superficial ulcerative gastritis following triparsamide therapy for syphilis

2
JouR. D.D. EINSEL---SUPERFICIAL ULCERATIVE GASTRITIS 191 JUNE, 1942 cent were below 0.5 mg. per cent and 4.2 per cent were below 0.3 mg. per cent and yet none of them showed any signs or symptoms of scurvy. In view of this evidence, the low values observed in the absence of clinical signs of scurvy can not be regarded as "sub- normal." Vitamin D: We found only one instance of rickets during childhood in a man who had a pigeon breast and beading of the ribs. Vitamin E a~d K: No significant observations were made relative to the Vitamin E and K status of the workmen examined. SUMMARY We have examined 1265 healthy adult men engaged in industrial work for evidence of vitamin deficiency disease. A detailed dietary and symptomatic history revealed that 24 out of 300 had a diet inadequate in Vitamin A. However, no instance of subclinical Vita- min A deficiency was observed. No instance of xero- phthalmia, night blindness or hyperkeratotic skin placules was observed in any of the 1265 men. No cases of muscle pains, paresthesia, polyneuritis suggesting Vitamin B 1 deficiency were seen. Gastro- intestinal symptoms (gas, heartburn and dyspepsia) were reported by 52 of the 300 questioned, but none of these were severe enough to cause a defective Vitamin B absorption nor could they be conclusively attributed to Vitamin B 1 deficiency. No cases of pigmented dermatitis, soreness of the mouth, redness of the tongue, indigestion, diarrhoea and disturbances of the central nervous system sug- gesting subclinical pellagra were seen. The cheilosis and conjunctivitis characteristic of riboflavin deficiency were not seen. Blood plasma ascorbic acid determinations upon 78 of the normal workmen showed that only 13 (15 per cent) of them had a level over 0.75 mg. per cent, while 64 per cent of them had plasma levels below 0.5 mg. per cent. The blood plasma ascorbic acid level corre- lated with the dietary intake of Vitamin C. None of the men showed any signs or symptoms of Vitamin C deficiency and all of them enjoyed good health and were physically able to do industrial work. These observations, together with others in the literature, indicate that plasma cevitamic acid saturation is not necessary for good health and that signs of scurvy will not develop even with plasma levels ranging from 0.1 mg. to 0.5 nag. per cent. Conversely there is no well-controlled experimental evidence upon human subjects which proves that tissue and plasma ascorbic acid saturation is necessary for normal good health. The estimated daily requirement of cevitamic acid therefore is considerably less than the 60-80 mg. advocated, and these smaller amounts in the diet are compatible with good health. The increasing number of reports upon the wide-spread prevalence of vitamin deficiency disease and its deleterious effect upon health should therefore not be viewed with too great alarm. REFERENCES 1. Mindlin, R. L. and Butler, A. M.: "Determination of Ascorbic Acid in Plasma, Macromethod and Micromethod." J. Biol. Chem., 122:673, 1938. 2. Frazier, C. N. and Hu, C. K.: "Cutaneous Lesions Associated with Deficiency in Vitamin A in Man." Arch. Int. Med., 48:507, 1931. 3. Youmans, J. B. and Corlette, M. B. : "Specific Dermatoses Due to Vitamin A Deficiency." Am. J. Med. Sci.. 195:644, 1938. 4. Scheer, M. and Keil, H.: "Follicular Lesions in Vitamin A and C Deficiencies." Arch. Dermut. and Syph., 30:177, 1934. 5. Jung, F. T. and Isaacs, B. L.: "The Measurement of Vitamin A Deficiency in Man." Proc. Inst. Med. of Chicago, 1939. 6. Thorson, J. A.: "Nutritional Xerophthalmia." J. A. M. A., 103:1438, 1934. 7. Hess, A. F. and Kerley, D. B.: "Incidence of Xerophthalmia and Night Blindness in the United States. Gauge of Vitamin A Deficiency." Am. J. Pub. Health, 23:935, 1933. 8. Meiklejohn, A. P.: "The Estimation of Vitamin B1 in Blood by a Modification of Schopfer's Test." Biochem. J., 31:1441, 1937. 9. Baudier, E.: "Quantitative Estimation of Nicotinic Acid in Urine." Bioehem. J., 33:1787, 1939. 10, Harris, L. J, and Raymond, W. D.: "Assessment of the Level of Nutrition. A Method for the Estimation of Nicotinic Acid in Urine." Biochem. J., 33:2037, 1939. 11, Vilter, S. P., Spies, T. D. and Mathews, A. P.: "A Method for the Determination of Nicotinic Acid, Nicotinamide, and Possibly Other Pyridine-like Substances in Human Urine." J. Biol. Chem., 125:85, 1938. 12. Spies, T. D., Vilter, R. W. and Ashe, W. F.: "Pellagra, Beriberi, and Riboflavin Deficiency in Human Beings; Diagnosis and Treatment." J. A. M. A., 113:931, 1939. 13. Spies, T. D., Bean, W. B., Vilter, R. W. and Huff, N. E.: "Endemic Riboflavin Deficiency in Infants and Children." Am. J. Med. Sci., 200:697, 1940. 14. Munsell, H. E.: "Planning the Day's Diet for Vitamin Content." J. Am. Diet. Ass'n, 15:639, 1939. 15. Farmer, C. J. and Abt, A. F.: "Determination of Reduced As- corbic Acid in Small Amounts of Blood." Proc. Soc. Exper. Biol. and Med,, 34:146, 1936. 16. Abt, A. F., Farmer, C. J. and Epstein, L M.: "Normal Cevitamie (Ascorbic) Acid Determination in Blood Plasma and Their Re- lationship to Capillary Resistance." J. Ped., 8:1, 1936. 17. Abt, A. F. and Farmer, C. J.: "Vitamin C: Pharmacology and Therapeutics." J. A. M. A., 111:1555, 1938. 18. Bryan, A. H., Turner, D. F., Huenemann, R. L. and Lotwin, G.: Am. J. Med. Sci., 202:77, 1941. 19. Croft, J. D. and Suorf, L. D.: "Cevitamic Acid Deficiency; Fre- quency in a Group of 100 Unselected Patients." Am. J. Med. Sci., 198:403, 1939. 20. Rohmer, P., Snaders, U. and Bezssouff, U. : "Synthesis of Vitamin C by the Infant." Nature, London, 134:142, 1934. 21. Crandon, J. H., Lund, C. C. and Dell, D. B.: "Experimental Human Scurvy." N. Eng. J. Med., 223:353, 1940. 22. Bartlett, M. K., Jones, C. M. and Ryan, A. E.: "Vitamin C Studies on Surgical Patients." Ann. Surg., 111:1, 1940. 23. Rhinehart, J. F., Greenberg, L. D., Baker, F., Mettier, S. K., Bruckman, F, and Choy, F.: "Metabolism of Vitamin C in Rheumatoid Arthritis." Arch. Int. Med., 61:537, 1938. Superficial Ulcerative Gastritis Following Triparsamide Therapy for Syphilis By I. H. EINSEL, M.D. CLEVELAND, OHIO T HE gastric upset associated with certain toxic states frequently involves pathological changes which ordinarily escapes detection. The following case emphasizes this fact and proves that a gastroscopic examination may demonstrate superficial ulcerative gastritis resulting from triparsamide medication for syphilis. Apparently such an observation has not previously been reported. Submitted September 30, 1941. CASE REPORT B. H., male, 43, referred by Dr. Vigor of Brecksville, Ohio, had heavy anti-luetic treatment followed by uncon- trollable vomiting of several weeks' duration. Syphilis was acquired many years previously but was untreated until central nervous system involvement supervened in 1933. He then received neoarsphenamine, bismuth and mercury therapy intermittently during the following five years. Late in 1938 triparsamide was administered; four injections of 1 gm. and two of 2 gm. each. Severe gastric

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JouR. D . D . E I N S E L - - - S U P E R F I C I A L U L C E R A T I V E G A S T R I T I S 191 JUNE, 1942

cent were below 0.5 mg. per cent and 4.2 per cent were below 0.3 mg. per cent and yet none of them showed any signs or symptoms of scurvy. In view of this evidence, the low values observed in the absence of clinical signs of scurvy can not be regarded as "sub- normal."

Vitamin D: We found only one instance of rickets during childhood in a man who had a pigeon breas t and beading of the ribs.

Vitamin E a~d K: No significant observations were made relative to the Vitamin E and K status of the workmen examined.

SUMMARY

We have examined 1265 healthy adult men engaged in industr ial work for evidence of vi tamin deficiency disease. A detailed die tary and symptomatic his tory revealed tha t 24 out of 300 had a diet inadequate in Vitamin A. However, no instance of subclinical Vita- min A deficiency was observed. No instance of xero- phthalmia, night blindness or hyperkeratot ic skin placules was observed in any of the 1265 men.

No cases of muscle pains, paresthesia, polyneuri t is suggest ing Vitamin B 1 deficiency were seen. Gastro- intest inal symptoms (gas, hear tburn and dyspepsia) were reported by 52 of the 300 questioned, but none of these were severe enough to cause a defective Vitamin B absorption nor could they be conclusively a t t r ibuted to Vitamin B 1 deficiency.

No cases of pigmented dermat i t is , soreness of the

mouth, redness of the tongue, indigestion, d iarrhoea and disturbances of the central nervous system sug- gest ing subclinical pel lagra were seen.

The cheilosis and conjunctivi t is character is t ic of riboflavin deficiency were not seen.

Blood plasma ascorbic acid determinat ions upon 78 of the normal workmen showed tha t only 13 (15 per cent) of them had a level over 0.75 mg. per cent, while 64 per cent of them had plasma levels below 0.5 mg. per cent. The blood plasma ascorbic acid level corre- lated with the d ie tary intake of Vitamin C. None of the men showed any signs or symptoms of Vitamin C deficiency and all of them enjoyed good health and were physically able to do industr ia l work. These observations, together with others in the l i terature , indicate that plasma cevitamic acid sa tura t ion is not necessary for good health and tha t signs of scurvy will not develop even with plasma levels ranging from 0.1 mg. to 0.5 nag. per cent. Conversely there is no well-controlled experimental evidence upon human subjects which proves tha t t issue and plasma ascorbic acid sa tura t ion is necessary for normal good health. The est imated daily requirement of cevitamic acid therefore is considerably less than the 60-80 mg. advocated, and these smaller amounts in the diet are compatible with good health. The increasing number of reports upon the wide-spread prevalence of vi tamin deficiency disease and its deleterious effect upon health should therefore not be viewed with too great alarm.

R E F E R E N C E S 1. Mindlin, R. L. and Butler, A. M.: "Determinat ion of Ascorbic

Acid in Plasma, Macromethod and Micromethod." J. Biol. Chem., 122:673, 1938.

2. Frazier , C. N. and Hu, C. K. : "Cutaneous Lesions Associated with Deficiency in Vi tamin A in Man." Arch. Int. Med., 48:507, 1931.

3. Youmans, J . B. and Corlette, M. B. : "Specific Dermatoses Due to Vi tamin A Deficiency." Am. J. Med. Sci.. 195:644, 1938.

4. Scheer, M. and Keil, H . : "Follicular Lesions in Vi tamin A and C Deficiencies." Arch. Dermut. and Syph., 30:177, 1934.

5. Jung , F. T. and Isaacs, B. L . : "The Measurement of Vi tamin A Deficiency in Man." Proc. Inst. Med. of Chicago, 1939.

6. Thorson, J . A. : "Nutr i t ional Xerophthalmia." J . A. M. A., 103:1438, 1934.

7. Hess, A. F. and Kerley, D. B. : "Incidence of Xerophthalmia and Night Blindness in the United States. Gauge of Vi tamin A Deficiency." Am. J. Pub. Health, 23:935, 1933.

8. Meiklejohn, A. P . : "The Est imation of Vi tamin B1 in Blood by a Modification of Schopfer 's Test ." Biochem. J., 31:1441, 1937.

9. Baudier, E . : "Quant i ta t ive Est imation of Nicotinic Acid in Ur ine ." Bioehem. J., 33:1787, 1939.

10, Harr is , L. J , and Raymond, W. D. : "Assessment of the Level of Nutri t ion. A Method for the Est imat ion of Nicotinic Acid in Ur ine ." Biochem. J., 33:2037, 1939.

11, Vilter, S. P., Spies, T. D. and Mathews, A. P . : "A Method for the Determination of Nicotinic Acid, Nicotinamide, and Possibly Other Pyridine-like Substances in Human Urine ." J. Biol. Chem., 125:85, 1938.

12. Spies, T. D., Vilter, R. W. and Ashe, W. F . : "Pel lagra, Beriberi,

and Riboflavin Deficiency in Human Beings; Diagnosis and Trea tment . " J . A. M. A., 113:931, 1939.

13. Spies, T. D., Bean, W. B., Vilter, R. W. and Huff, N. E . : "Endemic Riboflavin Deficiency in In fan t s and Children." Am. J. Med. Sci., 200:697, 1940.

14. Munsell, H. E . : "P lann ing the Day's Diet for Vi tamin Content." J. Am. Diet. A s s ' n , 15:639, 1939.

15. Farmer , C. J . and Abt, A. F . : "Determinat ion of Reduced As- corbic Acid in Small Amounts of Blood." Proc. Soc. Exper. Biol. and Med,, 34:146, 1936.

16. Abt, A. F., Farmer , C. J . and Epstein, L M.: "Normal Cevitamie (Ascorbic) Acid Determination in Blood Plasma and Their Re- lationship to Capillary Resistance." J . Ped., 8:1, 1936.

17. Abt, A. F. and Farmer , C. J . : "Vi t amin C: Pharmacology and Therapeut ics ." J . A. M. A., 111:1555, 1938.

18. Bryan, A. H., Turner , D. F., Huenemann, R. L. and Lotwin, G.: Am. J. Med. Sci., 202:77, 1941.

19. Croft, J . D. and Suorf, L. D. : "Cevi tamic Acid Deficiency; Fre- quency in a Group of 100 Unselected Pat ients ." Am. J. Med. Sci., 198:403, 1939.

20. Rohmer, P., Snaders, U. and Bezssouff, U. : "Synthesis of Vi tamin C by the In f an t . " Nature, London, 134:142, 1934.

21. Crandon, J . H., Lund, C. C. and Dell, D. B. : "Exper imenta l Human Scurvy." N. Eng. J. Med., 223:353, 1940.

22. Bartlett, M. K., Jones, C. M. and Ryan, A. E . : "Vi tamin C Studies on Surgical Pat ients ." Ann. Surg., 111:1, 1940.

23. Rhinehart , J . F., Greenberg, L. D., Baker, F., Mettier, S. K., Bruckman, F, and Choy, F . : "Metabolism of Vi tamin C in Rheumatoid Ar thr i t i s . " Arch. Int. Med., 61:537, 1938.

Superficial Ulcerative Gastritis Following Triparsamide Therapy for Syphilis By

I. H. EINSEL, M.D. C L E V E L A N D , OHIO

T HE gast r ic upset associated with cer tain toxic states frequently involves pathological changes

which ordinar i ly escapes detection. The following case emphasizes this fact and proves tha t a gastroscopic examination may demonstrate superficial ulcerative gas t r i t i s resul t ing from t r iparsamide medication for syphilis. Apparent ly such an observation has not previously been reported.

Submitted September 30, 1941.

CASE REPORT B. H., male, 43, referred by Dr. Vigor of Brecksville,

Ohio, had heavy anti-luetic treatment followed by uncon- trollable vomiting of several weeks' duration. Syphilis was acquired many years previously but was untreated until central nervous system involvement supervened in 1933. He then received neoarsphenamine, bismuth and mercury therapy intermittently during the following five years. Late in 1938 triparsamide was administered; four injections of 1 gm. and two of 2 gm. each. Severe gastric

192 AMERICAN JOURNAL OF DIGESTIVE DISEASES VOLUlY[I] 9 NUMBER 6

distress and nausea gradually supervened and then gradu- ally disappeared.

E X A M I N A T I O N X-ray examination, made two weeks a f te r stopping

t r iparsamide therapy, showed the gast ro- intes t inal t rac t normal except for thick gastr ic rugae, deep gastr ic peristaltic waves s ta r t ing close to the esopha- gus and slight spasm of descending colon. Gall bladder visualization with the dye was good. Gastroscopic ex- amination in three depths showed pyloric sphincter normal, the angulus was edematous with occasional superficial eroded areas. The gastr ic corpus contained

hundreds of eroded areas 2 to 4 mm. in diameter with a pearly white base and red edge. The lesions were chiefly on the anter ior and posterior wall and the grea ter curvature but were relatively scarce on the lesser curvature and at the cardiac end of the stomach. The mucosa was edematous and bled easily when touched by the gastroscope.

A second gastroscopic examination seven months la ter showed the gastr ic mucosa normal except for a slight edema which probably resulted f rom taking 30 grs. of acetylsalicylic acid for a severe headache the day before.

Gastroieiuno-Colic Fistula By

JUSTIN J. STEIN, M.D., F.A.C.S.t H I N E S , I L L I N O I S

T HE successful t rea tment of gastrojejuno-colic fistula is practically always of a surgical nature.

The patients generally become anemic and debilitated as a result of the nutri t ional disturbances brought about by the inability of the small intestines to assimi- late an adequate diet. Also Pfeiffer (1) has pointed out that the continued entrance of colon contents into the upper gastro-intest inal t ract is a very serious complication.

The purpose of this paper is to briefly discuss the general considerations of gastrojejuno-colic fistula, to report a successfully t reated case, and to stress the importance of per forming the operation in multiple stages. Since the surgical procedure consists in re- moving the gastroenteric stoma, closure of the colonic and jejunal fistulae, and re-establishment of gastro- intestinal continuity, the operative mortal i ty will be great ly reduced by multiple stage operations.

ETIOLOGY Since gastrojejuno-colic fistulas generally follow

jejunal ulcers which develop a f te r gastro-enterostomy, the etiological factors are essentially the same as those causing post-operative jejunal ulcer.

Hyperacidity, the application of t igh t intestinal clamps, the use of non-absorbable suture material, im- proper post~operative care, and other factors have been prominently mentioned as the causative agents for post-operative jejunal ulcer. Careful studies by different investigators have proven tha t these factors may be of some importance but that they have been great ly exaggerated since the ulcers occur where clamps have not been applied, absorbable suture ma- terial used, and a low gastr ic acidity is present. Er rors in surgical technique, such as improper location of the anastomosis, sharp angulation of the proximal and distal loops of the je junum at the site of anastomosis, and placing the sutures too close together in the mucosa, must not be minimized. Perhaps an inherited

~ F r o m the Su rg i ca l Service , V e t e r a n s A d m i n i s t r a t i o n Fac i l i ty , H ines , I l l inois.

Publ i shed w i t h the p e r m i s s i o n of t he Medical D i r ec to r of the V e t e r a n s A d m i n i s t r a t i o n who a s s u m e s no r e spons ib i l i t y fo r t he conclusions or op in ions expressed by the au tho r .

?On ac t ive du ty a t t he U. S. N a v a l Hosp i ta l , San Diego, Cal i forn ia . S u b m i t t e d October 20, 1941.

constitutional predisposition to form ulcer or an ulcer diathesis is th~ most important single factor since jejunal ulcers may develop under ideal conditions and in the best of hands. P r ima ry jejunal ulcer is rare, whereas post-operative jejunal ulcer is relatively common. As far as is known at the present time, the etiology of gastrojejunal ulcer is purely hypothetical.

AGE AND SEX In the ninety-five cases collected by Verbrugge (2),

one of the patients was a female. In the series of fifty cases of gastrojejuno-colic fistula and seventeen cases of impending fistula reported by Walters and Clagett (3), only one was a female. Rife (4) reported two females in his series of fourteen cases. Euster- man (5) places the proportion of males to females having gastr ic and duodenal ulcers as 3:1 and those with jejunal ulcers as 6:1. I t can therefore be readily assumed that gastrojejuno-colic fistula is a rare or unusual complication in the female sex. I t is interest- ing to note that in a study of one hundred and fifty cases of gastrojejunal ulcer by Walters and Clagett, only three of the patients were women.

The average age in the fourteen patients in Rife 's series was 46 years. The youngest pat ient was 31, and the oldest 72. In the series of fifty cases reported by Walters and Clagett, five were between 20 and 30, twenty-five between 40 and 50, and only two between 60 and 70.

I N C I D E N C E In a series of 6,214 gastro-enterostomies done at

the Mayo Clinic pr ior to January , 1924, Verbrugge reported tha t eighty-eight, or 1.41 per cent developed gastrojejunal ulcer. A gastrojejuno-colic fistula de- veloped in ten, or 11.36 per cent of the eighty-eight cases and in only 0.16 per cent, of the 6,214 cases in which gastro-enterostomy was performed. Walters and Clagett reported that gastrojejuno-colic fistula was present in twenty-three, or 13.6 per cent, or 169 cases of gastrojejunal ulcer in which operation was per- formed in the years 1933 to 1936 inclusive. Allen (6) found the incidence of gastrojejuno-colic fistula to be 14 per cent in thir ty-six cases of gastrojejunal ulcer'.