Cases reported "Diabetic Ketoacidosis"

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11/14. diabetes mellitus presenting with ketoacidosis following pentamidine therapy in patients with acquired immunodeficiency syndrome.

    patients with acquired immunodeficiency syndrome (AIDS) are at risk from many endocrine complications. pentamidine has been recognised for its potential to cause symptomatic, and even life-threatening hypoglycaemia. We report two cases of diabetes mellitus presenting with ketoacidosis 3 to 4 months after pentamidine therapy for pneumocystis carinii pneumonia (PCP), and review our experience of dysglycaemia in 58 patients with AIDS treated with pentamidine. These cases emphasise the potential for severe pancreatic toxicity in patients with AIDS. Hyperglycaemia during pentamidine therapy may be a marker for patients at increased risk of developing diabetes mellitus.
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keywords = deficiency
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12/14. Overwhelming strongyloidiasis in a diabetic patient following ACTH treatment and keto-acidosis.

    A non insulin-dependent Zairian patient developed ketoacidosis and then overwhelming strongyloidiasis following ACTH treatment. Severe cardiovascular and respiratory failure, associated with severe acute hypoprotidemia, preceded death, which occurred within three days. Pathologic examination revealed a massive parasitic infiltration of the gastro-enteric mucosa, mesenteric lymph nodes, and the pulmonary tissue and vessels. We suggest that ACTH treatment and keto-acidosis induced immune deficiency and triggered the acute parasitic episode, in a patient originating from an endemic area. Badly controlled diabetes should be known as a risk factor of hyperinfection by strongyloides stercoralis in latent carriers.
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13/14. Recurrent ketoacidosis in acquired, total lipodystrophy (lipoatrophic diabetes).

    The absence of ketoacidosis is thought to be characteristic of generalized lipoatrophic diabetes. It is widely believed that lipoatrophic diabetic patients are able to tolerate starvation and therapeutic insulin withdrawal, due to absence of subcutaneous body fat, the substrate essential for ketogenesis. In this article, we document nine episodes of acidosis and accelerated ketone body formation in a 24-yr-old woman whose deterioration followed episodes of dietary excesses without evidence of intercurrent infection or other identifiable forms of metabolic stress. serum c-peptide measurements demonstrated that an absolute insulin deficiency did not exist. During short-term, experimental, dietary manipulations, excess dietary calories worsened the hyperglycemia and hyperlipidemia but did not reproduce the ketoacidotic state. Excess fat added to the diet was the most poorly tolerated of the food groups, causing ketonuria, hypertriglyceridemia, and abdominal pain. Our experience with this patient suggests that increased food consumption, insufficient insulin relative to an insulin-resistant state, and increased amounts of insulin counterregulatory hormones (stress), acted in concert to cause acidosis and increased ketone body formation.
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14/14. acromegaly presenting with diabetic ketoacidosis.

    Diabetes in acromegaly is usually non-insulin dependent and is secondary to insulin resistance caused by growth hormone excess. diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. We describe a case of acromegaly presenting with diabetic ketoacidosis. We demonstrate that growth hormone excess can cause diabetic ketoacidosis in the presence of relative, but not absolute insulin deficiency.
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