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At least 667 records · Page 37Linked to original sources
PubMed1977

[Dr. Atkins' dietetic revolution: a critique].

Very fat people die earlier than people of normal weight because hypertension, diabetes and coronary disease are more frequent among the markedly obese. Most obese subjects, however, are only slightly overweight and their mortality is not elevated. Reasons for dieting are more often psychological than somatic. 2. Reducing diets are ineffective because the obese rarely follow them. Total fasting and intestinal bypass may provide better results, but are more dangerous. 3. Atkins' diet eliminates carbohydrates from food without restricting protein and fat intake. Deprived of carbohydrates, the body uses fat for fuel. A small part of metabolized fat is eliminated in the urine as ketone bodies, and this is why such diets are called "ketogenic". They have been known at least since 1863. 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the non-diabetic. It is maximal during total fasting and cannot be increased by a ketogenic diet. 5. In the short run, such diets produce rapid weight loss due to polyuria. On the other hand, refeeding carbohydrates causes water retention and weight gain. 6. The diet decreases appetite: patients eat less without feeling severe hunger and without measuring their food intake. 7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what Dr. ATKINS claims. 8. The diet increases plasma cholesterol and uric acid. It may be dangerous in diabetes (anorexia, acidosis) and in heart or kidney failure (hypokalemia). 9. The diet, though far from good, is better than the book. ATKINS' theories are at best half-truths, and the results he claims lack credibility. The obese subject's disappointment with traditional reducing diets and the book's hard-sell style account for ATKINS' success.

Acidosis↗
PubMed1996

[A rare case of rhinocerebral mucormycosis].

The authors describe a rare case of rhinocerebral mucormycosis. This is an acute, suppurative mycosis with poor prognosis. It has a particular affinity for rhinocerebral tissue and less frequently affects pulmonary tissue. Mucormycosis affects immunosuppressed patients and more than 75% of the cases involve patients suffering from acidosis, especially diabetic ketoacidosis. One characteristic feature is that the blood vessels are flooded causing thromboses, infarction and emboli. The disease is spread through the blood vessels or by expansion. The first clinical symptoms can be confused with an early stage of acute sinusitis with mucosanguineous rhinorrhea, facial tumescence and pain. In 50% of the cases there is rhinocerebral and orbital involvement. If the disease remains untreated it can prove fatal in 10 to 14 days. Effective treatment relies on an early diagnosis and prompt administration of intravenous amphotericin B as well as avulsion of the necrotic areas. To date only 200 cases of this severe pathology have been described. The present work is an attempt to throw further light on this disorder.

Adult↗
PubMed1999

Contrast media and metformin: guidelines to diminish the risk of lactic acidosis in non-insulin-dependent diabetics after administration of contrast media. ESUR Contrast Media Safety Committee.

The purpose of this study was to establish guidelines on how to avoid metformin-induced lactic acidosis following intravascular use of contrast media. We reviewed articles published in international journals. No conclusive evidence was found to indicate that the intravascular use of contrast media precipitated the development of metformin-induced lactic acidosis in patients with normal S-creatinine (< 130 mumol/l). The complication was almost always observed in non-insulin-dependent diabetic patients with decreased renal function before injection of contrast media. Guidelines for the use of contrast media in this group of patients are proposed.

Acidosis, Lactic↗
PubMedDate not supplied

[Lactic acidosis and severe hyperkalemia in a diabetic patient treated with metformin and enalapril: influence of acute renal disease and drugs].

A 71 year old hypertensive and non insulin-dependent diabetic patients with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkalemia, normal plasma level of beta-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable thanks to the treatment with the infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly assumed by the patient, could have played a iatrogenic role even if they were taken in low dosages. This event points out the importance of complying with the indications and especially the contraindications of these drugs, to avoid life threatening complications as that one occurred in this case.

Acidosis, Lactic↗
PubMed1985

Effects of diabetes, beta-hydroxybutyric acid and metabolic acidosis on the pituitary-thyroid axis in the rat.

Previous studies demonstrated alterations of thyroidal economy in untreated diabetes mellitus both in man and experimental animals. To test the role of beta-hydroxybutyric acid (BHB) and acidosis in generating such changes, we studied the pituitary-thyroid axis of streptozotocin-diabetic rats, BHB or ammonium chloride (NH4Cl)-treated normal rats. Serum TSH, pituitary content and pituitary concentration of TSH, serum T4, T3 and free T4 (FT4), were all measured by RIA. In short term (2 days) diabetic rats the pituitary content of TSH was normal whereas the concentration (per mg of protein) was elevated (p less than 0.05 versus control group). Serum TSH (p less than 0.05), serum T4 (p less than 0.05), serum T3 (p less than 0.01) and serum FT4 (p less than 0.05) were all significantly decreased. In long term (30 days) untreated diabetic rats serum changes were similar to the short term diabetic group, though the pituitary content of TSH was significantly decreased (p less than 0.05). Animals treated with NH4Cl had no variations from controls. However, rats treated with BHB displayed a significant decrease in pituitary content of TSH (p less than 0.05), pituitary concentration of TSH (p less than 0.05) and in plasma TSH (p less than 0.01), and normal thyroid hormones in serum. No significant changes were seen in the TSH response to TRH in 2 or 30 days untreated diabetic and in BHB - treated animals. The data suggest that BHB, although not NH4Cl acidosis, may be capable of inducing a moderate depression of pituitary and plasma TSH of a lesser magnitude of that accompanying the full, long term diabetic state in the rat.

3-Hydroxybutyric Acid↗
PubMed2003

Metformin-associated lactic acidosis and acute renal failure in a type 2 diabetic patient.

Metformin belongs to a class of drugs known as the biguanides that are widely used in the treatment of type 2 diabetes mellitus. Its association with lactic acidosis is well established, although rare. Metformin-associated lactic acidosis is recognized as a potentially lethal condition that can occur in patients with contraindications to the drug, such as renal dysfunction, liver diseases, alcoholism, and cardiopulmonary diseases. In these cases, the plasma concentration of metformin is not necessarily abnormally high. We describe a 75-year-old diabetic woman with acute renal failure and life-threatening lactic acidosis due to metformin intoxication. Clinical manifestations included vomiting, diarrhea, hypothermia, hypotension and transitory blindness. Her initial renal function was recovered after hemodialysis and she was discharged 3 months after admission.

Acidosis, Lactic↗
PubMed2005

Involvement of Ca2+/calmodulin-dependent protein kinase II in the modulation of indolamines in diabetic and hyperglycemic rats.

Hyperglycemia and acidosis are the key factors in diabetic complications. It has been shown that acute or chronic diabetes alters serotonin levels in brain. However, the mechanism of hyperglycemia- or acidosis-induced changes in serotonin levels remains poorly understood. Because Ca2+-dependent protein kinases play a major role in the regulation of serotonin synthesis and release, we investigated the effect of diabetes, hyperglycemia, and acidosis on the level of indolamines [5-hydroxytryptamine (5-HT) and/or 5-hydroxyindoleacetic acid (5-HIAA)] and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) enzyme activity or protein expression in different brain regions. Alloxan-induced (45 mg/kg bw) diabetic rats (30 days) showed increased level of 5-HT in striatum (ST; 183%), midbrain (MB; 199%), pons medulla (PM; 151%), cerebellum (CB; 214%), and cerebral cortex (CCX; 162%) compared with control (P < 0.05), and these changes were reversed after insulin administration. Rats treated with glucose (500 mg/kg bw) for 30 days showed a 146%, 183%, 208%, and 177% (P < 0.05) increase in 5-HT levels in ST, PM, CB, and CCX, respectively. 5-HIAA level increased in hippocampus (HC; 172%) and in MB (145%; P < 0.05). In addition, rats treated with sodium acetoacetate (NaAcAc) for 30 days (60 mg/kg bw) showed significant increases (P < 0.05) of 5-HT level in ST (152%) and MB (174%). However, the levels of 5-HIAA increased only in MB (151%, P < 0.05). Rats treated with NH4Cl, which induced acidosis (150 mg/kg bw), showed an increased level of 5-HT only in HC (165%, P < 0.05). The increased activity and protein expression of CaMKII in ST, MB, PM, CB, and CCX under diabetic conditions were correlated with the levels of indolamines changes during diabetic, hyperglycemic, or acidotic conditions. These results suggest that CaMKII may be involved in the regulation of indolamines in diabetic animals.

Acidosis↗
PubMed2006

Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood glucose concentration.

OBJECTIVE: To ascertain whether initial depression of conscious level in children with diabetic ketoacidosis (DKA) is related to hyperosmolality, acidosis or other factors. METHODS: In 225 episodes of DKA without evidence of cerebral edema, we examined the relationship between conscious level and initial biochemical variables. We contrasted these findings with those in 42 children who later developed cerebral oedema. RESULTS: On admission, 42/225 (19%) had mild (pH 7.26-7.35); 96 (44%) moderate (pH 7.11-7.25); and 80 (37%) severe DKA (pH <or= 7.10). Conscious level: alert and oriented (group 1, n=123), drowsy but oriented when woken (group 2, n=62), semi-conscious or confused/agitated (group 3, n=9), comatose (group 4, n=4). Glasgow Coma Score (GCS) was available in 65. pH varied significantly with conscious level; group 1, 7.20+/- 0.11(mean+/- SD); group 2, 7.10+/- 0.16; group 3, 6.96+/- 0.11; group 4, 6.88+/- 0.09 (anova, p<0.001). Blood glucose (BG) was not different between the groups. GCS was related to pH (r(s) = 0.49, p < 0.001), but not to BG or electrolyte levels. Age, sex, plasma sodium, corrected sodium and osmolality also varied with conscious level in a univariate model. Using multivariate analysis comparing groups 1 with groups 2-4, lower pH and younger age were the only independent determinants of impaired conscious level (p<0.001, p=0.036). Conscious level in the children with cerebral edema was also closely related to pH and not to other biochemical variables. pH was lower at each conscious level in the children with later cerebral edema. CONCLUSIONS: In children with DKA, initial conscious level is closely related to pH and weakly to age, but not to BG or plasma sodium level. Thus cerebral function in DKA is related to severity of acidosis even when there is no evidence of cerebral edema.

Adolescent↗
PubMed1997

Diabetes and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS): radiolabeled polymerase chain reaction is necessary for accurate detection of low percentages of mutation.

A 6-yr-old boy presented with muscle weakness, lactic acidemia, and insulin-dependent diabetes mellitus (IDDM). Using PCR and restriction enzyme analysis, he was found to have the classical A3248G mitochondrial DNA (mtDNA) mutation frequently associated with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). The mutation was confirmed by sequencing muscle mtDNA. The mutation in mtDNA from muscle, lymphoblasts, and blood was clearly demonstrable by standard methods using ethidium bromide staining. His mother also had IDDM, but no A3243G mutation could be detected in her blood or transformed lymphoblasts using the same PCR technique. When PCR was carried out in the presence of [32P]deoxycytidine triphosphate, subsequent autoradiography detected the presence of the mutation at low levels in mtDNA from the mother's lymphoblasts and blood. Study of the mother's muscle showed a mitochondrial myopathy, despite the fact that she was asymptomatic. We emphasize that the increased sensitivity of radiolabeled PCR may be necessary to detect small percentages of heteroplasmic A3243G mtDNA mutation in blood from diabetic subjects. Otherwise the incidence of mtDNA mutations in both IDDM and non-insulin dependent diabetes may be underestimated.

Adult↗
PubMed1978

[Haemodialysis in the treatment of biguanide-induced lactate acidosis (author's transl)].

Severe lactate acidosis developed in nine diabetics on biguanide. When lactate acidosis was diagnosed all patients had reduced renal function, six being oligoanuric. Pre-existing chronic renal failure as a factor in the development of lactic acidosis was excluded in five patients, normal renal function being restored later. All patients were dialysed, seven surviving. This mortality rate is lower than that reported by others for biguanide-induced lactate acidosis. Rapid biguanide elimination by dialysis was demonstrated both in vitro and in vivo. The in vivo clearance of buformin was 83 +/- 43 ml/min (mean +/- SD, n = 4), that of phenformin 68 +/- 33 ml/min (n = 7). The main advantages of haemodialysis in the treatment of biguanide-induced lactic acidosis are rapid removal of toxic biguanides and excess lactate and the ability to administer sodium bicarbonate adequately without risking hypernatraemia and fluid overload.

Acidosis↗