Clinical patterns of adverse drug reactions ppt
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Clinical patterns of adverse drug reactions ppt

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urticarial, purpuric, blistering, lichenoid, Exanthematic (maculopapular) reactions, Exfoliative dermatitis, Anaphylaxis and anaphylactoid reactions, Drug rash with eosinophilia and systemic symptoms ...

urticarial, purpuric, blistering, lichenoid, Exanthematic (maculopapular) reactions, Exfoliative dermatitis, Anaphylaxis and anaphylactoid reactions, Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome, Serum sickness, Fixed drug eruptions, Photosensitivity, Acute generalized exanthematous pustulosis (toxic pustuloderma)

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  • may be due to formation of antibody to a drug–capillary endothelial cell complex
  • Anaphylactoid reactions are those that clinically resemble an immediate immune response but in which the mechanism is undetermined.
  • Penicillin is the most common drug but other antibiotics including sulphonamides, cephalosporins and tetracyclines, as well as diuretics, tranquilizers, analgesics, muscle relaxants and anti hypertensives may be responsible. Morphine, codeine, doxorubicin, certain muscle relaxants like d-tubocurarine, and ionic radiocontrast dyes all cause mast cell degranulation.
  • Urticaria and angioedema due to aspirin and other cyclooxygenase inhibitors is probably due to an imbalance between prostaglandin and leukotriene production.
  • co-trimoxazole caused themaximum incidence (36.3%), followed by tetracycline (15.9%), pyrazolones (14.2%), sulfadiazine (12.4%), dipyrine (9.3%), paracetamol (7.9%), aspirin (1.7%), thioacetazone (0.88%) and levamisole (0.88%)
  • gold salts, antimalarials, diuretics, calcium channel blockers, heavy metals
  • Oral contraceptives may induce chloasma.Long-term (more than 4 months) antimalarial therapy may result in brownish or blue-black pigmentation, especially on the shin, face and hard palate or subungually.Yellowish discoloration ma occur with mepacrine (quinacrine) or amodiaquine. Long-term,high-dose phenothiazine (especially chlorpromazine) therapy results in a blue-grey or brownish pigmentation of sun-exposed areas, with pigment deposits in the lens and cornea cancer chemotherapeutic agents may be associated with pigmentation as follows [16]: skin pigmentation may be caused by bleomycin, busulfan, topical carmustine, cyclophosphamide, daunorubicin, fluorouracil, hydroxyurea, topical mechlorethamine, methotrexate, mithramycin, mitomycin and thiotepa.Gold may cause blue-grey pigmentation in light-exposed areas (chrysiasis) silver may cause a similar discoloration (argyria) Lead poisoning can cause a blue-black line at the gingival margin and grey discoloration of the skin. Clofazimine produces red-brown discoloration of exposed skin and the conjunctivae, together with red sweat, urine and faecesSlategrey to blue-black pigmentation may occur after long-term topical application of hydroquinone, causing ochronosis
  • Hydralazine [15,16] and procainamide [17,18], and c) [21], and quinidine
  • These include ampicillin, sulphonamides furosemide [4], thiazide diuretics, phenylbutazone and otherNSAIDs, quinidine, amiodarone [5], hydralazine [6], enalapril [7],propylthiouracil [8,9], mefloquine [10], cimetidine [11], coumadin[12,13], anticonvulsants including phenytoin
  • Other drugs have been associated with mycosis fungoides-likedrug eruptions, including allopurinol, antidepressants (e.g. fl uoxetine[14,15] and amitriptyline [15]), phenothiazines [16], thioridazine,benzodiazepines, methylphenidate hydrochloride [17],antihistamines [4], β-blockers (e.g. atenolol [18]), ACE inhibitors[19], calcium channel blockers, salazosulfapyridine [20], lipidloweringagents, mexiletine, ciclosporin [21], penicillamine,amiloride hydrochloride with hydrochlorothiazide, bromocriptine[22] and gemcitabine

Clinical patterns of adverse drug reactions ppt Clinical patterns of adverse drug reactions ppt Presentation Transcript

  • Clinical patterns of adverse drug reactions Moderator- Dr Vijay Paliwal
  • INTRODUCTION • An adverse reaction is a reaction which is noxious and unintended and which occurs at dosages normally used in man for prophylaxis, diagnosis or therapy of disease or for the modification of physiological function. • CADR found in 2-3 percent of hospitalised patients. • Ranges from common transient and benign erythema occurring 6–9 days after the introduction of a new drug, to the most severe forms which affect fewer than 1/10 000 users.
  • Exanthematic (maculopapular) reactions • Most frequent of all cutaneous reactions to drugs. • Can occur after almost any drug at any time up to 3 (but usually 2) weeks after administration. • Clinical features are variable, rash may be morbilliform or scarlatiniform or rubelliform. • Consist of profuse eruptions of small papules or purpuric lesions, which are usually associated with severe pruritus. View slide
  • • Distribution is also variable – generally symmetrical. – trunk and extremities are usually involved – face may be spared – relative sparing of pressure areas. – Palmar and plantar lesions may occur, and sometimes the eruption is generalized. • Usually fades with desquamation, sometimes with postinflammatory hyperpigmentation. • The main differential diagnosis is from viral rashes. View slide
  • • Ampicillin, amoxycillin and sulphonamides are amongst the most frequent causes. • Other common drugs include phenytoin, carbamazepine, NSAIDS and ciprofloxacin. • Less common drugs: cephalosporins, barbiturates, thiazides. INH, phenothiazines, naproxen and quinidine.
  • Purpura • Several mechanisms may be involved. – Altered coagulation – Allergic and non-allergic thrombocytopenia – Altered platelet function – Vascular causes • Cytotoxic drug therapy, Bleomycin (non allergic tcp) • Quinine, quinidine and chlorothiazide, heparin (allergic tcp) • Tissue plasminogen activator (alteplase) associated with painful purpura • Pigmented purpuric eruption/capillaritis -aspirin, carbromal, glipizide, pefloxacin, lorazepam, paracetamol,polyvinyl pyrrolidone, plasma expander, ciclosporin and griseofulvin.
  • Exfoliative dermatitis • It may follow exanthematous eruptions or may develop as erythema and exudation in the flexures, rapidly generalizing. • Serious condition and can be life threatening in elderly patients. • Takes 4 to 6 weeks to subside even after withdrawal of drugs. • Most frequently encountered drugs include sulfonamides, antimalarials, penicillin, INH, thioacetazone and a variety of homeopathic preparations. • Recently incriminated drugs are Captopril, Cefoxitin and Cimetidine.
  • Anaphylaxis and anaphylactoid reactions • A systemic reaction, usually develops within minutes to hours (mainly within the first hour), is often severe and may be fatal. • In less severe cases, there may be premonitory dizziness or faintness, skin tingling and reddening of the bulbar conjunctiva, followed by urticaria, angio-oedema, bronchospasm, abdominal pain and vasomotor collapse. • Usually develops on second exposure to a drug, but may develop during the first treatment. • Antibiotics (especially penicillin) and radiocontrast media are the most common known causes.
  • Urticaria • Second most common type of CADR. • Occurs within 24–36 h of drug ingestion. • Most commonly caused by penicillins, sulphonamides and NSAIDs (aspirin). • Urticaria manifests as severely pruritic circumscribed raised, oedematous and erythematous wheals widely scattered on the body. • As a rule, single lesions last less than 24 h, although new lesions may continue to arise. • Seen in association with anaphylaxis, angio-oedema and serum sickness.
  • • Angioedema - edema of the deep dermis or subcutaneous and submucosal areas. • Characterized by deep, skin-colored swelling, most commonly of the lips or eyes, that may last for several days. It may occur with urticarial lesions or arise independently. Eg- ACE inhibitors.
  • Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome • Synonymous to Drug hypersensitivity syndrome, Anticonvulsant hypersensitivity syndrome. • It is a severe idiosyncratic reaction, syndrome comprises of :1. Fever 2. Facial oedema with infiltrated papules, generalized papulopustular or exanthematous rash which may extend to exfoliative dermatitis. 3. Lymphadenopathy 4. Haematological abnormalities (hypereosinophilia in 90% of cases, atypical lymphocytes/mononucleosis in 40% of cases) 5. Organ involvement such as hepatitis, possible nephritis, pneumonitis, myocarditis and hypothyroidism, and encephalitis. • It usually develops 2-6 weeks after the drug is first administered.
  • • The drugs associated with this syndrome include antiepileptic agents- phenytoin, carbamazepine, phenobarbital and lamotrigine; dapsone; allopurinol, gold, trimethoprim– sulfamethoxazole, minocycline, procarbazine, terbinafine,abacavir and nevirapine and sorbinil. • The mortality is of the order of 10%. • The cutaneous histological pattern shows a lymphocytic infi ltrate, sometimes mimicking a cutaneous lymphoma. • Recovery is usually total but rash and hepatitis may persist for weeks. • Treatment with steroids has been widely advocated but controlled studies are lacking.
  • Serum sickness • Serum sickness, a type III immune complex-mediated reaction • Occur between 5 days and 3 weeks after initial exposure. • In its complete form, combines fever, urticaria, angio-oedema, joint pain and swelling, lymphadenopathy, and occasionally nephritis or endocarditis, with eosinophilia. • In minor forms, fever, urticaria and transitory joint tenderness may be the only manifestations. • Drugs implicated include heterologous serum , immunoglobulin, aspirin, antibiotics such as penicillin, amoxicillin , flucloxacillin , cefaclor , cefprozil , piperacillin, ciprofloxacin , cotrimoxazole, streptomycin, sulphonamides and sulfasalazine , thiouracils, intravenous streptokinase, Nacetylcysteine.
  • • Circulating immune complexes, low serum C4 and C3 levels, and elevated plasma C3a anaphylatoxin levels are found. • Direct immunofluorescence revealed the presence of immunoreactants including IgM, C3, IgE and IgA in the walls of dermal blood vessels.
  • Fixed drug eruptions • Characteristically recurs in the same site or sites each time the same drug is administered; with each exposure, however, the number of involved sites may increase. • Acute lesions usually develop 30 min to 8 h after drug administration. • Sharply marginated, round or oval itchy plaques of erythema and oedema becoming dusky violaceous or brown, and sometimes vesicular or bullous. • Eruption may initially be morbilliform, scarlatiniform or erythema multiforme-like. • As healing occurs, crusting and scaling are followed by pigmentation, which may be very persistent and occasionally extensive, especially in pigmented individuals.
  • • Distribution – the hands and feet, genitalia and perianal areas are favoured sites. – Perioral and periorbital lesions may occur. – Genital and oral mucous membranes may be involved in association with skin lesions, or alone.
  • Lichenoid eruptions • May develop weeks or months after initiation of therapy. • Morphology of lesions– similar to lichen planus – eczematous papules and generalized eczematous skin reactions with marked desquamation. – lesions are symmetrical, larger, and psoriasiform and often have a photo distribution. – Mucosa is less commonly involved • Long-lasting, deep hyperpigmentation, alopecia and skin atrophy with anhidrosis due to sweat gland atrophy. • Resolution of the skin eruption may be slow after cessation of therapy, on average from 1 to 4 months, but up to 24 months with gold.
  • • Histopathology - focal parakeratosis; focal interruption of the granular layer; cytoid bodies situated higher in the granular and cornified layers; presence of a few eosinophils; exocytosis of lymphoid cells into the upper epidermis; and a deeper perivascular infiltrate. Lichenoid photodermatitis occurring in a patient with a long history of thiazide ingestion.
  • Photosensitivity • General term used to describe individuals that exhibit an increased incidence of erythema upon exposure to ultraviolet radiation. • This may be manifested as an inflammatory reaction upon exposure to normally harmless levels of electromagnetic radiation or an exaggerated response to inflammation-inducing levels. • Eruptions on exposed areas • Sparing of upper eyelids, submental and retroauricular areas • May be phototoxic or photoallergic, cannot always be distinguished clinically. Phototoxic reactions • Commoner than photoallergic reactions, • Can be produced in almost all individuals given a high enough dose of drug and sufficient light irradiation. • Occur within 5–20 h of the first exposure, and resemble exaggerated sunburn. • Erythema, oedema, blistering, weeping, desquamation and residual hyperpigmentation occur on exposed areas; photo-onycholysis.
  • Photoallergic reactions • require a latent period during which sensitization occurs • usually appear within 24 h of re-exposure to drug and light in a sensitized individual • may spread beyond irradiated areas. • may occur as a result of local photocontact dermatitis to a topical photoallergen, relatively common cause of photosensitivity, accounting for 9% of cases. • Topical photoallergens include antihistamines, chlorpromazine, local anaesthetics, benzydamine, hydrocortisone, desoximetasone (desoxymethasone) and sunscreens containing p-aminobenzoic acid (PABA) and benzophenones.
  • Photorecall reactions • A curious photorecall-like eruption, occurs, restricted to an area of sunburn sustained previously, while on medication with certain drugs. • Cephazolin, gentamicin, piperacillin, tobramycin and ciprofl oxacin, site of pelvic radiotherapy for carcinomas, and Methotrexate. Photo-onycholysis • May be caused by tetracycline, psoralens and UVA (PUVA) therapy, and the fluoroquinolone antibiotics, pefloxacin and ofloxacin.
  • Pigmentation reactions Hyperpigmentation • Drug-induced alteration in skin colour may result from : 1. 2. 3. 4. increased melanin synthesis increased lipofuscin synthesis cutaneous deposition of drug-related material most commonly as a result of post-inflammatory hyperpigmentation (e.g. fixed drug eruption).
  • Flagellate pigmentation from bleomycin Minocycline pigmentation Amiodarone pigmentation Carotenemia due to anticonvulsants
  • Hypopigmentation • Occupational exposure to monobenzyl ether of hydroquinone, p-tertiary butylcatechol, p-tertiary-butylphenol, p-tertiary amylphenol, monomethyl ether of hydroquinone and hydroquinone • Hypopigmentation may result from phenolic detergent germicides and following use of diphencyprone for alopecia areata . • Depigmentation of the skin and hair occurred after a phenobarbital-induced eruption. • Photoleukomelanodermatitis occurred due to afloqualone for cervical spondylosis
  • Acneiform and pustular eruptions • Lesions are papulopustular but comedones are usually absent. • ACTH, corticosteroids , dexamethasone in neurosurgical patients, anabolic steroids for body-building , androgens (in females), oral contraceptives, iodides and bromides may produce acneiform eruptions. • Isoniazid may induce acne, especially in slow inactivators of the drug. • Others include production of acneiform rashes include dantrolene , danazol, quinidine , lithium and azathioprine.
  • Acute generalized exanthematous pustulosis (toxic pustuloderma) • A distinct reaction pattern commonly caused by β-lactam and macrolide antibiotics. • Especially ampicillin/amoxicillin + clavulanic acid, pristinamycin, quinolones, (hydroxy)chloroquine, anti-infective sulphonamides, terbinafine, diltiazem, carbamazepine and spiramycin, metronidazole. • Characterized by non-follicular based pustules on an erythematous background that arise within 2 weeks of drug exposure • The eruption usually begins on the face or intertriginous areas and spreads rapidly to affect the entire body. • In contrast to pustular psoriasis, polymorphous lesions, including EM-like lesions and purpura, are common • Fever and leukocytosis are also clinical clues to the diagnosis • Histology characteristically demonstrates an intraepidermal spongiform pustule with eosinophils.
  • Eczematous eruptions • A patient initially sensitized to a drug by way of allergic contact dermatitis may develop an eczematous reaction when the same, or a chemically related, substance is subsequently administered systemically - ‘systemic contact-type dermatitis medicamentosa’. • The eruption tends to be symmetrical, and may involve first, or most severely, the site(s) of the original dermatitis, before becoming generalized. • ‘baboon syndrome’ denotes a characteristic pattern of systemic allergic contact dermatitis, in which there is diffuse erythema of the buttocks, upper inner thighs and axillae, provoked by penicillin, ampicillin, amoxicillin, nickel, heparin, mercury (including that found in a homeopathic medicine) , terbinafine and hydroxyurea.
  • Erythema multiforme, Stevens–Johnson syndrome and toxic epidermal necrolysis • Widely accepted that EM minor, EM major, Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) were all part of a single “EM spectrum”. • Recently a consensus clinical classification was proposed, based on the pattern of skin lesions and the extent of epidermal detachment. • EM (minor or major) is mainly caused by herpes virus infection and other infectious diseases, but rarely, if ever by drugs. • SJS, TEN and overlap (SJS/TEN) are probably severe variants of a single disorder mainly caused by drugs.
  • • Diagnostic criteria for EM: – an acute self-limiting illness – Duration of episode less than four weeks – Symmetrically and acrally distributed lesions, typical or raised atypical target lesions. – Absent or limited mucosal involvement. – Recurrent episodes. • Stevens Johnson Syndrome – serious mucocutaneous illness with systemic symptoms and signs with significant mortality. – characterized by the presence of flat atypical target lesions or purpuric macules with blisters that are distributed mainly on the trunk or widespread – epidermal detachment <10% of body surface area (BSA). – Two or more mucosal sites can be involved.
  • • Toxic Epidermal Necrolysis – – life threatening illness characterized by high fever and confluent erythema followed by necrolysis – epidermal detachment is >30% of BSA. Patients with this condition may also have flat atypical target lesions (TEN with spots). – Rarely extensive epidermal necrosis occurs without any discrete target lesion (TEN without Spots) • In the overlap category (SJS/TEN) the area of epidermal detachment, is between 10 and 30% of the BSA. • Typically begin 1-3weeks after the initiation of therapy. • Suspected drug should be avoided lifelong.
  • Bullous eruptions Bullous eruption in drug overdosage • overdosage with barbiturates, methadone, meprobamate, imipramine, nitrazepam or glutethimide. • Bullae at pressure areas, usually in comatose patients. Drug-induced porphyria • excess destruction of haem or inhibition of haem synthesis by certain drugs exacerbate the acute hepatic porphyrias. Pseudoporphyria • porphyria-like blistering of exposed areas on the extremities occurs in the absence of abnormal porphyrin metabolism.
  • Drug-induced bullous pemphigoid • Clinically drug induced bullous pemphigoid usually resembles classic bullous pemphigoid with urticaria (hive)-like patches and tense clear blisters that do not break easily. • They usually appear suddenly. • Sometimes it can look more like erythema multiforme . • Rarely affects the mucous membranes. • Generally it occurs in a younger age group than classic idiopathic bullous pemphigoid, which is a disease of old age. • The skin biopsy histopathology and direct immunofluoresence is the same as for the classic disease.
  •  Drugs reported to cause this reaction include: • Analgesics • Antibiotics– including penicillins • Captopril • Diuretics – especially frusemide/furosemide, also spironolactone • Gold • D-penicillamine • Potassium iodide • Sulfasalazine
  • Drug-induced pemphigus • A number of drugs have been implicated in drug-induced pemphigus, usually of foliaceus type, although the erythematosus, herpetiformis and urticaria-like forms also occur; drug-induced pemphigus vulgaris is rare. • The skin lesions are flaccid blisters which break easily and often only erosions +/- crusting are seen. The Nikolsky sign can be positive. • In drug-induced pemphigus, mucous membranes are only involved in 10-15% of cases . • The onset of drug related pemphigus can be weeks to months after the drug was started. • Resolution occurs after drug withdrawal in drug-induced pemphigus but not if drug-triggered.
  •  Drug-induced pemphigus is caused by drugs with a thiol group such as: • D-penicillamine • Captopril • Gold sodium thiomalate • Pyritinol  Drug-triggered pemphigus follows nonthiol drug use including: • Antibiotics especially betalactams, rifampicin • Pyrazolone derivatives • Nifedipine • Propranolol • Piroxicam • Phenobarbital
  • Tense subepithelial blisters Well-demarcated crusted lesions scattered over the chest
  • Linear IgA disease • The drug related form usually resembles the idiopathic type with tense small and large blisters often in ring-shaped arrangements on the body, arms and legs. • It may involve the palms and soles and rarely mucous membranes. Rarely it may be more severe and resemble toxic epidermal necrolysis. • Skin biopsy shows the same histopathology and direct immunofluoresence (DIF) features as in the idiopathic form. • The reaction begins 1-2 weeks after starting the drug (range 24 hours to 15 days).
  • • When the offending drug is ceased, new blisters stop appearing 1-3 days later and the rash has usually cleared by 3 weeks. • Rechallenge with the drug results in a more severe reaction with a shorter latency time and longer time to clearance. • The most common drug associated with this reaction is vancomycin. • Others-amiodarone,ampicillin, atorvastatin , captopril , carbamazepine ,cefamandole (cephamandole), diclofenac, furosemide , glibenclamide, IFN-γ, iodine, lithium, penicillin, phenytoinand somatostatin, as well as tea-tree oil.
  • Lupus erythematosus-like syndrome • 5% of cases of SLE are drug induced. • Cutaneous involvement in drug-induced SLE may be vasculitic, bullous, erythema multiforme-like or resemble pyoderma gangrenosum. • Photosensitivity may be prominent, Constitutional symptoms may be present, and there may be evidence of Raynaud’s disease, arthritis or polyserositis. • Differenting features include – – occurs in an older age group – renal and central nervous system involvement are infrequent – antihistone antibodies are frequent – anti-DNA antibodies are absent and serum complement is normal. – deposition of immunoreactants in uninvolved skin is rare. • The condition usually, but not always, resolves after discontinuation of the drug.
  • • Commonly -Hydralazine ,procainamide, sulpha drugs • less commonly- β- blockers, methyldopa, isoniazid, most anticonvulsants in clinical use including phenytoin, carbamazepine, ethosuximide, trimethadione, primidone and valproate (but not phenobarbital or benzodiazepines) and quinidine. • Subacute LE with positive Ro/SSA antibodies has been reported in association with a number of drugs, including phenytoin, thiazide diuretics such as hydrochlorothiazide , ACE inhibitors, calcium channel blockers, terbinafine, griseofulvin , piroxicam, oxprenolol, interferons and statins. • A number of drugs may exacerbate pre-existing SLE, such as griseofulvin, β-blockers, sulphonamides, testosterone and oestrogens.
  • Vasculitis • Vasculitis of various morphological types can be caused by drug ingestion. • The clinical pattern is usually that of a superficial small vessel cutaneous leukocytoclastic vasculitis but other patterns, including systemic vasculitis, occur. • Drug-induced leukocytoclastic vasculitis presents with palpable purpura, petechiae, necrosis and urticarial lesions, indistinguishable from other causes of this pattern of vasculitis. • In the serum sickness-like reaction, the initial rash may be acral, with urticaria or purpura, followed by more generalized annular urticarial lesions. There may be fever, arthralgia, haematuria or proteinuria, lymphadenopathy and decreased complement.
  • • The patterns of polyarteritis nodosa, Henoch– Schönlein vasculitis and hypocomplementaemic vasculitis are not seen commonly with drugs. • Indistinguishable clinically from the same clinical picture occurring due to other causes. – Timing of the eruption in relation to starting a new drug may be informative. – Blood eosinophilia and tissue eosinophilia is found in almost 80% of patients. – Drug caused ANCA-associated vasculitides (cocaine) generally mimic the WG but with less systemic features, has multiple ANCA specificities or anti-HLE, rather than the more usual anti-MPO or anti-PR3 ANCA.
  • • Those most frequently implicated are penicillins, sulphonamides, quinolones, analgesics (including nonsteroidal anti-inflammatory drugs), thiazides and other diuretics, anticonvulsants, phenothiazines, allopurinol, and colony-stimulating factors. • Less commonly used drugs, but with a significant risk of causing vasculitis, include hydralazine, quinidine, thiouracils and various biological agents. • Suspected drug should be avoided.
  • Pseudolymphomatous drug hypersensitivity syndrome • Should be differentiated from DRESS, which has a more acute onset. • Develops between 2 weeks and 5 years after starting drug therapy, but usually within 7 weeks. • Skin involvement consist of erythematous plaques, multiple infiltrative papules or solitary nodules; there may be facial oedema. • Histopathologically, there is epidermotropism of atypical lymphocytes, often with Pautrier’s microabscess-like structures • Misdiagnosed as cutaneous lymphoma.
  • • Causative drugs - Phenytoin especially, but also phenobarbitone and carbamazepine, mephenytoin, trimethadione and sodium valproate. • Usually responds to drug withdrawal.
  • Pityriasis rosea-like reactions • The best-known drug cause of a pityriasiform rash is gold therapy but several other drugs have been implicated. • Includes metronidazole,aspirin , captopril , isotretinoin and omeprazole , angiotensin converting enzyme inhibitors, alone or in combination with hydrochlorothiazide, followed by one case each for hydrochlorothiazide plus sartan, allopurinol, nimesulide, and acetylsalicylic acid.
  • Psoriasiform eruptions • Psoriasiform eruptions are similar to idiopathic psoriasis and typically consist of erythematous plaques surmounted by large dry silvery scales. • The time course between initiation of the causative agent and exacerbation or formation of the eruption varies between drugs, from less than 1 month to more than 3 months. • One definite trigger is lithium, others are Terbinafine, chloroquine and hydroxychloroquine , beta-blockers. • Drug-associated or -exacerbated psoriasis is typically resistant to treatment indicated for idiopathic psoriasis. The causative agent should ideally be stopped or the dose reduced.
  • Widespread erythematous papulosquamous lesions on (a) the trunk and buttocks, and (b) both legs by lithium.
  • Widespread erythematous papulosquamous lesions on (a) the trunk and buttocks, and (b) both legs by lithium.