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  1. Re:lactation ketoacidosis-bmj case report

    Ketoacidosis is a direct result of exteremly low cellular magnesium levels. Gluconeogenesis is impaired at Glucose6 Phosphatase G6-Pase. G6- Pase is very magnesium dependent so if magnesium levels are severely reduced blood glucose levels plummet starving neurons of energy. The neurons in the hypothalamus signal the gut get more in 'the hunger pangs in Obesity'. Pyruvate carboxylase is also very magnesium dependent and if impaired by low magnesium levels and will also shutdown gluconeogenesis. Ketoacidosis is a direct result of beta oxidation of fat converting to AcetylCoA and Ketones. This continuous manufacture of ketones results in acid blood. Kidney failure in severe obesity and Diabetes-2 are other complications caused by a failure of gluconeogenesis. A magnesium sulphate injection would rectify the condition in amatter of minutes. If you require a comprehensive article please email. Arthur Henderson

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  2. Re:lactation ketoacidosis-bmj case report

    Thank you for your interest in our paper and for your comments. As was correctly pointed out in the letter, patients who are kept NPO should be given IV glucose supplementation. This was not done for our patient and this is indeed one of the reasons we decided to present her case in the Learning from errors section of the journal. We would like to clarify that it is in fact very unlikely for a non- breastfeeding patient to become significantly acidotic secondary to having no caloric intake for three days. Our bodies are normally well equipped to deal with short term starvation and only mild levels of acidosis develop in the starvation state when insulin levels are normal. In a small study published by Reidenberg et al., obese (non-lactating) women were starved for over a month and this produced only a mild metabolic acidosis of approximately 7.35 on arterial blood gas analysis. 1 On the other hand, Mohammad et al. showed that when lactating women are fasting for more than 42 hours, they begin to rely almost exclusively on gluconeogenesis as an energy substrate for milk production and are therefore at greater risk to develop a more profound metabolic acidosis compared to non-lactating women. 2 This distinction is key in our patient's case and emphasizes the unique nutritional needs of breastfeeding women. We hope this clarifies the issue. Adam Szulewski 1. Reidenberg MM, Haag BL, Channick BJ, et al. The Response of Bone to Metabolic Acidosis in Man. Metabolism 1966;15:236-241. 2. Mohammad MA, Sunehag AL, Chacko SK, et al. Mechanisms to conserve glucose in lactating women during a 42-h fast. Am J Physiol Endocrinol Metab 2009;297:E879-88.

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  3. lactation ketoacidosis-bmj case report

    It was indeed a very interesting report to read and was actually fascinated with the title initially. After reading the case report I am tempted to make some comments on the title which may be quite misleading .Even a normal person( meaning who is not breast feeding) will become ketotic if made nil by mouth for whatever reason for 3 days .But here the breast feeding probably aggravated the process further so it is difficult to say that the patient became ketotic because of breast feeding . I have been informed by the author that it is not their normal policy to keep a patient NPO for 3 days and not give any glucose so I am still not clear as to the reason for not giving IV glucose to this lady who wanted to continue breast feeding while she was NPO as that would not have been contraindicated .Yes I would agree with the author that this is a case of iatrogenic starvation acidosis but that would have developed in any person whether breast feeding or not after being kept NPO for 3 days .

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