sorbitol as a cryptic cause of diarrhea - hindawi1-att'd analysis of stoma effl uent revealed...

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Sorbitol as a cryptic cause of diarrhea

ANTHONYG. CATTO-S1v1ITH. MB, BS, FRACP, MRCP. R. BRENT SCOTT. MDCM. FRCPC, HELE!'-! M. MACHIDA. MD. FRCPC. 0. GRANT GALL. MD, FRCPC

ABSTRACT: Sorbitol is a poorly absorbed monosaccharide widely used as a sweetener for dietetic foods and as a drug vehicle. lngestion of sorbitol can lead to gastrointestinal complaints such as cramps and diarrhea. Two patients in whom unre· cognized sorbitol ingestion produced symptoms which mimicked an exacerbation of another underlying disorder are presented. The diagnosis of sorbitol induced symp· toms may be missed or delayed because patients do not appreciate that they are ingesting the compound in 'sugarless foods', and drug product information may not list its inclusion as a sweetener. Can J Gastroente rol 1988;2( 4 ): 140·2

Key Words: Crohn's disewe. Diarrhea, Exacerbation, Sorbitol, Tyrosinemia

S ORBITOI IS Wll)EI y usrn AS A SWEIT encr for dietetic foods and as ad rug

vehicle. It b a monosaccharide which i~ poorly absorbed from the intestine and ingestion can induce an osmotic diarrhea. Gryboski (I) w;is the first to describe the occurrence of this diarrhea in children consuming dietetic candies. Later, Hyams l2) ~tudied the effects o(

varying dose~ of sorbitol on healthy adult volunteers and demonstrated that the ingestion of even small amounts can lead to functional complaints such as cramps and bloating without diarrhea. Two cases in which cryptic sorbitol ingestion in hos· pitalized patients induced symptoms that mimicked exacerbation of their underlying medical cond itions arc presented .

Division of Pediatric Gastroenrerolog)' and Nutrition, Alberta Children's Hospital, University of Calgary, Calgary, Alberta

Correspondence and reprims: Dr D.G. Gall, lniestinal Disease Research Unit, University of Calgary, FaCHlry of Medicine, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N I. Telephone (403) 220-7370

Received/or publication May 30, 1988. Accepted Jul)' 15, 1988

140

CASE ONE In March 1987, an 18-ycar-old female

with an eight-year history ofCrohn'sdis· ease was admitted to hospital with a fourday history of severe colicky lower abdominal pain. nausea and decreased con· sistency of ileostomy outpu c. llcal Crohn's disease had been diagnosed at laparot· omy in 1979 and che subsequent clinical course had been one of chronic smoldering disease with acute exacerbations. ln 1984, recurrent bouts of intestinal obstruction required resection of a 55 cm strictured segment of jejunum. In 1986, a colectomy and ileostomy were carried out because of severe symptoms due to granulomatous colitis, unrcspon· sive to medical therapy. Following this the patient did well with minimal symptoms, although it was not possible to reduce the dose of prednisone below 10 mg per day. On admission to hospital the patient was afebrile w ith a non· d istended abdomen, mild lower abdom inal tenderness and a healthy matured ileostomy. Physical examination was othe rwise unremarkable.

An exacerbation o( Crohn's disea~e

CAN] GASTROENTEROL

or rarnal bowel ob,trucnon from Crohn', disease or adhesions were considered hkeh· diagnoses. The patient was placed <>n nil by mouth and ,tarted on total par· cnr~ral nutrition. However, her ilcoscomy output increased with volumes ranging trr,m 750 w 1500 ml of watery flt11d per day and the colicky lower abdominal pam continued. A barium contrast study rt calcJ muluplc arcn,of in\'ohed small lxiwcl There was no e\'1dence of ... 1gnificant ob truction. Endoscopic exmnina-11on o( the distal small bo\\'rl through the stoma was normal and h iopsics ,howed only mild nonspecific in flammatOr) changes Abdominal ulrra,ound \\'as nr,rmal and culture of urine and smma Ou1d revealed no pathogen~

lleostomy fluid output remained elc-1-att'd Analysis of stoma effluent revealed an osmolarity of282 mOsm/kg. sod ium 59mmoVL, potassium 6.6 mmoVL. chloride 27 mmol/L and an osmolar gap of 151 mOsm/kg. The patient was informed th,;r the symptoms migh t be due to the mg~suon of some agent which induced an osmotic diar rhea, but she denied mg,·suon of food, medication or laxamc, A room search failed to reveal any laxativeti. lleostomy fluid and urine ~creen~ for phenolphthalein and senna wm negative. The following day the pauent and her mother volunteered the addmonal information that she had for ,ome ume been chewing 14 to 28 sticks of Trident sugarless gum per day. Each su.:kcontains0.93 g of sorbicol, 0.40 g of xyhtol and 0.04 g of mannitol; a total of 131 g per stick. Total daily intake of sorbitol alone ranged between 13 and 26 g representing ingestion of 72 to 145 mOsml of poorly ahsorhablc solute pe r Jav

The patient ceased chcll'mg gum and owr the next 24 h there was ;1 cessation ot ahJominal cram rs and a decrcast' in 1lco,tomy output to less than 450 ml/day A normal diet was resumed, rarcn tera l nutnuon stopped and ileostomy cffluentrcmamcd appropriate in volume and con,1s1ency. There was no osmolar gap on repeat assessmen t

CASE TWO In June 1987 a six-month-old (cmalc

mfant with ryrosincmia was ad mined to ho,p1tal 1111th failure to thn Vl', vomiting .

\ol 2 No 4. November 1988

diarrhea and hepacosplenomegaly. There was bioche mical and radiological evidence of rickets T he d iagnosis of tyrosincmia was based on urmary and plasma amino acid ch romatography. The patient \\'as placed on nil by mouth and on total parenteral nutrition wtth parenteral calcium supplements because of the rickets. Vomiting and diarrhea resolved and the patient gained weight.

Following cl inical and biochemical impm\'ement , a low tyrosine d iet and oral medications were commenced O ral medications consisted of a calcium supplement (Calc1um-Sandm syrup; Anca Pharma, 23 ml qid) providing 506 mg elemental calcium per day, 1-25 d ihydroxycholccalc1ferol ( Rocaltrol; Roche. 125 µg bid), potassium phosphate 500 mg q1d, pyridoxme 2 5 mg daily, vitamin K 2. 5 mg daily, vitamin E 50 iu per Jay and -acerylcysteme 20";, 2 ml every 4 h

T he patient developed a recurrence of frequent watery stools, but was afebrile, not dehydrated and appeared co be improving clinically. Stool volume ranged fro m 285 to 420 ml/day. Stools were negative for reducing substances; stool virology and cu lture for bacteria fa iled to reveal the presence of pathogens. Metabolic control of the underlying ryrosinemia deteriorated with wide fluctuations in scrum tyrosine levels. The milk-free formula fed to the in fan t contained a mixture oflsomil (Ross Laboratories), 3200-AB (Mead-Johnson} and 80056 (Mead-Johnson ), balanced to provide essential amino acids at appropriate levels. Carbohydrate content was sucrose 7%. Feeds were discontinued and total parenteral nutrition recommenced, however, the loose, watery stools persisted.

E'\amination of prescribing 111forma·

Sorb ltol and d iarrhea

non available for the oral med1ca1mns made no mention of :-in osmmically active vehicle When ,pecific enquiries were made to the manufacturer it was learned that the sorbitol content of CalciumSando: syrup \\'as 0. 354 g/5 ml. The daily do,c of92 ml contamcd 6.5 g of sorhi tol representing an nsmt1t1c load ot' 16 mO,m per Jay The meJicatton was discontmued and replaced with calcium carbonat<.:. Watery d iarrhea ceased wnhin 12 hand feeds ll'erc recommenced 24 h later ll'tthout recurrence of diarrhea

DISCUSSION Sorb1tol is a hexahyd ric alcohol with

abou t half the sweetness of sucrOSl'. Its systemic toxici ty is vcrv low ( 3.4 ) even by the parenteral route ( 5,6). Small intestinal absorption of sorbitol is minimal ( 7 l. the majority of the drug reaching the large bowel Fcrmention by enteric bacteria further increases the osmolar load . lnge,tion of as little as 5 g can be detected hy excess breath hydrogen production ( 2 ). After an oral dose of 10 g, 71 ''o of adult subjects note mi ld gastrointesti nal distress with gas and bloating (8). A Cter 20 g. 57'';, develop abdominal cramps and diarrhea (H).

The Canad ian Society of Hospita l Pharmacists estimates that 31.5% of oral liquid pharmaceuticals marketed in Canada contain sorbitol (9). ln the two cases described the presence of sorbitol in the diet was not initially recognized and a number of investigative procedures were performed before the cause of the sym ptoms was established. In the fi rst case the symptoms induced by sorbitol ingestion mimicked an exacerbation of Crohn's disease. The unintention.il ad ministrauon of snrhitol to the second patient 111 the form of a drug \'Chicle resulted in d1ar-

Le sorbitol, une cause c ryptiquc de diarrhee RESUME: Le sorhitol est unc monosaccharinc diffici le a abwrbcr qui est largement uulist't' commt' succedanc du sucre ct comme vch1cule de medicament L'ingcst1on du s<1rhirol pt'Ut entrainer des troubles gastrointestmaux relics les crampcs ct ks diarrhccs. Nous prcsentons deux pat ients che:: q u i l'ingesuon non idcntificc de sor· hnol a pmduit de, sympti',mes 1111itant l'exacerbat1t1t1 d'un autre dcsordrt· ,ous·Jact·nt Le diagnostic correct peur ctrc manquc ou retardc parce quc lcs patients nc rcalisL'nt pas qu'ils absorben t k CtimpoM.: da ns les aliments 'sans sucrc'. D\1u 1rc par t, lcs re11,c1gnemcnts tourni, avec le, mt'.·dicamems n'inclucnt pas tnuinurs le sorhitol comme succt•dani• du sucre.

141

CATTO-SM! rH et al

rhc;i and ;i deterioration in tlw dicwry

control of plasma tyrosine levels.

ln summary, unrecognized sorbirnl

ingestion ~hould be kept in mind as ;i

pmcnti;il muse of di;irrhca when the cti-

ACK NOWLEDGEM ENTS: Dr AG Catro-Sm1th b tlw rcc1picnt nf an Alberta Children\ Hlhp1tal Fclk,w,h1p. The aurhnr~ thank Dr K Hegdc lt>r ,1llt,w1ng u, to p;1r11,1-patt· 1n the rnrc of p:tt1<'11t l, and Lauren Tokarek for typmg the manu,cnpt

REFER EN CES Gryhtisk1 JD Diarrhea Imm d1etct1c candit.·, N EnglJ Mc:d I%n.l7S:718.

l l lyamsJS. Sorhitol 1nwlcrancc An unapprcc1mcd cause tif functional gastrointestinal complaints. G;istrol'ntcrology J9HHH. 30-1 Reck SB. Chodo:. DJ Sorhitol induced diarrheal dines:, motkl ln1 J Clin

ology 1s not apparent ( 10,11). Sorbicol

ingestion can produce symptoms which

mimic the clinirnl features of other underlying disorders. The diagnosis of

sorhitol induced symptoms m;iy be

Pha rm;1eol Thcr Tt,x1,ol 1985 .2 l.-tO "\-'i 4 MacKen:1e KM. Hauck WN. \Vhcl·kr

AG, Roe FJC Thrce·gl'1wrn11on repnidut"t1on studv of r:us ingc,t1ng up 10 10'',, sorhitnl in the• diet and a brid rcviel\' of the roxicnlt,gicnl srntus ol ,orh1wl Br I Chem 'fox1rnl 1986;24- 191 200.

'i. Elli, F\V, Kr.int: JC Metabolism ,111d loXl<'ll\' ,tud1l'S with 111:mnitol and ,t,rh1tt1l 1n man and animnb J B1t1l Chem 1941.Hl.147-5-+

6 Scstnf1 L. An ernluauon of h1ochl'm1cal aspt·ct, of mtrnvenou, frunnsc, sorh1wl and xylitol admini,tration in man Acta An:w,thcs1ol Scand 198'i.l9 19-29

7 L1uwcr, A-M. Daunwrie C. Hcnquin JC. ln1c,unal absorruon t,t sorbi1ol :rnd

missed or delayed because patients J o

not appreciate that they arc ingesting the

compound in ~ugarlcss foods and drug

product information may not list its inclusion ;is a sweetener.

cffcns of n, ,1cutl' :1Jm1111,tr;111on on gluco,c homL'O>tnti, in normal rm,. Br .I Nutr 1985.51:5"\ 62 .

8 Jam NK. Rosenberg DB. Ulahannan MJ, Glasser MJ, Pitchumoni CS. Sorbitol intolerance in adults. AmJ Gastroentcrol 1985;80:678-81.

9 Naylor MJV Caloric and carbohydrate c~mtcnt of oral pharmaceutical rroducts in Canada The Canadian Society of Hospital PharmaciMs and Connaught Novo Ltd Willowdale: Connaught Novo Ltd, 1986.

10. Charney EB. Bodurth,1 JN. Intractable diarrhea associated with the usc of sorbitol. J Pediatr .1981 ;98: 157-8.

11 . Hill RE, Karnath RK. "Pink" diarrhea. Med J Aust 1982; I· 387-9.

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