eMedicine Specialties > Rheumatology > Metabolic and Bone Disease

Hypertrophic Osteoarthropathy: Treatment & Medication

Author: Richa Dhawan, MD, Faculty, Center of Excellence for Arthritis and Rheumatology, Louisiana State University Health Science Center at Shreveport
Coauthor(s): Mohammed Mubashir Ahmed, MD, Associate Professor, Department of Medicine, Division of Rheumatology, University of Toledo College of Medicine; Henri-Andre Menard, MD, Professor of Medicine, Director of Rheumatology, Department of Medicine, Division of Rheumatology, McGill University Health Center and McGill University; Director, The McGill Arthritis Center; Senior Physician, Shriner's Hospital for Crippled Children, Montreal
Contributor Information and Disclosures

Updated: Nov 7, 2008

Treatment

Medical Care

  • The only effective treatment for secondary hypertrophic osteoarthropathy (HOA) is treatment of the underlying condition, ie, surgery for cardiac anomalies or cancer and antibiotics for infections. Although removal of the primary tumor usually resolves this syndrome, effective treatment in patients with advanced lung cancer has not been established.
  • Recently, an orally active selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (gefitinib) provided clinical antitumor activity in a case report in Tokyo.
    • A 71-year-old male smoker with cough presented with clubbed fingers. A transbronchial lung biopsy (stage T2N3M1-IV) on a cavity lesion in the left lower lobe showed the features of adenocarcinoma, while bone scintigraphy revealed bilaterally symmetrical abnormal uptakes in the lower extremities, suggesting secondary hypertrophic osteoarthropathy.
    • The serum level of growth hormone was increased to 1.42 ng/mL. Chemotherapy (cisplatin, vinorelbine) was not effective. Gefitinib, as a second-line therapy, induced disappearance of the abnormal accumulation on bone scintigraphy and decrease of the cavity in the lung and of serum growth hormone. The presented case suggests that the EGFR inhibitor might be a promising option for the treatment of hypertrophic osteoarthropathy with advanced lung adenocarcinoma.45
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful for the painful osteoarthropathy in controlling the symptoms.
  • In those with primary hypertrophic osteoarthropathy, propranolol may be useful for hyperhydrosis, but the drug does not alter the natural course of the disorder. By adulthood, patients with primary hypertrophic osteoarthropathy are asymptomatic.
  • VEGF inhibitors such as octreotide have also been shown to have improved hypertrophic osteoarthropathy–related symptoms.
    • A 34-year-old man was admitted with bilateral leg pain. He had tetralogy of Fallot with pulmonary artery atresia. Surgical interventions had been performed in the past, with only transient success. The patient was rejected for cardiopulmonary transplantation. He had grade III dyspnea. In the last 2 months, progressive, severe pain along both legs and ankles developed, which had not responded to usual analgesics and impeded his sleep.
    • After informed consent had been obtained, subcutaneous octreotide 100 µg twice daily was added. After 3-4 days, complete pain relief was achieved and the other drugs could be withdrawn. No adverse events were recorded.
    • After 2 weeks, octreotide was tapered to 100 µg/d and the patient was discharged. After about 1 week, the pain reappeared and the patient was readmitted. His poor cardiorespiratory status was then rapidly deteriorating. Octreotide was increased to 100 µg twice daily, but, owing to untreatable dyspnea, multiple other palliative measures were needed, including morphine administration (thus precluding the evaluation of a specific response to octreotide), and the patient finally died.46
  • Bisphosphonates such as zoledronic acid and pamidronate are also effective for pain relief in hypertrophic osteoarthropathy.47 Bisphosphonates not only inhibit osteoclast activity, but some, including pamidronate, inhibit VEGF expression. One case report described a patient with hypertrophic osteoarthropathy of the lower extremities that developed secondary to congenital cyanotic heart disease. The major clinical manifestation was debilitating bilateral leg pain, which completely resolved following a single administration of 60 mg pamidronate.48

Surgical Care

  • In patients with primary hypertrophic osteoarthropathy, plastic surgery may be necessary to remove excess facial skin.
  • In patients with secondary hypertrophic osteoarthropathy, tumor resection results in spontaneous improvement within 2-4 weeks. In fact, hypertrophic osteoarthropathy may disappear completely by 3-6 months.

Medication

No drug effectively treats hypertrophic osteoarthropathy (HOA). Drugs such as NSAIDs may be used for symptomatic relief. Beta-blockers may be used for the treatment of hyperhidrosis of primary hypertrophic osteoarthropathy.

Nonsteroidal anti-inflammatory drugs

These agents have analgesic, anti-inflammatory, and antipyretic activities. The main mechanism of action is inhibition of COX activity and prostaglandin synthesis. These agents may also have other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions. NSAIDs such as ibuprofen, naproxen, indomethacin, piroxicam, diclofenac, and others are reasonable alternatives.


Ibuprofen (Ibuprin, Motrin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. Most common toxicities are nausea, dyspepsia, peptic ulcer disease, and renal and central nervous system toxicity.

Adult

400-800 mg PO tid/qid; not to exceed 3.2 g/d

Pediatric

20-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate; not to exceed 2.4 g/d

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of ACE inhibitors, beta-blockers, and other antihypertensive agents; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease (unless prophylaxis is adequate), renal insufficiency, anticoagulation or coagulopathy, or aspirin-sensitive asthma

Pregnancy

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Most common toxicities include GI manifestations (eg, nausea, abdominal pain, peptic ulcer disease) and renal insufficiency; category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy


Naproxen (Naprosyn, Naprelan, Anaprox, Aleve)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis.

Adult

250-500 mg PO bid; may increase to 1.5 g/d

Pediatric

10-20 mg/kg/d PO divided bid

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of ACE inhibitors, beta-blockers, and other antihypertensive agents; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease (unless prophylaxis is adequate), renal insufficiency, anticoagulation or coagulopathy, or aspirin-sensitive asthma

Pregnancy

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Most common toxicities include GI manifestations (eg, nausea, abdominal pain, peptic ulcer disease) and renal insufficiency; category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy


Celecoxib (Celebrex)

Inhibits primarily COX-2, which is considered an inducible isoenzyme induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek lowest effective dose for each patient.

Adult

200 mg PO qd

Pediatric

Not established

Coadministration with fluconazole may cause increased plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations

Pregnancy

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; may mask usual signs of infection; caution in presence of existing controlled infections; evaluate therapy when symptoms or lab results suggest liver dysfunction

Adrenergic beta-blockers

Beta-blockers are useful for treating hyperhidrosis, which may occur in primary hypertrophic osteoarthropathy.


Propranolol (Inderal, Betachron E-R)

Opposes multisystemic effects of excessive adrenergic tone.

Adult

Adults are asymptomatic; use is unnecessary

Pediatric

0.5 mg/kg/d PO divided bid/qid; increase gradually q3-7d; dosage range is 2-4 mg/kg/d divided bid; not to exceed 2 mg/kg/d

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; AV conduction abnormalities

Pregnancy

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

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Beta-blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely

More on Hypertrophic Osteoarthropathy

Overview: Hypertrophic Osteoarthropathy
Differential Diagnoses & Workup: Hypertrophic Osteoarthropathy
Treatment & Medication: Hypertrophic Osteoarthropathy
Follow-up: Hypertrophic Osteoarthropathy
Multimedia: Hypertrophic Osteoarthropathy
References
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Further Reading

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Keywords

hypertrophic osteoarthropathy, primary hypertrophic osteoarthropathy, primary HOA, HOA, secondary HOA clubbing, Hippocratic fingers, clubbed digits, pachydermoperiostosis, acroosteolysis, Touraine-Solente-Golé syndrome, Goldbloom's syndrome, Goldbloom syndrome, Pierre Marie-Bamberger's disease, Pierre Marie-Bamberger disease, osteoarthropathie hypertrophiante pneumique, hypertrophic pulmonary osteoarthropathy, HPOA, acropachy, hyperhidrosis, digital clubbing, periostosis, intrathoracic malignancy, intrathoracic infection, cyanotic cardiac disease, cyanotic heart disease, congenital clubbing, familial clubbing, osteosarcoma, thyroid acropachy, Crohn disease, Crohn's disease, polyposis, thymoma, achalasia, Graves disease, Graves' disease, thalassemia, POEMS syndrome

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Contributor Information and Disclosures

Author

Richa Dhawan, MD, Faculty, Center of Excellence for Arthritis and Rheumatology, Louisiana State University Health Science Center at Shreveport
Richa Dhawan, MD is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Physicians-American Society of Internal Medicine, and American College of Rheumatology
Disclosure: Nothing to disclose.

Coauthor(s)

Mohammed Mubashir Ahmed, MD, Associate Professor, Department of Medicine, Division of Rheumatology, University of Toledo College of Medicine
Mohammed Mubashir Ahmed, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and American Federation for Medical Research
Disclosure: Nothing to disclose.

Henri-Andre Menard, MD, Professor of Medicine, Director of Rheumatology, Department of Medicine, Division of Rheumatology, McGill University Health Center and McGill University; Director, The McGill Arthritis Center; Senior Physician, Shriner's Hospital for Crippled Children, Montreal
Henri-Andre Menard, MD is a member of the following medical societies: American College of Rheumatology, Canadian Medical Association, Canadian Rheumatology Association, and Quebec Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Bryan L Martin, DO, Chief, Allergy Immunology Department, Walter Reed Army Medical Center; Associate Professor of Medicine and Pediatrics, Uniformed Services University of the Health Sciences; United States Army Consultant in Allergy Immunology and Immunizations
Bryan L Martin, DO is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, American College of Osteopathic Internists, American College of Physicians, American Medical Association, and American Osteopathic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Lawrence H Brent, MD, Associate Professor of Medicine, Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center
Lawrence H Brent, MD is a member of the following medical societies: American Association of Immunologists, American College of Physicians, and American College of Rheumatology
Disclosure: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; Merck, Amgen, Biogen, Zimmer, Wyeth, Johnson&Johnson, Stryker, Medtronic, Zimmer.Abbott,  Ownership interest Other; West Penn Allegheny Health System Consulting fee Consulting; Alpharma Honoraria Consulting; Proctor&Gamble Grant/research funds Independent contractor

 
 
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