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Melanosis jejuni
with longstanding diabetes mellitus, n' 12 although the pathogenesis is quite different. Besides the sacral radiculopathy caused by the anogenital herpes infection, incontinence in a young woman of childbearing age could be due to a birth injury, in which symptoms could occur a few years from the injury. Trauma caused by anal sex could be another contributing factor, although t r a u m a has been associated with unwanted anal penetration but not with consensual anal intercourse, i3 Anal endosonography would differentiate the above condit i o n s 14 from transient nerve damage. However, in our patient, a complete resolution of sacral nerve dysfunction both symptomatically and manometrically after the cure of anogenital herpes supports strongly herpetic sacral nerve radiculopathy. REFERENCES 1. Black D, Stewart J, Melmed C. Sacral nerve dysfunction plus generalized polyneuropathy in herpes simplex genitalis. Ann Neurol 1983;14:692. 2. Caplan LR, Kleeman FJ, Berg S. Urinary retention probably secondary to herpes genitalis. N Engl J Med 1977;297:920-1. 3. Oates JK, Greenhouse PR. Retention of urine in anogenital herpetic infection. Lancet 1978;1:691-2. 4. Mertz G. Genital herpes simplex virus infections. Med Clin North Am 1990;74:1433-54.
5. Jacobs E. Anal infections caused by herpes simplex virus. Dis Colon Rectum 1976;19:151-7. 6. Baringer JR. Recovery of herpes simplex virus from human sacral ganglions. N Engl J Med 1974;291:828-30. 7. Wald A. Colonic and anorectal motility testing in clinical practice. Am J Gastroenterol 1994;89:2109-15. 8. Goligher JC, Hughes EJR. Sensibility of the rectum and colon: its role in the mechanism of anal continence. Lancet 1951;1:543-7. 9. Schuster MM. Motor action of rectum and anal sphincters in continence and defecation. In: Code CF, ed. Handbook of physiology. Section 6, vol. 4. Washington, DC: American Physiological Society, 1968:2121-46. 10. Whitehead WE, Engel BT, Schuster MM. Perception of rectal distention is necessary to prevent fecal incontinence. In: Adam G, Meszaros I, Banyai ET, editors. Advances in physiological sciences. Vol. 17. Brain and behavior, Budapest, Hungary: Akademia Kiado, 1981. 11. Schiller LR, Santa Ana CA, Schmulen AC, Hendler RS, Harford WV, Fordtran JS. Pathogenesis of fecal incontinence in diabetes mellitus: evidence for internal anal sphincter dysfunction. N Engl J Med 1982;307:1666-71. 12. Wald A, Tunuguntla AK. Anorectal sensorimotor dysfunction in fecal incontinence and diabetes mellitus. N Engl J Med 1984;310:1282-7. 13. Chun AB, Rose S, Silvestre T, Mitrani C, Wald A. Anal sphincter structure and function in homosexual males engaging in anoreceptive intercourse [abstract]. Gastroenterology 1996; 110:A648. 14. Sultan AH, Kamm MA, Hudson CN, Thomas TM, Bartram CT. Anal sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905-11.
Melanosis jejuni Jänos Banai, MD, PhD Andräs Fenyvesi, MD Gäbor Gonda, MD Ivän Petö, MD, PhD Melanosis of the gastrointestinal tract consists of pigment deposits in the mucosa. Dark pigmentation of t h e colon is a w e l l k n o w n a n d n o t r a r e c o n d i t i o n . M e l anosis or pseudomelanosis of the duodenum, ileum, and esophagus have also been described. In this report, we describe a case in which we observed melanosis of the jejunum.
CASE REPORT A 45-year-old woman was a d m i t t e d to our d e p a r t m e n t in November 1995. She h a d a history of d i a r r h e a since 1981 t h a t was diagnosed as ulcerative colitis in 1986. In 1988, total colectomy with proctomucosectomy was performed with From the First Department of Medicine, Gastroenterology Unit, Institute of Pathology, Imre Haynal University of Health Sciences, Budapest, Hungary. Reprint requests: Jänos Banai, MD, PhD, Gastroenterology Unit, Imre Haynal University of Health Sciences, Postgraduate Medical Faculty, Budapest, Szabolcs u. 35. H-1135 Hungary. 0016-5107/97/4505-043255.00 +0 GASTROINTESTINAL ENDOSCOPY Copyright © 1997 by the American Society for Gastrointestinal Endoscopy 37/4/79518
432 GASTROINTESTINAL ENDOSCOPY
Figure 1. Endoscopic appearance of the jejunal mucosa.
an ileoanal pouch. Ileostomy was closed a t the end of 1988. The reason for the p r e s e n t admission was fatigue, weakness, fecal incontinence, abdominal cramps, a n d bloating. A t home she h a d been t a k i n g 320 mg/day of ferrous sulphate, 2 to 6 mg/day of loperamide hydrochloride, v i t a m i n B complexes, and spasmolytics. On admission she was pale and thin with generalized t e n d e r n e s s over the abdomen. The liver was slightly enilarged (1 cm below the costal margin). L a b o r a t o r y tests showed normal blood count a n d n o r m a l chemistry results with the exception of a sedimentation r a t e of 58 m m / h and a serum-iron concentration of 6 Itmol/L. Electrocardiogram, VOLUME 45, NO. 5, 1997
Figure 2. Pigment laden macrophages in the connective tissue of the villi. (H&E, original magnification x250.)
chest x-ray, and abdominal ultrasound revealed no positive results. The abdominal CT scan showed a thickened small bowel wall with a narrowed lumen at the jejunoilealjunction in the right posterior quadrant of the abdomen. A marked prestenotic distension was also observed. The wall of the more proximal segments of the jejunum was also thickened. A small bowel barium study revealed a markedly distended segment of the jejunum but only indirect signs of stenosis were seen and the precise site of stenosis could not be determined. (A month later part of the ileum and the pouch were resected because of ileus caused by adhesions.) Jejunoscopy was performed to search for bacterial overgrowth and secondary villous atrophy. Endoscopy of the esophagus, stomach and proximal duodenum revealed no specific abnormalities. The duodenum near the duodenojejunal flexure demonstrated discrete signs of melanosis, but in the proximal part of the jejunum this pattern was more marked (Fig. 1). Diffuse, multiple, dark brown, discrete spots were observed on the intact mucosa. Jejunal fluid was aspirated for bacterial culture. Candida albicans but no bacteria was cultured from the jejunal fluid. Biopsy specimens were taken for light and electron microscopy from the jejunum 10 cm aboral to the duodenojejunal flexure. On stereomicroscopy the anatomy of the villi was normal, but the tips of almost all villi were discolored by a brownish pigment. The macroscopic appearance of the jejunum resembled that ofmelanosis coli. Five # m sections of the biopsy specimens were stained with H&E, oil-red O, Prussian blue, and periodic acid-Schiff (with and without amylase digestion). The ultrathin sections were examined with a Philips CM10 electron microscope. On light microscopy the structure of the jejunal mucosa was basically preserved, although in the connective tissue core of the villi numerous macrophages contained golden brown pigment granules in their cytoplasm (Fig. 2). The pigment was strongly positive with Prussian blue (Fig. 3), showed a moderately positive reaction with periodic acidSchiff (even after amylase digestion), and focal positivity with oil-red O. On electron microscopy the pigment granules were seen in the lysosomes. The overwhelming majority of the granules VOLUME 45, NO. 5, 1997
Figure 3. Positive Prussian blue reaction of the hemosiderin component. (Original magnification x250.)
Figure 4. Moderately electron dense hemosiderin and darker lipofuscin droplets. (Original magnification x39,000.)
showed the fine granular structure of hemosiderin; the minor component consisted of electron dense lipofuscin droplets. (Fig. 4). According to these results the pigment proved to be a compound material consisting ofhemosiderin and lipofuscin.
DISCUSSlON T h e t e r m m e l a n o s i s s u m m a r i z e s a condition characterized b y a n a b n o r m a l black, brown, or greyish p i g m e n t a t i o n in a n y p a r t of t h e h u m a n body (skin, mucosa, or l y m p h nodes). According to its classical m e a n i n g t h e p i g m e n t is produced b y m e l a n o c y t e s a n d is called m e l a n i n . H o w e v e r , t h e G r e e k w o r d m e l a n o sis m e a n s "b]ack condition," so this t e r m c a n b e u s e d to describe v a r i o u s conditions associated w i t h a n y k i n d of d a r k p i g m e n t a t i o n , a l t h o u g h t h e r e is a n e w t r e n d to u s e t h e t e r m p s e u d o m e ] a n o s i s instead. 1 W i t h t h e h e l p of h i s t o c h e m i s t r y a n d electron microscopy, some m a t e r i a l s t h a t occur in p i g m e n t g r a n GASTROINTESTINAL ENDOSCOPY 433
ules h a v e b e e n characterized, e.g., m e l a n i n , lipofuscin, h e m o s i d e r i n , a n d ferrous sulphide. B r o w n or black p i g m e n t a t i o n of t h e g a s t r o i n t e s t i n a l t r a c t w a s first described in the colonic m u c o s a b y Cruveilhier, b u t t h e t e r m " m e l a n o s i s coli" w a s first u s e d b y Virchow. 2 Melanosis fiel is a r a r e condition t h a t can be ass0ciated w i t h m e l a n o s i s coli or c a n occur s e p a r a t e l y . 1-5 Black p i g m e n t a t i o n of the e s o p h a g e a l m u c o s a h a s also b e e n m e n t i o n e d in t h e l i t e r a t u r e f l 2'6 Melanosis duodeni w a s first described in this j o u r n a l in 1976 b y Bisordi a n d K l e i n m a n , 7 a n d f u r t h e r cases w e r e published m o r e recently, s-23 D a r k p i g m e n t a t i o n of t h e d u o d e n u m is described in p a t i e n t s w i t h r e n a l failure. 7"9 Cowen a n d Humphries 1° h a v e described infilt r a t i o n of d u o d e n a l m u c o s a w i t h p s e u d o m e l a n i n , b u t t h e p i g m e n t h a s not b e e n f u r t h e r characterized. D u o d e n a l p i g m e n t w a s first c h a r a c t e r i z e d as ferrous s u l p h a t e by S t e c k m a n a n d Bozymski, 11 a finding l a t e r confirmed b y others. 12, 15-17,20, 22, 23 A n o t h e r type of p i g m e n t , lipofuscin, w a s also found in t h e m u c o s a of the d u o d e n u m a n d colon. 16, 20 A careful s e a r c h of t h e l i t e r a t u r e yielded no description of a n y t y p e of pigm e n t in the j e j u n a l m u c o s a s i m i l a r to our case. I n a r e c e n t p a p e r 1 the p i g m e n t s of the g a s t r o i n t e s t i n a l t r a c t are s u m m a r i z e d . Melanosis jejuni is not m e n tioned e i t h e r in isolated f o r m or in connection w i t h duodenal pigmentation. In our case p i g m e n t deposits w e r e seen endoscopically only in t h e j e j u n u m a n d aboral p a r t of the d u o d e n u m . T h e i l e u m w a s not affected, as proved b y t h e l a t e r l a p a r o t o m y . T h e endoscopic a p p e a r a n c e of m e l a n o s i s jejuni is v e r y s i m i l a r to m e l a n o s i s or p s e u d o m e l a n o s i s duodeni. The j e j u n a l m u c o s a h a s a b r o w n i s h - b l a c k speckled a p p e a r a n c e . T h e p i g m e n t deposits located m a i n l y in t h e tips of villi can be seen b y dissecting microscopy, f u r t h e r localized b y light microscopy in t h e m a c r o p h a g e s a n d b y electron microscopy in lysosomes. T h e p i g m e n t in our case w a s h e m o s i d e r i n a n d lipofuscin. T h e histologic a n d u l t r a s t r u c t u r a l findings w e r e identical to those of m e l a n o s i s ilei described b y G h a d i a l l y et al. 1, 5 B e c a u s e m o r p h o l o g y a n d function o f t h e j e j u n u m are s i m i l a r to t h a t of the d u o d e n u m , we s u p p o s e t h a t the c a u s e o f m e l a n o s i s is the s a m e . T h e r e h a v e b e e n speculations a b o u t t h e n a t u r e , origin, a n d significance of t h e p i g m e n t deposition. D u o d e n a l melanosis a p p e a r s to be associated w i t h g a s t r o i n t e s t i n a l bleeding, chronic r e n a l failure, c o n s u m p t i o n of differe n t d r u g s (hydralazine, propranolol, hydrochlorothiazide, furosemide, ferrous sulphate), or folic acid deficiency. I n our case l o n g - t e r m ferrous s u l p h a t e a d m i n -
434 GASTROINTESTINAL E N D O S C O P Y
i s t r a t i o n a n d v i t a m i n deficiencies could h a v e b e e n t h e m a j o r causes of p i g m e n t deposition. T h e clinical significance of this condition is u n c e r t a i n b u t t h e localization of the p i g m e n t deposition in this p a t i e n t is unique.
REFERENCES
1. Ghadially FN, Walley VM. Pigments of the gastrointestinal tract: a comparison of light microscopic and electron microscopic findings. Ultrastruc Patho] 1995;19:213-9. 2. Ghadially FN, Walley VM. Melanoses of the gastrointestinal tract. Histopathology 1994;25:197-207. 3. Won KH, Ramachand S. Melanosis of the ileum. Am J Dig Dis 1970;158:57-64. 4. Ghadia]ly FN, Boone SA, Walley VM. A comparison of the ultrastructure of pigment granules in me]anosis ilei and pulmonary lymph nodes. Histopathology 1993;23:167-72. 5. Ghadially FN, Boone SA, Walley VM. Melanosis (Haemosiderosis) ilei. J Submicrosc Cytol 1994;26:461-5. 6. Kimball MW. Pseudomelanosis of the esophagus. Gastrointest Endosc 1978;24:121-2. 7. Bisordi WM, Kleinman MS. Melanosis duodeni. Gastrointest Endosc 1976;23:37-8. 8. Ganju S, Adomavicius J, Salgia K, Steigmann F. The endoscopic picture of melanosis in the duodenum. Gastrointest Endosc 1980;26:44-5. 9. Breslaw L. Melanosis of the duodenal mucosa. Gastrointest Endosc 1980;26:45-6. 10. CowenML, Humphries TJ. Pseudomelanosis of the duodenum. Gastrointest Endosc 1980;26:107-8. 11. Steckman M, Bozymski EM. Hemosiderosis of the duodenum [abstract]. Gastrointest Endosc 1982;28:145. 12. Pounder DJ. The pigment of duodenal melanosis is ferrous sulfate [letter]. Gastrointest Endosc 1983;29:257. 13. Yamase H, Norris M, Gillies C. Pseudomelanosis duodeni: a clinico-pathologic entity. Gastrointest Endosc 1985;31:83-6. 14. Gupta TP, Weinstock JV. Duodenal pseudomelanosis associated with chronic renal failure. Gastrointest Endosc 1986;32: 358~60. 15. Lee HH, O'Donnell DB, Keven DF. Characteristics of melanosis duodeni: incorporation ofendoscopy, pathology and etiology. Endoscopy 1987;19:107-9. 16. Lin H-J, Tsay S-H, Chiang H, Tsui Y-T, Lee S-D, Yeh YS, et al. Pseudome]anosis duodeni. J Clin Gastroenterol 1988;10:155-9. 17. Rex DK, Jersild RA Jr. Further characterization ofthe pigment in pseudomelanosis duodeni in three patients. Gastroenterology 1988;95:177-82. 18. Sharp JR, Insalaco SJ, Johnson LF. Melanosis ofthe duodenum associated with a gastric ulcer and folic acid deficiency. Gastroenterology 1980;78:366-9. 19. Castellano G, Canga F, Lopez I, Colina F, Guttierez J, Costa R, et al. Pseudomelanosis of the duodenum. Endoscopic, histologic and ultrastructural study of a case. J Clin Gastroenterol 1988; 10:150-4. 20. West B. Pseudomelanosis duodeni. J Clin Gastroenterol 1988; 10:127-9. 21. Kuo YC, Wu CS. Duodenal melanosis. J Clin Gastroenterol 1988;10:160-4. 22. Kang JY, Wu AY, Chia JL, Wee A, Sutherland IH, Hori R. Clinical and ultrastructural studies in duodenal pseudomelanosis. Gut 1987;28:1673-81. 23. Minocha A, Fearneyhough PK, McClave SA, Parker JC Jr. Melanin-like pigmentation of the duodenum. Am J Gastroenterol 1995;90:1018-20.
VOLUME 45, NO. 5, 1997
5. Jacobs E. Anal infections caused by herpes simplex virus. Dis Colon Rectum 1976;19:151-7. 6. Baringer JR. Recovery of herpes simplex virus from human sacral ganglions. N Engl J Med 1974;291:828-30. 7. Wald A. Colonic and anorectal motility testing in clinical practice. Am J Gastroenterol 1994;89:2109-15. 8. Goligher JC, Hughes EJR. Sensibility of the rectum and colon: its role in the mechanism of anal continence. Lancet 1951;1:543-7. 9. Schuster MM. Motor action of rectum and anal sphincters in continence and defecation. In: Code CF, ed. Handbook of physiology. Section 6, vol. 4. Washington, DC: American Physiological Society, 1968:2121-46. 10. Whitehead WE, Engel BT, Schuster MM. Perception of rectal distention is necessary to prevent fecal incontinence. In: Adam G, Meszaros I, Banyai ET, editors. Advances in physiological sciences. Vol. 17. Brain and behavior, Budapest, Hungary: Akademia Kiado, 1981. 11. Schiller LR, Santa Ana CA, Schmulen AC, Hendler RS, Harford WV, Fordtran JS. Pathogenesis of fecal incontinence in diabetes mellitus: evidence for internal anal sphincter dysfunction. N Engl J Med 1982;307:1666-71. 12. Wald A, Tunuguntla AK. Anorectal sensorimotor dysfunction in fecal incontinence and diabetes mellitus. N Engl J Med 1984;310:1282-7. 13. Chun AB, Rose S, Silvestre T, Mitrani C, Wald A. Anal sphincter structure and function in homosexual males engaging in anoreceptive intercourse [abstract]. Gastroenterology 1996; 110:A648. 14. Sultan AH, Kamm MA, Hudson CN, Thomas TM, Bartram CT. Anal sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905-11.
Melanosis jejuni Jänos Banai, MD, PhD Andräs Fenyvesi, MD Gäbor Gonda, MD Ivän Petö, MD, PhD Melanosis of the gastrointestinal tract consists of pigment deposits in the mucosa. Dark pigmentation of t h e colon is a w e l l k n o w n a n d n o t r a r e c o n d i t i o n . M e l anosis or pseudomelanosis of the duodenum, ileum, and esophagus have also been described. In this report, we describe a case in which we observed melanosis of the jejunum.
CASE REPORT A 45-year-old woman was a d m i t t e d to our d e p a r t m e n t in November 1995. She h a d a history of d i a r r h e a since 1981 t h a t was diagnosed as ulcerative colitis in 1986. In 1988, total colectomy with proctomucosectomy was performed with From the First Department of Medicine, Gastroenterology Unit, Institute of Pathology, Imre Haynal University of Health Sciences, Budapest, Hungary. Reprint requests: Jänos Banai, MD, PhD, Gastroenterology Unit, Imre Haynal University of Health Sciences, Postgraduate Medical Faculty, Budapest, Szabolcs u. 35. H-1135 Hungary. 0016-5107/97/4505-043255.00 +0 GASTROINTESTINAL ENDOSCOPY Copyright © 1997 by the American Society for Gastrointestinal Endoscopy 37/4/79518
432 GASTROINTESTINAL ENDOSCOPY
Figure 1. Endoscopic appearance of the jejunal mucosa.
an ileoanal pouch. Ileostomy was closed a t the end of 1988. The reason for the p r e s e n t admission was fatigue, weakness, fecal incontinence, abdominal cramps, a n d bloating. A t home she h a d been t a k i n g 320 mg/day of ferrous sulphate, 2 to 6 mg/day of loperamide hydrochloride, v i t a m i n B complexes, and spasmolytics. On admission she was pale and thin with generalized t e n d e r n e s s over the abdomen. The liver was slightly enilarged (1 cm below the costal margin). L a b o r a t o r y tests showed normal blood count a n d n o r m a l chemistry results with the exception of a sedimentation r a t e of 58 m m / h and a serum-iron concentration of 6 Itmol/L. Electrocardiogram, VOLUME 45, NO. 5, 1997
Figure 2. Pigment laden macrophages in the connective tissue of the villi. (H&E, original magnification x250.)
chest x-ray, and abdominal ultrasound revealed no positive results. The abdominal CT scan showed a thickened small bowel wall with a narrowed lumen at the jejunoilealjunction in the right posterior quadrant of the abdomen. A marked prestenotic distension was also observed. The wall of the more proximal segments of the jejunum was also thickened. A small bowel barium study revealed a markedly distended segment of the jejunum but only indirect signs of stenosis were seen and the precise site of stenosis could not be determined. (A month later part of the ileum and the pouch were resected because of ileus caused by adhesions.) Jejunoscopy was performed to search for bacterial overgrowth and secondary villous atrophy. Endoscopy of the esophagus, stomach and proximal duodenum revealed no specific abnormalities. The duodenum near the duodenojejunal flexure demonstrated discrete signs of melanosis, but in the proximal part of the jejunum this pattern was more marked (Fig. 1). Diffuse, multiple, dark brown, discrete spots were observed on the intact mucosa. Jejunal fluid was aspirated for bacterial culture. Candida albicans but no bacteria was cultured from the jejunal fluid. Biopsy specimens were taken for light and electron microscopy from the jejunum 10 cm aboral to the duodenojejunal flexure. On stereomicroscopy the anatomy of the villi was normal, but the tips of almost all villi were discolored by a brownish pigment. The macroscopic appearance of the jejunum resembled that ofmelanosis coli. Five # m sections of the biopsy specimens were stained with H&E, oil-red O, Prussian blue, and periodic acid-Schiff (with and without amylase digestion). The ultrathin sections were examined with a Philips CM10 electron microscope. On light microscopy the structure of the jejunal mucosa was basically preserved, although in the connective tissue core of the villi numerous macrophages contained golden brown pigment granules in their cytoplasm (Fig. 2). The pigment was strongly positive with Prussian blue (Fig. 3), showed a moderately positive reaction with periodic acidSchiff (even after amylase digestion), and focal positivity with oil-red O. On electron microscopy the pigment granules were seen in the lysosomes. The overwhelming majority of the granules VOLUME 45, NO. 5, 1997
Figure 3. Positive Prussian blue reaction of the hemosiderin component. (Original magnification x250.)
Figure 4. Moderately electron dense hemosiderin and darker lipofuscin droplets. (Original magnification x39,000.)
showed the fine granular structure of hemosiderin; the minor component consisted of electron dense lipofuscin droplets. (Fig. 4). According to these results the pigment proved to be a compound material consisting ofhemosiderin and lipofuscin.
DISCUSSlON T h e t e r m m e l a n o s i s s u m m a r i z e s a condition characterized b y a n a b n o r m a l black, brown, or greyish p i g m e n t a t i o n in a n y p a r t of t h e h u m a n body (skin, mucosa, or l y m p h nodes). According to its classical m e a n i n g t h e p i g m e n t is produced b y m e l a n o c y t e s a n d is called m e l a n i n . H o w e v e r , t h e G r e e k w o r d m e l a n o sis m e a n s "b]ack condition," so this t e r m c a n b e u s e d to describe v a r i o u s conditions associated w i t h a n y k i n d of d a r k p i g m e n t a t i o n , a l t h o u g h t h e r e is a n e w t r e n d to u s e t h e t e r m p s e u d o m e ] a n o s i s instead. 1 W i t h t h e h e l p of h i s t o c h e m i s t r y a n d electron microscopy, some m a t e r i a l s t h a t occur in p i g m e n t g r a n GASTROINTESTINAL ENDOSCOPY 433
ules h a v e b e e n characterized, e.g., m e l a n i n , lipofuscin, h e m o s i d e r i n , a n d ferrous sulphide. B r o w n or black p i g m e n t a t i o n of t h e g a s t r o i n t e s t i n a l t r a c t w a s first described in the colonic m u c o s a b y Cruveilhier, b u t t h e t e r m " m e l a n o s i s coli" w a s first u s e d b y Virchow. 2 Melanosis fiel is a r a r e condition t h a t can be ass0ciated w i t h m e l a n o s i s coli or c a n occur s e p a r a t e l y . 1-5 Black p i g m e n t a t i o n of the e s o p h a g e a l m u c o s a h a s also b e e n m e n t i o n e d in t h e l i t e r a t u r e f l 2'6 Melanosis duodeni w a s first described in this j o u r n a l in 1976 b y Bisordi a n d K l e i n m a n , 7 a n d f u r t h e r cases w e r e published m o r e recently, s-23 D a r k p i g m e n t a t i o n of t h e d u o d e n u m is described in p a t i e n t s w i t h r e n a l failure. 7"9 Cowen a n d Humphries 1° h a v e described infilt r a t i o n of d u o d e n a l m u c o s a w i t h p s e u d o m e l a n i n , b u t t h e p i g m e n t h a s not b e e n f u r t h e r characterized. D u o d e n a l p i g m e n t w a s first c h a r a c t e r i z e d as ferrous s u l p h a t e by S t e c k m a n a n d Bozymski, 11 a finding l a t e r confirmed b y others. 12, 15-17,20, 22, 23 A n o t h e r type of p i g m e n t , lipofuscin, w a s also found in t h e m u c o s a of the d u o d e n u m a n d colon. 16, 20 A careful s e a r c h of t h e l i t e r a t u r e yielded no description of a n y t y p e of pigm e n t in the j e j u n a l m u c o s a s i m i l a r to our case. I n a r e c e n t p a p e r 1 the p i g m e n t s of the g a s t r o i n t e s t i n a l t r a c t are s u m m a r i z e d . Melanosis jejuni is not m e n tioned e i t h e r in isolated f o r m or in connection w i t h duodenal pigmentation. In our case p i g m e n t deposits w e r e seen endoscopically only in t h e j e j u n u m a n d aboral p a r t of the d u o d e n u m . T h e i l e u m w a s not affected, as proved b y t h e l a t e r l a p a r o t o m y . T h e endoscopic a p p e a r a n c e of m e l a n o s i s jejuni is v e r y s i m i l a r to m e l a n o s i s or p s e u d o m e l a n o s i s duodeni. The j e j u n a l m u c o s a h a s a b r o w n i s h - b l a c k speckled a p p e a r a n c e . T h e p i g m e n t deposits located m a i n l y in t h e tips of villi can be seen b y dissecting microscopy, f u r t h e r localized b y light microscopy in t h e m a c r o p h a g e s a n d b y electron microscopy in lysosomes. T h e p i g m e n t in our case w a s h e m o s i d e r i n a n d lipofuscin. T h e histologic a n d u l t r a s t r u c t u r a l findings w e r e identical to those of m e l a n o s i s ilei described b y G h a d i a l l y et al. 1, 5 B e c a u s e m o r p h o l o g y a n d function o f t h e j e j u n u m are s i m i l a r to t h a t of the d u o d e n u m , we s u p p o s e t h a t the c a u s e o f m e l a n o s i s is the s a m e . T h e r e h a v e b e e n speculations a b o u t t h e n a t u r e , origin, a n d significance of t h e p i g m e n t deposition. D u o d e n a l melanosis a p p e a r s to be associated w i t h g a s t r o i n t e s t i n a l bleeding, chronic r e n a l failure, c o n s u m p t i o n of differe n t d r u g s (hydralazine, propranolol, hydrochlorothiazide, furosemide, ferrous sulphate), or folic acid deficiency. I n our case l o n g - t e r m ferrous s u l p h a t e a d m i n -
434 GASTROINTESTINAL E N D O S C O P Y
i s t r a t i o n a n d v i t a m i n deficiencies could h a v e b e e n t h e m a j o r causes of p i g m e n t deposition. T h e clinical significance of this condition is u n c e r t a i n b u t t h e localization of the p i g m e n t deposition in this p a t i e n t is unique.
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VOLUME 45, NO. 5, 1997