Henry Ford Hospital Medical Journal

Volume 19 | Number 1 Article 4

3-1971 The linicC al Course of Duodenal Ulcer Associated with Melvin A. Block

Boy Frame

Thomas A. Fox Jr.

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Recommended Citation Block, Melvin A.; Frame, Boy; and Fox, Thomas A. Jr. (1971) "The lC inical Course of Duodenal Ulcer Associated with Hyperparathyroidism," Henry Ford Hospital Medical Journal : Vol. 19 : No. 1 , 21-26. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol19/iss1/4

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp. Med. Journal Vol. 19, No. 1, 1971

The Clinical Course of Duodenal Ulcer Associated with Hyperparathyroidism

Melvin A. Block, M.D.*; Boy Frame, M.D.**; and Thomas A. Fox, Jr., M.D.***

In 98 patients with primary hyperparathyroidism, 15 had objective evidence of duodenal ulcer disease. Following operative correction of the hyperparathyroidism, improvement of duodenal ulcer disease occurred usually, but not uniformly, if un­ associated with non-beta islet cell tumors. Correction of hyperparathyroidism in patients with the Zollinger-Ellison syndrome does not significantly influence the peptic ulcer which should be given primary aggressive surgical treatment.

Although the association is not fre­ symptoms which may be compatible quent, there appears to be an increased with duodenal ulcer disease and which incidence of duodenal ulcer disease in may disappear after surgical correction patients having primary hyperparathy­ of the hyperparathyroidism. However, roidism. A natural question is the in­ unless the presence of a duodenal ulcer fluence of correction of the hyperpara­ was confirmed by x-ray such patients thyroidism and its associated hyper­ were omitted from this study. Also calcemia on the course of demonstrated omitted was one patient with labora­ duodenal ulcer disease. It led to this tory evidence of hyperparathyroidism review of our experience. at the time of operative treatment for Clinical Experience duodenal ulcer because surgical explor­ ation of the parathyroids, to confirm Through 1969, of 98 patients for the diagnosis of hyperparathyroidism, whom the diagnosis of primary hyper­ was not performed. parathyroidism had been confirmed, 15 The clinical course of the 15 patients also had evidence of duodenal ulcer with the association of duodenal ulcer disease demonstrated by radiologic disease and primary hyperparathyroid­ study, operation, or autopsy. Patients ism is outlined in Table I. Of the total with primary hyperparathyroidism fre­ group, 8 were females and 7 males, 3 quently complain of digestive tract of the females having, in addition, non- beta islet cell tumors of the pancreas. *Division V, Department of General Sur­ As is evident from Table I, the clini­ gery. cal course necessitated separation of **Division V, Department of Medicine. patients with duodenal ulcer disease ***Division III, Department of General Sur­ gery. and hyperparathyroidism into two ma-

21 Table I

CLINICAL COURSE IN 15 PATIENTS OF DUODENAL ULCER DISEASE ASSOCIATED WITH PRIMARY HYPERPARATHYROIDISM

STATUS OF ACTIVITY OF DUODENAL ULCER NO. PTS. AGE OF PTS. COURSE AFTER SURGICAL CORRECTION OF HYPERPARATHYROIDISM Recurrence Duration Died of Ulcer Recurrence Required Follow-up Ulcer Prior Improved Operation in Years to Operation a on f'arathy. o Range Ave. Range Ave.

Not associated with islet cell tumors 3 of pancreas Ulcer active at time of operative correction of hyperparathyroidism 38-68 44 1-11 6 -n o Ulcer inactive at time of operative X correction of hyperparathyroidism 49-69 60 1-5 3 Ulcer operation required prior to recognition of hyperparathyroidism 69

II. Associated with non-beta islet cell tumor of pancreas (ulcer active) 39-53 46 Duodenal Ulcer Associated with Hyperparathyroidism jor groups on the basis of the presence tumor and for the subsequent or absence of islet cell tumors produc­ nine years. ing manifestations of the Zollinger- A single parathyroid tumor was Ellison syndrome. Although the total found in all of the patients with duo­ number of patients involved does not denal ulcer disease unassociated with permit a valid statistical analysis, the islet cell tumors. Abnormalities in virulence of the duodenal ulcer disease multiple parathyroid glands were pres­ associated with non-beta islet ceU ent in the three patients with the Zol- tumors is obvious in this experience, linger-EUison syndrome. and conforms with recognized char­ acteristics of the ZoUinger-EUison syn­ Discussion drome. Even though in one such pa­ This study conforms with previous tient the associated hyperparathyroid­ reports indicating a small increase in ism was corrected first, severe duodenal the incidence of duodenal ulcer disease ulcer disease continued untU total gas­ in patients with primary hyperparathy­ trectomy was accomplished. Two other roidism, However, our experience patients succumbed from complications emphasizes the clinical necessity of related to perforation of peptic ulcers separating patients having concomitant before surgical consideration could be duodenal ulcer disease and primary given to associated hyperparathyroid­ hyperparathyroidism into two groups ism. on the basis of the presence or absence Duodenal ulcer disease unassociated of non-beta islet cell tumors. with the Zollinger-Ellison syndrome For patients not demonstrating fea­ was less severe and usually improved tures of the ZoUinger-EUison syn­ symptomatically following surgical cor­ drome, our experience, although not rection of associated primary hyper­ statistically firm, corroborates that of parathyroidism. However, one of eight others in indicating that correction of patients in whom the ulcer appeared to primary hyperparathyroidism usually be active at the time of the parathyroid results in the amelioration of duodenal operation required surgical correction ulcer disease.* "-" However, the over- four years later for a recurrent sympto­ aU experience suggests that duodenal matic, bleeding duodenal ulcer. There ulcer disease in patients with primary was no evidence of recurrent hyper­ hyperparathyroidism unassociated with islet cell tumors is not particularly ag­ parathyroidism in this patient. Al­ gressive and probably runs a course not though active ulcer disease had been gready dissimUar from that unassoci­ present previously in three patients, the ated with hyperparathyroidism. ulcer was clinically quiescent at the Correction of hyperparathyroidism time of removal of a parathyroid does not guarantee freedom from seri­ tumor. One other patient had under­ ous difficulty from a duodenal ulcer. gone operative correction of a duo­ This was shown by one patient who denal ulcer and had no further diffi­ later required operation for further culty with peptic ulcer disease for the complications from his ulcer. Further­ 13 years prior to removal of a para­ more, in three patients a previously ac-

23 Block, Frame and Fox tive duodenal lUcer was mactive at the hormone since administration of this time of the parathyroid operation. agent has no predictable influence on Variations occur in the severity of duo­ gastric secretion.^- Hypercalcemia in denal ulcer disease in patients with man produces elevated blood levels of hyperparathyroidism. Not all patients , particularly in patients with having primary hyperparathyroidism duodenal ulcers, and this then is the demonstrate excessive gastric secre­ likely cause of -induced in­ tion, The hypercalcemia and other creased gastric acid secretion. It ap­ effects of primary hyperparathyroid­ pears that the influence of hypercal­ ism, although aggravating factors, are cemia on the secretion of gastric acid probably not major determinants in is mediated in some manner through the etiology of duodenal ulcer disease the vagus nerve.^" -^ There does appear in these patients. to be a direct relationship between the Correction of hypercalcemia does level of serum calcium and gastric se­ not appear to significantly alter the cretion.These effects of hypercalce­ course of duodenal ulcer disease in pa­ mia, however, are based on acute or tients with non-beta islet cell tumors of short-term studies, so that long term the pancreas.^^"^*^ Although hypercalce­ results in patients with hypercalcemia mia conceivably exaggerates duodenal are not conclusive.Nevertheless, ulcer disease in these patients, other basal gastric secretory studies show a factors are more important in produc­ reduction following operative cor­ ing the extreme virulence of the ulcer rection of primary hyperparathyroid- in the Zollinger-Ellison syndrome. Hy­ ism.i--a« perparathyroidism should be given Duodenal ulcer disease, unassociated secondary consideration in such pa­ with other than hy­ tients since aggressive surgical control perparathyroidism, usually does not ap­ by total gastrectomy as early as possi­ pear particularly serious. But, if se­ ble is indicated. Aggravation of duo­ vere, it does require therapy on the denal ulcer disease by other endocrine basis of usual indications. The behav­ lesions was not evident in this study. ior of ulcer disease associated with hy­ Experimental studies support the perparathyroidism may follow one of view that hypercalcemia influences gas­ three general patterns: tric secretion, although it is probably 1. Heals spontaneously, or after not a critical factor. Species differences gastric operation, with persistent make animal studies of questionable hyperparathyroidism. significance for man." Evidence indi­ cates that in man hypercalcemia results 2. Persists with temporary remis­ in an increased basal secretion of hy­ sions but heals after correction of hyperparathyroidism. drochloric acid as well as an increase in the volume of gastric juice, a de­ 3. Persists or recurs after operative crease in pepsin secretion, and an in­ correction of hyperparathyroid­ crease in mucous secretion."'!""^* ism; in such patients the co­ These changes do not appear to be the existence of the Zollinger-Ellison result of direct effects of parathyroid syndrome should be considered.

24 Duodenal Ulcer Associated with Hyperparathyroidism

Summary and Conclusions disease in the absence of the ZoUinger- 1. Of 98 patients with primary hy­ EUison syndrome usually improves fol­ perparathyroidism, the clinical course lowing operative correction of associ­ of an associated duodenal ulcer pres­ ated primary hyperparathyroidism, this ent in 15 depended primarUy on the is not uniformly true. Hypercalcemia presence or absence of co-existent non- appears to be only one factor, and not beta islet ceU tumors of the pancreas. always a dominant etiologic factor in 2. Although hypercalcemia may the duodenal ulcer disease which varies exaggerate the virulence of duodenal in severity in these patients. ulcer disease in patients with the Zol- 4. In patients with active duodenal linger-EUison syndrome, correction of ulcer disease associated with primary hypercalcemia does not significantly hyperparathyroidism in the absence improve the duodenal ulcer. Operative of the Zollinger-Ellison syndrome, the treatment, consisting of a total gastrec­ ulcer should be treated on the basis of tomy in nearly all instances, should be its own merits with consideration given urgently provided for such patients to correction first of the hyperparathy­ prior to operative consideration for the roidism if usual surgical indications for hyperparathyroidism. the ulcer do not exist. 3. Although active duodenal ulcer

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