Gastroesophageal Reflu and Ascorbic Acid Insufficiency

Transcription

1 Gastroesophageal Reflu and Ascorbic Acid Insufficiency Clement A. Hiebert, M.D. ABSTRACT The incidental discovery of scurvy in a patient with a symptomatic hiatal hernia has led to the identification of 9 other individuals with chemically proved vitamin C deficiency secondary to an expressed aversion to acid food in any form. These patients were screened with capillary fragility tests and serum ascorbic acid determinations from approximately 200 hiatal hernia and reflux patients. With resumption of a normal vitamin C intake, scattered deficiency symptoms disappeared and both capillary fragility tests and serum ascorbic acid levels returned toward normal. There were no wound healing problems. The chance recognition in 1967 of a scorbutic rash in a patient with a symptomatic hiatal hernia has led to the identification of 9 other instances of ascorbic acid deficiency resulting from aversion to acid food in any form. Case Report Patient 1, a 47-year-old phlegmatic retired Army major had complained of heartburn, regurgitation, and dysphagia for fifteen years. His medical record showed that several efforts had been made to dilate a lower esophageal ring, but swallowing continued to be distressed, and he complained of burning, tightening, and sticking in the subxiphoid area. He appeared mentally depressed. (Years later he indicated he had been considering suicide for no remembered reason.) Incidental to physical examination, the skin over the upper portion of the right calf was noted to be erythematous (Fig 1). He commented that the change in skin color was a predictable sequel From the Department of Surgery, Maine Medical Center, Portland, ME. I wish to thank Professor Herman Baker of the New Jersey College of Medicine for the tissue ascorbic acid determinations and Marilyn van Saun for helpful technical assistance. Presented at the Thirteenth Annual Meeting of The Society of Thoracic Surgeons, Jan 24-26, 1977, San Francisco, CA. Address reprint requests to Dr. Hiebert, 321 Brackett St, Portland, ME to being seated with his legs crossed for a spell while waiting for his doctor to appear. The rash did not blanch on pressure and was seen to consist of myriad punctate hemorrhages, each one surrounding a hair follicle. Initial reluctance to accept the possibility of this being scurvy was erased when the patient conceded that his diet for much of the last decade had been soft peanut butter, mashed potatoes, and bland baby food. Acid food such as fruit and fruit juices were an anathema. He took no vitamins. The patient s history was pursued with a new bias. He admitted that his skin itched and bruised after minimal trauma. As a security officer in Korea, he had once been bitten on the left wrist, and his entire forearm had turned purple. Within the previous year a superficial scalp laceration had taken six weeks to heal. His gums bled whenever he brushed his teeth. Inspection of the mouth confirmed the presence of hemorrhagic and inflamed gingival margins, from which blood trickled when touched with a tongue depressor (Fig 2). The capillary fragility test was strongly positive. A low plasma ascorbic acid level of 0.63 mg per 100 ml was recorded (normal, > 0.7 mgllo0 ml). (We were then ignorant of the possibility of verifying suspected vitamin C deficiency with cellular ascorbate measurements.) An upper GI series showed a small, sliding hiatal hernia with a 5 mm Schatzki ring. When viewed endoscopically, the lower 10 cm of gullet was reddened and bled on touch but was not primarily ulcerated. A biopsy was not taken. No narrowing could be visualized, and the scope passed into the stomach without discernible resistance. An esophageal perfusion study (Bernstein test) was positive, and a swallow of viscous xylocaine ameliorated the patient s substernal burning. The hemoglobin was 15.3 gm. The patient was treated with ascorbic acid, 100 mg daily. Within two weeks his capillary fragility test produced only 12 petechiae in a

2 109 Hiebert: Gastroesophageal Reflux and Ascorbic Acid Insufficiency hernia, have been taken. Only one further dilation has been required, that being done more or less prophylactically on the ninth anniversary of his first office visit. His capillary fragility test (6 petechiae) has remained normal though his serum ascorbic acid level is still borderline (0.5 to 0.7 mglloo ml). Fig 1. Spontaneous capillary fragility test. Perifollicular hemorrhagic rash on calf after sitting with legs crossed for30 minutes (Patient 1). Method of Subsequent Study Since 1969, all patients with symptoms of gastroesophageal reflux, peptic stricture, esophageal spasm, or disordered motor activity have been questioned for dietary eccentricities and scrutinized for clinical stigmata of ascorbic acid deficiency. Individuals with suspicious history or findings are then screened with a capillary fragility test. The upper arm sphygmomanometer cuff is inflated midway between systolic and diastolic pressures for five minutes, cm circle as opposed to too many to count before treatment. Gums ceased to bleed and limbs to bruise. After two months of treatment he was consuming a varied diet, including acid food. He said that he now felt normally fit and declined the offer of an operation to restore competency to his gastroesophageal junction. In 1970 he underwent abdominoperineal resection for rectal cancer and made an uneventful recovery. During the ensuing years routine roentgenograms, displaying the original ring and hiatal Fig2. Hemorrhages ingingival margin of left lower incisor and bicuspid teeth (Patient 1). Fig3. Strongly positive capillary fragility test, with more than 100 petechiae in a 2.5 cm circle (normal, < 12).

3 110 The Annals of Thoracic Surgery Vol 24 No 2 August 1977 Principal Findings in 10 Patients Capillary Fragilitya Serum Ascorbic Acida m c Ascorbic Patient Deficiency Pretreat- Posttreat- Pretreat- Posttreat- Acid Level No. Diagnosis Symptoms ment ment ment ment before Treatments 1 Hiatal hernia, Bruising, Florid ring bleeding, 2300 scaly skin, slow wound healing, depression 2 Reflux without Easy bruising, hiatal hernia mental changes, fatigue 3 Reflux after hernia repair Hiatal hernia, mg 5 Hiatal hernia, Easy bruising Hiatal hernia Neuropathy "g 7 Hiatal hernia, Easy bruising, 120 I, CA esophagus purpura 8 Hiatal hernia, Depression, esophagospasm, joint swelling 9 Reflux only Easy bruising > Hiatal hernia, Easy bruising, ring mental changes "Normal values: capillary fragility, 42; serum ascorbic acid, >0.7 mg/loo ml; WBC level before treatment, mg/loo gm bpatient died; posttreatment findings unavailable. after which the number of petechiae in a 2.5 cm circle of antecubital skin is counted. The presence of 12 or more petechiae is considered a positive result (Fig 3). Such individuals subsequently have had blood samples assayed for ascorbic acid [41. In several instances, tissue stores have been determined by the method of Baker and Frank [ll. Patients deficient in vitamin C are given ascorbic acid, generally 50 to 100 mg daily. When patients are capable of accepting a normal diet, vitamin supplements are discouraged. Treatment for esophageal problems is based on usual criteria. Results Twenty-two of approximately 200 patients with hiatal hernia or gastroesophageal reflux had a dietary history suggesting vitamin C deprivation. They were screened with capillary fragility tests. Of the 17 who had a positive result, 9 had serum ascorbic acid levels between 0.2 and 0.7 mg per 100 ml (normal, > 0.7 mglloo ml). A tenth patient (Patient 6 in the Table) with a florid capillary fragility test and an apparently normal serum ascorbic acid level of 1.2 mg per 100 ml, was included in the study when her cellular as- corbic acid was found to be zero. (One other patient with a serum level of 0.1 mg per 100 ml is not included because of incomplete data.) In 5 instances when tissue stores were mea- 4 s + ) \ z 75- h Q 60- B 0: n " Tourniquet Tests in G E Reflux Pre Post 8 Fig 4. Capillary fragility test results before and after ascorbic acid treatment.

4 111 Hiebert: Gastroesophageal Reflux and Ascorbic Acid Insufficiency Pre 5( Post px Fig5. Ascorbicacid levels before and after treatment. Normal > 0.7 rngilo0 ml. The contradictory line is almost certainly spurious. Initial cellular ascorbate in this patient (No. 6) was zero. sured, levels ranged from 0 to 14 mg per 100 gm of white cells (normal, mg/100 gm). All but 1 patient had severe gastroesophageal reflux, which was complicated in 3 by, in 1 by esophagospasm, and in another by esophageal cancer. While only Patient 1 was classically scorbutic, several others exhibited isolated symptoms of easy bruising, mental changes, and peripheral neuropathy. Ascorbic acid and dietary treatment reversed capillary fragility tests and ascorbic acid levels (Figs 4, 5) and resulted in improvement, if not outright elimination of symptoms ascribed to the deficiency. A prominent exception was Patient 8, who had uncorrected diffuse spasm of the esophagus, for which reason she continues to limit her ingestion of food containing vitamin C. A total of 9 patients underwent operation. There were no wound healing problems. Comment While only the initial patient had clinical scurvy, the remainder of the group exhibited an occa- sional clue; the most frequent was evidence of fragile capillaries. Consistent reversal of this sign following ascorbic acid ingestion was striking and suggests that the tourniquet test may be a more valuable screening examination than had been supposed [21. Similarly, normalization of the serum ascorbic acid level after treatment seems to support the validity of the diagnosis. Serum levels, however, do not necessarily reflect total body reserves [l, 21, being analogous in this respect to serum potassium values as opposed to intracellular stores. Measurement of tissue ascorbate is now possible and remains the definitive laboratory test. It requires 100 to 200 mg of packed washed leukocytes, the routine securing of which, however, has posed some technical problems. An interesting speculation is whether the dramatic improvement in reflux symptoms experienced by Patient 1 was the result of a salubrious effect on the esophageal mucosa, nerve supply, or lower sphincter, or merely a reflection of his overall enhanced sense of well-being. Esophageal biopsies before and after treatment in Patient 8 were examined by light microscopy and showed no alteration of the grade I nonulcerated. The study of human scurvy can be frustratingly slow in an affluent society that ranks freedom from avitaminosis-c high on the list of national goals. Indeed, health bureaucrats, orange growers, food processors, and concerned spouses have made it all but impossible to avoid ingestion of the "recommended daily allowance" before breakfast is half over. To their determined ranks must be added the megadose vitamin takers, whose credo, "If a little is good, more will be better," has made ascorbic acid gorging a national pastime. We urge that all studies on an individual suspected of vitamin C depletion be done immediately upon admission. Several excellent candidates, abetted by nurses, aides, and spouses, ate or drank their way out of the study before testing was complete! Finally, what, if any, is the surgical significance of these observations? In experimental human scurvy, between one and four months of a diet totally deficient in vitamin C are required

5 112 The Annals of Thoracic Surgery Vol 24 No 2 August 1977 before abnormal signs develop [l-31. Failure of wound healing takes approximately 90 days of deprivation [2]. Physicians have known all along that starved patients generally do well over the short haul without vitamin supplements, but the discovery of partially depleted stores in this selected group of individuals, who have restricted their diets before seeing the doctor, suggests that a nutritional history on occasion can be unexpectedly illuminating. References 1. Baker H, Frank 0: Clinical Vitaminology Methods and Interpretation. New York, Interscience, 1968, p Crandon JH, Lund CC, Dill DB: Experimental human scurvy. N Engl J Med 223:353, Hodges RE, Hood J, Canham JE, et al: Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr 24:432, Roe JH, Kuether CA: Determination of ascorbic acid in whole blood and urine. J Biol Chem 147:399, 1943