Correspondence.

(Letters to the Editor are welcomed. They may report new clinical or laboratory observations and new developments in medical care or may contain comments on recent contents of the Journal. They will be published, if found suitable, as space permits. Like other material submitted for publication, letters must be typewritten, double-spaced, and submitted in duplicate. They must not exceed two typewritten pages in length. No more than five references and one figure or table may be used. See "Information for Authors" for format of references, tables, and figures. Editing, possible abridgment, and acceptance remain the prerogative of the Editors.)

The H-index: A Measure of Ideal Weight From Height Alone

To the Editor. Body mass index (BMI) is widely accepted as the most useful measure of weight adjusted for height in health surveys. Values in the range of 18.5 to 24.9 are suggested as the ideal BMI for both men and women. (1) Many people cannot readily calculate their own BMI or understand the BMI charts, however. (2)

In the Middle East, a method of calculating a target weight range from height alone is provided from the simple rule of thumb that the lower end of the target range for men and the upper end of the target range for women can be calculated as follows: Target Weight = Height - 100, where weight is measured in kilograms and height is measured in centimeters; a 5 kg range in the target weight can then be calculated (eg, for subjects 165 cm tall, this range would be 65 to 70 kg for men and 60 to 65 kg for women). We have compared this approach with BMI values and found that for tall men the target range includes values above BMI 25, while for short women, the target range includes values below 18.5. We calculated the target weight without the 5 kg adjustment, however, using the range of height from the fifth to the 95th percentile of men and women in the United Kingdom, as reported by Gregory et al. (3) This value, which we call the El-index, is equivalent to a BMI of 23.7 to 24.9 for men in the height range 163.0 to 185.8 cm, and a BMI of 22.5 to 24.3 cm for women in the height range 151.8 to 172.1 cm (Figure). Although the BMI value equivalent to the H-index increases with height, all values lie within the upper half of the normal range of BMI proposed by the World Health Organization. We therefore suggest that the H-index could be a useful guide to target weight for many nonprofessionals unable to easily estimate their ideal BMI.

Emad G. Kamel, MSc

Geraldine McNeill, PhD

Department of Medicine and Therapeutics

Foresterhill

University of Aberdeen AB25 2ZD

Aberdeen, Scotland, United Kingdom

[Graph omitted]

References

(1.) The World Health Organization: Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation on Obesity, Geneva, June 3-5, 1997. Geneva, Switzerland, World Health Organization, 1998

(2.) Health Education Authority: Obesity and Overweight. London, United Kingdom, Health Education Authority, 1991

(3.) Gregory J, Foster K, Tyler H, et al: The Dietary and Nutritional Survey of British Adults. London, United Kingdom, Her Majesty's Stationery Office, 1990

Pituitary Apoplexy After Administration of Heparin and Isosorbide Dinitrate

To the Editor. A 68-year-old man with a history of hypertension treated with atenolol (25 mg/day) and diabetes mellitus treated with metformin (850 mg twice daily) was admitted with an acute inferior-wall myocardial infarction. Results of physical examination were unremarkable. Routine laboratory test results were unremarkable, except for elevation of the cardiac enzyme levels: aspartate aminotransaminase, 112 U/L; alanine aminotransaminase, 32 U/L; and creatine kinase (CK), 780 U/L, 10% of which was CK-MB isoenzyme.

Treatment was begun with propranolol (10 mg, 3 times daily), captopril (25 mg, 3 times daily), intravenous isosorbide dinitrate (3 mg/hr), intravenous heparin (25,000 U/24 hours), and aspirin (100 mg/day). After 2 days of treatment, the patient suddenly complained of a severe headache and started to vomit. Blood pressure was 200/110 mm Hg. Findings from computed tomography (CT) of the brain were reported as normal. Both isosorbide dinitrate and heparin infusions were stopped; the headache continued, and 24 hours later ptosis of the right eyelid developed. On examination, there was dilatation of the right pupil, right oculomotor-nerve palsy, and bitemporal superior-quadrant defects, but no meningeal signs. Repeated CT and subsequent magnetic resonance imaging (MRI) of the brain revealed a pituitary macroadenoma (2.2 x 1.8 cm) with hemorrhage. Serum cortisol level was 173 nmol/L (normal, 193 to 690 nmol/L); subsequent synacthen test showed a baseline cortisol level of 49 nmol/L, which increased to 67 nmol/L aft er 30 minutes and 558.2 nmol/L after 60 minutes. Testosterone level was 0.4 nmol/L (normal, 9.4 to 37.0 nmol/L), luteinizing hormone level was 1.0 IU/L (normal, 0.5 to 10.0 IU/L), follicle stimulating hormone level was 5.4 IU/L (normal, 1 to 7 IU/L), prolactin level was <30 mU/L (normal, 35 to 380 mU/L) and dehydroepiandrosterone sulfate (DHEAS) level was <0.81 [micro]mol/L (normal, 2.2 to 15.2 [micro]mol/L). A neurosurgeon recommended continuing with conservative therapy at this stage and the patient was treated with intravenous hydrocortisone (100 mg 3 times daily). The hydrocortisone was tapered to 5 mg/day, and the patient subsequently made a complete recovery, except for a slight residual ptosis. Significant tumor shrinkage (from 2.2 to 1.1 cm) was shown on repeated MRI. Treatment with testosterone and levothyroxine was initiated, and the patient remained well at last follow-up.

The development of pituitary apoplexy after the intravenous administration of isosorbide dinitrate and heparin is a rarely described event. We believe that our patient had a previously undiagnosed macroadenoma of the pituitary that, because the initial CT scan of the brain was not specifically directed toward the pituitary fossa, was not visualized. In addition, initial laboratory tests showed evidence of pituitary dysfunction, with low levels of cortisol, testosterone, and DHEAS. The low prolactin level suggested that there may have been destruction of the lactotrophs.

Pituitary apoplexy is a clinical syndrome in which a pituitary adenoma undergoes sudden enlargement as a result of hemorrhage, infarction, or both. It may occur in 10% to 15% of adenomas,' though the majority of cases of pituitary apoplexy occur in patients with adenomas that were previously undiagnosed; (1) thus, an apopleptic episode is often the presenting feature of a pituitary tumor.

Pituitary tumors are particularly prone to hemorrhage and necrosis. In some series, rates of hemorrhagic degeneration of 9.5% to 15.8% have been reported. (1) It is unclear why pituitary tumors have this tendency to hemorrhage. Some have suggested that a rapidly growing adenoma outstrips its blood supply, and the resulting ischemic necrosis progresses to hemorrhage. (1) Another theory is that there is direct compression of the infundibulum by an expanding tumor mass that renders the whole lobe ischemic and produces a secondary hemorrhage. Other suggested mechanisms include the inherent fragility of tumor blood vessels and atherosclerotic embolization. Pituitary apoplexy has been described in association with a wide variety of medications, procedures, and pathologic states, though the reason for many of these associations is unclear. Coughing and sneezing, which may produce a transient increase in intracranial pressure, have been linked to pituitary apoplexy, as has minor head trauma. (1) Other conditions that have been linked to pitutiary apoplexy include an elevated estrogen concentration (eg, pregnancy, exogenous administration), certain diagnostic procedures (eg, angiography, pneumoencephalography, CT scans), as well as dynamic testing of the pituitary using gonadotropin-releasing hormone (GnRH). (1) Although therapeutic modalities for treating pituitary adenomas, such as bromocriptine administration and pituitary irradiation, have been associated with pituitary hemorrhage, and a case has been reported in an intravenous-drug abuser after lumbar laminectomy and hemodialysis, the majority of cases of pituitary apoplexy are without an identifiable trigger. (1)

There is, however, a connection between anticoagulation and pituitary apoplexy. In 1965, hemorrhage into a pituitary adenoma during anticoagulant therapy was reported. (2) More recently, there have been reports of apoplexy after spontaneous hemorrhage associated with thrombolytic therapy (3) or heparin therapy4 some of these patients received additional antithrombotic therapy, such as ticlopidine hydrochloride and antibody to platelet receptor IIb-IIIa. There are also reports of patients having pituitary apoplexy after intraoperative anticoagulation during coronary bypass surgery. (1) One case of pituitary apoplexy due to the administration of isosorbide mononitrate, which our patient also received, has been reported. (5)

The mechanism for a connection between anticoagulation and apoplexy is unclear. These tumors have a propensity for spontaneous necrosis, and any concomitant hemodynamic compromise related to a myocardial event may exacerbate this tendency. Concomitant anticoagulation may then exacerbate any minor hemorrhage. Use of anticoagulant, antithrombotic, and fibrinolytic therapy in the treatment of coronary artery disease has been steadily increasing in recent years. Since the majority of patients with pituitary macroadenomas are asymptomatic, it may be anticipated that there will be an increase in the incidence of pituitary apoplexy. A high index of suspicion on the part of the attending physician is essential to make a fast and accurate diagnosis of this condition and to obtain an urgent neurosurgical consultation. As our case shows, headache in a patient receiving nitrates and heparin is not necessarily just a minor side effect of the medication.

Svetalna Korotinsky, MD

Pierre Smadja, MD

Sorel Goland, MD

Marina Somin, MD

Malka Attali, MD

Taiba Zhornicky, MD

Stephen D. H. Malnick, MA(Oxon), MSc, MBBS (Lond)

Department of Internal Medicine C

Kaplan Medical Center

Rehovot 76100, Israel

References

(1.) Rolih CA, Ober K.P: Pituitary apoplexy. Endocrinol Metab Clin North Am 1993; 22:291-302

(2.) Nourizadeh AR, Pius FW: Hemorrhage into pituitary adenoma during anticoagulant therapy. JAMA 1965; 193:623-625

(3.) Fuchs 8, Been R, Hasin Y, et al: Pituitary apoplexy as a first manifestation of pituitary adenomas following intensive thrombolytic and antithrombotic therapy. AmJ Cardiol 1998; 81:110-111

(4.) Oo MM, Krishna AY, Bonavita CJ, et al: Heparin therapy for myocardial infarction: an unusual trigger for pituitary apoplexy. Am J Med Sci 1997; 314:351-353

(5.) Bevan JS, Oza AM, Burke CW: Pituitary apoplexy following isosorbide administration. J Neurol Neurosurg Psychiatry 1987; 50:636-637