eMedicine Specialties > Rheumatology > Systemic Rheumatic Disease

Undifferentiated Connective-Tissue Disease: Treatment & Medication

Author: Bernard A Hildebrand Jr, MD, Staff Rheumatologist, Department of Rheumatology, San Antonio Military Medical Center, San Antonio, Texas
Coauthor(s): Daniel F Battafarano, DO, FACP, FACR, Clinical Professor of Medicine, University of Texas Health Science Center, San Antonio, Texas; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences, F Edward Hebert School of Medicine; Chief of Rheumatology Service, San Antonio Military Medical Center, San Antonio, Texas.
Contributor Information and Disclosures

Updated: Jul 24, 2009

Treatment

Medical Care

A patient with undifferentiated connective-tissue disease (UCTD) can be evaluated and treated primarily as an outpatient.

Surgical Care

Surgery for patients with UCTD is not routinely necessary and should be initiated only when indicated for diagnosis or treatment.

Consultations

  • A rheumatologist should be consulted.
  • Consultations with other specialists may be clinically indicated, including with a dermatologist, ophthalmologist, pulmonologist, cardiologist, neurologist, physical medicine specialist, physical therapist, and/or occupational therapist.

Diet

No special diet is recommended for patients with UCTD.

Activity

  • In general, activities are not restricted in the absence of specific functional limitations associated with UCTD.
  • Patients with photosensitivity should minimize prolonged exposure to sunlight and should use protective clothing and sunblock lotions/creams to protect against ultraviolet light.
  • Patients with severe Raynaud phenomenon should avoid prolonged exposure to severe cold temperatures (<40° F) to avoid digital vasospasm. Layered clothing, hats, and gloves help to maintain a warm core body temperature and decreased vasospastic symptoms. Tobacco use should be avoided.

Medication

Nonsteroidal anti-inflammatory drugs (NSAIDs), antimalarials (eg, hydroxychloroquine), and corticosteroids are the mainstay of therapy in patients with undifferentiated connective-tissue disease (UCTD). Immunosuppressive drugs are generally reserved for treating specific clinical manifestations and when there is major organ involvement.

Mosca et al (2008) found that 93% of patients with UCTD were initially treated with corticosteroids and/or antimalarials, and 2% were started on immunosuppressive medications. After 10 years of follow-up, 16% of patients were no longer receiving therapy, 36% were being treated with hydroxychloroquine plus corticosteroids, 10% were taking corticosteroids alone, and no patients were receiving cytotoxic immunosuppressive therapy.17

Bodolay et al (2003) prescribed low-dose corticosteroids only when NSAIDs were deemed ineffective.15 Common indications for systemic corticosteroids included recurrent serositis, skin vasculitis, and synovitis. Antimalarials were administered for photosensitivity and severe rash. The authors concluded that aggressive immunosuppressive therapy for "true" UCTD is neither necessary nor justified.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs may be beneficial for analgesic, antipyretic, anti-inflammatory, or antiplatelet effects. These medications inhibit the enzyme cyclooxygenase, resulting in a generalized decrease in prostaglandin production, ultimately reducing pain and inflammation. Other mechanisms may also exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Arthritis and arthralgias may respond to NSAIDs alone or in combination with an antimalarial (see below).


Naproxen (Naprosyn)

For relief of mild-to-moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis.

Adult

250-500 mg PO bid

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Reports suggest that NSAIDs may diminish the antihypertensive effect of angiotensin-converting enzyme (ACE) inhibitors; concomitant administration of aspirin increases the risk of GI complication; may interfere with beneficial antiplatelet effect of aspirin; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase the bleeding risk in patients taking other anticoagulants; monitor the prothrombin (PT) closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

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

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

Precautions

Some studies suggest there is an increased risk of myocardial infarction or stroke in patients taking certain NSAIDs; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Nonsteroidal Anti-Inflammatory Drug (NSAID), Cox-2 Selective

The inducible cyclooxygenase-2 (COX-2) isoenzyme is produced during inflammatory conditions, resulting in increased production of proinflammatory prostaglandins that cause pain and swelling. COX-2 inhibitors selectively block the COX-2 isoenzyme and may minimize adverse effects associated with traditional NSAIDs (eg, gastrointestinal bleeding).


Celecoxib (Celebrex)

Selectively inhibits cyclooxygenase-2 and reduces prostaglandin synthesis

Adult

100-200 mg PO bid

Pediatric

Not established

Reports suggest that NSAIDs may diminish antihypertensive effect of angiotensin-converting enzyme (ACE) inhibitors; concomitant administration of aspirin increases rate of GI ulceration or other complications; concomitant administration of fluconazole at 200 mg daily resulted in 2-fold increase in celecoxib plasma concentration; NSAIDs can reduce natriuretic effects of furosemide and thiazides in some patients; lithium plasma levels increase approximately 17% when administered concomitantly; celecoxib does not alter anticoagulant effects of warfarin as determined by prothrombin time

Documented hypersensitivity to celecoxib or sulfonamides; preoperative pain prior to coronary artery bypass surgery

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

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

Precautions

Studies suggest high doses of celecoxib are associated with increased cardiovascular risk; elderly patients may require lower doses; caution in hepatic and renal impairment

Antimalarials

These agents may inhibit the chemotactic properties of pro-inflammatory leukocytes (eg, polymorphonuclear cells, lymphocytes). They may also interfere with intracellular processing of autoantigenic peptides.

Antimalarials may be used with or without NSAIDs to control arthralgias/arthritis, constitutional symptoms, and mucocutaneous manifestations.


Hydroxychloroquine (Plaquenil)

Inhibits chemotaxis of eosinophils and locomotion of neutrophils and impairs complement-dependent antigen-antibody reactions. Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Adult

200 mg PO bid for several weeks depending on response
Prolonged maintenance therapy: 200-400 mg PO qd (not to exceed 6.5 mg/kg/d)

Pediatric

5 mg base/kg/d PO qd or divided bid; not to exceed 7 mg/kg/d

Serum levels increase with cimetidine; magnesium trisilicate may decrease absorption

Documented hypersensitivity; retinal and visual field changes attributable to 4-aminoquinolones

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

Caution in hepatic disease, G-6-PD deficiency, psoriasis, and porphyria; not recommended for long term in children; perform periodic (6 mo) ophthalmologic examinations; test periodically for muscle weakness

Corticosteroids

Corticosteroids inhibit the cascade of inflammatory and immune mechanisms at the cellular level, resulting in profound anti-inflammation and modification of the immune response. The pharmacologic effects and adverse effects of corticosteroids are influenced by the drug preparation, dose, dosing schedule, and route of administration. They vary with the individual patient and disease process.

These drugs are commonly used in combination with other medications to control the signs and symptoms of inflammation.


Prednisone (Deltasone, Orasone, Meticorten)

Immunosuppressant for treatment of autoimmune disorders. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Adult

5 mg PO qd, titrate up to 1 mg/kg/d PO in divided doses

Pediatric

Administer as in adults

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

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

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

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, cognitive impairment, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use, particularly at high doses (>20 mg/d); patients on glucocorticoids for extended periods should be evaluated for osteoporosis and treated according to published guidelines

Immunosuppressant agents

These agents suppress key factors of the immune system and are typically reserved for severe manifestations of UCTD.


Methotrexate (Rheumatrex, Folex PFS)

Unknown mechanism of action. Analog of folic acid and inhibits dihydrofolate reductase and, ultimately, DNA synthesis. Methotrexate also inhibits the enzyme 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) transformylase, leading to intracellular accumulation of AICAR and extracellular adenosine release. The adenosine has anti-inflammatory properties.
Methotrexate is very effective in the treatment of inflammatory arthritis and other systemic manifestations of UCTD. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness).
Available as 2.5-mg tab or 25-mg/mL vial.

Adult

7.5-25 mg PO/IM/SC weekly

Pediatric

Administer as in adults

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral methotrexate (MTX); charcoal lowers MTX levels; coadministration with etretinate may increase hepatotoxicity of MTX; folic acid 1 mg/d or its derivatives contained in some vitamins may decrease response to MTX; coadministration with NSAIDs may be fatal; indomethacin and phenylbutazone can increase MTX plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity of MTX; may increase plasma levels of thiopurines

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC count monthly and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); follow published guidelines for performing liver biopsy; MTX has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood counts occurs; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly with MTX


Azathioprine (Imuran)

A purine analog that interferes with the synthesis of adenosine and guanine resulting in inhibited synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells and may be effective for treatment of articular and extra-articular manifestations of connective-tissue disease.

Adult

1-2.5 mg/kg/d PO

Pediatric

Up to 1 mg/kg/d PO

Toxicity increases with coadministration of allopurinol (allopurinol reduces the metabolism of azathioprine; reduce azathioprine dose by 75%); concurrent use with ACE inhibitors may induce severe leukopenia; may increase levels of methotrexate metabolites and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine

Pregnancy

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

Precautions

Prior treatment with alkylating agents may increase risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur

Calcium channel blockers

These agents relax vascular smooth muscle and decrease peripheral vascular resistance. They may help control the signs and symptoms of Raynaud phenomenon.


Nifedipine (Procardia, Procardia XL, Adalat CC)

During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle.

Adult

10-30 mg PO tid
Alternatively, 30-90 mg PO qd (ER form)

Pediatric

Not established

Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 blockers (cimetidine) may increase toxicity

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 cause lower extremity edema; allergic hepatitis has occurred but is rare; excessive hypotension, peripheral edema, or significant left ventricular dysfunction


Diltiazem (Cardizem, Cardizem SR)

During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle.

Adult

30 mg PO qid
Alternatively, 60-120 mg PO qd (SR dosage)

Pediatric

Not established

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when administered with beta-blockers, may increase cardiac depression; cimetidine may increase diltiazem levels

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

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

Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur; cardiac conduction abnormalities

More on Undifferentiated Connective-Tissue Disease

Overview: Undifferentiated Connective-Tissue Disease
Differential Diagnoses & Workup: Undifferentiated Connective-Tissue Disease
Treatment & Medication: Undifferentiated Connective-Tissue Disease
Follow-up: Undifferentiated Connective-Tissue Disease
References
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Further Reading

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Keywords

undifferentiated connective-tissue disease, UCTD, undifferentiated connective-tissue syndromes, UCTS, early connective-tissue disease, rheumatoid arthritis, RA, systemic lupus erythematosus, SLE, systemic sclerosis, SSc, polymyositis, PM, dermatomyositis, DM, mixed connective-tissue disease, MCTD, Sjögren's syndrome, Sjögren syndrome, SS

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Contributor Information and Disclosures

Author

Bernard A Hildebrand Jr, MD, Staff Rheumatologist, Department of Rheumatology, San Antonio Military Medical Center, San Antonio, Texas
Bernard A Hildebrand Jr, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel F Battafarano, DO, FACP, FACR, Clinical Professor of Medicine, University of Texas Health Science Center, San Antonio, Texas; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences, F Edward Hebert School of Medicine; Chief of Rheumatology Service, San Antonio Military Medical Center, San Antonio, Texas.
Daniel F Battafarano, DO, FACP, FACR is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.

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; West Penn Allegheny Health System None Board membership

 
 
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