Fowlerʼs Solution as an Etiologic Agent in Cirrhosis

Franklin, Murray; Bean, William B.; Hardin, Robert C.

doi:10.1097/00000441-195006000-00001

Cited by 66 publications

(21 citation statements)

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“…In four of our cases there was unequivocal evidence of chronic arsenic poisoning, with death from lung cancer in two (Robson and Jelliffe, 1963). It is tempting to suggest that arsenic was also responsible for the liver lesion, and indeed Fowler's solution has been incriminated in the genesis of cirrhosis (Franklin, Bean, and Hardin, 1950), but the cases were poorly documented. Jaundice has also been associated with parenteral arsenic administration but this was presumably related to an associated serum hepatitis.…”

Section: Discussionmentioning

confidence: 65%

Prolonged survival after portal decompression of patients with non-cirrhotic intrahepatic portal hypertension

Zeegen¹,

Stansfeld²,

Dawson³

et al. 1970

Gut

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SUMMARY In a series of 251 good-risk patients undergoing portal decompression for intrahepatic portal hypertension, one fifth have been found not to have hepatic cirrhosis. Of these, 44 had only minor changes in hepatic architecture, and the clinical features and subsequent course have been compared and contrasted with a group of 201 cirrhotic patients who underwent portal decompression for similar indications.The degree of portal hypertension was comparable in both groups and it was not possible confidently to differentiate the condition from hepatic cirrhosis on either clinical or biochemical grounds in the individual case.The histological lesion was not progressive in the non-cirrhotic group and this was reflected in the far better survival of these patients. After five years 83 % (30 of 36) of this group were alive compared with 43 % (65 of 152) of the cirrhotic patients. After 10 years the cumulative survival was 77% (20 of 26) for those without cirrhosis, contrasted with 22% (19 of 87) for the cirrhotic patients.

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Section: Discussionmentioning

confidence: 65%

Prolonged survival after portal decompression of patients with non-cirrhotic intrahepatic portal hypertension

Zeegen¹,

Stansfeld²,

Dawson³

et al. 1970

Gut

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“…However, insulin treatment again increased their activity, showing no improvement in liver function. Several studies have suggested that iAs induces direct toxic liver injury [49][50][51]. Alloxan is also known to induce perilobular necrosis and endothelial damage [52].…”

Section: Discussionmentioning

confidence: 99%

Effect of Insulin on Arsenic Toxicity in Diabetic Rats—Liver Function Studies

Singh

Rana²

2009

Biol Trace Elem Res

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Arsenic (iAs)-induced diabetic mellitus has been debated by several workers. However, role of insulin in iAs-induced diabetes is yet to be investigated. Present report suggests that iAs promotes insulin secretion in diabetic rats and inhibits hyperglycemia. Whereas, reverse effects were recorded after insulin treatment to diabetic and iAs-treated rats. These conditions affect accumulation of iAs in liver. It decreased in diabetic and iAs-treated rats but increased after insulin treatment. Reciprocal effects were observed on serum transaminases and total bilirubin. Nevertheless, activity of glucose-6-phosphatase in the liver was stimulated by insulin treatment to diabetic and arsenic-fed rats. These results suggest that manifestations of arsenic-induced diabetes mellitus are not modulated or reversed by insulin. Observations on liver function further suggest that iAs is less toxic in diabetic rats. This protective effect has been attributed to noninsulin-dependent carbohydrate regulatory mechanisms. Diabetes certainly alters the pharmacodynamics and pharmacokinetics of iAs in rat.

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“…Franklin et al (1950) drew attention to the development of fibrosis and cirrhosis in four patients taking Fowler's solution for therapeutic purposes.…”

Section: Discussionmentioning

confidence: 99%

Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India.

Datta¹,

Mitra²,

Chhuttani³

et al. 1979

Gut

103

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SUMMARY Estimates were made of the arsenic concentration in liver specimens from nine patients having idiopathic portal hypertension (IP), and in four livers these were found to be significantly higher than those in patients with cirrhosis and in control subjects. The splenovenogram revealed extensive portosystemic collateral circulation. Corrected sinusoidal pressure and blood flow studies showed higher levels in four patients than in normal subjects. Microscopic examination of liver tissues revealed periportal fibrosis. The higher hepatic arsenic levels that were found were due to the inadvertent drinking of water contaminated with arsenic, adulterated opium, and indigenous medicines. A history of opium intake was not forthcoming but two patients had drunk water contaminated with arsenic and two others had taken bhasams (Ayurvedic medicines prepared by repeated oxidation of ores). Though the aetiology of idiopathic portal hypertension is not known, it is possible that arsenic intake may be one of the factors.Idiopathic portal hypertension (IP) has recently been recognised as a new entity (Ramalingaswami et al., 1962;Boyer et al., 1967;Basu Mallik et al., 1967;Sama et al., 1971;Datta, 1975;Datta, 1976a). In this condition haematemesis and splenic enlargement are common features, and solenovenographic studies reveal collaterals in 80% of cases. The aetiology of the syndrome is unknown and it has been suggested that there may be several causes (Datta, 1975;Mahajan and Datta, 1976 Received for publication 27 February 1979 Methods SUBJECTSThe livers of nine patients with idiopathic portal hypertension (IP) and seven with cirrhosis were investigated for their content of arsenic. A piece of liver (about 2 g) was obtained by wedge biopsy at laparotomy in six patients and the same quantity from necropsy in three patients. The gross and microscopic examination of 18 patients who showed no evidence of hepatic disease and who died from non-hepatic causes served as controls in our studies.Nine liver tissues were obtained from newborn infants. In addition, 105 livers were obtained through

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Fowlerʼs Solution as an Etiologic Agent in Cirrhosis

Cited by 66 publications

References 0 publications

Prolonged survival after portal decompression of patients with non-cirrhotic intrahepatic portal hypertension

Prolonged survival after portal decompression of patients with non-cirrhotic intrahepatic portal hypertension

Effect of Insulin on Arsenic Toxicity in Diabetic Rats—Liver Function Studies

Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India.

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