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Reactive Hypoglycemia Mechanisms and Management

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Reactive Hypoglycemia Mechanisms and Management MEDICAL STAFF CONFERENCE Reactive Hypoglycemia Mechanisms and Management These discussions are selected from the weekly staff conferences in the Depart- ment of Medicine, University of California, San Francisco. Taken from tran- scriptions, they are prepared by Drs. Sydney E. Salmon-and Robert W. Schrier, Assistant Professors of Medicine, under the direction of Dr. Lloyd H. Smith, Jr., Professor of Medicine and Chairman of the Department of Medicine. DR. SLEISENGER: * Grand Rounds today involves cose tolerance test. There was no known family an interesting disorder of carbohydrate homeo- history of diabetes. stasis-hypoglycemia. The patient with this syn- Results of physical examination, including neu- drome will be presented by Dr. Norman Coleman. rological testing, were entirely within normal lim- DR. COLEMAN:t A 26-year-old Caucasian woman its. The blood pressure was 120/70 mm of mer- was admitted to the hospital with a six-year his- cury and the pulse regul at 76 beats per minute. tory of headaches which had increased in fre- Hemoglobin was 12.4 gra'ns per 100 ml and leu- quency over the nine months before admission. kocytes numbered 4,900 per cu mm with normal Although they lasted several days each time, the differential. Results of urinalysis, electrocardio- headaches were never' severe enough to cause her gram, x-ray films of chest and skull, and an elec- to stay home from work. They commenced in the troencephalogram were all within normal limits. neck, progressed to the side of the head and were A 24-hour urine measurement of 17-hydroxy- and not relieved by aspirin. Associated symptoms in- 17-ketosteroid excretion was normal. A morning cluded sleepiness, slurred speech, chills, tremu- plasma cortisol level was 44 micrograms per 100 lousness, occasional diaphoresis and nausea, but ml, while an early afternoon level the same day no vomiting. The symptoms were unrelated to was 17 micrograms per 100 ml. Dexamethasone menses. There was no history of scotomata, loss (2 mg) was administered at 11 p.m. the same day, of consciousness, seizures or other neurological and the plasma cortisol level was 4.5 mg per 100 symptoms during these episodes. There was no ml on the following morning. The elevated plasma clear relationship to meals, although food did help cortisol was considered compatible with the his- the headaches. Past medical history included tory of oral contraceptive therapy, since the pitui- some nervousness which had been treated with tary-adrenal axis showed normal suppression. The chlordiazepoxide hydrochloride (Librium®). The oral glucose tolerance test showed the following patient had been taking norethindrane with me- results: stranol (Orthonovum®) birth control pills for the Time (hours) . 0 3 1 2 3 past year. A 32-year-old sister a 13 4 5 had history of Plasma glucose headaches and hypoglycemia documentgd by glu- (mg per 100 ml)...92 200 210 140 100 52 70 75 *Marvin H. Sleisenger, M.D., Professor of Medicine. tNorman C. Coleman, M.D., Assistant Resident in Medicine. At the third and fourth hour periods of the glu- 64 MAY 1971 * 114 * 5 cose tolerance test the patient complained of perinsulinism. While most readers in the scientific headache similar to that she had experienced in community would accept that Mr. Pezet's weak- the past. Reactive hypoglycemia was diagnosed ness, nervousness and fatigue could have been ex- and the patient was discharged with prescription plained by the reactive hypoglycemia, it was more of a high protein, low carbohydrate diet. On this difficult to accept the second half of the book dietary regime she has been asymptomatic for the wherein the cure of his asthma, hay fever and two months since discharge from the hospital. allergies, as well as the cure of peptic ulcers, rheu- DR. SLEISENGER: This patient with hypoglycemia matic fever and arthritis in other patients, was presents a difficult problem in diagnosis and treat- attributed to stabilization of the blood sugar level. ment. Dr. John Karam will discuss some of these Nevertheless, the book remains quite popular, de- aspects. spite its shortcomings, and a foundation located DR. KARAM:* Patients who have rather nonspe- in New York distributes it nationally to its mem- cific complaints and no abnormalities on physical bers who suffer in common from hypoglycemia. examination are always a difflcult management In the patient presented today the obvious ques- problem. A succession of normal laboratory tests tion is whether the headaches, nervousness and usually confirms the initial impression that or- other nonspecific symptoms had any correlation ganic disease is not present, and the symptoms are with the documented measurement of a plasma then attributed to the tensions of modem living. sugar level of 52 mg per 100 ml recorded three Usually the only form of therapy given is reassur- hours after 100 grams of glucose was administered ance, and since it does not often succeed the pa- orally. Many physicians do not consider a blood tient often consults a number of physicians and glucose level above 40 mg per 100 ml or a plasma tries a succession of tranquilizers without benefit. glucose above 46 mg per 100 ml to be low enough Inevitably the question of hypoglycemia is raised, to cause hypoglycemic symptoms. In one study, frequently by the patients themselves owing to continuous automatic monitoring of blood glucose wide publicity in the lay press. "Health food" demonstrated that nine out of twelve asympto- store shelves are lined with current books para- matic subjects had a blood glucose between 44 phrasing the original classic, Body, Mind, and and 58 mg per 100 ml at some time during an oral Sugar,' which emphasizes an almost mystical role glucose tolerance test.2 However, the glucose re- of low blood sugar in many of the physical ills of sponse of the present patient must be considered our times. This book, written in 1951 and unre- in context with the clinical problem. The general vised since the original publication, has been re- pattern of the oral glucose tolerance test was ab- printed almost every year and remains a best normal, with initial hyperglycemia (200 mg per seller. The authors of this book are a physician, 100 ml in the first half hour) and a relatively rapid E. M. Abrahamson, and one of his patients, A. W. fall in plasma glucose to 52 mg per 100 ml by three Pezet, who had multiple complaints including hours. As continuous monitoring was unavailable, nervousness, weakness, and fatigue which per- we cannot ascertain the exact minimal level to sisted despite attempts at management by numer- which plasma glucose may have fallen in this pa- ous physicians. It was only after Dr. Abrahamson tient. The development of her chief complaint, performed a glucose tolerance test and demon- headache, at the time of the lowest measured strated a reduced blood sugar at three to four plasma sugar level and her own observation that hours that sucoessful therapy was begun. This food often relieved her headaches were additional therapy consisted of frequent, small feedings of a points suggesting an etiological relationship be- low carbohydrate, high protein diet. With the tween symptoms and blood glucose levels. help of his patient, who was a professional jour- The pattern of response to the oral glucose tol- nalist, Dr. Abrahamson wrote a very entertaining erance test is a great help in classifying patients and expressive story of the dramatic results ob- with hypoglycemia.3 The presence of a "reactive" tained in this and other cases. rather than a "fasting" hypoglycemia in this pa- The first half of the book gave an excellent and tient makes it unlikely that the diagnosis is the remarkably accurate scientific description of car- result either of autonomous production of insulin bohydrate homeostasis with emphasis on the role by an insulinoma or of heterogenous factors in- of insulin in its regulation and the hazards of hy- volved in the hypoglycemia related to nonpancre- *John H. Karam, M.D., Assistant Professor of Medicine. atic tumors. CALIFORNIA MEDICINE 65 The Western Journal of Medicine REACTIVE HYPERINSULINISM 250 - ACCELERATED (alimentary) -DELAYED (diabetic) ,/"E ~~~~(a) 150 E 50 E 250 E SUSTAINED (obese nondiabetic) SUSTAINED (pseiudo dia'be-tic) E 150 a _ \ z ~~~~(c) .fftf-\ftf.. ui -Ij LI) SO z -J WITHOUT HYPERINSULINISM 0V . ,XCOUNTER REGULATORY DEFICIENCY IDIOPATHIC I,v LJ ,___ (f) LI) 0 50 4 2%3%4 - co eI I 1 2 3 4 S 1 2 3 4 5 TIME IN HOURS Chart 1.-Patterns of Reactive Hypoglycemia: Reactive hypoglycemia with reactive hyperinsulinism (a,b,c,d). Reactive hypoglycemia with normal insulin response (e,f). The abscissa records time after ingestion of 100 gm of glucose. Classification of Reactive Hypoglycemia TABLE 1.-Classification of Reactive Hypoglycemia With the establishment of a "reactive" type of "Early" Hypoglycemia hypoglycemia by clinical history, as well as by Postgastrectomy plasma glucose measurements, it is then useful to Increased vagal tone determine whether the pattern of response to the "Late" Hypoglycemia oral glucose load is one of "early" or "late" hypo- Diabetic reactive hypoglycemia glycemia. A typical "early" hypoglycemia occurs Nondiabetic 'late" hypoglycemia Obesity within three hours of the ingestion of glucose, Pseudodiabetes whereas 'late" hypoglycemia occurs three to five Counter regulatory deficiency hours after receiving the glucose. The patho- Idiopathic reactive hypoglycemia genetic mechanisms and management of these re- sponses are quite different. "Early" Hypoglycemia. The present patient though serum insulin levels were not measured demonstrated a pattern of glucose response in the in this patient, they almost invariably reach very first hour that is characteristic of the alimentary high levels in the first hour when associated with type (Chart 1,a). There was an exaggerated rise this particular type of plasma glucose response.
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