1/8. hypernatremia in a non insulin dependent (type 2) diabetic patient with central diabetes insipidus.We describe a patient with central diabetes insipidus who presented with hyperosmolar, non-ketotic hyperglycaemia. The role in this case of reduced thirst sensation with decreased water intake and abnormal AVP production illustrates the importance of these protective mechanisms in normal physiology regarding maintenance of normal plasma osmolality. Despite the complex pathophysiology in this patient, fluid resuscitation aimed at normalisation of the water deficit resulted in full recovery.- - - - - - - - - - ranking = 1keywords = water (Clic here for more details about this article) |
2/8. metformin as a cause of late-onset chronic diarrhea.metformin is an effective and commonly administered drug for controlling plasma glucose concentrations in patients with type 2 diabetes mellitus. Gastrointestinal adverse effects such as abdominal pain, nausea, dyspepsia, anorexia, and diarrhea are common and widely accepted when occurring at the start of metformin therapy. diarrhea occurring long after the dosage titration period is much less well recognized. Our patient began to experience nausea, abdominal cramping, and explosive watery diarrhea that occasionally caused incontinence after several years of stable metformin therapy A trial of metformin discontinuation resolved all gastrointestinal symptoms. A review of the literature revealed two reports that suggest diarrhea occurring long after the start of metformin therapy is relatively common, based on surveys of patients with diabetes. metformin-induced diarrhea is differentiated from diabetic diarrhea, which is clinically similar, except diabetic diarrhea is rare in patients with type 2 diabetes. patients with type 2 diabetes who are taking metformin and experience diarrhea deserve a drug-free interval before undergoing expensive and uncomfortable diagnostic tests, even when the dosage has been stable over a long period.- - - - - - - - - - ranking = 0.5keywords = water (Clic here for more details about this article) |
3/8. Does the use of insulin in a patient with liver dysfunction increase water retention in the body, i.e. cause insulin oedema?A 68-year-old female with mild diabetes mellitus was admitted because of acute liver dysfunction due to autoimmune hepatitis. While 40 mg/day of prednisolone improved hepatic dysfunction dramatically, her diabetic milieu deteriorated seriously. The induced hyperglycaemia could not be controlled sufficiently, despite a high dose of insulin (> 110 units/day), suggesting the existence of insulin insensitivity and hyperinsulinaemia. Soon after introduction of insulin therapy, she developed severe anasarca, including marked peripheral oedema, ascites and pleural effusion. Anasarca eventually subsided within 4 weeks with the use of a diuretic agent. We conjectured that the side effects of insulin, such as anti-natriuresis and increased vascular permeability, might be pronounced in the presence of the hepatic dysfunction that accompanies insulin insensitivity, hyperinsulinaemia and hypoalbuminaemia.- - - - - - - - - - ranking = 2keywords = water (Clic here for more details about this article) |
4/8. Unilateral macular oedema secondary to retinal venous congestion without occlusion in patients with diabetes mellitus.OBJECTIVE: To identify fundus characteristics associated with intraocular and intra-individual variations in the distribution of macular oedema in patients with diabetes. methods: A review was carried out of fundus photographs and fluorescein angiograms from 226 diabetes patients who received photocoagulation treatment for macular oedema. Cases with strictly unilateral clinically significant macular oedema were identified. RESULTS: Strictly unilateral macular oedema was identified in five patients with non-proliferative diabetic retinopathy, three of whom demonstrated angiographic leakage confined to a single venous drainage unit, and two of whom demonstrated leakage confined to two adjacent venous drainage units opposing one another on either side of the temporal circulatory watershed. Involved drainage units were delimited by arteriovenous crossings displaying signs of venous compression. Affected eyes had more frequent and more severe crossing signs involving macular drainage than fellow eyes. Although all patients had been examined regularly, no patient had had branch retinal vein occlusion and no patient developed such occlusion during 5 years of follow-up. CONCLUSION: In the present study, unilateral macular oedema in patients with diabetes was associated with angiographic leakage from venous drainage units where compression signs indicated a higher than normal likelihood of upstream congestion being present. Presumably, a modest increase in venous pressure induced macular oedema because of an underlying abnormal vascular vulnerability induced by diabetes.- - - - - - - - - - ranking = 0.5keywords = water (Clic here for more details about this article) |
5/8. The value of urine specific gravity in detecting diabetes insipidus in a patient with uncontrolled diabetes mellitus: urine specific gravity in differential diagnosis.When a patient with diabetes mellitus presents with worsening polyuria and polydipsia, what is a sensible, cost-effective approach? We report the unique coincidence of type 2 diabetes mellitus and diabetes insipidus. A 46-year-old woman with poorly controlled type 2 diabetes complained of polyuria with a daily output of 5 L. Although urinalysis demonstrated significant glucosuria, diabetes insipidus was suspected owing to a low urine specific gravity (1.008). The low specific gravity persisted during a water deprivation test. Ultimately, diabetes insipidus was confirmed when urine specific gravity and urine osmolality normalized following desmopressin administration. This case emphasizes the importance of accurately interpreting the urine specific gravity in patients with polyuria and diabetes mellitus to detect diabetes insipidus.- - - - - - - - - - ranking = 0.5keywords = water (Clic here for more details about this article) |
6/8. Possible gliclazide-induced water retention with azotemia.An 80-year-old woman with diabetes mellitus was treated with gliclazide. Prior to the gliclazide administration, her urinary excretion of albumin, serum urea nitrogen and serum creatinine were normal. After the medication, oliguria, edema and azotemia developed. On the twenty-fourth day when the edema was severe and generalized, gliclazide administration was terminated. On the following day urinary volume increased suddenly (5,740 ml/day). polyuria persisted for five days. edema improved and urea nitrogen and creatinine were normalized thereafter. Though the mechanism is not known, the clinical course suggests that gliclazide is the principal causative factor in the water retention and azotemia in this patient.- - - - - - - - - - ranking = 2.5keywords = water (Clic here for more details about this article) |
7/8. Possible involvement of hypersecretion of ADH in hyponatremia in a diabetic patient complicated with severe neuropathy.The present case was a 44-year-old man who had been diagnosed as having noninsulin-dependent diabetes mellitus 2 years before admission. He gradually showed severe neuropathy and emaciation because of poor control of his blood glucose levels. He was admitted to our hospital because of disturbance of consciousness with hyponatremia. The endocrinological findings including thyroid and adrenal functions revealed no abnormalities. Insufficiency of water diuresis was noted in the water loading test. Severe orthostatic hypotension was noted during the standing up test, and an excessive response in the plasma ADH level was also noted. These findings demonstrated that excessive ADH secretion occurred to compensate for the fall in blood pressure because of the breakdown of homeostatic regulation in blood pressure due to diabetic neuropathy. It is suggested that hyponatremia seemed to be subsequently induced by hypersecretion of ADH.- - - - - - - - - - ranking = 1keywords = water (Clic here for more details about this article) |
8/8. Two survival cases of alcoholic lactic acidosis complicated with diabetes mellitus and alcoholic liver disease.We have experienced two patients with alcoholic lactic acidosis complicated with liver disease and diabetes mellitus who were successfully treated. They developed hypoglycemia, dehydration, lactic acidosis, and renal failure after drinking a large volume of alcohol without eating for 1 week before onset. acidosis was thought to be directly related to excessive alcoholic intake, because it was no associated with severe liver failure and rhabdomyolysis. During monitoring of respiratory and circulatory functions, a rapid infusion of fluids adjusting to water and electrolyte imbalance was performed. A mixture of physiological saline and 5% glucose solution was thought to be effective in these cases. patients recovered from renal failure and lactic acidosis without hemodialysis. Our experience will hopefully provide a key to successful treatment of fatal alcoholic lactic acidosis.- - - - - - - - - - ranking = 0.5keywords = water (Clic here for more details about this article) |