with those drugs available in the United States (e.g., Sectral, Tenormin, Inderal, Toprol).
Anticonvulsants prevent epileptic seizures and may result in positive ANA tests. Nearly all clinical cases of lupus attributed to phenytoin (Dilantin) occurred in children. Occasional reports have been associated with carbamazepine
(Tegretol), but phenobarbital has not been connected with DILE. Up to 15 per-
cent of patients with lupus experience epileptic seizures. None of these drugs
will cause flareups of lupus and there is no reason not to take any of them.
Isoniazid (INH) is an antituberculosis agent similar in structure to hydralazine.
Its long-term administration may result in positive ANA tests in up to 25 percent of those taking the drug, but only a few cases of clinical lupus have been
published. Drugs that treat psychosis in the phenothiazine family (e.g., Thora-
[54]
What Causes Lupus?
zine, Stelazine, Mellaril) may convert patients to ANA positivity up to 26 per-
cent of the time, but lupus-related symptoms are extremely unusual. Certain
preparations used to treat hyperthyroidism (e.g., propylthiouracil, or PTU) only in rare instances cause a lupus-like syndrome.
D- penincillamine is used to manage rheumatoid arthritis and scleroderma.
About 1 percent of the time, these patients may develop myasthenia gravis or
SLE from the drug. Since those taking D-penicillamine already have an auto-
immune disease, sorting things out can be problematic. Your doctor should
consider consulting a rheumatologist. Was the diagnosis of scleroderma or rheu-
matoid arthritis correct all along, or could the diagnosis have been lupus? D-
penicillamine has no place in the treatment of lupus and should be stopped in
anyone suspected of having SLE.
TNF blocking medicines prescribed for rheumatoid arthritis (e.g., Remicade, Humira, Enbrel) can flare lupus if it is also present, or if a lupus patient has been misdiagnosed with rheumatoid arthritis. It rarely causes clinical lupus. TNF
blockers induce the formation of autoantibodies, particular anti-DNA in 20–40
percent of users. This is clinically relevant in a minority of patients and is not by itself a reason to stop taking it.
How Can We Tell DILE From SLE?
While taking a lupus-causing drug, the DILE patient displays many of the signs
and symptoms seen in the patient with lupus. However, DILE patients rarely
have symptoms involving the many organ systems of the body. (In other words,
the central nervous system, heart, lung, and kidneys are not usually involved.) In these patients, we do find antihistone antibodies (in fact, they are found on blood testing in more than 95 percent of patients with DILE; the problem is
that 40 percent with SLE also develop these antibodies). The patient with DILE
does not have the other typical lupus antibodies reviewed in Chapter 6. Normal
complement levels are also present in DILE patients. Further, upon discontin-
uing the drug, DILE improves or resolves within days to weeks in these patients.
Even though antihistone antibodies decrease, the ANA test may remain positive
for years.
Your doctor must differentiate DILE from bacterial or viral infections, po-
lymyalgia rheumatica, SLE, rheumatoid arthritis, or Dressler’s syndrome (fever
with pericarditis in patients who have had a recent heart attack). Blood tests and cultures usually distinguish among these diseases.
How Do We Treat DILE?
If the offending drug is withdrawn as soon as symptoms present themselves, no
therapy may be necessary. Approximately one-third of the time, my patients
have benefited from several weeks to months of aspirin or other NSAID med-
Drugs That May Cause Lupus or Produce Flareups
[55]
ications (such as ibuprofen, naproxen, or indomethacin). If serious complications develop (e.g., pericardial tamponade or kidney disease) or the symptoms are
severe (e.g., disabling arthritis, pleurisy with shortness of breath), I usually prescribe several weeks