flexor carpi ulnaris tendinitis

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97 Finally, Drs. Fishbein and Alarcon-Segovia sug- gest that we “disregard” the genetic polymorphism of acetyl transferase activity. In fact our Figure 2 clearly shows a classic bimodal distribution with values similar to those in control populations. JOHN S. SERGENT, MD RAYMOND L. WOOSLEY, MD, PhD Department of Medicine Vanderbilt University School of Medicine Nashville, Tennessee 3 7232 REFERENCES I. Fishbein E, Alarcon-Segovia D: Phenotypically low acetyl transferase activity: a characteristic of SLE (abst). Arthritis Rheum 19:796, 1976 2. Reidenberg MM, Martin JH: The acetylator phenotype of patients with systemic lupus erythematosus. Drug Metab Dispos 2:7 1-73, 1974 3. Gelber R, Peters JH, Gordon GR, Glayko AJ, Leby L: The polymorphic acetylation of dapsone in man. Clin Pharm Thes 12:225-238, 1971 Flexor carpi ulnaris tendinitis To the Editor: Recently I attended a 34-year-old married man with acute wrist pain. He had awakened the previous night with acute swelling in the left wrist. He had been seen in the emergency room of a local hospital 2 days earlier for discomfort in the wrist and had been placed on Butazolidin and aspirin without improvement. He was employed as a youth director and specifically de- nied extramarital coitus, urethritis, conjunctivitis, or skin rash. He had had no fever, chills, sore throats, re- cent skin infections, or trauma. He was an avid jogger and had no prior history of joint complaints or family history of arthritis or gout. On examination he was afebrile. His left wrist was held in a flexed position and supported by his right hand. Complete physical examination showed unre- markable results except that the patient complained of extreme pain on motion of the wrist. The left wrist was red, warm, and swollen over the volar medial aspect. Tenderness was maximum at the volar aspect of the dis- tal ulna and there was a suggestion of subcutaneous cre- pitus. Laboratory data revealed a hemoglobin of 16, a white blood cell count of 8,700 with a normal differen- tial. Sedimentation rate was 10 mm/hr by the West- ergren method. A uric acid was 7.1. Figure 1. X-ray of the left wrist (Figure 1) revealed a round calcified body distal to the ulna. No fluid, pus, or other material cocld be obtained from the wrist with at- tempted aspiration. The point of maximum tenderness was injected with 20 mg of Hydeltra TBA, the wrist splinted, and Butazolidin continued. Three days later, the wrist had markedly improved. Two weeks after the second visit, the patient was asymptomatic. The wrist was normal on examination. Hand x-ray demonstrated no evidence of osteomyelitis, and the calcific body was absent (Figure 2). Calcific tendinitis of the hand and wrist is rare and has been reported to occur in about 2% of all cases of calcific tendinitis (1). When the wrist is involved, the most frequently observed areas of acute calcific tendi- nitis are the points of insertion of the flexor carpi ulnaris tendon into the pisiform bone or the flexor carpi radialis into the base of the second metacarpal bone (2-4). Less commonly, the long digital flexors and extensors in the

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Page 1: Flexor carpi ulnaris tendinitis

97

Finally, Drs. Fishbein and Alarcon-Segovia sug- gest that we “disregard” the genetic polymorphism of acetyl transferase activity. In fact our Figure 2 clearly shows a classic bimodal distribution with values similar to those in control populations.

JOHN S. SERGENT, MD RAYMOND L. WOOSLEY, MD, PhD Department of Medicine Vanderbilt University School of Medicine Nashville, Tennessee 3 7232

REFERENCES

I . Fishbein E, Alarcon-Segovia D: Phenotypically low acetyl transferase activity: a characteristic of SLE (abst). Arthritis Rheum 19:796, 1976

2. Reidenberg MM, Martin JH: The acetylator phenotype of patients with systemic lupus erythematosus. Drug Metab Dispos 2:7 1-73, 1974

3. Gelber R, Peters JH, Gordon GR, Glayko AJ, Leby L: The polymorphic acetylation of dapsone in man. Clin Pharm Thes 12:225-238, 1971

Flexor carpi ulnaris tendinitis To the Editor:

Recently I attended a 34-year-old married man with acute wrist pain. He had awakened the previous night with acute swelling in the left wrist. He had been seen in the emergency room of a local hospital 2 days earlier for discomfort in the wrist and had been placed on Butazolidin and aspirin without improvement. He was employed as a youth director and specifically de- nied extramarital coitus, urethritis, conjunctivitis, or skin rash. He had had no fever, chills, sore throats, re- cent skin infections, or trauma. He was an avid jogger and had no prior history of joint complaints or family history of arthritis or gout.

On examination he was afebrile. His left wrist was held in a flexed position and supported by his right hand. Complete physical examination showed unre- markable results except that the patient complained of extreme pain on motion of the wrist. The left wrist was red, warm, and swollen over the volar medial aspect. Tenderness was maximum at the volar aspect of the dis- tal ulna and there was a suggestion of subcutaneous cre- pitus.

Laboratory data revealed a hemoglobin of 16, a white blood cell count of 8,700 with a normal differen- tial. Sedimentation rate was 10 mm/hr by the West- ergren method. A uric acid was 7.1.

Figure 1.

X-ray of the left wrist (Figure 1) revealed a round calcified body distal to the ulna. No fluid, pus, or other material cocld be obtained from the wrist with at- tempted aspiration. The point of maximum tenderness was injected with 20 mg of Hydeltra TBA, the wrist splinted, and Butazolidin continued. Three days later, the wrist had markedly improved. Two weeks after the second visit, the patient was asymptomatic. The wrist was normal on examination. Hand x-ray demonstrated no evidence of osteomyelitis, and the calcific body was absent (Figure 2).

Calcific tendinitis of the hand and wrist is rare and has been reported to occur in about 2% of all cases of calcific tendinitis (1). When the wrist is involved, the most frequently observed areas of acute calcific tendi- nitis are the points of insertion of the flexor carpi ulnaris tendon into the pisiform bone or the flexor carpi radialis into the base of the second metacarpal bone (2-4). Less commonly, the long digital flexors and extensors in the

Page 2: Flexor carpi ulnaris tendinitis

98

Figure 2.

region of the wrist may be involved (5). A history of trauma or stress to the hand is unusual and no voca- tional groups have been dominant except perhaps housewives (5). Typically the onset is abrupt, often awakening the patient from a sound sleep, and local in- flammatory response is so intense as to suggest gout (1,5,7), acute gonococcal arthritis,(5), septic arthritis or osteomyelitis (1,3), acute cellulitis (1,2), and trauma (5). Generally with rest, the acute symptoms subside within a few days and the calcification disappears in most cases within a few weeks (2,3,7). Antiinflammatory drugs, heat, ultrasound, and local corticosteroid injections may be beneficial (7).

In view of its rarity, it is likely that many physi- cians may not be aware of calcific tendinitis of the wrist (8,9). This patient serves as a reminder, not only of the condition, but that it may be initially misdiagnosed as another more common rheumatic disease, such as acute gonococcal tenosynovitis or arthritis, other septic arthri-

tides, or even gout. Awareness of this entity, therefore, may obviate unnecessary expense, diagnostic proce- dures, and therapeutic interventions.

JOHN G. PATY, JR. MD Appalachian Arthritis Center and Section of Rheumatology Department of Medicine University of Tennessee Clinical Education Center Chattanooga, Tennessee

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REFERENCES Martin JF, Brogdon BG: Peritendinitis calcarea of the hand and wrist. J Radiology 78:74-85 Aitken AP, Magill HK: Calcareous tendinitis of the flexor carpi ulnaris. N Engl J Med 244:434-435, 1951 Pinals RS, Short CL: Calcific periarthritis involving mul- tiple sites. Arthritis Rheum 9566-573, 1966 Cowan 11, Stone JR: Painful periarticular calcifications at wrist and elbow: diagnosis and treatment. JAMA 149530- 533, 1975 Carroll RE, Sinton W, Garcia A: Acute calcium deposits in the hand. JAMA 157:422426, 1955 Thompson GR, Ming Ting Y, Riggs GA, Fenn ME, Den- ning RM: Calcific tendinitis and soft-tissue calcification re- sembling gout. JAMA 203:122-130, 1968 Hollander J, McCarty DJ: Arthritis and Allied Conditions. Eighth edition. Philadelphia, Lea & Febiger, p 1405 Yelton CL, Dickey LE Jr.: Calcification about the hand and wrist. South Med J 51:489-495, 1958 Hauptrnan HA: Acute tendinitis calcarea. NY Stat J Med 955-961, (1970)

Uric acid excretion in patients with gout To the Editor:

Do the kidneys of gouty men “handle” urate in an abnormal way? The answer to this question has re- mained elusive despite significant gains in our under- standing of the renal mechanisms involved (1). One ap- proach to the problem has been to repeat measurements of uric acid excretion in normal and gouty individuals at varying levels of serum urate. The data from six such studies (2-7) have been collected and reanalyzed here.

In both normal and gouty subjects, data were ob- tained under basal conditions, after oral purine loading or during allopurinol therapy. Age, sex, and racial back- ground were not stated in all sources, although most ob- servations were made in white males. An estimate of the glomerular filtration rate (GFR) was available in each study from concurrent determination of the inulin clear- ance. For both normal and gouty subjects, uric acid ex-