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Pachydermoperiostosis Medication

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD  more...
Updated: Jun 21, 2016

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.


Nonsteroidal anti-inflammatory drugs

Class Summary

These medications have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action in pachydermoperiostosis or primary hypertropic osteoarthropathy is not known. In general, NSAIDs inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist; these include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ibuprofen (Ibuprin, Motrin, Advil, Excedrin IB)


Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Indomethacin (Indocin, Indochron E-R)


Indomethacin is rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation; it inhibits prostaglandin synthesis.

Meloxicam (Mobic)


Meloxicam decreases the activity of cyclo-oxygenase, which, in turn, inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Celecoxib (Celebrex)


Celecoxib primarily inhibits COX-2. COX-2 is an isoenzyme induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI tract toxicity. At therapeutic concentrations, the COX-1 isoenzyme is not inhibited, thus GI tract toxicity may be decreased. Seek the lowest dose for each patient.

Naproxen (Aleve, Naprosyn, Naprelan, Anaprox)


Naproxen is used for the relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase and prostaglandin synthesis.


Antidote, Hypercalcemia

Class Summary

These agents inhibit bone resorption and increase renal calcium excretion.

Pamidronate (Aredia)


Pamidronate acts principally by inhibiting osteoclastic bone resorption.


Bisphosphonate Derivative

Class Summary

These agents inhibit osteoclastic bone resorption.

Risedronate (Actonel)


Risedronate is a potent aminobisphosphonate. It inhibits bone resorption via actions on osteoclasts or osteoclast precursors. Supplementation with adequate calcium and vitamin D is required for effectiveness.

Risedronate has been shown to reduce bone resorption and increase bone mineral density of the spine by 5% and femoral neck by 1.6%. It has also has been shown to reduce the incidence of vertebral fractures by 41% and nonvertebral fractures by 39% over a period of 3 years in postmenopausal women.

In men with osteoporosis, significant mean increases in bone mineral density at the lumbar spine, femoral neck, trochanter, and total hip compared with placebo were shown after 2 years of treatment. It is indicated for prevention or treatment of osteoporosis.


Antineoplastic Agent, Hormone Antagonist

Class Summary

These agents inhibit estrogen effects.

Tamoxifen (Nolvadex, Tamofen, Tamone)


Tamoxifen competitively binds to the estrogen receptor, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects.

Contributor Information and Disclosures

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


Supriya Goyal, MD Consulting Dermatologist

Supriya Goyal, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Gregory M Richards, MD Clinical Assistant Professor, Department of Human Oncology, University of Wisconsin School of Medicine and Public Health

Gregory M Richards, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, American Medical Association, American Roentgen Ray Society, American Society for Radiation Oncology, Radiological Society of North America, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Rajiv Goyal, MD Radiologist, Department of Radiology, Kaiser Permanente Medical Center

Rajiv Goyal, MD is a member of the following medical societies: American Medical Association, MedChi The Maryland State Medical Society, Radiological Society of North America, Maryland State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Van Perry, MD Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

Van Perry, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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