eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Nummular Dermatitis: Treatment & Medication

Author: Jami L Miller, MD, Assistant Professor, Division of Dermatology, Department of Internal Medicine, Vanderbilt University Medical School; Director of Phototherapy Unit, Vanderbilt University Medical Center; Consulting Attending Physician, Nashville Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Aug 3, 2009

Treatment

Medical Care

Treatment is aimed at rehydration of the skin and repair of the epidermal lipid barrier, reduction of inflammation and treatment of any infection.

  • Lukewarm or cool baths or showers reduce itching and help rehydrate the skin. Patients should be instructed to bathe 1-2 times a day at least, followed by the application of moisturizers or medicated topical preparations to seal the water in the skin. The "soak-and-smear" therapeutic regimen includes a 20-minute plain water soak each night followed by application of steroid ointment or petrolatum to wet skin and includes alteration of cleansing habits so that soap is applied only to the axilla and groin. One study showed greater than 90% response in 27 of 28 patients with refractory chronic pruritic eruptions when the regimen was followed as directed.17
  • Wet wrap treatments are often helpful. This involves dampening the skin with lukewarm water until it is well hydrated (usually 10 min). Then, petrolatum or steroid ointment is applied liberally, followed by occlusion for 1 hour with damp pajamas or a nonbreathable sauna suit. For small areas of involvement, plastic wrap may be used to occlude the area. This process may be repeated 5-6 times a day with petrolatum. Caution must be used when prescription steroid medications are used because overuse of these medications can cause striae, thinning of the skin, and, rarely, enough systemic absorption of steroid to affect the hypothalamic-pituitary-adrenal axis.
  • Steroids are the most commonly used therapy to reduce inflammation.
    • Topical steroids are effective. Less erythematous, less pruritic lesions may be treated with low-potency (class III-VI) steroids. Severely inflamed lesions with intense erythema, vesicles, and pruritus require high-potency (class I-II) preparations. Penetration of the medication is enhanced by occlusion or presoaking in a tub of plain water followed immediately (without drying) by application of the steroid-containing ointment.
    • Application of the medicine to damp skin allows more effective penetration and faster healing.
    • Ointments are usually more effective than creams because they are more occlusive, form a barrier between the skin and the environment, and more effectively hold water into the skin.
    • Emollients and topical class I-III topical steroids may be used short term.
    • Oral, intramuscular, or parenteral steroids may be required in cases of severe, generalized eruptions.
  • Tar preparations are helpful to decrease inflammation, particularly in older, thickened, scaly plaques.
  • Topical immune modulators (tacrolimus and pimecrolimus) also reduce inflammation. These are often initiated a few days after the topical steroid to decrease the risk of a burning sensation that may occur when applied to extremely irritated skin.
  • When eruptions are generalized and prolonged, phototherapy (generally UVB) may be helpful.18
  • Oral antihistamines or sedatives may help reduce itching and improve sleep.
  • Oral antibiotics, such as dicloxacillin, cephalexin, or erythromycin, should be used in cases of secondary infection. Swab cultures of the skin guide selection of antibiotics.
  • Once the eruption has resolved, ongoing aggressive hydration may decrease the frequency between flares, particularly in dry climates. Heavy moisturizers (preferably a sensitive-skin formulation) or petroleum jelly applied to damp skin after showering may be helpful.

Consultations

Because lesions are persistent and may be difficult to treat, consultation with a dermatologist in an outpatient setting may be advisable.

Activity

Activities that heat or dry the skin worsen the pruritus and the eruption.

  • Resting in a cool, moist environment is therapeutic.
  • Heat, drying conditions, and irritating activities should be avoided.
  • Sunlight or phototherapy may be beneficial, particularly in chronic cases. Ultraviolet radiation helps reduce the inflammatory activity within the skin. The risk of heat worsening the pruritus and of ultraviolet light inducing cutaneus malignancies must be weighed against the potential benefits.

Medication

A potent-to-intermediate potency steroid may be applied 2-4 times daily to the affected areas. They are most effective when used in ointment form (rather than cream) and applied to damp skin. Once lesions improve, a lower-potency steroid or moisturizer should be prescribed to avoid skin atrophy.

If the patient has an overt infection, a combination of a topical antibiotic and a steroid ointment applied twice daily is usually very effective. This therapy decreases inflammation and colonization by staphylococci.

Use of sedating antihistamines at night helps with sleep.

Severe or generalized flares may be treated with tap water–moistened dressings on top of the steroid ointment. Oral or parenteral steroids may be used in severe flares, followed by topical therapy.

Oral antibiotics, such as dicloxacillin, cephalexin, or erythromycin, should be used in cases of secondary infection.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, modify the body's immune response to diverse stimuli.


Triamcinolone (Aristocort)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. A good choice once lesions stabilize and the threat of secondary infection has passed. Use 0.025-0.1% strength.

Adult

Apply thin film to affected area bid

Pediatric

Not established

Documented hypersensitivity; fungal, viral, or bacterial skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prolonged use may induce skin atrophy; avoid use in sensitive areas (eg, groin, axillae, face); prolonged use, applications over large areas, and use of potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria


Prednisone (Deltasone, Meticorten, Orasone)

For severe generalized flares. May decrease inflammation by reversing increased capillary permeability and suppressing PMN leukocyte activity.

Adult

40-60 mg PO qd with rapid taper

Pediatric

0.14 mg/kg or 4-6 mg/m2 PO in divided doses

May decrease oral anticoagulant effectiveness; increases metabolism of isoniazid and salicylates; coadministration with estrogens may decrease clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral, fungal, tubercular skin, or connective-tissue infections; peptic ulcer disease; hepatic dysfunction

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur; adjust dose in persons with hypoglycemia and in those on insulin


Clobetasol propionate (Clobex, Cormax)

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Decreases inflammation by stabilizing lysosomal membranes, inhibiting PMN and mast cell degranulation.

Adult

Apply bid for up to 2 wk; not to exceed 50 g/wk

Pediatric

Not established

Documented hypersensitivity; viral or fungal skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy

Immune modulators

Reduces inflammation.


Pimecrolimus 1% cream (Elidel)

First nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus. Selectively inhibits production and release of inflammatory cytokines from activated T-cells by binding to cytosolic immunophilin receptor macrophilin-12. Resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids. Indicated only after other treatment options have failed.

Adult

Apply topically to affected areas bid; short-term and intermittent use only

Pediatric

<2 years: Not established
>2 years: Administer as in adults
Short-term and intermittent use only

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Potential exacerbation of existing infection at site of application; may cause burning and irritation; product insert revised and contains a boxed warning stating long-term safety of calcineurin inhibitors has not been established; although a causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported


Tacrolimus 0.03% or 0.1% ointment (Protopic)

The mechanism of action of tacrolimus in atopic dermatitis is not known. Reduces itching and inflammation by suppressing the release of cytokines from T cells. Also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, may inhibit release of preformed mediators from skin mast cells and basophils, and down-regulate expression of FCeRI on Langerhans cells. Can be used in patients as young as 2 y. Drugs of this class are more expensive than topical corticosteroids. Available as an ointment in concentrations of 0.03 and 0.1%. Indicated only after other treatment options have failed.

Adult

Apply thin layer to affected skin areas bid and rub in gently and completely; continue treatment for 1 wk after clearing of signs and symptoms
Short-term and intermittent use only

Pediatric

<2 years: Not recommended
2-15 years: Apply 0.03% ointment bid to affected area(s)
>15 years: Administer as adults
Short-term and intermittent use only

Documented hypersensitivity to tacrolimus or components of ointment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use with occlusive dressings; may be associated with an increased risk of folliculitis in adults; may cause local burning sensation, stinging, soreness, or pruritus (typically improve as lesions heal); for external use only; minimize exposure to natural or artificial sunlight (eg, tanning beds or UVA/B treatment); be sure skin is completely dry before application; product insert was revised in January 2006 and contains a boxed warning stating long-term safety of calcineurin inhibitors has not been established; although a causal relationship has not been established, rare cases of malignancy (eg, skin and lymphoma) have been reported; only 0.03% ointment is indicated for use in children aged 2-15 y.

Antihistamines

To help with sleep. Caution must be used because even the traditionally nonsedating classes may cause somnolence.


Hydroxyzine (Atarax, Vistaril, Vistazine)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Piperazine type of antihistamine that has fewer sedating effects compared with diphenhydramine and is effective. Usually well tolerated in most individuals.

Adult

25-100 mg PO qd/qid

Pediatric

2 mg/kg/d PO; 0.6 mg/kg/dose PO q6h

CNS depression may increase with alcohol or other CNS depressants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for porphyric patients); ECG abnormalities (alterations in T-waves) may occur; may cause drowsiness

Antibiotics

Used for severe exudative flares with infection. Empiric antimicrobial therapy should cover S aureus and other likely pathogens in the context of the clinical setting.


Sulfamethoxazole and trimethoprim (Bactrim)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa. For MRSA infections.

Adult

160 mg TMP/800 mg SMZ PO q12h for 10-14 d

Pediatric

<2 months: Do not administer
>2 months: 10-20 mg TMP/kg/d PO/IV divided tid/qid for 14 d

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Documented hypersensitivity; megaloblastic anemia due to folate deficiency; age <2 mo

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use during last trimester of pregnancy due to potential toxicity to newborn (eg, jaundice, hemolytic anemia, kernicterus)
Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: Recommended IV dose q18h
CrCl 50-10: Recommended IV dose q24h
CrCl <10: Not recommended
Hemodialysis: 4-5 mg/kg after hemodialysis
During peritoneal dialysis: 0.16-0.8 g q48h
Discontinue at first appearance of rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in persons with G-6-PD deficiency; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation


Dicloxacillin (Dynapen, Pathocil, Dycill)

Binds to 1 or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected.

Adult

125-500 mg PO qid for 7-10 d

Pediatric

Not established

May decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients with renal impairment


Erythromycin (E.E.S., E-Mycin, Eryc)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.

Adult

500 mg PO bid for 7-10 d

Pediatric

Not established

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Documented hypersensitivity; hepatic impairment

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, or abdominal colic occurs


Cephalexin (Biocef, Keflex, Keftab)

First-generation cephalosporin arrests bacterial growth by inhibiting synthesis of bacterial cell walls. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora. Used for skin infections or prophylaxis in minor procedures.

Adult

250-500 mg PO qid for 7-10 d

Pediatric

25-50 mg/kg/d PO divided qid (125 or 250 mg/5 mL)

Probenecid may increase effect of cephalosporins; tetracyclines may decrease effect of cephalosporins with concurrent use

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function

More on Nummular Dermatitis

Overview: Nummular Dermatitis
Differential Diagnoses & Workup: Nummular Dermatitis
Treatment & Medication: Nummular Dermatitis
Follow-up: Nummular Dermatitis
Multimedia: Nummular Dermatitis
References

References

  1. Aoyama H, Tanaka M, Hara M, Tabata N, Tagami H. Nummular eczema: An addition of senile xerosis and unique cutaneous reactivities to environmental aeroallergens. Dermatology. 1999;199(2):135-9. [Medline].

  2. Ozkaya E. Adult-onset atopic dermatitis. J Am Acad Dermatol. Apr 2005;52(4):579-82. [Medline].

  3. Moore MM, Elpern DJ, Carter DJ. Severe, generalized nummular eczema secondary to interferon alfa-2b plus ribavirin combination therapy in a patient with chronic hepatitis C virus infection. Arch Dermatol. Feb 2004;140(2):215-7. [Medline].

  4. Shen Y, Pielop J, Hsu S. Generalized nummular eczema secondary to peginterferon Alfa-2b and ribavirin combination therapy for hepatitis C infection. Arch Dermatol. Jan 2005;141(1):102-3. [Medline].

  5. Horsmanheimo L, Harvima IT, Jarvikallio A, Harvima RJ, Naukkarinen A, Horsmanheimo M. Mast cells are one major source of interleukin-4 in atopic dermatitis. Br J Dermatol. Sep 1994;131(3):348-53. [Medline].

  6. Jarvikallio A, Naukkarinen A, Harvima IT, Aalto ML, Horsmanheimo M. Quantitative analysis of tryptase- and chymase-containing mast cells in atopic dermatitis and nummular eczema. Br J Dermatol. Jun 1997;136(6):871-7. [Medline].

  7. Jarvikallio A, Harvima IT, Naukkarinen A. Mast cells, nerves and neuropeptides in atopic dermatitis and nummular eczema. Arch Dermatol Res. Apr 2003;295(1):2-7. [Medline].

  8. Patrizi A, Rizzoli L, Vincenzi C, Trevisi P, Tosti A. Sensitization to thimerosal in atopic children. Contact Dermatitis. Feb 1999;40(2):94-7. [Medline].

  9. Pigatto PD, Guzzi G, Persichini P. Nummular lichenoid dermatitis from mercury dental amalgam. Contact Dermatitis. Jun 2002;46(6):355-6. [Medline].

  10. Bendl BJ. Nummular eczema of statis origin. The backbone of a morphologic pattern of diverse etiology. Int J Dermatol. Mar 1979;18(2):129-35. [Medline].

  11. Adachi A, Horikawa T, Takashima T, Ichihashi M. Mercury-induced nummular dermatitis. J Am Acad Dermatol. Aug 2000;43(2 Pt 2):383-5. [Medline].

  12. Flendrie M, Vissers WH, Creemers MC, de Jong EM, van de Kerkhof PC, van Riel PL. Dermatological conditions during TNF-alpha-blocking therapy in patients with rheumatoid arthritis: a prospective study. Arthritis Res Ther. 2005;7(3):R666-76. [Medline].

  13. Sakurane M, Shiotani A, Furukawa F. Therapeutic effects of antibacterial treatment for intractable skin diseases in Helicobacter pylori-positive Japanese patients. J Dermatol. Jan 2002;29(1):23-7. [Medline].

  14. Pietrzak A, Chodorowska G, Urban J, Bogucka V, Dybiec E. Cutaneous manifestation of giardiasis - case report. Ann Agric Environ Med. 2005;12(2):299-303. [Medline].

  15. Khurana S, Jain VK, Aggarwal K, Gupta S. Patch testing in discoid eczema. J Dermatol. Dec 2002;29(12):763-7. [Medline].

  16. Krupa Shankar DS, Shrestha S. Relevance of patch testing in patients with nummular dermatitis. Indian J Dermatol Venereol Leprol. Nov-Dec 2005;71(6):406-8. [Medline].

  17. Gutman AB, Kligman AM, Sciacca J, James WD. Soak and smear: a standard technique revisited. Arch Dermatol. Dec 2005;141(12):1556-9. [Medline].

  18. Gambichler T. Management of atopic dermatitis using photo(chemo)therapy. Arch Dermatol Res. Mar 2009;301(3):197-203. [Medline].

  19. Bukhari IA. Successful treatment of chronic persistent vesicular hand dermatitis with topical pimecrolimus. Saudi Med J. Dec 2005;26(12):1989-91. [Medline].

  20. Clark RA, Hopkins TT. The other eczemas. In: Moschella SL, Hurley HJ, eds. Dermatology. Vol 1. 3rd ed. Philadelphia, Pa: WB Saunders; 1992:482-4.

  21. Cowan MA. Nummular eczema. A review, follow-up and analysis of a series of 325 cases. Acta Derm Venereol. 1961;41:453-60. [Medline].

  22. Hellgren L, Mobacken H. Nummular eczema--clinical and statistical data. Acta Derm Venereol. 1969;49(2):189-96. [Medline].

  23. Krogh HK. Nummular eczema. Its relationship to internal foci of infection. A survey of 84 case records. Acta Derm Venereol. 1960;40:114-26. [Medline].

  24. Krueger GG, Kahn G, Weston WL, Mandel MJ. IgE levels in nummular eczema and ichthyosis. Arch Dermatol. Jan 1973;107(1):56-8. [Medline].

  25. Le Coz C. Contact nummular (discoid) eczema from depilating cream. Cont Dermat. 2002;46:111-112.

  26. O'Loughlin S, Diaz-Perez JL, Gleich GJ, Winkelmann RK. Serum IgE in dermatitis and dermatosis: an analysis of 497 cases. Arch Dermatol. Mar 1977;113(3):309-15. [Medline].

  27. Soter NA. Nummular eczematous dermatitis. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, Fitzpatrick TB, eds. Fitzpatrick's Dermatology in General Medicine. 5th ed. New York, NY: McGraw-Hill; 1999:1480.

  28. White JW. Eczematous reaction patterns: nummular eczema. In: Sams WM, Lynch PJ, eds. Principles and Practice of Dermatology. 2nd ed. New York, NY: tone: Churchill Livings; 1996:443.

Further Reading

Keywords

nummular dermatitis, discoid eczema, nummular eczema, nummular eczema, coin-shaped eczema, coin-shaped dermatitis, nummular pruritus, Staphylococcus aureus, S aureus, staphylococcal skin infection, staphylococcal dermatitis

Contributor Information and Disclosures

Author

Jami L Miller, MD, Assistant Professor, Division of Dermatology, Department of Internal Medicine, Vanderbilt University Medical School; Director of Phototherapy Unit, Vanderbilt University Medical Center; Consulting Attending Physician, Nashville Veterans Affairs Medical Center
Jami L Miller, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

John D Wilkinson, MD, MBBS, MRCS, FRCP, Chairman, Clinical Director, Department of Dermatology, Amersham Hospital and High Wycombe Hospital, UK
John D Wilkinson, MD, MBBS, MRCS, FRCP is a member of the following medical societies: American Academy of Dermatology and Royal College of Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.