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Hyperosmolar coma
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Bradwell AR, Harvey TC. Control of hypercalcaemia of parathyroid carcinoma by immunisation. Lancet 1999; 353: 370–73. 2 Nestle FO, Alijagic S, Gilliet M. Vaccination of melanoma patients with peptide- or tumor lysate-pulsed dendritic cells. Nat Med 1998; 4: 328–32. 3 Hsu FJ, Benike C, Fagnoni F. Vaccination of patients with B-cell lymphoma using autologous antigen-pulsed dendritic cells. Nat Med 1996; 2: 52–58. 4 Sallusto F, Lanzavecchia A. Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor alpha. J Exp Med 1994; 179: 1109–11.
Hyperosmolar coma Sir—In 1995, we reviewed a case of refractory lithium-induced nephrogenic diabetes insipidus (LINDI) in a woman who presented with hyperglycaemic, hypernatraemic coma.1 Although her name had been altered, the same patient was transferred to our intensive-care unit after a multiple-drug overdose, complicated by self-inflicted stab wounds to the rectum. She was lethargic with decreased respirations, and was orally intubated, followed by gastric lavage with return of pill fragments. Potentially toxic concentrations of acetaminophen (1602 mol/L; 246 g/mL), were treated wtih N-acetyl-cysteine. Her initial serum sodium was 140 mmol/L, and the initial glucose was 12·2 mmol/L. The patient underwent diverting colostomy with Hartmann’s pouch and repair of the posterior wall of the uterus without complications. It was noted during the operation that her urine output exeeded 250 mL/h, and this trend continued upon her return to the intensive-care unit. Within 12 h of returning from the operating room, the patient’s cumulative fluid intake was 6·2 L (4 L of normal saline and 2·2 lactated Ringer’s solution), and urine output was 5·9 L. Serum sodium was 152 mmol/L. Once the patient was extubated and her sensorium had cleared sufficiently for a more complete history and physical examination to be done, she informed us that she was the same person we had treated for LINDI 4 years earlier. After review of the previous hyperglycaemic and hyperosmolar complications of providing this patient with large volumes of intravenous dextrose in water solutions, we chose to begin enteral administration of water at an initial rate of 150 mL/h, gradually increasing to 300 mL/h. Serum sodium peaked at 154 mmol/L,
THE LANCET • Vol 353 • April 3, 1999
glucose concentrations remained below 17 mmol/L, and by the third postoperative day the patient had begun oral liquid (water) intake in excess of 8 L daily in addition to meals. When the patient was transferred to the psychiatric unit, her electrolytes and glucose concentrations were normal, liver enzymes had not risen, surgical sites were healing, and urine output and fluid intake were each about 10 L daily. This patient shows that LINDI can be permanent, even in the complete absence of further ingestion of the drug. Alterations in consciousness, whether induced by disease, medication, or medical procedures (such as surgery) may result in rapid dehydration, hypernatraemia, and lifethreatening hyperosmolality, unless water replacement is continued. Solute restriction combined with nonsteroidal anti-inflammatory drugs and thiazide diuretics will help modulate the volume losses that occur in the kidneys of affected patients,2,3 but the primary mechanism of fluid and electrolyte homeostasis remains the ingestion of large volumes of water. *Drew A MacGregor, Sylvia Y Dolinski Departments of *Anesthesiology and Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA 1
MacGregor DA, Baker AM, Appel RG, Ober KP, Zaloga GP. Hyperosmolar coma due to lithium-induced diabetes insipidus. Lancet 1995; 346: 413–17. 2 Walker RG. Lithium nephrotoxicity. Kidney Int Suppl 1993; 32: S93–98. 3 Boton R, Gaviria M, Batlle DC. Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy. Am J Kidney Dis 1987; 10: 329–45.
Coeliac disease in Saharawi children in Algerian refugee camps Sir—Over the past few years, there has been a great deal of research on the epidemiology of coeliac disease. The disease has a worldwide distribution, even if the highest prevalence is supposed to be in western countries. Prevalence of coeliac disease among Italian schoolchildren is reported to be as high as 1 in 305.1 Gianfranco Meloni and colleagues (Jan 2, p 37)2 report a prevalence of subclinical coeliac disease of 1 in 100 schoolchildren in Northern Sardinia. The prevalence of coeliac disease among Arab children has been the subject of only a few reports. The incidence of overt clinical coeliac disease in Palestinian children living in Kuwait is 1 in 2400, compared with
1 in 6500 among Kuwaitis; an incidence of 1 per 2800 livebirths has been found in Jordanian children.3 We report the results of a preliminary sceening study among Saharawi children with chronic diarrhoea and failure to thrive living in refugee camps in the Algerian desert. Saharawi people have an ethnic background of autochthon Berber and Bedouin tribes mixed with YemeniteArab populations. Since 1975 when Mauritanian and Moroccan forces occupied the Western Saharan territory, most of the civilian Saharawi population live in refugee camps in the South West Algerian desert around the oasis town of Tindouf. As part of an humanitarian programme, a group of Saharawi children came to stay in our region of Tuscany, in Italy, usually during the summer holidays from June to September. In 1995, Italian families gave hospitality to 300 Saharawi children. Some of the children had chronic diarrhoea and were failing to thrive and were referred to the paediatric gastroenterology units of Pisa and Florence. Ten Saharawi children were found to have coeliac disease by means of serological tests and intestinal biopsy. Prompted by this observation, one clinical investigator (TF) went, in May, 1996, to the Tindouf refugee camps in Algeria. Over 3 days, she visited three refugee camps and completed physical examinations of 150 children. IgA antiendomisium antibodies (AEA) were tested in serum samples from 54 children. Blood samples were taken from 54 children (23 boys and 31 girls aged from 18 months to 14 years). All of them were affected by chronic diarrhoea and most of them were failing to thrive and had abdominal distension. 22 (40·7%) serum samples from 11 boys and 11 girls were positive for AEA. We were not able to perform an intestinal biopsy in these children because of local difficulties. Since AEA test gives an almost 100% sensitivity and specificity for coeliac disease,4 Del Rosario suggested that small-bowel biopsy may be unnecessary in AEA-positive patients in whom this condition is suspected.5 The most likely explanation is that coeliac disease affected all AEApositive Saharawi children, even without a diagnosis confirmed by biopsy. These data suggest that among Saharawi people there is a particularly high prevalence of coeliac disease. In this population, wheat consumption is high and one hypothesis is that in a proportion of children, symptoms
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Bradwell AR, Harvey TC. Control of hypercalcaemia of parathyroid carcinoma by immunisation. Lancet 1999; 353: 370–73. 2 Nestle FO, Alijagic S, Gilliet M. Vaccination of melanoma patients with peptide- or tumor lysate-pulsed dendritic cells. Nat Med 1998; 4: 328–32. 3 Hsu FJ, Benike C, Fagnoni F. Vaccination of patients with B-cell lymphoma using autologous antigen-pulsed dendritic cells. Nat Med 1996; 2: 52–58. 4 Sallusto F, Lanzavecchia A. Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor alpha. J Exp Med 1994; 179: 1109–11.
Hyperosmolar coma Sir—In 1995, we reviewed a case of refractory lithium-induced nephrogenic diabetes insipidus (LINDI) in a woman who presented with hyperglycaemic, hypernatraemic coma.1 Although her name had been altered, the same patient was transferred to our intensive-care unit after a multiple-drug overdose, complicated by self-inflicted stab wounds to the rectum. She was lethargic with decreased respirations, and was orally intubated, followed by gastric lavage with return of pill fragments. Potentially toxic concentrations of acetaminophen (1602 mol/L; 246 g/mL), were treated wtih N-acetyl-cysteine. Her initial serum sodium was 140 mmol/L, and the initial glucose was 12·2 mmol/L. The patient underwent diverting colostomy with Hartmann’s pouch and repair of the posterior wall of the uterus without complications. It was noted during the operation that her urine output exeeded 250 mL/h, and this trend continued upon her return to the intensive-care unit. Within 12 h of returning from the operating room, the patient’s cumulative fluid intake was 6·2 L (4 L of normal saline and 2·2 lactated Ringer’s solution), and urine output was 5·9 L. Serum sodium was 152 mmol/L. Once the patient was extubated and her sensorium had cleared sufficiently for a more complete history and physical examination to be done, she informed us that she was the same person we had treated for LINDI 4 years earlier. After review of the previous hyperglycaemic and hyperosmolar complications of providing this patient with large volumes of intravenous dextrose in water solutions, we chose to begin enteral administration of water at an initial rate of 150 mL/h, gradually increasing to 300 mL/h. Serum sodium peaked at 154 mmol/L,
THE LANCET • Vol 353 • April 3, 1999
glucose concentrations remained below 17 mmol/L, and by the third postoperative day the patient had begun oral liquid (water) intake in excess of 8 L daily in addition to meals. When the patient was transferred to the psychiatric unit, her electrolytes and glucose concentrations were normal, liver enzymes had not risen, surgical sites were healing, and urine output and fluid intake were each about 10 L daily. This patient shows that LINDI can be permanent, even in the complete absence of further ingestion of the drug. Alterations in consciousness, whether induced by disease, medication, or medical procedures (such as surgery) may result in rapid dehydration, hypernatraemia, and lifethreatening hyperosmolality, unless water replacement is continued. Solute restriction combined with nonsteroidal anti-inflammatory drugs and thiazide diuretics will help modulate the volume losses that occur in the kidneys of affected patients,2,3 but the primary mechanism of fluid and electrolyte homeostasis remains the ingestion of large volumes of water. *Drew A MacGregor, Sylvia Y Dolinski Departments of *Anesthesiology and Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA 1
MacGregor DA, Baker AM, Appel RG, Ober KP, Zaloga GP. Hyperosmolar coma due to lithium-induced diabetes insipidus. Lancet 1995; 346: 413–17. 2 Walker RG. Lithium nephrotoxicity. Kidney Int Suppl 1993; 32: S93–98. 3 Boton R, Gaviria M, Batlle DC. Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy. Am J Kidney Dis 1987; 10: 329–45.
Coeliac disease in Saharawi children in Algerian refugee camps Sir—Over the past few years, there has been a great deal of research on the epidemiology of coeliac disease. The disease has a worldwide distribution, even if the highest prevalence is supposed to be in western countries. Prevalence of coeliac disease among Italian schoolchildren is reported to be as high as 1 in 305.1 Gianfranco Meloni and colleagues (Jan 2, p 37)2 report a prevalence of subclinical coeliac disease of 1 in 100 schoolchildren in Northern Sardinia. The prevalence of coeliac disease among Arab children has been the subject of only a few reports. The incidence of overt clinical coeliac disease in Palestinian children living in Kuwait is 1 in 2400, compared with
1 in 6500 among Kuwaitis; an incidence of 1 per 2800 livebirths has been found in Jordanian children.3 We report the results of a preliminary sceening study among Saharawi children with chronic diarrhoea and failure to thrive living in refugee camps in the Algerian desert. Saharawi people have an ethnic background of autochthon Berber and Bedouin tribes mixed with YemeniteArab populations. Since 1975 when Mauritanian and Moroccan forces occupied the Western Saharan territory, most of the civilian Saharawi population live in refugee camps in the South West Algerian desert around the oasis town of Tindouf. As part of an humanitarian programme, a group of Saharawi children came to stay in our region of Tuscany, in Italy, usually during the summer holidays from June to September. In 1995, Italian families gave hospitality to 300 Saharawi children. Some of the children had chronic diarrhoea and were failing to thrive and were referred to the paediatric gastroenterology units of Pisa and Florence. Ten Saharawi children were found to have coeliac disease by means of serological tests and intestinal biopsy. Prompted by this observation, one clinical investigator (TF) went, in May, 1996, to the Tindouf refugee camps in Algeria. Over 3 days, she visited three refugee camps and completed physical examinations of 150 children. IgA antiendomisium antibodies (AEA) were tested in serum samples from 54 children. Blood samples were taken from 54 children (23 boys and 31 girls aged from 18 months to 14 years). All of them were affected by chronic diarrhoea and most of them were failing to thrive and had abdominal distension. 22 (40·7%) serum samples from 11 boys and 11 girls were positive for AEA. We were not able to perform an intestinal biopsy in these children because of local difficulties. Since AEA test gives an almost 100% sensitivity and specificity for coeliac disease,4 Del Rosario suggested that small-bowel biopsy may be unnecessary in AEA-positive patients in whom this condition is suspected.5 The most likely explanation is that coeliac disease affected all AEApositive Saharawi children, even without a diagnosis confirmed by biopsy. These data suggest that among Saharawi people there is a particularly high prevalence of coeliac disease. In this population, wheat consumption is high and one hypothesis is that in a proportion of children, symptoms
1189