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类型医科大学精品课件:Drug eruption.ppt

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    医科大学精品课件:Drug eruption 医科大学 精品 课件 Drug
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    1、Drug Eruption,Liangchun Wang Department of Dermatology, Sun Yat-Sen Memorial Hospital 15.10.16,Adverse Drug Reactions,Over 2 MILLION serious ADRs yearly 100,000 DEATHS yearly ADRs 4th leading cause of death ahead of pulmonary disease, diabetes, AIDS, pneumonia, accidents and automobile deaths Nursin

    2、g home patients ADR rate350,000 yearly,Drug eruption,Gastrointestinal tract events 22.1% (colchicine) Electrolyte/renal 16.7% (Amphotericin B, Cyclosporin A) Hemorrhagic 12.7% (warfarin) Metabolic/endocrine 9.5% (corticosteroid) Dermatologic (skin) /allergic 7.9%,Medical administration pathways that

    3、 induce drug eruption,Ingestants: substances that enter the body by mouth Inhalants: the allergen is breathed in through the nose or mouth Injected: enter the body through puncture Contact Allergies: enter the body through the skin,Pathogenesis,Type A:,Nonimmunologic mechanisms -sometimes predictabl

    4、e,Over dose Cumulative toxicity Drug-drug interactions Exacerbation of disease Pharmacological side effects,Type A:,Idiosyncratic with a possible immunologic mechanism-unpredictable,DRESS TEN/SJS- allopurinol /HLA-B*5801; Carbamazepine/ HLA-A*3101 Drug reaction in the setting of HIV infection Drug i

    5、nduced lupus,Type B:,Response by the patients to the drug or its metabolite Four types of hypersensitivity,Type I hypersensitivity,Type I hypersensitivity,Systemic Anaphylaxis (Allergic shock) Anaphylactic shock drug allergy, e.g. penicillin toxin from bee, seafood Localized Anaphylaxis: Breathe tra

    6、ct allergy: allergic rhinitis, allergic asthma Digest tract allergy (food) Skin allergy: urticaria, angioedema,Type II hypersensitivity,Red cells: Penicillin, chloropromazine, phenacetin Granulocytes: Quinidine, amidopyrine Platelets: sulphonamides, thiazides,Type II hypersensitivity,Infusion reacti

    7、on Neonate hemolysis(Rh blood group antigen) Drug reactions hemolytic anemia, thrombocytopenic purpura , granulocytopenia Graves disease,Type III hypersensitivity,Characterized by fever, chills, skin rash,Type III hypersensitivity(2),Type IV hypersensitivity,Clinical manifestation,The most frequent

    8、cutaneous patterns: exanthemas urticarial eruptions/angioedema fixed drug eruptions Acneiform eruptions Photosensitivity,Bullous drug reactions: Erythema multiforme SJS v. TEN (life threatening),Most common form of adverse cutaneous eruption Lesions first appear proximally - especially groin and axi

    9、lla, generalizing within 1-2 days Pruritus: usual, prominent, a distinguishing factor from a viral exanthem Occur first 2 weeks of tx but may occur later Most common cause: Antibiotics, especially semi-synthetic penicillin & sulfamethoxazole /trimethoprim,Exanthemas,Differential diagnosis (DDx),Vira

    10、l eruption,Presentation: wheals, angioedema, or part of severe anaphylactic reactions with bronchospasm, laryngospasm, or hypotension Types: Nonimmunologic Aspirin and NSADS are the most common cause. They alter prostaglandin metabolism, enhancing degranulation of mast cells. Immunologic Most common

    11、ly associated with penicillin and related beta-lactam antibiotics Skin test: penicillin exposure Cross reaction with cephalosporins,Urticaria,DDx,Papular urticaria,urticaria,A complication of ACE inhibitors Dose dependent, dose resolve ACE users: one episode; a 10x risk of a second episode , more se

    12、vere. Mechanism :Blocking of kinkiness II by ACE inhibitors may increase tissue kinin levels?,Angioedema,Fixed drug eruption,Unknown pathogenesis Variant: Nonpigmented fixed drug eruption Large, tender, often symmetrical erythematous plaques Resolve completely weeks, Recur on re-ingestion of offendi

    13、ng drug Pseudoephedrine by far most common.,Variant: pigmented fixed drug eruption Unknown pathogenesis Present anywhere on body (50% occur on oral and genital mucosa) Presentation: Six or less lesions occur, typically one. A red patch an iris or target lesion (EM) blister & erode. Postinflammatory

    14、hyperpigmentation results.,Topical corticosteroids may induce allergic contact dermatitis . Eczematous dermatitis: worse or is refractory to topical steroid tx. Systemic corticosteroid administration may be tolerated, but in some pts there is a cross reaction manifested by whole-body allergic dermat

    15、itis Steroid Acne, perioral dermatitis,Acneiform eruptions,Photosensitivity,Meds may cause phototoxic, photoallergic UVA range Common drugs: NSAIDs, sulfamethoxazole/trimethoprin, thiazide diuretics and related sulfonylureas, quinine and quinidine, and certain tetracyclines,Phototoxic reactions: (su

    16、nburn) Dose-related Does not require prior exposure or participation by the immune system Appear from hrs to days after to exposure Phototoxic: Drug accumulates in skin absorbs light photochemical reaction photobiological reaction tissue damage TX: May include dose reduction and photoprotection,Phot

    17、oallergic reactions Typically eczematous, pruritic, and occur after some period of drug exposure. Immune system(+), positive photopatch testing (+) In general, not dose dependent Photoallergic: drug cell mediated immune response contact dermatitis on exposure to light. Eg sulfonamides, griseofulvin

    18、etc.,Bullous drug eruption,Uncommon: 0.4 - 1.2 per million person years for TEN (Toxic epidermal necrolysis) 1.2 to 6.0 per million person years for Stevens-Johnson syndrome. Definition: SJS(Stevens-Johnson syndrome) 30 % TEN Likely a disease spectrum:,J AM ACAD DERMATOL 2013, 68:693,Erythema multif

    19、orme,“target” or “iris” lesion,SJS/TEN,Causes: Most common: sulfamethoxazole(1-3/100,000), sulfadoxine with pyrimethamine (10/100,000), carbamazepine(14/100,000). Antibiotics (especially long-acting sulfa drugs and penicillins). Other: anticonvulsants, anti-inflammatory and allopurinol are also caus

    20、es. Mechanism: genetic background?,Presentation: Spread rapidly: within 4 days maximum extent Initial lesions: macular, iris lesions and bullae desquamation slough. Mucosal surfaces: difficult swallowing(GI), painful urination, photophobia, respiratory and alimentary tract Workup: Skin bx DDX: Paran

    21、eoplastic pemphigus (excluded with DIF). Graft-versus host disease (hx) and SSSS ( superficial blister).,TEN advanced clinical and laboratory knowledge,J AM ACAD DERMATOL 2013, 69:173e1-e13 J AM ACAD DERMATOL 2013, 69:187e1-e15,Etiology,Majority: drug Minority: infection Mycoplasma P. CMV Dengue vir

    22、us,Immunopathogenesis,Keratinocytes death mediated meanly by CD8 T cells CD8 T cell activation: granzyme B, perforin and granulysin Antigen Pro-hapten HLA : HLA-B*1502: Aromatic antiepileptic agents=carbamazepine, phenytoin, oxcarbazapine, and lamotrigine Han-Chinese, Thai, Malaysianand South Indian

    23、 but not in Japanese, Korean, or European HLA -B*5801: Allopurinol European descent HLA -B*5701: abacavir,Clinical features,An extensive slough both internal and external mucocutaneous membranes. Kidney: URT: microalbuminuria + renal tubular enzymes His: glomerular structure + proximal tubular damag

    24、e Pathogenesis: cytokines + stress + hypovolemia + low cardiac output Pulmonary: 25% Hypoxemia, ARDS, BO, Subcutaneous emphysema GI: Abdominal pain, diarrhea, transiently elevated liver enzymes, hepatitis, Others: Myocarditis; Encephalopathy; Anemia, Leukopenia; Hypoalbuminemia, Hyponatremia,DDx,Pro

    25、gnosis,Mortality rate: 25-30% Common cause: sepsis leading to multiorgan failure Other causes: GI bleeding, pulmonary embolism/edema, mycardial infarction,Management,Similar to an extensive burn Fluid and electrolyte imbalances, bacteremia from loss of protective skin barrier, hypercatabolism, and s

    26、ometimes ARDS IVIG in 10 pts in doses up to 0.75 g/kg/day for 4 days led to response in 48 hrs and skin healing within 1 week No adverse rxns where observed,Previous general experience with the drugs Latent periods: The rash begins 5 to 10 days (range, 1 day to 4 weeks) after beginning the drug and

    27、may occur after the drug is terminated. Clinical manifestation Skin testing (penicillin, vaccine et al.),Diagnosis,Management,Discontinue the offending agent Administer appropriate Tx Glucocorticoids: as early as possible, full dose Antibiotics: Supportive care e.g., hydration, warm / cold compresses, analgesics or antipruritics Topical treatment,

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