Case Report Open Access
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Apr 28, 2008; 14(16): 2599-2601
Published online Apr 28, 2008. doi: 10.3748/wjg.14.2599
Extreme gastric dilation caused by chronic lead poisoning: A case report
Vesna Begovic, Darko Nozic, Clinic of Infectious and Tropical Diseases, Military Medical Academy, Crnotravska 17, Belgrade 11000, Serbia
Srdjan Kupresanin, Institute of Radiology, Military Medical Academy, Crnotravska 17, Belgrade 11000, Serbia
Dino Tarabar, Clinic of Gastroenterology, Military Medical Academy, Crnotravska 17, Belgrade 11000, Serbia
Author contributions: Begovic V and Nozic D contributed equally to this work and wrote the paper; Kuprtesanin S performed the radiological examination; Tarabar D performed the endoscopic examination and explained the data.
Correspondence to: Professor Darko Nozic, Clinic of Infectious and Tropical Diseases, Military Medical Academy, Crnotravska 17, Belgrade 11000, Serbia. darkonozic@yahoo.com
Telephone: +381-11-3609112
Fax: +381-11-2666164
Received: December 24, 2007
Revised: March 6, 2008
Published online: April 28, 2008

Abstract

Lead is a toxic metal that affects many organ systems and functions in humans. In the majority of adults, chronic lead poisoning comes from exposures to work places and can occur in numerous work settings, such as manufacturing, lead smelting and refinement, or due to use of batteries, pigments, solder, ammunitions, paint, car radiators, cable and wires, certain cosmetics. In some countries, lead is added to petrol. We present a rare case of gastric dilation caused by long-term petrol ingestion. A 16-year-old young man was admitted to our hospital due to a 6-mo history of exhaustion, dizziness, nausea, abdominal cramps and constipation. X-ray examination revealed dilated stomach descending into the pelvis and small bowel distension. After a long clinical observation, we found that the reason for the chronic lead poisoning of the patient was due to a 3-year history of petrol ingestion. The patient spontaneously recovered and stomach returned to its normal position and size. Lead poisoning should be taken into consideration in all unexplained cases of gastric dilation.

Key Words: Lead; Petrol; Stomach; Poisoning; Gastric dilation



INTRODUCTION

Lead is a toxic metal that affects many organ systems and functions in humans. In the majority of adults, chronic lead poisoning comes from exposures to work places and can occur in numerous work settings, such as manufacturing, lead smelting and refinement or due to use of batteries, pigments, solder, ammunitions, paint, car radiators, cable and wires, certain cosmetics[1]. In some countries, lead is added to petrol. Inorganic lead is absorbed from the respiratory or gastrointestinal tract. Approximately 30%-40% of inhaled lead is absorbed into the blood stream[2]. Gastrointestinal absorption varies depending on nutritional status and age. Iron is believed to impair lead uptake in the gut, while iron deficiency is associated with increased blood lead concentrations in children. Once absorbed, 99% of circulating lead is bound to erythrocytes for approximately 30-35 d (only 1% of absorbed lead is found in plasma and serum) and is dispersed into the soft tissues of liver, renal cortex, aorta, brain, lungs, spleen, teeth, and bones in the following 4-6 wk. The clinical manifestations can vary from individual to individual. Diagnosis of lead toxicity is mainly based on the elevated blood lead levels (BLL). There is a general correlation between toxic effects of lead and BLL. New data implicate that lower blood lead levels, previously considered normal, can cause cognitive dysfunction, neurobehavioral disorders, different neurological damages, hypertension and renal impairment[36].

Toxicity of petrol is usually associated with inhalation of vapor leading to dysfunction of the central nervous system. Ingestion of petrol by adults is rare and happens accidentally during siphoning of petrol tanks. The incidence of petrol ingestion in children is relatively low. An accidental ingestion of petrol causes acute symptoms of gastrointestinal tract including abdominal pain, nausea, vomiting and diarrhea. We report a rare case of extreme gastric dilation caused by long-term petrol ingestion.

CASE REPORT

A previously healthy 16-year-old young man was admitted to our hospital due to a 6-mo history of exhaustion, dizziness, nausea, abdominal cramps and constipation. He was not drug addictive. At admission to our hospital, he was pale, with slightly icteric eyes, normal heart and lungs, generalized abdomen tenderness, but no hepatosplenomegaly. Neurological examination was normal. Laboratory investigation revealed normocytic anemia, 117 g/L hemoglobin, 7 &mgr;mol/L iron (normal 11-30 &mgr;mol/L), 26 &mgr;mol/L bilirubin (normal 0-20 &mgr;mol/L), 21 &mgr;mol/L unconjugated bilirubin, 41 IU/L AST (normal 0-30 IU/L), 56 IU/L ALT (normal 0-41 IU/L). Blood tests showed that white blood cells, platelets, urea, creatinine, acid uric, albumin, HBsAg, anti-HCV, anti-HIV, and urine were normal or negative. Chest radiography and abdominal ultrasound were normal. X-ray examination of the stomach revealed extreme gastric dilation (Figure 1A). The stomach descended into the pelvis. Gastroscopy showed chronic erosive gastritis. Colonoscopy was normal. After supportive therapy, the patient was discharged without explanation for gastric dilation. Control hospitalization in our hospital was four months later. During that time, he was feeling well and had no abdominal pains. Physical examination at admission was normal. Laboratory investigations displayed that hemoglobin was decreased to 111 g/L and iron to 8 &mgr;mol/L while bilirubin was increased to 32 &mgr;mol/L (unconjugated 30 &mgr;mol/L). Red blood cells, white blood cells, aminotransferases, urea, creatinine, acid uric and urine returned to normal. Coombs test was negative. Stool examination was negative for parasites. X-ray examination of stomach was the same as in previous hospitalization. Then we intended to do more aggressive medical examinations but the patient told that he was selling petrol on the street before he had symptoms three years ago. It was an illegal work and the patient was afraid to admit it before. During the siphoning, he often swallowed a small amount of petrol. We, therefore, determined his lead blood level (BLL) which was 30 mcg/dL (normal < 10.0 mcg/dL). Urinary excretion of aminolevulinic acid was normal. It was obvious that the patient had chronic lead poisoning but we did not treat him because his condition was good due to no longer lead exposure. We saw the patient four years later during his military service. In that period, he sometimes felt nausea and paresthtesia in fingers and toys. Physical examination was normal. Laboratory analyses were normal except for an increased bilirubin value of 43 &mgr;mol/L (unconjugated 37 &mgr;mol/L). Serum lead concentration was normal (2.66 mcg/dL). X-ray examination revealed that his stomach retuned to its normal size and position (Figure 1B). Nerve conduction studies showed mixed sensory-motor polyneuropathy.

Figure 1
Figure 1 X-ray examination showing dilated stomach descending into the pelvis (A) and the stomach having returned to its normal size and position (B).
DISCUSSION

Lead is widely dispersed in the environment. In the world, the main sources of lead exposure are gasoline additives, food-can soldering, lead-based paints, ceramic glaze and drinking water systems, cosmetic and folk remedies. In literature, there are single reports on long-term lead exposure and few reports on lead poisoning from retained bullets[78]. Two-year consumption of homemade wine can cause lead poisoning[9]. Chronic lead poisoning has many symptoms and signs, including pains, numbness or tingling of the extremities, muscular weakness, headache, loss mood disorders, reduced sperm count, and abnormal sperm. Our patient had mixed sensory-motor polyneuropathy and anemia. Lead has effects on cell membrane, interfering with various energy and transport systems, which may explain why it can shorten erythrocyte survival time and cause anemia. Peripheral blood smear could show basophilic stippling in several red cells from a patient with lead poisoning. Lead can interfere with the heme synthetic pathway especially enzyme delta-aminolevulinic acid dehydratase causing accumulation of aminolevulinic acid and increasing urinary excretion. Since aminolevulinic acid could be detected in urine only when BLL exceeds 35 mcg/dL, it is not a marker of low lead toxicity[10]. Our patient had a lower BLL and normal urinary aminolevulinic acid excretion. Gastrointestinal manifestations of lead poisoning include chronic or recurrent abdominal pain, nausea, vomiting, constipation, bloating, anorexia and weight loss[1113]. These symptoms associated with anemia could lead to toxic etiology especially in the absence of other causes. Our patient had a 6-mo history of unexplained abdominal cramps after stopping petrol ingestion. Generally, all toxic effects of petrol are associated with vapor inhalation. A few minutes after vapor inhalation, symptoms resembling alcohol intoxication (dizziness, excitement, incoordination, etc) occur[14]. Accidental ingestion of petrol is very rare and may cause symptoms of acute gastrointestinal irritation. The main health effect associated with petrol exposure is pneumonitis, resulting from pulmonary aspiration of vomitus following ingestion[1516]. No report on long-term petrol ingestion is available. In addition to a number of potentially neurotoxic chemicals (benzene, toluene, ethyl benzene, n-hexane, etc), lead in petrol is a main additive. Since 2000 in most countries, petrol has only been commercially available in unleaded form, but our patient in Serbia, was selling petrol with lead. When lead is inhaled or absorbed through skin, it is toxic to humans. We could not find any other similar case of extreme gastric dilation caused by lead. Srebocan et al[17] have described gastric dilation in a dog with lead poisoning. The pathogenesis of such dilation remains uncertain, but it seems that lead has a paralytic action on gastrointestinal system. Normal gastrointestinal motor function is a complex series of events that require coordination of the sympathetic and parasympathetic nervous systems, neurons within the stomach and intestine, and the smooth muscle cells of the gut. Abnormalities of this process can delay gastric emptying (gastric stasis) and gastric tonus (gastric ptosis). It seems that reduction of heme body pool caused by lead impairs cyto-dynamics impairing nerve conduction and paralysis of stomach. Diagnostic evaluation of adults with potential lead toxicity includes medical and environmental history, searching for potential sources of exposure, signs and symptoms of lead poisoning, and laboratory examination. BLL is essential for the diagnosis of lead poisoning. However, BLL measures current exposure to lead, but lead may also be incorporated into bone due to prior exposures not shown in BLL until this bone-lead becomes "mobilized" through pregnancy or fracture healing. X-ray fluorescence (XRF) equipment can be used to measure lead concentrations in bones[18]. The standard elevated BLL is above 25 mcg/dL in adults and above 10 mcg/dL in children. BLL was 30 mcg/dL in our patient ten months after stopping petrol ingestion. The decision to treat it with chelating agents depends on a number of factors, including presence of lead-related symptoms, current BLL, duration of excessive lead exposure and symptoms. Patients with BLL over 80 mcg/dL should be treated[19]. Chelation therapy is recommended for individuals with blood lead levels between 40 mcg/dL and 80 mcg/dL if they have lead-related symptoms. The main chemicals used in chelation therapy are ethylenediaminetetraacetic acid (EDTA) administered through injection and oral drug dimercaprol (BAL). Since our patient had a lower BLL, he could recover by avoiding exposure to lead.

In conclusion, this case illustrates that lead poisoning should be taken into consideration in all unexplained cases of gastric dilation.

Footnotes

Peer reviewer: Hitoshi Asakura, Director, Emeritus Professor, International Medical Information Center, Shinanomachi Renga Bldg.35, Shinanomachi, Shinjukuku, Tokyo 160-0016, Japan

References
1.  Patrick L. Lead toxicity, a review of the literature. Part 1: Exposure, evaluation, and treatment. Altern Med Rev. 2006;11:2-22.  [PubMed]  [DOI]  [Cited in This Article: ]
2.  Philip AT, Gerson B. Lead poisoning--Part I. Incidence, etiology, and toxicokinetics. Clin Lab Med. 1994;14:423-444.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Philip AT, Gerson B. Lead poisoning--Part II. Effects and assay. Clin Lab Med. 1994;14:651-670.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Shih RA, Glass TA, Bandeen-Roche K, Carlson MC, Bolla KI, Todd AC, Schwartz BS. Environmental lead exposure and cognitive function in community-dwelling older adults. Neurology. 2006;67:1556-1562.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  Lin JL, Lin-Tan DT, Hsu KH, Yu CC. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes. N Engl J Med. 2003;348:277-286.  [PubMed]  [DOI]  [Cited in This Article: ]
6.  Marsden PA. Increased body lead burden--cause or consequence of chronic renal insufficiency? N Engl J Med. 2003;348:345-347.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  McQuirter JL, Rothenberg SJ, Dinkins GA, Manalo M, Kondrashov V, Todd AC. The effects of retained lead bullets on body lead burden. J Trauma. 2001;50:892-899.  [PubMed]  [DOI]  [Cited in This Article: ]
8.  Akhtar AJ, Funnye AS, Akanno J. Gunshot-induced plumbism in an adult male. J Natl Med Assoc. 2003;95:986-990.  [PubMed]  [DOI]  [Cited in This Article: ]
9.  Mangas S, Visvanathan R, van Alphen M. Lead poisoning from homemade wine: a case study. Environ Health Perspect. 2001;109:433-435.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  Somashekaraiah BV, Venkaiah B, Prasad AR. Biochemical diagnosis of occupational exposure to lead toxicity. Bull Environ Contam Toxicol. 1990;44:268-275.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Janin Y, Couinaud C, Stone A, Wise L. The "lead-induced colic" syndrome in lead intoxication. Surg Annu. 1985;17:287-307.  [PubMed]  [DOI]  [Cited in This Article: ]
12.  Hart SP, McIver B, Frier BM, Agius RM. Abdominal pain and vomiting in a paint stripper. Postgrad Med J. 1996;72:253-255.  [PubMed]  [DOI]  [Cited in This Article: ]
13.  Jongnarangsin K, Mukherjee S, Bauer MA. An unusual cause of recurrent abdominal pain. Am J Gastroenterol. 1999;94:3620-3622.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Wang CC, Irons GV Jr. Acute gasoline intoxication. Arch Environ Health. 1961;2:714-716.  [PubMed]  [DOI]  [Cited in This Article: ]
15.  Banner W Jr, Walson PD. Systemic toxicity following gasoline aspiration. Am J Emerg Med. 1983;1:292-294.  [PubMed]  [DOI]  [Cited in This Article: ]
16.  Litovitz T, Greene AE. Health implications of petroleum distillate ingestion. Occup Med. 1988;3:555-568.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Srebocan E, Pompe-Gotal J, Harapin I, Capak D, Butkovic V, Stanin D. Lead poisoning in a dog--a case report. Berl Munch Tierarztl Wochenschr. 2001;114:216-217.  [PubMed]  [DOI]  [Cited in This Article: ]
18.  Hu H, Shih R, Rothenberg S, Schwartz BS. The epidemiology of lead toxicity in adults: measuring dose and consideration of other methodologic issues. Environ Health Perspect. 2007;115:455-462.  [PubMed]  [DOI]  [Cited in This Article: ]
19.  Fischbein A. Occupational and environmental exposure to lead. Philadelphia: Lippincott-Raven Publishers 1998; 973.  [PubMed]  [DOI]  [Cited in This Article: ]