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Home , Abfraction, Actinic cheilitis, Amelogenesis imperfecta, Contact stomatitis, Dentigerous cyst, Epithelial dysplasia

EPITHELIAL FROM A TO Z and Systemic Considerations: What Every Clinician Should Know

Theresa Sullivan Gonzales, DMD, MS Colonel, United States Army Director, Orofacial Pain Management Tripler Army Medical Center Honolulu, Hawaii 96859 Diplomate, Oral and Maxillofacial Pathology

The 15 Most Common Oral Pathoses (Based on examination of 23,616 U.S. adults; excludes caries & periodontitis) Number of per 1,000 Adults Diagnosis Rank Males Females Both 1 42.5 13.1 23.7

Torus palatinus 2 13.2 21.7 18.7 Irritation 3 13.0 11.4 11.9 Fordyce granules 4 17.7 5.2 9.7 5 9.6 7.9 8.5 Leaf-shaped fibroma (under denture) 6 0.4 12.9 6.7 Hemangioma 7 8.4 4.1 5.6 Inflammatory ulcer 8 5.4 5.1 5.2 Inflammatory 9 4.5 4.8 4.7 Papilloma 10 5.3 4.2 4.6 fissuratum 11 3.4 4.4 4.0 Lingual varicosities 12 3.5 3.4 3.5 Fissured 13 3.5 3.1 3.3 14 3.4 3.0 3.1 Papillary of 15 1.7 3.8 3.0

References: Bouquot JE. J Am Dent Assoc 1986; 112:50-57; www.oralpath.com Differential DX

Deferential DX Differential Diagnosis  M – Metabolic

 I – Inflammatory

 N – Neoplastic

 D - Developmental

Clefts Oral and Maxillofacial Pathology Fordyce Granules Categories Osteogenesis Imp. Developmental CleidocranialFissured Tongue Paget’sDentigerousHairy Disease Tongue Odontogenic CGCGOKC/KOTTori BFOLCOC Teeth/Pulpal/Perio OsteomaOdontoma Erosion// Mucosal Osteosarcoma AOT Imperfecta Chondrosarcoma CEOT Dentinogenesis Imperfecta Ewing’s Sarcoma Myxoma Gemination/Fusion Salivary Pulpal/Periapical Dis. Periodontal Dis. Allergy/Immunologic Rec. Apthous Others Sarcoidosis Manifes of PhysicalWegner’s Granulomatosis Heme Dermatologic Forensics LichenSystemic Planus Dis. ChemicalAngioedemaPemphigus ContactErythema Stomatitis Multiforme Erythema Migrans Ectodermal Dysplasia Cowden Syndrome Oromaxillofacial Pathology Categories Developmental

Odontogenic

Teeth/pulpal perio

Mucosal

Infections

Salivary Amyloidosis Vitamin Deficiency Diabetes Bone Hyperparathyroidism Inborn Errors of Metabolism Addison’s Disease Crohn’sAllergy/Immunologic Disease Iron Def. Anemia

Others

Manifes of Physical Heme Dermatologic Forensics Systemic Dis. Chemical Oral Mucosal Lesions

Epithelial Soft Tissue

Neoplastic Reactive Reactive Neoplastic

Benign Malignant Benign

SCC Papillary/ Malignant Verruciform VerrucousFibroma C. Spindle Cell C. Basaloid SCC3 P’s Pigmented EphelisAdenosquamosEpulis Fissuratum ActinicBCC LentigoIPH Leurkoplakia/ MelasmaNasopharyngeal OralCarc Melanotic of Max. Macule Sin MelanoacanthomaMerkel Cell Smoker’sMelanoma Melanosis Nevi Oral Mucosal Lesions

Epithelial Soft Tissue

Neoplastic Reactive Reactive Neoplastic

Benign Malignant Benign Frictional Linea Alba Pre-malignant Malignant Morsicatio Linguarum Cotton Roll Aspirin Burn SDK Radiation Mucositis Oral Submuc. Fibrosis Physical/ Sanguinaria-ass. Nicotine Stomatitis? Chemical Pyrophosphate-ass. keratosis Solar Keratosis Hyperplastic Candidiasis Leukoplakia Actinic ? Infectious PVL Diagnosis – “through knowledge”

… A solid knowledge of the basic principles of the various disease processes is essential for obtaining a good history. As Goethe stated: "The eyes see what the mind knows." Consider

Anatomical Location

Biological Plausibility Patient History

Taking the patient's history is traditionally the first step in virtually every clinical encounter.

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Multiplicity of Presentation

 Systemic Disease  Syndromic Presentation A

Recurrent

 “aphthous ulcerations”  “canker sores”  Prevalence in the general population 5% to 66% with a mean of 20%  Mucosal destruction – T-cell mediated immunologic reaction Etiologic Factors

 Allergies  Genetic predisposition  Nutritional deficiencies – B12, B6, Fe ++  Hematological abnormalities  Hormonal influences  Infectious agents  Trauma  Stress Four Principal Categories

 Primary immunodysregulation  Decrease of the mucosal barrier  Increase in antigenic exposure  Genetic predisposition / HLA-12, HLA - B51 and Cw7 Systemic Disorders Associated with Recurrent Aphthous Stomatitis

 Behcet’s syndrome  Celiac disease   Nutritional deficiencies  IgA deficiency  Immunoincompetence  Inflammatory bowel disease Three Clinical Variations

 Minor  Major – Sutton’s disease or PMNR (periadenitis mucosa necrotica recurrens)  Herpetiform Minor Aphthous Ulcerations

 Non-keratinized mucosa  Prodromal symptoms – burning, itching, stinging  Erythematous macule – fibrinopurulent membrane with a erythematous halo * except in immunocompromised

Major Aphthous Ulcerations

 Larger - 1 to 3 cm  Deeper  Clinically persistent  Develop post pubertal  Recurrences for up to 20 years or more Herpetiform Aphthous Ulcerations

 Greatest number of lesions  Increased frequency of occurrence  Superficial resemblance to viral  Any mucosal surface may be involved Behcet’s Syndrome

“the silk route” Behcet’s Syndrome

 1937 – Turkish dermatologist –Hulusi Behcet described this condition

 Ocular Inflammation  Orogenital Inflammation  Multisystem Disorder Behcet’s Disease

 Highest Prevalence – Middle East and Japan  Oral Involvement – primary manifestation in 25% to 75% of the cases  All three forms of aphthous stomatitis may be seen Behcet’s Disease

 Genital lesions are clinically similar to oral lesions  75% of the patients demonstrate the genital lesions  Genital lesions are generally more symptomatic in males Behcet’s Disease Criteria for the Diagnosis of Behcet’s Disease (International Study Group)

 Recurrent oral ulceration  Plus two of the following:  Recurrent genital ulcerations  Eye lesions –anterior/posterior uveitis  Skin lesions  + pathergy – read by 24-48 hours Behcet’s Disease Treament

 Topical or intralesional corticosteriods  Oral colchicine  Thalidomide  Low-dose methotrexate  Systemic corticosteriods  Cyclosporine  Interferon alpha2A Treatment

 Triamcinolone 0.1% in Orabase (Kenalog in Orabase) Apply to dried ulcer two to four times daily until healed  Randomized, controlled studies show decreased pain  Dexamethasone elixir, 0.5 mg per 5 ml Swish and spit with 5 mL every 6 hours  As above B

Burning Syndrome

About 1.3 million American adults, mostly postmenopausal women, are afflicted with , a chronic often debilitating condition whose cause remains a medical mystery. Burning Mouth Syndrome The main symptom of burning mouth syndrome is a burning sensation involving the tongue, , , palate, throat or widespread areas of the whole mouth. People with the syndrome may describe the sensation in the affected areas as hot or scalded, as if they had been burned with a hot liquid. Burning Mouth Syndrome

 Dry mouth  Sore mouth  A tingling or numb sensation in your mouth or on the tip of your tongue  A bitter or metallic taste Causes

 Dry mouth (xerostomia).  Nutritional deficiencies  Allergies.  Psychological factors.  Nerve disturbance or damage (neuropathy).

Treatments Potentially efficacious medicines include: * tricyclic antidepressants (like amitriptyline - brand name, Elavil) * benzodiazepines (like clonazepam - brand name, Klonopin; or *chlordiazepoxide brand name - Librium) * even anticonvulsants have proven effective in some cases. BMS: Treatment Tricyclic antidepressants Amitriptyline (Elavil)10 to 150 mg per day 10 mg at bedtime; increase dosage by 10 mg every 4 to 7 days until oral burning is relieved or side effects occur BMS: Treatment Benzodiazepines Clonazepam (Klonopin)0.25 to 2 mg per day0.25 mg at bedtime; increase dosage by 0.25 mg every 4 to 7 days until oral burning is relieved or side effects occur; as dosage increases, medication is taken as full dose or in three divided doses BMS: Treatment Anticonvulsants Gabapentin (Neurontin) 300 to 1,600 mg per day100 mg at bedtime; increase dosage by 100 mg every 4 to 7 days until oral burning is relieved or side effects occur; as dosage increases, medication is taken in three divided doses C

Candidiasis Oral thrush and other Candida infections occur when your immune system is weakened by disease or drugs such as prednisone, or when antibiotics disturb the natural balance of microorganisms in the body. Predisposing factors for infection

 Infancy or old age

 Serious underlying disease, such as or infection with HIV

 Dry mouth due to disease of the salivary glands or medications e.g. antihistamines, diuretics

(especially if they are not regularly cleaned or fit badly) Predisposing factors for infection

 Smoking

 Injury to the mouth

 Nutritional deficiency e.g. iron &/or B-vitamin deficiency

 Inhaled corticosteroids used to treat asthma e.g. beclometasone, budesonide, fluticasone. Drink water after inhalation to reduce this complication Clinical features

 Acute pseudomembranous candidiasis. There are white patches on gums, tongue & inside the mouth that can be peeled off leaving a raw area.  Acute atrophic candidiasis. There are smooth red shiny patches on the tongue. The mouth is very sore.  Chronic atrophic candidiasis. This is common in those with dentures. The underlying mucosa is red and swollen. Clinical features

. There are sore red splits at each side of the mouth, more likely if there is overhang of the upper over the lower lip causing a moist deep furrow. Angular cheilitis due to candida and/or Staphylococcus aureus arises frequently in those taking the medication for acne; this medication dries the lips.  Chronic hyperplastic candidiasis. This is a type of oral leukoplakia (white patch) inside the cheeks or on the tongue with persistent nodules or lumps. It usually affects smokers and is pre-malignant. Red patches (erythroplakia) as well as white patches may indicate malignant change. Clinical features

 Chronic mucocutaneous candidiasis presents as a chronic pseudomembranous infection. The skin and nails are also affected.  Median rhomboid - there is diamond- shaped inflammation at the back of the tongue.  Severe infections may extend down the throat (esophageal infection). Rationale for Treatment: Topical vs. Systemic Drugs

 Topical antifungals are usually the drug of choice for uncomplicated, localized candidiasis in patients with normal immune function.  Systemic antifungals are usually indicated in cases of disseminated disease and/or in immunocompromised patients. Suggested Medications for the Treatment of Candidiasis:

Rx: Clotrimazole troches, 10 mg Disp: 70 troches Sig: Let 1 troche dissolve in mouth 5 times per day for 14 days. Do not chew. NPO 1/2 hour. Suggested Systemic Medications for the Treatment of Candidiasis:  Rx: Ketoconazole tablets, 200 mg Disp: 14 tablets Sig: Take 1 tab q.d. with a meal or orange juice for 14 days  Rx: Fluconazole tablets, 100 mg Disp: 15 tablets Sig: Take 2 tablets stat, then 1 tablet q.d. for 14 days  Rx: Itraconazole tablets, 100 mg Disp: 28 tablets Sig: Take 1 tablet b.i.d. with a meal or orange juice for 14 days CA Head and Neck Cancer

 Squamous Cell

 Intraoral Melanoma

Intraoral Melanoma The five year survival rate for oral melanoma is less than 20 % as compared to 75% for Cutaneous melanomas. The average time of first local recurrence for oral melanoma is less than one year and metastatic disease is usually diagnosed within three months of the recurrence. The average survival rate after is typically less than 6 months.

Extranodal Lymphoma Extranodal usually develop as a rapidly growing mass of the palate or posterior tongue (area of Waldeyer’s ring). Pain may or may not be a presenting sign. Clinically, the may present as an erythematous mass with a boggy consistency. The average survival rate for AIDS patients with an intraoral lymphoma is eight months.

Squamous Cell Carcinoma

Second primary – field cancerization

Incidence & Mortality H&N Ca

 41,000 new cases annually  13,000 affected will die of disease  Rates constant over last 20yrs  < 5% of neoplasias U.S.  Highest incidence southeastern & south- central Asia Disease in Women

 Prior to 1940 male:female ratio - 10:1  1980s ratio 3:1  Reason: tobacco use among women in early decades of the century  Habits have stabilized – male:female incidence normalized Tobacco Use

 1956 Wynder et al H&N Ca 10-fold increase among smokers  Most studies 5-fold to 25-fold increase intensity and duration of tobacco consumption  80-90% of H&N Ca patients use tobacco Alcohol

 Odds ratio increases 3- to 15-fold for H&N Ca, after adjusting for tobacco use, with consumption of alcohol  Multiplicative effect with tobacco and alcohol  Location of cancer – oral, pharyngeal,(topical mechanism) Alcohol

 Promotional effects independent of initiation  -prostaglandin synthesis, lipid peroxidation, free radical oxygen, enhance cell turnover  Enhances cell permeability  Defective repair mechanisms  Depressed immunity 4 RF

Dz 3 RF

2 RF

1 RF RISK FACTORS (RF) The concept of

INFECTION TUMOR PAIN locallocal T regional N systemic M

CERVICAL LYMPH NODE ENLARGEMENT

INFECTION •bacterial •< 40 yrs: lymphoma •viral (local / systemic) •> 40 yrs: metastatic SCC •fungal •postinfect. fibrosed node

OTHERS

•leukemia •connective tissue diseases (e.g. lupus) •sarcoidosis Importance of early diagnosis of

40% 60% stage I & II stage III & IV

80-90% cure 2/3 recurrence < 2 yrs

< 1/3 survive 3 yrs.

Second primary tumor in successfully treated patients within 5-7 years: up to 40% !!! Follow-up important!!! Squamous Cell Carcinoma

 Mortality (8000) deaths per year  Mortality by Site  Tongue 43.2%  Salivary 13.0%  Floor of mouth 9.50%  Lip 2.4%  Other 31.9% Premalignant Lesions

 Leukoplakia  Erythroplakia  Erythroplasia   Verrucous Leukoplakia  Tobacco patch keratosis  Actinic cheilosis  Mouth wash (Viadent) dysplasia

Leukoplakia Erythroplakia

 Defined as a red patch that can not be clinically or pathologically diagnosed as any other condition  Almost all erythroleukoplakia demonstrate dysplasia or CIS  Etiology is similar to oral SCC  May occur in conjunction with leukoplakia Erythroplakia

 Risk of malignant transformation in erythroleukoplakia about 4x greater than homogenous leukoplakia  Predominately disease of older men with peak prevalence of 65 to 74 years  Floor of mouth, tongue, and are most common sites of involvement Erythroplakia The Management of Head and Neck Cancer Major advances  Conservative or partial resections  Micro vascular free-tissue transfer in reconstruction  Better definition of the roles of chemotherapy and radiotherapy Despite these advances, the treatment of loco regional recurrence remains a major challenge  success rates for salvage therapy are poor. Treatment

 Radiotherapy

 Chemotherapy

 Immunotherapy* at present the role of immunotherapy remains investigational Chemotherapy

Several randomized and non-randomized trial have evaluated chemotherapy for the treatment of head and neck cancer  Various agents have been shown to produce a response  No agents , either alone or in combination have demonstrated an improvement in survival* *cisplatin and 5 - FU  Uses  Inoperable tumors  Salvage therapy for recurrent tumors Treatment

 The main treatment modalities for head and neck cancer remain : surgery and radiotherapy  Patient factors that merit consideration  Impact on the quality of life  Medical condition – “co - morbidities”  Patient preference  Treatment cost and convenience  Compliance Treatment

Early stage disease (stage I and II) can be treated with either surgery or radiotherapy with equivalent control rates  Small lesions of the oral cavity wide local excision is preferred over radiotherapy  Radiotherapy can be delivered to a site generally only once  Reserve this modality for less operable lesions Treatment: Combined Modality Surgery and Radiotherapy Indications for post operative radiotherapy : Primary Tumor  Advance T stage  High histologic grade  Positive surgical resection margins  Lymphatic permeation  Vascular invasion  Perineural spread Radiotherapy

 Daily dose of 180 cGy to 200 cGy  5,000 cGy over a five week period  T1 – 6,000 to 6,600 cGy  T2 - 6,600 to 7,000 cGy  T3/T4 - > 7,000 cGy  “shrinking field technique”  hyperfractionation technique 200 cGy per day for 25 days followed by 400 cGy per day for 5 days D

Desquamative is a clinical term to describe red, painful, glazed and friable gingivae which may be a manifestation of some mucocutaneous conditions such as or the vesiculobullous disorders. Clinical features of

 Fiery, red, friable gingiva  Painful, desquamates easily  Buccal aspect of anterior attached gingiva affected  Marginal gingiva spared  Not significantly improved by measures alone Differential Diagnosis

 Erosive Lichen Planus  Immune-mediated blistering diseases  Intra-epithelial   Subepithelial  Pemphigoid  Linear IgA disease  Dermatitis herpetiformis  Epidermolysis bullosa 

Treatment: Topical Corticosteroids

 Recurrent aphthous ulcers  • Oral manifestations of Behçet's disease, Reiter's syndrome, acute vulvar ulcer, MAGIC syndrome. PFAPA syndrome, ulcerative colitis,  Crohn's disease, Melkersson-Rosenthal syndrome, Sweet's syndrome, among others  • Drug-induced ulcerations mediated by an immune mechanism  • Lichen planus  • Cicatricial pemphigoid  • pemphigoid  • Bullous pemphigoid  • Erythema multiforme  • Linear IgA dermatosis  • Pemphigus vulgaris Topicals

 Temovate, cream 0.05% Clobetasol propionate  Halog, cream 0.1% Halcinonide  Lidex, cream 0.05% Fluocinonide  Topicort, cream 0.25% Desoximethasone  Lidex, gel 0.05% Fluocinonide  Aristocort, cream H-P 0.5% Triamcinolone acetinode  Diprosone, cream 0.05% Betamethasone dipropionate  Florone, cream 0.05% Diflorasone diacetate  Maxiflor, cream 0.05% Diflorasone diacetate  Synalar, cream H-P 0.2% Fluocinolone acetonide Topicals

 Tropicort-LP, cream 0.05% Desoxymethasone  Benisone, cream 0.025% Betamethasone benzoate  Cordran, cream 0.025% Flurandenolide  Kenalog, cream 0.1% Triamcinolone acetonide  Locoid, cream 0.1% Hydrocortisone butyrate  Synalar, cream 0.025% Fluocinolone acetonide  Valisone, cream 0.1% Betamethasone valerate  Tridesilon, cream 0.05% Desonide  Locorten, cream 0.03% Flumetasone pivalate  1% Hydrocortisone Topical Corticosteroids Used to treat oral lesions.

Clobetasol (Temovate) -- Suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Class I superpotent topical steroid useful in treating oral lesions. Topical corticosteroids commonly are used intraorally for oral manifestations of autoimmune blistering skin diseases. Since these diseases are chronic inflammatory in nature, topical corticosteroids are very useful as an adjunct treatment. Patients with disease confined to the gingiva should see a dentist to have a custom-made soft tray to carry the medication H

How does herpes simplex develop?

 overexposure to  overexposure to wind  colds, influenza and similar infections  heavy alcohol use  fever from any cause  the menstrual period  physical stress  emotional stress Symptoms

 Primary (Initial) HSV I  Fever  Adenopathy  Ulcers deep in mouth  Secondary (Later) HSV I (Recurrent labial lesions)  Fever form on outer vermillion border  Cold Sores form on inner lip  Initial: Vesicle  Next: Crust  Last: Healing in 10-14 days

Differential Diagnosis

 Differs from Aphthous Ulcers in that:  Found on keratinized (bound-down) intraoral mucosa  Vesicles rupture into coalescing ulcers  HSV lesions are anterior compared with:   Hand Foot and Mouth Disease

Specific antiviral drugs: Herpes Oral acyclovir (Zovirax) or the recently developed drugs, valacyclovir (Valtrex) or famciclovir (Famvir), lessen the symptoms and frequency of fever recurrences for some patients. These drugs prevent HSV from multiplying and are effective when taken in pill form prior to an outbreak of the . Systemic Antivirals

 Acyclovir  Dose: 15 mg/kg (max: 200 mg) PO 5x/day for 7 days  Shortens first HSV infection by 6 days in children

 Famciclovir  Shortens healing time by 2 days in UV-induced cases  Spruance (1999) J Infect Dis 179:303-10  Valacyclovir (FDA approved for age 12 and older)  Adult dose: 2 g PO bid for one day Specific antiviral drugs: Herpes Topical antiviral creams containing acyclovir (Zovirax) or penciclovir (Denavir) may also help in limiting the extent or duration of lesions if applied promptly to affected areas. Topical Treatments

 Penciclovir (Denavir) heals HSV-1 sores on average about half a day faster than without treatment, stops viral shedding, and reduces the duration of the pain. Ideally, the patient should apply the cream within the first hour of symptoms, although benefits have also been noted with later application. It is continued for four consecutive days and should be reapplied every two hours while awake.  Docosanol cream (Abreva) is an over-the-counter agent for oral-facial herpes. It helps resist infection by inhibiting the ability of the virus to become fully active after it has attached itself to the host cell. It is applied five times a day, beginning at the first sign of tingling or pain. Studies have been mixed on it benefits. Topical Treatments

 Acyclovir cream (Zovirax) has been approved. It may speed healing of oral herpes lesions and lessen the duration of pain, particularly if it is applied early on (at the first sign of pain or tingling).  Lidex is a gel that contains a fluocinonide, as corticosteroid. Corticosteroids, commonly called steroids, are anti-inflammatory agents and not ordinarily used for herpes. Some evidence suggests it may be effective in combination with oral famciclovir. Topical Treatments

 Over-the-counter topical anesthetics may provide modest relief. They include Anbesol gel, Blistex lip ointment, Campho-phenique, Herpecin-L, Viractin, and Zilactin. In one study, Viractin reduced the duration of the attack compared to placebo by two days. It also relieved itching but had little effect on other symptoms. In general, however, few studies have been conducted on any of these products. X

Xerostomia Xerostomia is not a disease but can be a symptom of certain diseases. It can produce serious negative effects on the patients quality of life, affecting dietary habits, nutritional status, speech, taste, tolerance to dental prosthesis and increases susceptibility to dental caries. The increase in dental caries can be devastating in many patients and therefore special care must be made to control this condition. Causes for Xerostomia include:

 -Medications - Several hundred current medications can cause xerostomia. antihypertensives, antidepressants, analgesics, tranquilizers, diuretics and antihistamines c.  -Cancer Therapy - Chemotherapeutic drugs can change the flow and composition of the saliva. Radiation treatment that is focused on or near the salivary gland can temporarily or permanently damage the salivary glands.  -Sjogren's syndrome - An autoimmune disease, causes xerostomia and dry eyes. Causes for Xerostomia include:

 -Other conditions -such as bone marrow transplants, endocrine disorders, stress, anxiety, depression, and nutritional deficiencies may cause xerostomia.  -Nerve Damage - Trauma to the head and neck area from surgery or wounds can damage the nerves that supply sensation to the mouth. While the salivary glands may be left intact, they cannot function normally without the nerves that signal them to produce saliva. Treatment: Identify the xerostomic condition and the cause. Some of the causes may be ameliorated and this will aid therapy. But in many situations, it will be difficult to eliminate the causes. Thus, it will be necessary for the Dentist to control the results of xerostomia. This is especially true about the increase in dental caries. Treatment:

 -pilocarpine (Salagen) 5mg, qid, prescription required.  -special food preparation - blended and moist foods are easier to swallow  artificial saliva (available over-the-counter).  -sipping plain water is usually preferred over artificial saliva by most patients.  -Biotene brand, over-the-counter, dry mouth products (toothpaste, alcohol- free mouth rinse and Oralbalance lubricating gel).  -avoidance of alcohol-based mouth rinses  -use of water and glycerin mixed in a small aerosol spray bottle. RX:

Contains sorbitol, sodium carboxymethlcellulose, and methylparaben in a pleasantly flavored solution.

120 mL (4.06 fl oz) Z

Treatment

 Acyclovir (Zovirax)†800 mg orally five times daily for 7 to 10 days 10 mg per kg IV every 8 hours for 7 to 10 days‡  $174 to 248 (129 to 200)  Famciclovir (Famvir)†500 mg orally three times daily for 7 days  $140 Treatment

 Valacyclovir (Valtrex)†1,000 mg orally three times daily for 7 days  $84  Prednisone (Deltasone)30 mg orally twice daily on days 1 through 7; then 15 mg twice daily on days 8 through 14; then 7.5 mg twice daily on days 15 through 21 Treatment

 Lotions containing calamine (e.g., Caladryl) may be used on open lesions to reduce pain and pruritus.  Once the lesions have crusted over, capsaicin cream (Zostrix) may be applied.  Topically administered lidocaine (Xylocaine) and nerve blocks have also been reported to be effective in reducing pain.

 Amitriptyline (Elavil) -- By inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentration in CNS. Useful as analgesic for certain types of chronic and neuropathic pain.  Adult DoseEarly in course of HZ: 25 mg/d PO hs to prevent PHN After PHN develops: 30-100 mg PO qhs Postherpetic Neuralgia

 Capsaicin cream (Dolorac, Capsin, Zostrix) -- Natural chemical derived from plants of Solanaceae family. By depleting and preventing reaccumulation of substance P in peripheral sensory neurons, may render skin and joints insensitive to pain. Substance P thought to be chemomediator of pain transmission from periphery to CNS.  Adult DoseCream: Apply to skin tid/qid for 3-4 consecutive wk and evaluate efficacy; not to exceed 4 applications/d Postherpetic Neuralgia

 Lidocaine (DermaFlex gel, Lidoderm 5% patch) -- Several recent studies have advocated topical administration of lidocaine as treatment of PHN. Lidocaine gel (5%) in placebo-controlled study showed significant relief in 23 patients studied. Lidocaine tape also decreases severity of pain.  Adult DoseGel (5%): Apply to affected area prn Patch (5%): Apply to most painful area up to 3 patches per application; patch may remain in place for up to 12 h in any 24 h period Postherpetic Neuralgia

 Gabapentin (Neurontin) -- This medication has been approved by the FDA for the treatment of PHN. Has properties common to other anticonvulsants and antineuralgic effects. Exact mechanism of action is not known. Structurally, gabapentin is related to GABA, but it does not interact with GABA receptors. Believed to have a binding site at the alpha 2-delta protein, an auxiliary subunit of voltage- gaited calcium channels. In the rat brain, binding is localized on neuronal dendritic areas. Relevance of these observations to treatment of PHN is not known.  Adult Dose100 mg PO tid; titrate dose prn; recommended dose is 900-1800 mg PO qd; not to exceed 900 mg PO qid