Jul-Sep, 2012 - Indian Journal of Pharmacy Practice

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Mahendra Kumar BJ - Drug Induced Syndromes: An Overviewand symptoms of infection. Use of Vasoactive agents(Pentoxyphylline) together with hyperbaric oxygen may bebeneficial considering the vascular pathogenesis. Vasospasmmay be relieved by the phosphodiesterase inhibiting action ofpentoxyphylline. Topical corticosteroids are effective foracute tissue inflammation. Wound care, debridement,dressings, and flap reconstruction are ideal surgical measures.Failure to recognize the extent of fat necrosis and poor bloodsupply leads to inadequate debridement and poor woundhealing. The patients are then prone to repetitive cycles ofinfection leading to extensive scarring, soft tissue23indentation, and unsightly skin grafts.Warfarin-Induced Skin Necrosis: Warfarin-induced skinnecrosis due to oral anti-coagulation therapy causes injury tothe skin. Cutaneous injury from warfarin begins as localizedparesthesias with an erythematous flush, progresses topetechiae and hemorrhagic bullae, and may eventually result24in full-thickness skin necrosis.24, 25, 26Causative drug: Warfarin.Symptoms: Patients may initially experience localparesthesias with an erythematous flush followed by intensepain and rapid development and coalescence of petechiae,with concomitant accumulation of subcutaneous edemaresulting in a peaud'orange appearance. During the first 24hours after the first sign of skin lesions, hemorrhagic bullaemay occur, which signals irreversible tissue injury. Full-24thickness skin necrosis is the end stage of cutaneous injury.(Fig 5)Treatment: Vitamin K intravenously and fresh frozen plasma(FFP) can be given to the patient to reverse the effects of the24warfarin.Sweet Syndrome: Sweet syndrome is a condition associatedwith autoimmune phenomena including relapsingpolychondritis, drug-induced lupus, and development of27Anti-Neutrophil Cytoplasmic Antibodies (ANCAs).Causative drugs: Abacavir, All-Trans Retinoic Acid,Bortezomib, Carbamazapine, Celecoxib, Clozapine,Diclofenac, Diazepam, Furosemide, Hydralazine, Imatinib,Lenalidomide, Minocycline, Nitrofurantoin, Norfloxacin,Ofloxacin, Pegfilgastrin, Propylthiouracil, Quinupristin,27Dalfopristin, Trimethoprim-Sulfamethoxazole.Symptoms: Rapid onset of fever, leukocytosis, painfulerythematous and edematous papules, plaques and nodules27infiltrated by neutrophils.Treatment: Causative drugs should be suspended andsystemic corticosteroids can be given to the patient for the28management of lesions.Stevens - Johnson syndrome (SJS): SJS is a wellrecognizedimmune complex mediated hypersensitivityreaction that affects all age groups. It has classic systemic,29mucosal and dermatologic manifestations.Causative drugs: Ibuprofen, Allopurinol, Chloroquine,Penicillamine, Sulfasalazine, Carbamazepine, Etosuximide,Phenobarbital, Phenytoin, Valpoic Acid, Amoxicillin,Imipenem, Ciprofloxacin, Clindamycin, Doxycyclin,Erythromycin, Sulfadiazine, Sulfamethoxazole-Trimethoprim, Dapsone, Fluconazole, Nystatin, Nevirapine,Abacavir, Efavirenz, Tamoxifen, Verapamil, Enalapril,30,31,32Acetazolamide.Symptoms: Erythema with bullous, eroded lesions of skin and29mucous membrane and cholestatic liver disease.Treatment: Withdrawal of the causative drugs, rapidlyinitiating supportive care in an appropriate setting and themanagement of fluid and electrolyte requirements. Treatmentstarted with IV fluids and combination of corticosteroid is29used.Toxic Epidermal Necrolysis (Lyell Syndrome/TEN): TENis a severe adverse cutaneous drug reaction thatpredominantly involve the skin and mucous membranes. It isan autoimmune blistering disease, including linear IgAdermatosis and paraneoplastic pemphigus but alsopemphigus vulgaris and bullous pemphigoid, acutegeneralized exanthematous pustulosis (AGEP), disseminatedfixed bullous drug eruption and staphyloccocal scalded skinsyndrome (SSSS).Causative drugs: Sulfonamides, Pyrazolones, Barbiturates,Ibuprofen, Allopurinol and Carbamazepine.Symptoms: Hyper and hypopigmentation of the skin, naildystrophies, ocular complications, trichiasis, symblepharon,distichiasis, visual loss, entropion, ankyloblepharon,lagophthalmos and corneal ulceration.Treatment: Prompt identification and withdrawal of thecausative drug, systemic steroids, high-dose intravenousimmunoglobulin Ciclosporin, and Cyclophosphamide31(CPP).Rabbit's Syndrome (RS): RS is a rare movement disordergenerally associated with prolonged use of antipsychoticscharacterized by involuntary, rhythmic, fast and finemovements of the oral and masticatory muscles along thevertical axis of the mouth. It takes its name from an unusual33resemblance to the chewing motions of rabbits.Causative drugs: Methotrimipramine, Benzotropine,M e s o r i d a z i n e , C l o r a z e p a t e , C h l o r p r o m a z i n e ,Trifluoperazine, Lithium, Clocapramine, Propericiazine,Levopromazine, Bromperidol, Sulpiride, Thioridazine,Indian Journal of Pharmacy Practice Volume 5 Issue 3 Jul - Sep, 2012 15
Mahendra Kumar BJ - Drug Induced Syndromes: An OverviewHaloperidol, Zuclopentixol, Biperidene, Perphenazine,Amitriptyline, Paroxetine, Risperidone, Clozapine,33Olanzapine, Aripiprazole.Symptoms: RS is characterized by involuntary and rhythmicmovements along the vertical axis of the mouth occur at afrequency of approximately 5 Hz. The oral movements areoften accompanied by a popping sound that is produced by therapid smacking on one's lips. This syndrome is limitedexclusively to the territory of the oral and masticatory34muscles and does not involve the tongue.Treatment: Rabbit's Syndrome typically responds favorablyto anticholinergic agents such as Benztropine, Biperiden,Procyclidine and Trihexyphenidyl. This Syndrome typicallydisappears few days after the introduction of ananticholinergic agent, but can, on occasion, reappear after34stopping anticholinergic medications.Vanishing Bile Duct Syndrome (VBDS): VBDS is a rarecause of progressive cholestasis and is mostly related withdrugs. Drugs act as a hapten and produce autoantibodiesagainst cytokeratin which is in the bile duct, skin,conjunctival epithelium and orogenital mucosa.Autoantibodies destroy biliary apparatus with resultantdisappearance of intrahepatic bile duct.Causative drugs: Anticonvulsants, Sulfonamides, Penicillins,Allopurinol, Nonsteroidal Anti-Inflammatory Drugs.Symptoms: Cholestasis, pruritis, weight loss, malaise,disappearance of intrahepatic bile ductTreatment: The therapy involves mainly the withdrawal of thecausative agent, supportive care, and the usage ofimmunosuppressants. Steroids, choleretic agents are also29useful for the management purpose.H a n d - F o o t S y n d r o m e ( P a l m a r - P l a n t a rE r y t h r o d y s a e s t h e s i a / H F S ) : P a l m a r - P l a n t a rErythrodysaesthesia is a relatively common adverse effect ofchemotherapeutic drugs.Causative drugs: 5-Fluorouracil, Doxorubicin, Docetaxel,Idarubicin, and Cytarabine.Symptoms: Erythema, tenderness, tingling, numbness, dryrash and desquamation over the palms and soles. (Fig 6)Treatment: The management of hand-foot syndrome entailsimmediate discontinuation of the causative drug andsymptomatic care. Steroids and pyridoxine show goodresponse in patients. The causative drug may be cautiously re-35introduced in a lower dose.Purple Glove Syndrome (PGS): Purple Glove Syndrome iscaused by intravenous administration of phenytoin resultingin soft tissue injury at the site of injection leading to oedemaand purplish-black discoloration of the hand.Causative drugs: Phenytoin.Symptoms: Intense pain, purplish black discoloration andoedema at the site of injection.Treatment: The management of PGS is mainly conservative,which includes limb elevation and physiotherapy. Use of lowconcentration local anaesthetic for brachial plexus block hasan added advantage of preserving motor function to facilitatephysiotherapy in addition to providing adequate analgesia36and relief of vasospasm.Creutzfeldt-Jakob like Syndrome (CJS): CJS syndromecommonly with lithium products is characterisized bydementia and periodic complexes on EEG.Causative drugs: Lithium with Levodopa, Lithium, Lithiumwith Nortriptyline, Amitriptyline.Symptoms: Dementia, confusional state, myoclonus,Parkinson's syndrome, dystonia, grimacing, dysarthria,oculogyric crisis, blepharospasm, swallowing difficulties,torticollis and trismus.Treatment: patients are advised to discontinue the causativedrugs. When the patients are treated with high potencyantipsychotic drugs a low starting dose is recommended toreduce the risk of acute dystonia compared with a standard37dose.Fetal valproate syndrome (FVS): Valproic acid is acommonly used anticonvulsant and also used in the treatmentof bipolar affective disorder. Although, its teratogenic effectsare well known, the exact mechanism is unclear which resultin multiple birth defects, dysmorphic facies, developmentaldelay, learning difficulties and/or behavioural problems.Fetal valproate syndrome is the term used to encompass theseteratogenic effects.Causative drug: Sodium valproate.Symptoms: Neural tube defects, trigonocephaly, radial raydefects, pulmonary abnormalities,coloboma of iris/optic, low verbal IQ, autism and autisticspectrum disorder.Treatment: High dose folic acid (4 mg/day) is recommendedduring pregnancy, starting at least 6 weeks pre-conceptionand continuing through the first trimester. Folic acidsupplements are thought to be protective againstmalformations, in particular against neural tube defects.Some clinicians are of the opinion that it may be advisable forpregnant women to continue folic acid until delivery, due tothe continued development of the fetal brain throughout thepregnancy. Serum α-feto-protein levels in the secondtrimester may be helpful in picking up open neural tubedefects. Antenatal scans should be able to pick up most majormalformations, especially if specific attention is being paid38towards anomalies known to be associated with FVS. (Fig 7)Pseudolymphoma Syndrome (PS): PS is a rare form ofadverse cutaneous drug reaction.Causative drugs: Anti-arrhythmic, anti-hypertensive, anti-Indian Journal of Pharmacy Practice Volume 5 Issue 3 Jul - Sep, 2012 16
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Aishwaryalakshmi K - Assessment of
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Instructions to AuthorsIntroduction
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Instructions to AuthorsElectronic j
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