Skip to main content
Annals of Saudi Medicine logoLink to Annals of Saudi Medicine
. 2015 Mar-Apr;35(2):165–167. doi: 10.5144/0256-4947.2015.165

Unusual presentation of arsenic poisoning in a case of celiac disease

Rana M Hasanato a, AbdulKareem M Almomen b,
PMCID: PMC6074129  PMID: 26336025

Abstract

Arsenic poisoning may occur from sources other than drinking water such as rice, seafood, or insecticides. Symptoms and signs can be insidious, non-specific, atypical, and easily overlooked. We present a 39-year-old woman with celiac disease who was on gluten-free diet for 8 years and presented with diarrhea, headache, insomnia, loss of appetite, abnormal taste, and impaired short-term memory and concentration, but with no skin lesions. Arsenic concentration in her 24-hour urine was 682.77 μg/g creatinine (normal <15). She responded very well to chelation therapy with dimercaptosuccinic acid given orally and recovered within 2 weeks. The suspected source of arsenic poisoning was rice, as drinking contaminated ground water is not known in Saudi Arabia and she had not taken seafood. Therefore, arsenic poisoning should be suspected based on the meticulous medical history in cases of patients with celiac disease whose main food is rice and who present with unusual symptoms.


Arsenic poisoning is known to occur in areas with contaminated drinking ground water such as Bangladesh, India, Taiwan, and United States.14 Other sources may include certain industries, particularly, carpenters dealing with pressure-treated wood that has been treated with arsenic-containing wood preservative. Other sources include food (sea food and rice), insecticides, and drugs.517 Arsenic poisoning can easily be overlooked because of atypical symptoms and signs, lack of awareness, and unavailability of the arsenic level test. We present a case of arsenic poisoning who presented with atypical signs and symptoms and was overlooked, and treatment was delayed for several months. We present this case to illustrate that such cases can be easily diagnosed and treated if arsenic poisoning is suspected and not overlooked.

CASE

Our case is a 39-year-old housewife, known with celiac disease for 8 years, who presented with progressive fatigue, profound watery diarrhea (12 times/d), palpitation, dry mouth, poor appetite, poor taste, sleeplessness, impaired concentration, and short-term memory. She was on gluten-free diet (mainly rice and corn derivatives) and vitamin and mineral supplements. She had not eaten sea food for almost 1 month prior to this admission. She continued to have regular menstrual periods. She was married with 4 healthy children. She had no other illnesses, and her medical history was unremarkable. No other family members had celiac disease or similar symptoms. On physical examination, she looked ill, exhausted, and anxious. Her height was 160 cm, weight 47 kg, pulse 110/min, regular, and blood pressure 110/70 mm Hg. No pallor or skin lesions were observed, and her abdominal, cardiovascular, and neurological examinations were normal. At this point, we thought that she was not compliant with her gluten-free diet, and probably she had a mixture of multiple deficiencies (e.g., calcium, magnesium, zinc, iron, vitamin B12) and depression. Laboratory tests were as follows: white blood cells 8.9×109/L, Hb 94 g/L, mean corpuscular volume 76.6 fl, platelets 397×106/L, erythrocyte sedimentation rate 41 mm, fasting glucose 4.7 mmol/L, urea 3.6 mmol/L, creatinine 40 μmol/L, albumin 31 g/L, globulins 36 g/L, total bilirubin 5 μmol/L, alkaline phosphatase 153 U/L, alanine aminotransferase 70 U/L, aspartate aminotransferase 30 U/L, gamma glutamyl transferase 25 U/L, zinc 7.3 μmol/L (normal 7.65–22.9), corrected calcium 2.29 mmol/L, magnesium 0.9 mmol/L, ferritin 97.2 ng/mL, vitamin B12 157.8 pmol/L, gliadin antibodies immunoglobulin (Ig) G 114 (positive >20), and anti-human tissue transglutaminase IgA 53 (positive >20). IgA anti-gliadin, anti-endothelium, and anti-reticulin were negative. Patient was started on intravenous fluids and 24-hour urine were collected and sent to Micro Trace Minerals (Micro Trace Minerals GmbH, Rohrenstrasse-91217, Hersbruck, Germany, www.microtrace.de) for metal analysis. The results of the 24-hour urine showed arsenic concentration 682.77 μg/g creatinine (normal <15). Therefore, the diagnosis of arsenic poisoning was made, and the patient was started on chelation therapy with dimercaptosuccinic acid 30 mg/kg orally every 8 hours along with multivitamin and mineral supplements for 3 days. Her chemistry tests (liver functions, kidney functions, calcium, magnesium, zinc, and copper) were monitored twice/d. She showed a rapid response with gradual improvement of her symptoms over the next 2 weeks, and a repeat of arsenic concentration in the 24-hour urine was 26 μg/g and 12 μg/g creatinine after 7 days and 2 weeks, respectively. The source of arsenic poisoning could not be identified, but rice was the suspected source.

Other possible sources could be insecticides, pressure-wood furniture, supplements, or cosmetics. Drinking water is not suspected because the main water supply is desalination or mineral water. Arsenic is not known in well water in Saudi Arabia.

DISCUSSION

Arsenic is a naturally occurring toxic metalloid that combines with other elements such as oxygen, sulfur, chloride, hydrogen, and carbon.18 Due to its poisonous properties, arsenic has been used throughout the history as a homicidal and suicidal poison.19,20 In the past century, arsenic became very important insecticide, herbicide, and algaecide.7 Besides, arsenic is used in several industries such as copper smelting, wood preservation, and medicine. Arsenic trioxide is currently used in the treatment of acute promyelocytic leukemia.9,10 Exposure to arsenic occurs through drinking water from contaminated wells, inhaling smoke from pressure-treated wood, or inhaling vapors from insecticides, herbicides, algaecides or drugs. High levels of arsenic has been found recently in seafood, particularly bivalves and rice. Exposure to arsenic leads to several health problems that affect the gastrointestinal tract, respiratory system, cardiovascular system, nervous system, and skin.1826 Several malignancies have been attributed to arsenic such as cancer of the skin, bladder, and lung; cancers are caused due the strong carcinogenicity of arsenic.2126 Patients with celiac disease are at a high risk of arsenic exposure, because their gluten-free diet is composed mainly of rice.1317,27 Our patient is known with celiac disease who is compliant with gluten-free diet, consuming abundance of rice. Arsenic from seafood was excluded, because she had a poor appetite and did not take any seafood for 1 month prior to admission. Other causes cannot be excluded such as inhalation of vapors from insecticides, pressure-treated wood, and may be some cosmetics. In addition, arsenic may contaminate other grains and supplements. Our patient was unusual, because she lacked classical skin lesions, and the other symptoms were non-specific. Arsenic concentration in the urine is more reliable because blood levels are normal in persons with chronic arsenic poisoning.28,29 She responded very well and rapidly to chelation therapy with oral DMSA, which is a safe agent for chelation therapy of heavy metals.3032 We conclude that exposure to arsenic may not be rare, and that it has to be suspected and looked for in high risk persons

In conclusion, chronic arsenic poisoning can present with atypical signs and symptoms. It should be suspected in high risk persons based on their health status, occupation, diet, and life style.

Footnotes

Conflict of interest

None.

REFERENCES

  • 1.Argos M, Kalra T, Rathouz P, Chen Y, Pierce B, Parvez F, et al. Arsenic exposure from drinking water, and all-cause and chronic-disease mortalities in Bangladish (HEALS): a prospective cohort study. Lancet. 2010;376:252–8. doi: 10.1016/S0140-6736(10)60481-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Mitra S, Guha Mazumder D, Basu A, Block G, Haque R, Samanta S, et al. Nutritional factors and susceptibility to arsenic-caused skin lesions in West Bengal, India. Environ Health Perspect. 2004;112:1104–9. doi: 10.1289/ehp.6841. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Chang C, Ho S, Tsai S, Yang C. Ischemic heart disease mortality reductuion in an arsenosis-endemic area in Southwestern Taiwan after a switch in the tap-water supply system. J Toxicol Environ Health. 2004;67:1353–61. doi: 10.1080/15287390490471451. [DOI] [PubMed] [Google Scholar]
  • 4.United States Geological Survey. Arsenic in ground water in the United States. Reston, VA: 2005. [accessed 2009 September 14]. updated 2009 June 16. Available from: http://water.usgs.gov/nawaqa/trace/pubs/geo-v46n11/fig3.html. [Google Scholar]
  • 5.Weis P, Weis J, Coohill Toxicity to estuarine organisms of leachates from chromated copper arsenate treated wood. Arch Environ Contam Toxico. 1991;20:118–24. doi: 10.1007/BF01065337. [DOI] [PubMed] [Google Scholar]
  • 6.Baptist D, Leslie N. Children playing with poison: Arsenic exposure from CCA-treated wood. J Nurse Practitioners. 2008;4:48–53. [Google Scholar]
  • 7.Jones K, Huang WH. Evaluation of toxicity of the pesticides, chlorpyrifos and arsenic, in the presence of compost humic substances in aqueous systems. J Hazardous Materials B. 2003;103:93–105. doi: 10.1016/s0304-3894(03)00227-9. [DOI] [PubMed] [Google Scholar]
  • 8.Chakraborti D, Mukherjee SC, Saha KC, Chaudhury UK, Rahman MM, Sengupta MK. Arsenic toxicity from homeopathic treatment. J Toxicol Clin Toxicol. 2003;41:963–7. doi: 10.1081/clt-120026518. [DOI] [PubMed] [Google Scholar]
  • 9.Antman KH. Introduction: the history of arsenic trioxide in cancer therapy. The Oncologist. 2001;6:1–2. doi: 10.1634/theoncologist.6-suppl_2-1. [DOI] [PubMed] [Google Scholar]
  • 10.Iland HJ, Seymour JF. Role of arsenic trioxide in acute promyelocytic leukemia. Curr Treat Options Oncol. 2013;14:170–84. doi: 10.1007/s11864-012-0223-3. [DOI] [PubMed] [Google Scholar]
  • 11.Liu J, Lu Y, Wu Q, Goyer RA, Waalkes MP. Mineral arsenicals in traditional medicines: orpiment, realgar, and arsenolite. JPET. 2008;326:363–8. doi: 10.1124/jpet.108.139543. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Barak J, Hosgood HD. Seafood arsenic: implications for human risk assessment. Regul Toxicol Pharmacol. 2007;47:204–12. doi: 10.1016/j.yrtph.2006.09.005. [DOI] [PubMed] [Google Scholar]
  • 13.Bae M, Watanabe C, Inaoka T, Sekiyama M, Sudo N, Bokul MH, Ohtsuka R. Arsenic in cooked rice in Bangladesh. Lancet. 2002;360:1839–40. doi: 10.1016/S0140-6736(02)11738-7. [DOI] [PubMed] [Google Scholar]
  • 14.Williams PN, Raab A, Feldmann J, Meharg AA. Market basket survey shows elevated levels of As in South Central U.S. processed rice compared to California: consequences for human dietary exposure. Environ Sci Technol. 2007;41:2178–83. doi: 10.1021/es061489k. [DOI] [PubMed] [Google Scholar]
  • 15.Jorhem L, Astrand C, Sundström B, Baxter M, Stokes P, Lewis J, Grawé KP. Elements in rice from the Swedish market: 1. Cadmium, lead and arsenic (total and inorganic) Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008;25:284–92. doi: 10.1080/02652030701474219. [DOI] [PubMed] [Google Scholar]
  • 16.Sun GX, Williams PN, Carey AM, Zhu YG, Deacon C, Raab A, Feldmann J, Islam RM, Meharg AA. Inorganic arsenic in rice bran and its products are an order of magnitude higher than in bulk grain. Environ Sci Technol. 2008;42:7542–46. doi: 10.1021/es801238p. [DOI] [PubMed] [Google Scholar]
  • 17.Rahman MA, Hasegawa H. High levels of inorganic arsenic in rice in areas where arsenic-contaminated water is used for irrigation and cooking. Sci Total Environ. 2011;409:4645–55. doi: 10.1016/j.scitotenv.2011.07.068. [DOI] [PubMed] [Google Scholar]
  • 18.U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry. Toxicological profile for arsenic. Atlanta GA: 2007. [accessed 2008 January 14]. Updated 2007 August. Available from: http://atsdr.cdc.gov/toxprofils/tp2.html. [Google Scholar]
  • 19.Massey EW, Wold D, Heyman A. Arsenic: homicidal intoxication. South Med J. 1984;77:848–51. [PubMed] [Google Scholar]
  • 20.Yilmaz Y, Armagan E, Olmez O, Esen M, Alkis N, Dolar E. Acute arsenic self-poisoning for suicidal purpose in a dentist: a case report. Hum Exp Toxicol. 2009;28:63–5. doi: 10.1177/0960327108097432. [DOI] [PubMed] [Google Scholar]
  • 21.Hughes MF, Beck BD, Chen Y, Lewis AS, Thomas DJ. Arsenic Exposure and Toxicology: A Historical Perspective. Toxicol Sci. 2011;123:305–32. doi: 10.1093/toxsci/kfr184. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Mazumder G. Chronic arsenic toxicity: clinical features, epidemiology, and treatment: experience in West Bengal. J Environ Sci Health. 2003;38:141–63. doi: 10.1081/ese-120016886. [DOI] [PubMed] [Google Scholar]
  • 23.Tsuchiya K. Various effects of arsenic in Japan depending on type of exposure. Environ Health Perospect. 1977;19:35–42. doi: 10.1289/ehp.771935. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.Ratnaike RN. Acute and chronic arsenic toxicity. Postgrad Med J. 2003;79:391–396. doi: 10.1136/pmj.79.933.391. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Chen CJ, Chen CW, Wu MM, Kuo TL. Cancer potential in liver, lung, bladder and kidney due to ingested inorganic arsenic in drinking water. Br J Cancer. 1992;66:888–92. doi: 10.1038/bjc.1992.380. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26.Binder HJ, Solitare GB, Spiro HM. Neuromuscular disease in patients with steatorrhoea. Gut. 1967;8:605–11. doi: 10.1136/gut.8.6.605. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Murray JA. The widening spectrum of celiac disease. Am J Clin Nutr. 1999;69:354–65. doi: 10.1093/ajcn/69.3.354. [DOI] [PubMed] [Google Scholar]
  • 28.Valentine JL, Kang HK, Spivey G. Arsenic levels in human blood, urine, and hair in response to exposure via drinking water. Environ Res. 1979;20:24–32. doi: 10.1016/0013-9351(79)90082-3. [DOI] [PubMed] [Google Scholar]
  • 29.Abdelghani AA, Anderson AC, Jaghabir M, Mather F. Arsenic levels in blood, urine, and hair of workers applying monosodium methanearsonate (MSMA) Arch Environ Health. 1986;41:163–9. doi: 10.1080/00039896.1986.9935772. [DOI] [PubMed] [Google Scholar]
  • 30.Miller AL. Dimercaptosuccinic Acid (DMSA), A non-toxic, water-soluble treatment for heavy metal toxicity. Altern Med Rev. 1998;3:199–207. [PubMed] [Google Scholar]
  • 31.Shum S, Whitehead J, Vaughn L, Shum S, Hale Chelation of organoarsenate with dimercaptosuccinic acid. Vet Hum Toxicol. 1995;37:239–42. [PubMed] [Google Scholar]
  • 32.Bradberry S, Sheehan T, Vale A. Use of oral dimercaptosuccinic acid (succimer) in adult patients with inorganic lead poisoning. Q J Med. 2009;102:721–32. doi: 10.1093/qjmed/hcp114. [DOI] [PubMed] [Google Scholar]

Articles from Annals of Saudi Medicine are provided here courtesy of King Faisal Specialist Hospital and Research Centre

RESOURCES