Williams' textbook of endocrinology. Philadelphia: WB Saun- ders, 1985; 682-815. 4. Hegediis L, Hansen JM, Karstrup S: High incidence of normal thyroid gland ...
LETTERS TO THE EDITOR
THYROTOXICOSIS
IN THE VERY
TABLE
OLD
To the Editor: In a recent report, Tibaldi et al (Am J Med 1986; 81: 619-622) drew attention to the lack of symptoms and signs of hypetthyroidism in old persons. Although their study was retrospective, limiting the value of recordings of signs and symptoms of hyperthyroidism, we agree with most of their conclusions and offer the following extension of objective data regarding thyroid size in a consecutive group of patients with untreated hypet-thyroidism. Thyroid gland volume, ultrasonically determined [I], was investigated in 312 consecutive untreated patients with hyperthyroidism. Thirty patients (10 percent) were older than 75 years of age. Median age was 78 years (range, 76 to 86 years). Other pertinent data are given in Table I. It is well accepted that the clinical evaluation of thyroid size is very inaccurate and nonreproducible [2]. Furthermore, little is known regarding “normal thyroid size” in different populations. In a previous study, we attempted such a definition of a normal thyroid size in a Danish population [ 11. Ultrasonically determined normal thyroid volume was found to be 9.3 to 27.7 ml in that study. Of the 312 consecutive hyperthyroid patients, 95 (30 percent) had a thyroid volume of less than 27.7 ml. This is not different from the number of patients without thyroid enlargement who were older than 75 years (seven of 30,23 percent). Thus, our finding is not totally in agreement with the data of Tibaldi et al, who observed that 68 percent of their patients had no thyroid gland enlargement. It is, however, important to stress that a large number of patients with hyperthyroidism do not have thyroid enlargement and that our objective data suggest that this is not more frequent in very old persons. Although it has been stated [3] that only approximately 3 percent of hyperthyroid patients do not have goiter, we have shown by an objective ultrasonic technique (in addition to palpation) that this is approximately a IO-fold underestimation [4]. Recently, this was verified in a study in which only palpation of the thyroid was performed [5]. The latter authors, in accordance with Tibaldi et al, found the absence of a goiter to be more frequent in old patients. We conclude that, independent of whether the number of patients with hyperthyroidism but no thyroid enlargement increases with increasing age, it is important not to refrain from suspecting hyperthyroidism despite the absence of a clinically detectable goiter. Furthermore, the recent finding of irreversible intellectual impairment in patients with hyperthyroidism [6] should increase efforts to diagnose this ailment in elderly persons, since this age group might very well be the most susceptible to the cerebral effect of hyperthyroidism. LASZLO HEGEDUS, JENS M. HANSEN,
DK-2730,
I
Pertinent Clinical Data in 30 Consecutive Patients Older Than 75 Years of Age with Hyperthyroidism
Diffuse Number of patients Sex (F/M) No goiter Normal volume Median thyroid volume (ml) (range)
1.
2.
3.
4.
5. 6.
Type 01 Thyroid Gland MultiToxic nodular Adenoma
7
18 15/3 5 2
6/i 4 3
5 5/O 0 2
(16%7)
(233-577)
Hegedus L, Perrild H, Poulsen LR, et al: The determination of thyroid volume by ultrasound and its relationship to body weight, age and sex in normal subjects. J Clin Endocrinol Metab 1983; 56: 260-263. Tannahill AJ, Hooper MJ, England M, Ferriss JB, Wilson GM: Measurement of thyroid size by ultrasound, palpation and scintiscan. Clin Endocrinol 1978; 8: 483-486. lngbar SH: The thyroid gland. In: Wilson JD, Foster DW, eds. Williams’ textbook of endocrinology. Philadelphia: WB Saunders, 1985; 682-815. Hegediis L, Hansen JM, Karstrup S: High incidence of normal thyroid gland volume in patients with Graves’ disease. Clin Endocrinol 1983; 19: 603-607. Greenwood RM, Daly JG, Himsworth RL: Hyperthyroidism and the impalpable thyroid gland. Clin Endocrinol 1985; 22: 583-587. Perrild H, Hansen JM, Arnung K, Olsen PZ, Danielsen U: Intellectual impairment after hyperthyroidism. Acta Endocrinol 1986; 112: 185-191. Submitted
January
29, 1987, and accepted
ORTHOSTATIC HYPOTENSION AND ATENOLOL
February
11, 1987
DUE TO QUINIDINE
To the Editor: Loon et al (Am J Med 1986; 81: 1101-1104) recently reported the first case of orthostatic hypotension due to combined treatment with quinidine and propranolol, whereas either agent alone did not cause any clinically significant problem. We have also observed a similar case and wish to bring attention to this potential side effect that may arise when quinidine is combined with any of the beta-blocking agents (atenolol in our case). A 56-year-old woman was followed in our clinic for angina pectoris, which was treated with isosorbide dinitrate 40 mg four times a day, diltiazem 90 mg four times a day, and atenolol 50 mg twice a day. In late October 1986, she was found to have atrial fibrillation. Treatment with digoxin and warfarin was begun, and five weeks later she was admitted to New England Medical Center for elective cardioversion. Treatment with quinidine sulfate 300 mg four
M.D. M.D.
Herlev Hospital Herlev, Denmark
May
1987
The American
Journal
of Medicine
Volume
82
1083
LETTERS
TO THE EDITOR
SWEET’S SYNDROME SOLID TUMORS
times a day was initiated, and sinus rhythm was restored 36 hours later, thus obviating the need for direct current cardioversion. During this two-day hospitalization, atenolol was withheld because of excessive bradycardia. Upon discharge, the patient misunderstood instructions and did not resume atenolol therapy at a lower dose. She was subsequently seen in the clinic one month later still in sinus rhythm and receiving isosorbide dinitrate, diltiazem, and quinidine at the same aforementioned doses. Treatment with atenolol was then resumed at 50 mg once a day. Three days later, the patient reported symptoms of orthostatic hypotension with dizziness, lightheadedness, and faintness upon standing, which occurred after the second dose of atenolol and disappeared when she assumed a supine position. With the third dose of atenolol, she almost fell on standing up, and her daughter, who is a nurse, documented a pulse rate of 44 beats/minute and a palpable blood pressure of 120 mm Hg while she was supine and 90 mm Hg while she was sitting in a chair. She subsequently stopped taking atenolol, and symptoms resolved over the next two days. Our patient clearly had tolerated either agent alone very well, and it was only when they were combined that symptoms developed. The other two vasodilatory drugs (nitrate and diltiazem) the patient was receiving cannot be implicated, as they had been tolerated well all along; in combination with either atenolol or quinidine, they had not caused any symptoms and their dosage had not been changed. As suggested by Loon et al, beta-blockade alone inhibits reflex tachycardia on standing but does not usually cause orthostatic hypotension, as peripheral vasoconstriction is maintained. When quinidine is added, vasodilation precipitates symptomatic postural hypotension. The reverse sequence as demonstrated in our patient had similar results: peripheral vasodilation caused by quinidine-induced alpha-adrenergic blockade did not pose a clinical problem; symptomatic orthostatic hypotension ensued when reflex tachycardia was inhibited by atenolol. Indeed, orthostatic hypotension is more commonly seen with combined alpha- and betablockade caused directly or indirectly by single sympatholytic agents, e.g., guanethidine, reserpine, methyldopa, labetalol [ 11. (We recently observed profound postural symptoms caused by amiodarone, which also possesses both alpha- and beta-blocking properties) [2]. A similar effect is to be expected when this blockade is caused by combination therapy as demonstrated by these two cases. ANTONIS S. MANOLIS, N. A. MARK ESTES,
2.
M.D.
Weiner N: Drugs that inhibit adrenergic nerves and block adrenergic receptors. In: Goodman-Gilman A, Goodman LS, Gilman A, eds. The pharmacological basis of therapeutics. New York: Macmillan, 1980; 176-210. Polster P, Broekhuysen J: The adrenergic antagonism of amiodarone. Biochem Pharmacol 1976; 25: 131-134. Submitted
1084
May
February
1987
5, 1987, and accepted
The
February
American Journal of Medicine
11, 1987
Volume
WITH
To the Editor: Sweet’s syndrome is a rare dermatologic condition characterized by fever, neutrophilic dermatosis, granulocytosis, and raised, painful plaques on the limbs, face, and neck [ 11. Systemic manifestations, including arthralgias, arthritis, conjunctivitis, episcleritis, and renal involvement, have been described [2,3]. The syndrome occurs in an isolated form in association with myeloproliferatlve disorders, leukemia [3,4], and, rarely, in patients with solid tumors 15-61. We report Sweet’s syndrome in a patient with vaginal carcinoma. A 3%year-old white woman received radiation therapy for stage II-A squamous cell carcinoma of the vagina. One year later, systemic methotrexate chemotherapy was begun for painful bone metastases, which improved. Seven months afterward, she had fever, and small, painful papules, which blanched with pressure, and vesicles developed on the forearms. Skin biopsy showed mononuclear cells surrounding small vessels of the superficial and deep dermis. The leukocyte count was 4.4 X log/liter with 71 percent polymorphonuclear cells and 18 percent lymphocytes. Topical steroid creams resulted in no benefit, and several more papules developed. All lesions spontaneously cleared within 21 days, and fever disappeared. Two weeks later, the painful papules and a few pustules reappeared on the forearms and on the skin overlying the right scapula (Figure 1). The patient complained of night sweats and fever. She was treated with oral tetracycline, but had no response. Skin biopsy performed a second time showed intense neutrophilic infiltration of the skin, consistent with Sweet’s syndrome (Figure 2). Both the fever and the papules spontaneously resolved within four weeks, but recurred a few weeks later. Prednisone (10 mg orally for 14 days) was associated with prompt resolution of rash and fever. Despite continuation of methotrexate for persistent metastatic cancer for the past 20 months, Sweet’s syndrome has not recurred in this patient. Sweet’s syndrome has been described in association with metastatic cancer. In a case reported by Shapiro et al [7], Sweet’s syndrome antedated a diagnosis of testicular carcinoma by six weeks. The skin lesions were controlled with orally administered prednisone, and the testicular tumor was treated with surgery and chemotherapy. Green et al [5] reported Sweet’s syndrome concurrent with the diagnosis of metastatic adenocarcinoma in bone and soft tissue in a young man. The skin lesions resolved spontaneously over a two- to three-week period. In other cases of Sweet’s syndrome, skin lesions followed the diagnosis of neoplasm. Nguyen et al [6] described a woman with clear cell carcinoma of the ovary. Sweet’s syndrome appeared one week after chemotherapy was discontinued and resolved with prednisone therapy. Rash recurred when prednisone was discontinued. Schwartz et al [8] described a man with diffuse histocytic lymphoma. Two years following chemotherapy and radiation, Sweet’s syndrome developed and resolved spontaneously. No evidence of recurrent lymphoma was found.
Ill, M.D. Cardiac Electrophysiology Tufts/New England Medical Center 750 Washington Street Boston, Massachusetts 02111 1.
IN ASSOCIATION
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