Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The range of diseases in which intravenous immunoglobulin (IVIG) is effective has expanded significantly since its initial use in primary antibody deficiency. There are at present at least 17 preparations of IVIG in use worldwide with similar profiles of adverse effects. Infusion-related effects range in severity. Mild adverse reactions (headache, flushing, low backache, nausea, wheezing) are often associated with a fast infusion rate, and respond rapidly on slowing the infusion. Very rare episodes of life-threatening anaphylaxis may occur, particularly in those IgA-deficient patients with anti-IgA antibodies; such patients should receive an IgA-depleted preparation of IVIG. There are concerns with any blood product about safety in regard to viral transmission. The 4 outbreaks of non-A non-B hepatitis (probably hepatitis C) in the 1980s were associated with the use of particular batches of IVIG. The more recent exclusion of all anti-hepatitis C virus positive individuals from the donor pool, and the introduction of specific antiviral steps in the manufacture of IVIGs, should prevent further outbreaks. The human immunodeficiency virus (HIV) is effectively inactivated during the manufacturing process itself and HIV transmission has not been reported with IVIG. Rarely, haematological (Coombs' test positive haemolysis), neurological (aseptic meningitis) or renal (transient rises in serum creatinine) adverse effects may be seen when high doses of IVIG are used for immunomodulatory purposes. Haemolysis, due to passive transmission of blood group antibodies (anti-A, anti-D), may be prevented by selecting IVIG batches that give a negative cross-match between the recipient's red cells and IVIG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effects of intravenous immunoglobulin. 826 Jan 19

A 30-year-old incarcerated man was sprayed with the "tear gas" ortho-chlorobenzylidene malononitrile (CS). He was hospitalized 8 days later with erythroderma, wheezing, pneumonitis with hypoxemia, hepatitis with jaundice, and hypereosinophilia. During the subsequent months he continued to suffer from generalized dermatitis, recurrent cough and wheezing consistent with reactive airways dysfunction syndrome, and eosinophilia. These abnormalities responded to brief courses of systemic corticosteroid but recurred off therapy. The dermatitis resolved gradually over 6-7 months, but the patient still had asthma-like symptoms a year following exposure. Patch testing confirmed sensitization to CS. The mechanism of the patient's prolonged reaction is unknown but may involve cell-mediated hypersensitivity, perhaps to adducts of CS (or a metabolite) and tissue proteins. This is the first documented case in which CS apparently caused a severe, multisystem illness by hypersensitivity rather than direct tissue toxicity. Both the ethics and safety of CS use remain controversial, in part because of the difficulty documenting sporadic injuries received in the field, and also because the charged circumstances surrounding CS use may lead to both underreporting and exaggerated claims of medical harm. The medical literature on CS focuses mainly on its immediate irritant effects and on transient dermal and ocular injuries, with only 2 prior case reports of acute lung injury related to CS exposure. Given the paucity of documented lasting effects despite its widespread use for more than 3 decades, CS appears to be safe when deployed (outdoors) in a controlled manner, but it can cause important injuries if misused or if applied to a sensitized individual.
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PMID:Medical hazards of the tear gas CS. A case of persistent, multisystem, hypersensitivity reaction and review of the literature. 1094 52

Hypersensitivity syndrome associated with teicoplanin has rarely been reported. We report a case with a preceding episode of vancomyin-related neutropenia. A 47-year-old female with cervical spine infection was treated with vancomycin. Neutropenia occurred after 17 days of vancomycin therapy. Vancomycin was changed to teicoplanin, and the neutropenia resolved 4 days later. After 11 days of teicoplanin therapy, a new episode of hypersensitivity syndrome manifested as fever, bilateral neck lymphadenopathy, mild wheezing, hepatitis and increased CRP occurred. Neutropenia and thrombocytopenia developed 3 days later. The patient's symptoms settled over 1 week following withdrawal of teicoplanin. Naranjo's ADR algorithm categorized the neutropenia associated with vancomycin and the hypersensitivity syndrome associated with teicoplanin as 'probable'.
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PMID:Teicoplanin-induced hypersensitivity syndrome with a preceding vancomycin-induced neutropenia: a case report and literature review. 2105 66