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Fetal alloimmune thrombocytopenia
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Neonatal AIT is usually a self-limiting disorder, often resolving over the course of several weeks, as maternal antiplatelet antibodies disappear from the neonatal circulation. The most serious and feared complication is ICH, and until recently it had been believed that the greatest risk of ICH was at the time of labor and delivery. Hence, obstetric management had focused on the peripartum period and elective cesarean section at term was advocated (13,14). In the neonatal period, the goal was to replenish the neonate’s circulating platelets in order to prevent complications secondary to bleeding. These infants should receive compatible antigen-negative platelets from either the mother or compatible donors (15). If the mother’s platelets are used, they must be carefully washed in order to avoid introducing additional antiplatelet antibodies into the neonatal circulation. High-dose intravenous immunoglobulin therapy (1–2g/kg over 1–5 days) may provide an additional or alternative therapy (16,17) especially when matched platelets are unavailable.
Thymectomy
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Most patients with MG are on anticholinesterase therapy and may be on steroids as well. These medications need to be maximized and monitored closely both pre- and postoperatively. Depending on the severity of muscle weakness and respiratory compromise, plasmapheresis may be indicated preoperatively to try to diminish postoperative respiratory issues. Intravenous immunoglobulin therapy can also be instituted to diminish the necessity for postoperative ventilation.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
GBS, an acute demyelinating disease of the PNS, often presents after a bacterial illness. It is a rare neurological condition in which the body’s immune system attacks its peripheral nervous system. Macrophages attack myelinated axons, stripping away the myelin sheath. Its symptoms can range from a mild condition, tingling sensation or weakness at the periphery, to severe condition, paralysis in which the respiratory muscles could be affected. GBS can progress rapidly over a few days and up to four weeks, and the severity of the muscle weakness or paralysis is different in each individual. When the patient’s respiratory muscle is affected or become totally paralysed, this is a life-threatening condition, as the breathing can be affected and even the blood pressure and heart rate could be compromised (National Institute of Neurological Disorders and Stroke 2019). If respiratory muscles are affected, patients may require intubation and ventilation. Treatment is directed towards the immune system using plasmapheresis (plasma exchange) and intravenous immunoglobulin therapy.
Acute motor axonal neuropathy following SARS-CoV-2 infection in the third trimester of pregnancy
Published in Baylor University Medical Center Proceedings, 2022
Mohamed M. G. Mohamed, Amar Jadhav, Polo Banuelos, Alexandre Lacasse, Vikas Kumar
On arrival, the patient was noted to have rapid, shallow, labored breathing; therefore, she was intubated and mechanically ventilated. In a few hours, spontaneous premature vaginal delivery of a viable male infant ensued. Motor weakness and paresthesia rapidly became global. Dysautonomia was also observed, with her heart rate ranging from 60 to 140 beats/min and systolic blood pressure ranging from 60 to 180 mm Hg. Of note, acetylcholine receptor binding, blocking, and modulating antibodies were negative. Campylobacter jejuni antibody was equivocal at 0.99 (with <0.90 not detected, >1.10 detected). Anti-GQ1 antibody was negative, but anti-GD1a antibody was positive. Electromyography with a nerve conduction study was consistent with multifocal axonal motor polyneuropathy without demyelinating features or active denervation. A 5-day course of intravenous immunoglobulin therapy (IVIG) (0.4 mg/kg/day) was completed. On hospital day 10, she was extubated. On discharge at day 16, she had a score of 3–4/5 on the Medical Research Council scale for upper and lower extremities. Tingling and numbness remarkably improved. She was able to walk 300 feet with assistance and a walker. She was discharged to an acute rehabilitation facility, where she spent 4 weeks.
Cancer-Associated Retinopathy and Treatment with Intravenous Immunoglobulin Therapy. A Seldom Used Approach?
Published in Ocular Immunology and Inflammation, 2021
Luis Ramos-Ruperto, Carmen Busca-Arenzana, Ana Boto-de los Bueis, Arnelle Schlincker, Francisco Arnalich-Fernández, Ángel Robles-Marhuenda
Cancer-associated retinopathy (CAR) is a paraneoplastic syndrome of the central nervous system (CNS)1 that causes a bilateral and progressive vision loss that can result in blindness. The diagnosis is based on the history of neoplasia, although it may precede, and on the alteration of visual examination tests. The determination of antibodies (Ab) against some retinal antigens is confirmatory, but their absence does not exclude the diagnosis.1 Recoverin was the first antigen to be described. It is a 23-kDa calcium-binding protein that can be found in photoreceptors in the retina and may be expressed by the tumoral cells in patients affected by CAR.2 As this syndrome may compromise the patient sight, a quick diagnosis and an early start of the treatment are of great importance.3 However, treatment continues presenting a challenge as no protocol has been set yet and the response to different types of therapies are hetero-geneous.3 Thus, concerning our case and through a literature review, we wanted to evaluate the response of CAR to intravenous immunoglobulin therapy (IVIG). We believe that it is a good option with respect to other immunosuppressants, taking into account the adverse effects of current chemotherapies and their immunomodulatory profile without adding immunosuppressive risk.
Successful treatment with etanercept in a case of seronegative rheumatoid arthritis with corticosteroid/methotrexate-resistant pemphigus erythematosus
Published in Modern Rheumatology Case Reports, 2018
Naoaki Ohkubo, Kazuhisa Nakano, Ippei Miyagawa, Shigeru Iwata, Shunsuke Fukuyo, Satoshi Kubo, Yasutaro Tamaki, Shingo Nakayamada, Yoshiya Tanaka
Bullous skin diseases such as pemphigus erythematosus are autoimmune diseases, in which acantholysis is caused by autoantibodies targeting desmoglein (Dsg), one of the desmosome components that bind epidermal keratinocytes to each other, and intraepidermal blisters are formed. The pathological conditions vary depending on which Dsg the autoantibodies target. It is known that anti-Dsg-1 antibody causes fragile blisters and pemphigus foliaceus that forms crust with desquamation, and anti-Dsg-3 antibody causes pemphigus vulgaris that forms flaccid blisters on the entire body including mucous membranes. Pemphigus erythematosus is considered to be a subtype of pemphigus foliaceus, characterised by intraepidermal blisters that develop on seborrheic sites such as the face, chest and back, and butterfly rashes on the face. It is treated with oral corticosteroids or immunosuppressive drugs targeting anti-Dsg antibodies. Severe or intractable cases are treated with high-dose intravenous immunoglobulin therapy, intravenous cyclophosphamide pulse therapy, plasma exchange or rituximab. Although some case reports show that anti-tumor necrosis factor α (anti-TNF-α) inhibitors successfully treat pemphigus, others show that administration of anti-TNF-α inhibitors cause the appearance of blisters on the skin in patients with rheumatoid arthritis (RA). Thus, the reported findings on the effect of anti-TNF-α inhibitors on pemphigus have been inconsistent. In this study, we report on the case of a patient who was successfully treated with etanercept (ETN) in both the short and long terms after RA developed during treatment of pemphigus erythematosus.