treatment should also include an antibiotic that inhibits toxin production. Clindamycin or linezolid are often added to intravenous benzylpenicillin. Intravenous immunoglobulin (IVIG) may be considered in toxic shock syndrome.
Therapeutic issues in Guillain–Barré syndrome
Published in Expert Review of Neurotherapeutics, 2023
Intravenous immunoglobulin (IVIG) is a medication that is derived from human plasma. It is produced by pooling, purifying, and concentrating plasma from thousands of healthy donors in order to obtain a high concentration of antibodies, mostly IgG. IVIG is used to treat many autoimmune and inflammatory conditions. Its exact mechanism of action remains debated but probably involves several pathways in the innate and adaptative immune system, involving the Fab- and Fc fragments [55]. Its efficacity in GBS was suspected in 1988 after a small open-label study [56]. First, a patient with what we now call treatment-related fluctuation (TRF) after a series of five PE improved markedly on the second day of IVIG treatment. Subsequently, the authors decided to treat six consecutive patients with IVIG alone. Five of them improved their MRC sum score after IVIG without a plateau phase.
Corneal Ulcers with NOD2 Mutations Presenting with Mixed Syndromic Phenotype
Published in Ocular Immunology and Inflammation, 2023
Travis Scott Schofield, Chang Sup Lee, Brian Patrick Peppers, Thomas Mauger
She was evaluated by neurology, infectious disease, and immunology services, while she was admitted. Her neurology work-up included an MRI, lumbar puncture, and EMG. Her MRI showed bilateral T1 shortening of the basal ganglia, which was likely caused by chronic metabolic conditions, and symmetric thickening at the brachial plexus after exiting the neural foramina and at the L4 and L5 nerves. Her lumbar puncture revealed normal CSF content without organisms. Her EMG showed prolongation of all distal latencies with bilateral decreases in amplitudes in the upper extremities. Concentric needle examination showed fibrillations in the vastus lateralis, tibialis anterior, and medial gastrocnemius muscles. These assessments ruled out cauda equina syndrome or infection and supported a diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) or peripheral neuropathy due to her poorly controlled diabetes. Upon discharge, CIDP was the proposed diagnosis, and our neurology service referred the patient for further outpatient evaluation and management with our allergy and immunology department. High dose intravenous immunoglobulin (IVIG) therapy was started with a transient but dramatic improvement in her symptoms.
Adverse transfusion reactions and what we can do
Published in Expert Review of Hematology, 2022
Yajie Wang, Quan Rao, Xiaofei Li
Post-transfusion purpura (PTP) is a rare syndrome caused by alloimmunization of human platelet-specific antigens (mostly HPA-1a), resulting in severe thrombocytopenia and bleeding within 2–14 days after blood transfusion [144]. PLT alloantibodies in the patient are preformed due to previous pregnancy or blood transfusion, and PLT alloimmunization can lead to the PLT refractoriness associated with the clinical symptoms. The incidence is about 1:50,000–100,000 transfusions and multiparous women are most often to be affected [145]. The diagnosis of PTP may be challenging, because these patients are usually post-surgery or critically ill, and there are alternative understandings for thrombocytopenia, such as drugs, infections, etc. Generally, it can be confirmed by detecting the platelet-specific alloantibodies in the serum [146]. Patients may experience purpura, petechial, or mucosal bleeds, since antibodycoated PLTs are severe destroyed by macrophages (<10 × 109/L). Fortunately, the majority of patients are self-limited and the PLT count will recover within 3 weeks. However, it has a mortality rate of 10–20% for cases with a secondary high bleeding risk [147]. Intravenous immunoglobulins (IVIGs) are the primary treatment, which has a rapid onset of action and response rate of 75–95%. Alternatively, corticosteroids may be managed together with IVIG, although the reaction seems unpredictable. Plasmapheresis is occasionally regarded as a second-line treatment [10,144]. PLT transfusions, especially with units lacking the antigen, may be useful for individuals with severe bleeding.