Henry Ford Hospital Medical Journal

Volume 19 | Number 1 Article 4

3-1971

The Clinical Course of Duodenal Ulcer Associatedwith HyperparathyroidismMelvin A. Block

Boy Frame

Thomas A. Fox Jr.

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

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 un­associated 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 fre­quent, there appears to be an increased incidence of duodenal ulcer disease in patients having primary hyperparathy­roidism. A natural question is the in­fluence of correction of the hyperpara­thyroidism and its associated hyper­calcemia on the course of demonstrated duodenal ulcer disease. It led to this review of our experience.

Clinical Experience

Through 1969, of 98 patients for whom the diagnosis of primary hyper­parathyroidism had been confirmed, 15 also had evidence of duodenal ulcer disease demonstrated by radiologic study, operation, or autopsy. Patients with primary hyperparathyroidism fre­quently complain of digestive tract

*Division V, Department of General Sur­gery.

**Division V, Department of Medicine. ***Division I I I , Department of General Sur­

gery.

symptoms which may be compatible with duodenal ulcer disease and which may disappear after surgical correction of the hyperparathyroidism. However, unless the presence of a duodenal ulcer was confirmed by x-ray such patients were omitted from this study. Also omitted was one patient with labora­tory evidence of hyperparathyroidism at the time of operative treatment for duodenal ulcer because surgical explor­ation of the parathyroids, to confirm the diagnosis of hyperparathyroidism, was not performed.

The clinical course of the 15 patients with the association of duodenal ulcer disease and primary hyperparathyroid­ism is outlined in Table I . Of the total group, 8 were females and 7 males, 3 of the females having, in addition, non-beta islet cell tumors of the pancreas.

As is evident from Table I , the clini­cal course necessitated separation of patients with duodenal ulcer disease and hyperparathyroidism into two ma-

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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

Not associated with islet cell tumors of pancreas

Ulcer active at time of operative correction of hyperparathyroidism

Ulcer inactive at time of operative correction of hyperparathyroidism

Ulcer operation required prior to recognition of hyperparathyroidism

Range Ave.

38-68 44

49-69 60

69

Recurrence Ulcer Recurrence Required

Improved Operation

Duration Died of Follow-up Ulcer Prior in Years to Operation

on f'arathy.

Range Ave.

1-11 6

1-5 3

a o

3

-n o X

I I . 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 or absence of islet cell tumors produc­ing manifestations of the Zollinger-Ellison syndrome. Although the total number of patients involved does not permit a valid statistical analysis, the virulence of the duodenal ulcer disease associated with non-beta islet ceU tumors is obvious in this experience, and conforms with recognized char­acteristics of the ZoUinger-EUison syn­drome. Even though in one such pa­tient the associated hyperparathyroid­ism was corrected first, severe duodenal ulcer disease continued untU total gas­trectomy was accomplished. Two other patients succumbed from complications related to perforation of peptic ulcers before surgical consideration could be given to associated hyperparathyroid­ism.

Duodenal ulcer disease unassociated with the Zollinger-Ellison syndrome was less severe and usually improved symptomatically following surgical cor­rection of associated primary hyper­parathyroidism. However, one of eight patients in whom the ulcer appeared to be active at the time of the parathyroid operation required surgical correction four years later for a recurrent sympto­matic, bleeding duodenal ulcer. There was no evidence of recurrent hyper­parathyroidism in this patient. A l ­though active ulcer disease had been present previously in three patients, the ulcer was clinically quiescent at the time of removal of a parathyroid tumor. One other patient had under­gone operative correction of a duo­denal ulcer and had no further diffi­culty with peptic ulcer disease for the 13 years prior to removal of a para­

thyroid tumor and for the subsequent nine years.

A single parathyroid tumor was found in all of the patients with duo­denal ulcer disease unassociated with islet cell tumors. Abnormalities in multiple parathyroid glands were pres­ent in the three patients with the Zol-linger-EUison syndrome.

Discussion

This study conforms with previous reports indicating a small increase in the incidence of duodenal ulcer disease in patients with primary hyperparathy­roidism, However, our experience emphasizes the clinical necessity of separating patients having concomitant duodenal ulcer disease and primary hyperparathyroidism into two groups on the basis of the presence or absence of non-beta islet cell tumors.

For patients not demonstrating fea­tures of the ZoUinger-EUison syn­drome, our experience, although not statistically firm, corroborates that of others in indicating that correction of primary hyperparathyroidism usually results in the amelioration of duodenal ulcer disease.* "-" However, the over-aU experience suggests that duodenal ulcer disease in patients with primary hyperparathyroidism unassociated with islet cell tumors is not particularly ag­gressive and probably runs a course not gready dissimUar from that unassoci­ated with hyperparathyroidism.

Correction of hyperparathyroidism does not guarantee freedom from seri­ous difficulty from a duodenal ulcer. This was shown by one patient who later required operation for further complications from his ulcer. Further­more, in three patients a previously ac-

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Block, Frame and Fox

tive duodenal lUcer was mactive at the time of the parathyroid operation. Variations occur in the severity of duo­denal ulcer disease in patients with hyperparathyroidism. Not all patients having primary hyperparathyroidism demonstrate excessive gastric secre­tion, The hypercalcemia and other effects of primary hyperparathyroid­ism, although aggravating factors, are probably not major determinants in the etiology of duodenal ulcer disease in these patients.

Correction of hypercalcemia does not appear to significantly alter the course of duodenal ulcer disease in pa­tients with non-beta islet cell tumors of the pancreas.̂ "̂̂ *̂ Although hypercalce­mia conceivably exaggerates duodenal ulcer disease in these patients, other factors are more important in produc­ing the extreme virulence of the ulcer in the Zollinger-Ellison syndrome. Hy­perparathyroidism should be given secondary consideration in such pa­tients since aggressive surgical control by total gastrectomy as early as possi­ble is indicated. Aggravation of duo­denal ulcer disease by other endocrine lesions was not evident in this study.

Experimental studies support the view that hypercalcemia influences gas­tric secretion, although it is probably not a critical factor. Species differences make animal studies of questionable significance for man." Evidence indi­cates that in man hypercalcemia results in an increased basal secretion of hy­drochloric acid as well as an increase in the volume of gastric juice, a de­crease in pepsin secretion, and an in­crease in mucous secretion."'!""^* These changes do not appear to be the result of direct effects of parathyroid

hormone since administration of this agent has no predictable influence on gastric secretion.^- Hypercalcemia in man produces elevated blood levels of gastrin, particularly in patients with duodenal ulcers, and this then is the likely cause of calcium-induced in­creased gastric acid secretion. It ap­pears that the influence of hypercal­cemia on the secretion of gastric acid is mediated in some manner through the vagus nerve.̂ " -̂ There does appear to be a direct relationship between the level of serum calcium and gastric se­cretion.These effects of hypercalce­mia, however, are based on acute or short-term studies, so that long term results in patients with hypercalcemia are not conclusive.Nevertheless, basal gastric secretory studies show a reduction following operative cor­rection of primary hyperparathyroid-ism.i--a«

Duodenal ulcer disease, unassociated with endocrine disease other than hy­perparathyroidism, usually does not ap­pear particularly serious. But, if se­vere, it does require therapy on the basis of usual indications. The behav­ior of ulcer disease associated with hy­perparathyroidism may follow one of three general patterns:

1. Heals spontaneously, or after gastric operation, with persistent hyperparathyroidism.

2. Persists with temporary remis­sions but heals after correction of hyperparathyroidism.

3. Persists or recurs after operative correction of hyperparathyroid­ism; in such patients the co­existence of the Zollinger-Ellison syndrome should be considered.

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Duodenal Ulcer Associated with Hyperparathyroidism

Summary and Conclusions 1. Of 98 patients with primary hy­

perparathyroidism, the clinical course of an associated duodenal ulcer pres­ent in 15 depended primarUy on the presence or absence of co-existent non-beta islet ceU tumors of the pancreas.

2. Although hypercalcemia may exaggerate the virulence of duodenal ulcer disease in patients with the Zol-linger-EUison syndrome, correction of hypercalcemia does not significantly improve the duodenal ulcer. Operative treatment, consisting of a total gastrec­tomy in nearly all instances, should be urgently provided for such patients prior to operative consideration for the hyperparathyroidism.

3. Although active duodenal ulcer

disease in the absence of the ZoUinger-EUison syndrome usually improves fol­lowing operative correction of associ­ated primary hyperparathyroidism, this is not uniformly true. Hypercalcemia appears to be only one factor, and not always a dominant etiologic factor in the duodenal ulcer disease which varies in severity in these patients.

4. In patients with active duodenal ulcer disease associated with primary hyperparathyroidism in the absence of the Zollinger-Ellison syndrome, the ulcer should be treated on the basis of its own merits with consideration given to correction first of the hyperparathy­roidism if usual surgical indications for the ulcer do not exist.

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