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undertaken in the noncompliant patient, as requirements for so-

dium restriction and diuretic therapy generally continue after

shunting. Finally, candidates for OLT should also be excluded,

given the general prohibition against abdominal surgery in these

patients, as well as the significant risk of morbidity and mortality

after shunt placement. Our patients case clearly illustrates the

latter point.

Alternative management options for the patient with refractoryascites include OLT, large volume paracentesis (5, 6), and tran-

sjugular intrahepatic portosystemic shunt (9). OLT is definitive

treatment for refractory ascites. UNOS data from 1995 indicate an

overall 1-yr survival of 84% after OLT, which is the only available

therapy that improves both patient quality of life and survival. The

availability of alternative therapies mandate that the risks and

benefits of PVS be carefully weighed before its use is advocated.

Reprint requests and correspondence: Paul Martin, M.D., UCLA CHS77-132 CHS, UCLA School of Medicine, Los Angeles, CA 90045-1744.

REFERENCES

1. Forns X, Gines A, Arroyo V. Management of ascites and renal failurein cirrhosis. Sem Liver Dis 1994;14:8296.

2. LeVeen HH, Christoudias G, Moon IP, et al. Peritoneovenous shunting

for ascites. Ann Surg 1974;180:58091.3. Shah KH, Stulic JP, Hoy GR, et al. Coronary sinus perforation from

placement of a LeVeen shunt in a child. Chest 1982;82:1979.4. Bories P, Compean G, Michel H, et al. The treatment of refractory

ascites by the LeVeen shunt; a multi-center controlled trial. J Hepatol

1986;3:2128.5. Stanley MM, Ochi S, Lee KK, et al. Peritoneovenous shunting as

compared with medical treatment in patients with alcoholic cirrhosis

and massive ascites. N Engl J Med 1989;321:16328.6. Gines P, Arroyo V, Vargas V, et al. Paracentesis with intravenous

infusion of albumin as compared with peritoneovenous shunting incirrhosis with refractory ascites. N Eng J Med 1991;325:82935.

7. Moscovitz M. The peritoneovenous shunt: Expectations and reality.

Am J Gastroenterol 1990;85:91729.8. Scholz DG, Nagorney DM, Lindor KD. Poor outcome from peritone-

ovenous shunts for refractory ascites. Am J Gastroenterol 1989;84:5403.

9. Ochs A, Rossle M, Haag K, et al. The transjugular intrahepatic porto-

systemic stent-shunt procedure for refractory ascites. N Eng J Med1995;332:11927.

A CASE OF HEPATOCELLULAR CARCINOMA

ASSOCIATED WITH TROUBLESOME

HYPOGLYCEMIA: MANAGEMENT BY

CYTOREDUCTION USING PERCUTANEOUS

ETHANOL INJECTION

S. Saigal, M.D., D.M., H.P. Nandeesh, M.D., D.M.,V. Malhotra, M.D., and S.K. Sarin, M.D., D.M.

Department of Gastroenterology, G.B. Pant Hospital,New Delhi, India

Hypoglycemia is a well known paraneoplastic manifestation

of hepatocellular carcinoma. However, hypoglycemia as the

first presentation is extremely uncommon. We herein report a

case of HCC presenting with severe, uncontrollable hypogly-

cemia that was managed with percutaneous ethanol injection

therapy. (Am J Gastroenterol 1998;93:13801381. 1998 by

Am. Coll. of Gastroenterology)

INTRODUCTION

Hypoglycemia is a well known paraneoplastic manifestation of

hepatocellular carcinoma (HCC) (1). However, hypoglycemia as

the first presentation of HCC is very uncommon. Except for

glucose infusion, no definitive treatment for correcting hypogly-

cemia is known. We report here, probably for the first time,

percutaneous ethanol injection as a palliative treatment for treating

HCC-associated refractory hypoglycemia.

CASE REPORTA 24-yr-old woman was admitted with a history of recurrent

episodes of unconsciousness over the previous 2 months. During

these episodes, she was discovered to be hypoglycemic; she would

regain normal sensorium after i.v. 25% dextrose. She was anicteric

and there were no stigmata of chronic liver disease. The liver was

enlarged 6 cm below the right costal margin, with a hard, nodular

surface. Minimal ascites was detected. The serum AST and ALT

were 130 IU/L and 106 IU/L, respectively (normal, 40 IU/L).

The serum alkaline phosphatase was 261 IU/L (normal, 170

IU/L) and serum bilirubin was normal. The serum alpha fetopro-

tein was raised to 14,674 ng/ml (normal, 20 ng/ml). She tested

negative for HBsAg and anti-HCV.

A CT scan (Fig. 1) showed a large mass in the right lobe of theliver and multiple nodular metastatic deposits in the lungs. A

US-guided fine needle aspiration was diagnostic of HCC. During

her hospital stay, she developed frequent hypoglycemic episodes

with neuroglycopenic symptoms. She was kept on a 24-h infusion

of 20% dextrose, which intermittently needed to be supplemented

with 50% glucose. The lowest blood sugar value obtained was 15

mg/dl. The serum insulin level during one of the hypoglycemic

attacks was 3.6 IU/ml (normal, 0 to 30 IU/ml). She showed no

response to a high dose of vitamin K and tamoxifen. Because of her

worsening hypoglycemia, she was offered a palliative cytoreduc-

tion therapy using percutaneous ethanol injection (PEI). The PEI

was done under US guidance, as described previously (2), and 10

Received Sep. 12, 1997; accepted Apr. 24, 1998.

FIG 1. Contrast-enhanced CT scan of the abdomen showing a large massin the right lobe of the liver.

1380 BRIEF CASE REPORTS AJG Vol. 93, No. 8, 1998

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ml of absolute alcohol was injected on three occasions on a weekly

basis. Following the third session of PEI, the hypoglycemic attacks

became infrequent and the intravenous glucose requirement mark-

edly decreased.

DISCUSSION

The reported prevalence of hypoglycemia in HCC varies from

4% in North American cases to 27% in Chinese patients fromHongkong (3). HCC-associated hypoglycemia has been divided

into two types (4). In the more common type A tumors, which are

poorly differentiated, hypoglycemia of mild to moderate severity is

a late event. In contrast, in the less common type B tumors, which

are well differentiated and slowly growing, hypoglycemia is se-

vere, occurs early, and is difficult to control. Our patient clearly

had a type B tumor.

Types A and B hypoglycemia probably have different mecha-

nisms. Production of insulin or insulin-like substances has not been

substantiated as yet. The serum insulin is usually low or undetect-

able during the hypoglycemic attack. Recently, more emphasis has

been placed on the role of insulin-like growth factor II (IGF-II) as

an important mediator of hypoglycemia (5). Also, there are reportsof raised Pro-IGF-II level and its abnormal processing to IGF-II in

patients of HCC with hypoglycemia (5, 6). Such hormonal play

may be more likely in type B tumors.

There is no definitive treatment for refractory hypoglycemia

occurring with unresectable HCC. We used an innovative approach

of cytoreduction using PEI, which probably led to a reduction in

the amount of hormonal mediators released by the tumor. As a

result, our patient showed symptomatic improvement and a de-

crease in the daily glucose requirement. In conclusion, this initial

observationthat PEI could be useful in tackling tumor hypogly-

cemiahighlights cytoreduction as a new approach for treating

the paraneoplastic syndromes associated with HCC.

REFERENCES

1. Schiff L, Schiff ER. Diseases of the liver, 7th edition. Philadelphia: J.B.

Lippincott, 1993:123676.

2. Sarin SK, Sreenivas DV, Saraya A, et al. Improved survival with

percutaneous ethanol injection in patients with large hepatocellular

carcinoma. Eur J Gastroenterol Hepatol 1994;6:9991003.

3. Marchesini G, Bianchi G. Carbohydrate metabolism in hepatocellular

carcinoma: Where does the glucose go? Hepatology 1989;10:2535.

4. McFadzean AJS, Yeung RTT. Hypoglycemia in primary carcinoma of

liver. Arch Intern Med 1956;98:72031.

5. Hunter SJ, Daughaday WH, Callender ME, et al. A case of hepatoma

associated with hypoglycemia and over production of IGFII (E-21):

Beneficial effects of treatment with growth hormone and intrahepatic

adriamycin. Clin Endocrinol 1994;41:397401.6. Daughaday WH, WU JC, Lee SD, et al. Abnormal processing of

pro-IGF-II in patients with hepatoma and in some hepatitis B virus

antibody-positive asymptomatic individuals. J Lab Clin Med 1990;116:

55562.

ESOPHAGOGASTRIC FISTULA: A COMPLICATION

OF CROHNS DISEASE

Case Report and Review of the Literature

MAJ James C. Rholl, M.D., Robert T. Yavorski, M.D.,COL Christopher P. Cheney, M.D., Ph.D., and

COL Roy K.H. Wong, M.D.

Department of Gastroenterology, Walter Reed Army Medical

Center, Washington, DC and Uniformed Services University of

the Health Sciences, Bethesda, Maryland

Esophagogastric fistula formation as a complication of

esophageal Crohns has been reported in only one case in the

literature. In addition, only eight cases of esophageal fistulae ofany type have been reported in the setting of Crohns disease.

Unlike the more often described superficial, aphthous disease

of the esophagus, response of fistulae to medical therapy has

been disappointing, and recurrence and progression are likely.

Surgery remains the primary modality for refractory disease.

The roles of salicylates, antibiotics, immunosuppressive agents,

sealants, and intralesional steroid injections have not been well

defined. We present a case of severe, refractory Crohns dis-

ease with fistula formation between the esophagus and stom-

ach, and concomitant involvement of the oropharynx, duode-

num, terminal ileum, and cecum. (Am J Gastroenterol 1998;

93:13811383. 1998 by Am. Coll. of Gastroenterology)

INTRODUCTION

Esophageal involvement in Crohns disease (CD) is uncommon.

Since the first description of regional esophagitis by Franklin

and Taylor in 1950 (1), there have been relatively few cases

reported. The true prevalence is not known. Recent reviews have

suggested that up to 1.8% of adults and 6.5% of pediatric patients

with CD may have involvement of the esophagus (2). Two pro-

spective studies in children with documented CD reported evi-

dence of esophageal disease in 25.8% (3) and 42.5% (4), respec-

tively. Whether such findings universally represent esophageal CD

remains controversial (5). Establishing the specific diagnosis of

esophageal CD can be difficult. The symptoms and histopathology

are often nonspecific, and the characteristic granulomas and giant

cells are found in 25% (5). The majority of patients have had

concomitant ileocolonic disease, which is often severe (6). Rarely,

patients may present with recognizable disease limited to the

esophagus (7).

Most reports of esophageal CD describe superficial lesions with

nonspecific inflammation, erosions, or shallow ulcerations (1).

Such lesions are typically responsive to treatment with corticoste-

roids, although clinical relapses are likely (6). The precise role of

antisecretory medications in such cases has yet to be defined. Beck

et al. described a patient with symptomatic response and healing of

esophageal ulcerations after treatment with proton pump inhibitors

(2). Others, however, have reported persistent endoscopic and

histological disease activity, despite symptomatic response using

omeprazole (2, 8).

Rarely, esophageal CD may be complicated by stricture forma-

tion and fistulae. Such complicated esophageal CD has been less

responsive to medical therapy than have the more typical superfi-

cial lesions. Surgery has remained the primary treatment modality

for refractory disease. In this communication, we present a case of

an esophagogastric fistula in a patient with previously documented

Crohns disease of the cecum, terminal ileum, duodenum, and

oropharynx.

Received July 18, 1997; accepted Apr. 24, 1998.

AJG August 1998 BRIEF CASE REPORTS 1381