• Annals of Clinical Neurophysiology
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• v.6 no.2
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• pp.92-97
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• 2004

Background: There were several studies comparing prognostic factors in Guillain-Barre syndrome treated with intravenous immunoglobulin and plasmapheresis. However, there were controversies in what were significant factors and there were few studies so far comparing the therapeutic outcomes in patients treated with immunoglobulin. This study was aimed to determine the prognostic factors which affected the therapeutic outcome of Guillain-Barre syndrome treated with intravenous immunoglobulin. Method: We retrospectively reviewed the medical records of patients with Guillain-Barre syndrome admitted to our hospital between January 1999 and March 2004. All patients were treated with intravenous immunoglobulin. Outcome and prognosis were followed up after four weeks using the overall disability sum score. Results: Thirty-six patients were enrolled in this study. According to the clinical and electrophysiological findings, 17 patients were AIDP, 10 were axonal forms, two were mixed and seven had electrophysiologically no evidence of abnormalities. At a follow-up of four weeks, disabilities at the nadir (p<0.001) and admission (P<0.012), initial manifestations of bulbar symptom (P<0.024) and electrodiagnostic features (P<0.013) were significantly correlated with outcome in patients treated with intravenous immunoglobulin. But only disabilities at the nadir (P<0.033) and electrodiagnostic features (P<0.018) were significant in the multivariate logistic regression analysis. Conclusion: Among the patient treated with intravenous immunoglobulin, the outcomes were significantly different according to the neurological status at the nadir. Therefore early diagnosis, administration of intravenous immunoglobulin and preventing complications during acute stages are essential to minimize neurological deficit and shorten the periods of recovery.

• Clinical and Experimental Pediatrics
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• v.62 no.4
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• pp.119-123
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• 2019

Kawasaki disease (KD) is a systemic vasculitis that mainly affects younger children. Intravenous immunoglobulin (IVIG) resistant cases are at increasing risk for coronary artery complications. The strategy on prediction of potential nonresponders and treatment of IVIG-resistant patients is now controversial. In this review the definition and predictors of IVIG-resistant KD and current evidence to guide management are discussed.

• Pediatric Infection and Vaccine
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• v.21 no.1
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• pp.29-36
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• 2014

Purpose: The objective of this study was to find the predictors and generate a prediction scoring model of nonresponse to intravenous immunoglobulin in patients with Kawasaki disease. Methods: We examined 573 children diagnosed with KD at the Severance Children's Hospital between January 2009 and december 2012. We retrospectively reviewed their medical records. These patients were divided into 2 groups; the experimental group (N=433) and the validation group (N=140). Each group were divided into 2 groups the intravenous immunoglobulin nonresponders and the responders. Multivariate logistic regression analysis identified predictive factors of intravenous immunoglobulin nonresponders which make predictive scoring model. We practice internal validation and external validation. Results: Multivariate logistic regression analysis identified male, cervical lymphadenopathy, changes of the extremities, platelet, total bilirubin, alkaline phophatase, lactate dehydrogenase, C-reactive protein as significant predictors for nonresponse to intravenous immunoglobulin. We generated prediction score assigning 1 point for (1) male, (2) cervical lymphadenopathy, (3) changes of the extremities, (4) platelet (${\leq}368,000/mm^3$), (5) total bilirubin (${\geq}0.4mg/dL$), (6) alkaline phophatase (${\geq}227IU/L$), (7) lactate dehydrogenase (${\geq}268IU/L$), (8) C-reactive protein (>77.1 mg/dL). Using a cut-off point of 4 and more with this prediction score, we could identify the intravenous immunoglobulin nonresponder group. Sensitivity and specificity were 52.5% and 82.4% in experimental group and 37.8% and 81.8% in validation group, respectively. Conclusion: Our predictive scoring models had high specificity and low sensitivity in Korean patients. Therefore it is useful in predicting nonresponse to intravenous immunoglobulin with Kawasaki disease.

• Journal of Yeungnam Medical Science
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• v.18 no.2
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• pp.246-252
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• 2001

We report the result of a high-dose intravenous immunoglobulin therapy in a Henoch-Schnlein purpura patient with severe abdominal pain and nephrotic syndrome who did not respond to methylprednisolone pulse therapy. Kidney biopsy showed diffuse mesangial cell proliferative glomerulonephritis with fibrocellular crescent formation in approximately 50% of glomeruli. Mesangium of all glomeruli were strong positive for IgA and C3 antibodies. High-dose intravenous immunoglobulin treatment was introduced and dramatic improvement of gastrointestinal symptom and proteinuria as well as hematuria was noted. Immunoglobulin administration should be considered in Henoch-Schnlein purpura patients with steroid-resistant intractable gastrointestinal manifestation and renal involvement.

• Annals of Clinical Neurophysiology
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• v.14 no.1
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• pp.49-51
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• 2012

• Childhood Kidney Diseases
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• v.12 no.2
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• pp.233-238
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• 2008

It has been suspected that various infections, including cytomegalovirus(CMV) infection, are associated with IgA nephropathy. In case of CMV infection, ganciclovir is known to be a treatment of choice for severe CMV infection in general. But ganciclovir has a lot of severe toxicity, so children with normal immunity are seldom treated by ganciclovir when CMV infection is suspected. On the other hand, intravenous immunoglobulin can also be used to treat CMV infection. We report a case of CMV-associated IgA nephrophaty, who was treated with deflazacort and Intravenous immunoglobulin therapy. An 11 years old boy suffered from gross hematuria for 3 days. He had proteinuria, thrombocytopenia(104,000/$mm^3$), antiplatelet antibody(＋), impaired renal function and low serum albumin. His CMV serology was CMV-IgM/IgG(＋/-) and urine CMV-PCR was positive. The renal histological findings revealed IgA nephropathy, WHO class II. His proteinuria persisted despite of deflazacort therapy(2.5 mg/kg/day). Later, intravenous immunoglobulin(1 g/kg) was administered twice. In two years, he showed no gross and microscopic hematuria, and his laboratory findings were also normalized.

• Journal of Veterinary Clinics
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• v.30 no.1
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• pp.61-65
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• 2013

An American Cocker Spaniel (3-year-old, intact female, 6.0 kg) was referred to the Veterinary Medical Teaching Hospital of Chungnam National University for evaluation of pustules and crusts in the periocular region, dorsal and ventral region of the trunk, and digits. Complete blood count (CBC) revealed leukocytosis with mature neutrophilia, and a serum biochemistry profile revealed hypoalbuminemia. Tape strip tests identified numerous neutrophils and acatholytic cells. Histopathology identified intraepithelial pustules with neutrophils and acantholytic keratinocytes. Definitive diagnosis of pemphigus foliaceus (PF) was made by direct immunofluorescence (DIF) test with goat anti-canine IgG antibody. The human intravenous immunoglobulin (IVIG) was administered at a rate of 15 ml/h over 6 hours for 4 days. After that, the dog was maintained on prednisolone (2.2 mg/kg, PO, SID) and azathioprine (2.0 m/kg, PO, SID). An infusion of IVIG (0.5 g/kg) was repeated 3 days after 4 weeks. After 10 weeks, the dog showed the remarkable regression of lesions.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.6-15
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• 2006

Intravenous immunoglobulin (IVIg) is the treatment of choice for many autoimmune neuropathic disorders such as Guillain-Barre syndrome (GBS), chronic inflammatory Demyelinating neuropathy (CIDP), and multifocal motor neuropathy (MMN). IVIg is preferred because the adverse reactions are milder and fewer than the other immune-modulating methods such as steroid, other immunosuppressant such as azathioprine, and plasmapheresis. IVIg also has been used in other autoimmune neuromuscular disorders (inflammatory myopathy, myasthenia gravis, and Lambert-Eaton myasthenic syndrome) and has been known as safe and efficient agent in these disorders. Since IVIg would get more indications and be used more commonly, clinicians need to know the detailed mechanism of action, side effects, and practical points of IVIg.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.48-52
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• 2006

Background: Intravenous immunoglobulin (IVIg) has been administered for various immune-mediated neurological diseases such as autoimmune neuropathy, inflammatory myopathies, and other autoimmune neuromuscular disorders. The purpose of this study is to investigate side effects and complications of IVIg therapy in neuromuscular disorders. Methods: We enrolled 29 patients (age 8~63 years) with IVIg therapy for various neurological diseases including Guillain-Barre syndrome, myasthenia gravis, dermatomyositis, polymyositis, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy. IVIg therapy was used at a dose of 0.4 g/kg body weight/day for 5 consecutive days. Results: 10 patients (34%) had adverse events. There are adverse events in 16 courses (11%) among total 145 courses. The majority of patients presented with mild side effects, mostly asymptomatic laboratory changes. Rash or mild headache occurred in 3 patients. One patient showed a serious side effect of deep vein thrombosis. Conclusions: IVIg therapy is safe for a variety of immune-mediated neurological diseases in our study.

• Annals of Clinical Neurophysiology
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• v.18 no.1
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• pp.14-17
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• 2016

Intravenous immunoglobulin (IVIG) is a safe treatment to treat various neurological disorders, but fatal thrombotic events as rare complications have been reported. A 54-year-old woman with Guillain-Barre syndrome complained of dyspnea during IVIG treatment. She was finally diagnosed with pulmonary thromboembolism. To the best of our knowledge, this is the first case of pulmonary thromboembolism associated with IVIG treatment in a Korean patient with Guillain-Barre syndrome.