Hypercalcaemia and metabolic alkalosis with betel nut chewing: emphasis on its integrative pathophysiology

Lin, Shih Hua

doi:10.1093/ndt/17.5.708

Cited by 48 publications

(29 citation statements)

References 27 publications

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“…Even with vitamin D supplementation as high as 800 IU/d, 25-hydroxyvitamin D levels have been reported to be normal or even low (13,15) (as reported in patient 1). In the small number of serum calcitriol values reported, 11 were low and four were low normal (13,15,17,18,131) (as reported in patient 2). Therefore, it could be argued that in a minority of patients, the failure to suppress calcitriol levels fully could contribute to the development of the milk alkali syndrome in a setting in which the ingestion of calcium is high.…”

Section: Vitamin Dmentioning

confidence: 77%

Milk Alkali Syndrome and the Dynamics of Calcium Homeostasis

Felsenfeld¹,

Levine²

2006

Clinical Journal of the American Society of Nephrology

107

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Section: Vitamin Dmentioning

confidence: 77%

Milk Alkali Syndrome and the Dynamics of Calcium Homeostasis

Felsenfeld¹,

Levine²

2006

Clinical Journal of the American Society of Nephrology

107

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“…H + can react with HCO 3 – in the portal vein and thereby cause a rise in the P L-lactate and P CO 2 in that location (52 ± 2.2 mm Hg; table 4), which can lead to a high P CO 2 in the hepatic vein (51 ± 1 mm Hg; table 4). Second, there is also CO 2 formed due to bacterial fermentation (many short-chain fatty acids are formed daily and their H + may react with P HCO 3 or in the lumen of the gastrointestinal tract [21]). In contrast, the P CO 2 in the femoral vein was significantly lower (45 ± 1.6 mm Hg, p < 0.05); hence the bicarbonate buffer system in resting muscles should remove fewer of these H + .…”

Section: Discussionmentioning

confidence: 99%

An Acute Infusion of Lactic Acid Lowers the Concentration of Potassium in Arterial Plasma by Inducing a Shift of Potassium into Cells of the Liver in Fed Rats

Cheema‐Dhadli¹,

Chong²,

Kamel³

et al. 2012

Nephron Physiol

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Background: Potassium (K⁺) input occurs after meals or during ischemic exercise and is accompanied by a high concentration of L-lactate in plasma (P_L-lactate). Methods: We examined whether infusing 100 µmol L-lactic acid/min for 15 min would lead to a fall in the arterial plasma K⁺ concentration (P_K). We also aimed to evaluate the mechanisms involved in normal rats compared with rats with acute hyperkalemia caused by a shift of K⁺ from cells or a positive K⁺ balance. Results: There was a significant fall in P_K in normal rats (0.25 mM) and a larger fall in P_K in both models of acute hyperkalemia (0.6 mM) when the P_L-lactate rose. The arterial P_K increased by 0.8 mM (p < 0.05) 7 min after stopping this infusion despite a 2-fold rise in the concentration of insulin in arterial plasma (P_Insulin). There was a significant uptake of K⁺ by the liver, but not by skeletal muscle. In rats pretreated with somatostatin, P_Insulin was low and infusing L-lactic acid failed to lower the P_K. Conclusions: A rise in the P_L-lactate in portal venous blood led to a fall in the P_K and insulin was permissive. Absorption of glucose by the Na⁺-linked glucose transporter permits enterocytes to produce enough ADP to augment aerobic glycolysis, raising the P_L-lactate in the portal vein to prevent postprandial hyperkalemia.

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“…In our survey of 37 Bangladeshis, we found an average of 3.5 betel quids per day with a range of 1-30 per day (manuscript submitted). Other studies have also reported that people can chew up to 30 quid per day [17,18]. In our study, we chose a more modest intake of six quids per day for the various calculations.…”

Section: Figurementioning

confidence: 99%