Q J Med 2004; 97: 105-106
© Association of Physicians 2004; all rights reserved.
Correspondence |
Flatulence and carpopedal spasm: more than social embarrassment
Sir,A 61-year-old female of mixed Asian and African descent was admitted to our institution in December 2001, because of carpopedal spasms. She had been well until 13 months prior to admission, when she began to lose weight progressively, to a total of 20 pounds. She denied any loss of appetite, change in vision or bleeding. On examination, her vital signs were stable. Her abdomen was unremarkable. There were spasms of her hands and feet, and slight ankle oedema. Her stools were negative for occult blood on many occasions. Her blood results were as follows: sodium 134 mmol/l, chloride 104 mmol/l, potassium 3.6 mmol/l, bicarbonate 20 mmol/l, blood urea nitrogen 2.28 mmol/l (8 mg/dl), creatinine 26 µmol/l (0.3 mg/dl), calcium 1.35 mmol/l (5.4 mg/dl), albumin 26 g/l, haemoglobin 87 g/l with an MCV of 62 fl, white blood cell count 7000/mm3, phosphate 1.23 mmol/l (3.8 mg/dl), and a prothombin time of 15 s (N 11–13).
An electrocardiogram revealed sinus bradycardia at 60 bpm and a prolonged QT interval. Intravenous calcium gluconate was administered. Serum 25-hydroxy vitamin D was 12.48 nmol/l (N 20–200). Vitamins D and K were administered. The patient denied ever having diarrhoea or any loose bowel movements. She had severe flatulence that was persistently foul-smelling, causing social embarrassment. She was evaluated for coeliac sprue. Her serum antigliadin antibodies, both IgG and IgA, were markedly elevated. Endoscopic evaluation of her gastrointestinal tract revealed a normal colon and stomach. A proximal jejunal biopsy (Figure 1) showed severe villous flattening with crypt hypertrophy, and chronic inflammatory infiltrate in the lamina propria. No granulomas, parasites or malignant cells were seen. The patient was placed on a gluten-free diet. Her clinical response to treatment was dramatic: 18 months after discharge, she had gained 35 pounds, had little flatulence that was no longer malodorous and her laboratory values had returned to the normal range.
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Coeliac sprue is a relatively common disease in patients of Northern European ancestry, with a prevalence rate of 1:300, but its epidemiology is not well established in patients of African or Asian origin.1 It is strongly associated with selected HLA class II antigens HLA-DR3 and HLA-DQw2. In the genetically-susceptible host, gluten (found in wheat, rye, barley and oats but not rice and corn) triggers both humoral and cell-mediated inflammatory responses that result in mucosal destruction. The diagnosis is often delayed because of the variable presentation.2 The diarrhoea and weight loss often seen in children is rarely seen in adults.2 In a series of 30 consecutive patients, 25 had no gastrointestinal complaints and anaemia was the most frequent presentation.3 Coeliac-related antibodies are now readily available, and should help in screening patients before jejunal biopsy. Treatment of coeliac sprue is of course life-long abstention from gluten-rich foods. Coeliac sprue can be complicated by malignancies, with intestinal T-cell lymphoma occurring in more than 10% of patients, and other autoimmune diseases such as lupus, Graves disease and type 1 diabetes. Our patient presented with late-onset coeliac sprue with only flatulence as her initial symptom before developing carpopedal spasms as a result of hypocalcaemia.
Flatulence is usually a benign symptom when it is secondary to compulsive aerophagia. It is usually of low volume, composed of nitrogen and responds to non-specific modifications in diet and behavior. However, flatus that is malodorous and of large volume suggests the presence of methane, hydrogen and carbon dioxide, which are produced (together with the characteristic sulphides) by the action of colonic bacteria on unabsorbed polysaccharides and glycoproteins.4,5 Such patients should not have their symptoms flatly dismissed, but rather should be evaluated for possible malabsorption.
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Department of Medicine Department of Pathology Department of Gastroenterology Department of Endocrinology New York Hospital Medical Center of Queens e-mail: aryel_nicoleau_md{at}yahoo.com
References
1. Cole SG, Kagnoff MF. Celiac disease. Ann Rev Nutr 1985; 5:241.[Medline]
2. Malnick SD, Lurie Y, Beergabel M, Bass DD. Celiac disease. Postgrad Med 1997; 101:239–44.[Medline]
3. Hin H, Bird G, Mahy N, Jewell D. Coeliac disease in primary care: case finding study. Br Med J 1999; 318:164–7.
4. Levitt MD, Lasser RB, Schwartz JS, Bond JH. Studies of a flatulent patient. N Engl J Med 1976; 295:260.[Medline]
5. Perman JA, Modler S. Glycoproteins as substrates for production of hydrogen and methane by colonic flora. Gastroenterology 1982; 83:388.[Medline]
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