1588 LETTERS

Corticosteroids in Cogan’s syndrome To the Editor:

Although our paper on Cogan’s syndrome (1) did not directly address itself to the problem of deaf- ness, total deafness was the end result in both of our reported cases despite liberal use of prednisone, 60 to 80 mg every day for 2 weeks, in each case. This finding is at variance with that reported by Haynes et al in the March 1981 issue of Arthritis and Rheumutism ( 2 ) .

One of our patients did respond to 60 mg prednisone given daily beginning 18 hours after deaf- ness occurred. However, on a subsequent occasion, she remained totally deaf despite institution of the same therapy 8 hours after onset.

Our other patient became totally deaf and re- mained so despite 80 mg prednisone daily for 2 weeks begun 24 hours after onset.

I think we can agree that the therapy may be beneficial, but very cautious optimism should be ex- erted. We agree with the caution expressed by Haynes and his colleagues.

THOMAS G . KANTOR, MD New York University School ojMedicine New York, N Y

1 . Gelfand ML, Kantor TG, Gorstein F: Cogan’s syndrome with cardiovascular involvement: aortic insufficiency. Bull NY Acad Med 48:647-660, 1972

2. Haynes BF, Pikus A, Kaiser-Kupfer M, Fauci A: Suc- cessful treatment of sudden hearing loss in Cogan’s syndrome with corticosteroids. Arthritis Rheum 24501- 503. 1981

Pro-Banthine for hypertrophic osteoarthropathy To the Editor:

In the July 1980 issue of Arthritis and Rheumu- tism, Lopez-Enriquez et a1 (Lopez-Enriquez E, Mo- rales AR, Robet F: Effect of atropine sulfate in pulmo- nary hypertrophic osteoarthropathy. Arthritis Rheum 23:822-824, 1980) described the use of atropine sulfate in pulmonary hypertrophic osteoarthropathy ( 1). Their patient had subjective improvement of joint symptoms with the use of subcutaneous atropine, and he was then switched to oral Pro-Banthine (propantheline

bromide). This is a preliminary report of the successful use of Pro-Banthine by itself for symptomatic treat- ment of hypertrophic osteoarthropathy .

My patient is a 37-year-old man who has had inflammatory bowel disease since 1973. lnitial treat- ment with high-dose corticosteroids was quite effec- tive. Steroids were ultimately discontinued, and his bowel disease has been only mildly active recently. In addition, the patient has had chronic, active hepatitis with cirrhosis and he has had three episodes of hepatic encephalopath y .

In 1977, finger clubbing was noted and perioste- al thickening of long bones was seen on roentgeno- gram. He was asymptomatic at that time and no therapy was administered for this condition. In Febru- ary 1980, he began to notice stiffness and aching in his knees, and by April 1980, he had become markedly disabled because of pain and swelling in the knees, ankles, toes, wrists, and hands.

Initial treatment with Tylenol and Darvon was not very successful. Treatment with antiinflammatory agents was considered somewhat risky because of his cirrhosis and the fear that even small amounts of gastrointestinal bleeding might result in hepatic coma. On October 6, 1980, he was started on Pro-Banthine 40 mg four times a day, and he described rather striking results over the next 3 to 4 days. In mid-November, Pro-Banthine was discontinued on a trial basis, and after 2 days, the number of painful joints had in- creased, so Pro-Banthine was restarted. When seen on December 19, 1980, he continued to have swelling of knees and ankles, but grip strength had improved and there was no active synovitis of small finger joints. His only side effect has been slight dryness of his mouth. He has continued to be symptomatically improved and is able to work fulltime.

In many patients with hypertrophic osteoarth- ropathy, the underlying cause cannot be corrected and symptomatic treatment becomes necessary. Thera- peutic approaches that have been reported to be successful in relieving symptoms include vagotomy, adrenergic blockade, atropine, and nonsteroidal an- tiinflammatory drugs. This case documents the posi- tive results with the use of Pro-Banthine, an oral parasympathetic blocking agent.

HARVEY A. SCHWARTZ, MD, FACP Assistant Clinicul Professor of Medicine Georgetown University Washington, DC