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PubMed2002

Phenotypes and mitochondrial DNA substitutions in families with A3243G mutation.

OBJECTIVE: To clarify the relationship between mitochondrial DNA (mtDNA) sequence variations and phenotypes in patients with A3243G mutation. MATERIALS AND METHODS: We studied whole mtDNA sequences in two families with A3243G mutation and characteristic clinical features. Two brothers in Family 1 had shown thiamine deficiency and mitochondrial myopathy without central nervous system involvement. In Family 2, a 16-year-old woman showed the symptoms of mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Her mother had had diabetes mellitus and died at the age of 42. The proportion of A3243G mtDNA in blood was 87 and 89% in the patients of Family 1, and 25% in the patient and less than 5% in the mother of Family 2. RESULTS: The mtDNA analysis revealed the following homoplasmic substitutions: T1520C and C12153T found only in Family 1, and A15954G found only in Family 2. These substitutions were not detected in seven other MELAS patients or in 50 controls. CONCLUSION: These substitutions might be specific to these families and could be one of the factors that modulate their clinical features together with the A3243G mutation.

Adolescent↗
PubMed1992

[Mucormycosis].

Mucormycosis, which is caused by a group of fungi found in rotting fruit and vegetables, can be fatal. The fungi do not cause disease in healthy individuals, but attack those with immunodepression. The usual patient is a diabetic in ketoacidosis, but also those with other causes of metabolic acidosis, such as AIDS, burns, and gastrointestinal tract ulcers, may be affected. When the disease results in infection of the sinuses, the patient may present with orbital apex syndrome: exophthalmos, IInd, IIIrd, IVth and VIth nerve involvement, conjunctival chemosis and central artery or vein occlusion. The presence of necrotic tissue in the nose should alert the physician to the possibility of mucormycosis. Prognosis is poor if it spreads to the brain or cavernous sinus and if treatment does not include surgery. We present 3 typical cases: a 71-year-old women and men aged 62 and 73, respectively. The first 2 died soon after the diagnosis was established. They had been conservatively treated and the disease had spread to the brain. The third survived after several months of treatment which included surgical debridement.

Aged↗
PubMed2003

[Cardiomyopathy showing progression from diffuse left ventricular hypertrophy to dilated phase associated with mitochondrial DNA point mutation A3243G: A case report].

A 44-year-old man was admitted to our hospital because of congestive heart failure. He had various symptoms caused by insulin-dependent diabetes mellitus, sensorineural deafness, Wolff-Parkinson-White syndrome and cardiomyopathy associated with mitochondrial DNA point mutation A3243G. Echocardiography had showed symmetrical hypertrophy of the left ventricular wall and normal cardiac function (ejection fraction 55%) at age 32 years. However, echocardiography showed cardiac transformation, consisting of posterior wall thinning and significantly reduced cardiac function (ejection fraction 11%), at age 44 years. Electrocardiography showed lowered R-wave in the chest leads and QRS widening. Both lactic acid and pyruvate serum levels were increased. Mitochondrial respiratory enzyme analysis in gastrocnemius muscle tissue indicated a partial deficiency of rotenone-sensitive NADH cytochrome C reductase. He was discharged from our hospital, and medically treated with coenzyme Q10(30 mg/day). He had no progression of cardiomyopathy or congestive heart failure. However, he suddenly died of lactic acidosis at age 47 years.

Acidosis, Lactic↗
PubMed2002

Influence of age on the presentation and outcome of acidotic and hyperosmolar diabetic emergencies.

BACKGROUND: Diabetic emergencies associated with ketoacidosis (DKA) and a hyperosmolar, hyperglycaemic state (HHS) are both acute life-threatening metabolic disturbances. Traditionally, DKA and HHS have been classified as distinct entities but there is evidence to suggest that patients can present with elements of both conditions. AIMS: To examine the presentation profiles, mortality rates and prognostic factors associated with a fatal outcome for diabetic patients admitted with ketoacidosis and/or hyperosmolarity. METHODS: A retrospective analysis of 312 admissions to an Australian tertiary referral hospital between 1986 and 1999. RESULTS: Of the patients surveyed, DKA was the diagnosis for 171 presentations (55%), HHS was the diagnosis for 47 presentations (15%) and combined DKA and HHS (DKA-HHS) was diagnosed for 94 presentations (30%). Age at presentation for DKA patients (33+/-1.2 years) was significantly less (P< 0.01) than DKA-HHS patients (44+/-2.4 years). This, in turn, was significantly less (P < 0.01) than HHS patients (69+/-1.7 years). There were 15 deaths for the 312 presentations, resulting in an overall mortality rate of 4.8%. Combined mortality rates according to age at presentation were: (i) 0/134 for patients aged <35 years, (ii) 1/85 (1.2%) for patients aged 35-55 years and (iii) 14/93 (15.0%) for patients aged >55 years. For the three categories of diabetic emergencies, mortality rates were: (i) 2/171 (1.2%) for DKA, (ii) 5/94 (5.3%) for DKA-HHS and (iii) 8/47 (17%) for HHS. For all presentations associated with ketoacidosis - regardless of the degree of hyperosmolarity - the mortality rate was 7/264 (2.7%), however for all presentations with hyperosmolarity regardless of the degree of acidosis - the mortality rate was 13/141 (9.2%). When the associations between age, category of diabetic emergency, serum osmolarity and various other biochemical parameters with mortality were assessed by logistic regression analysis, age and the degree of hyperosmolarity were found to be the most powerful predictors of a fatal outcome. In particular, patients aged >65 years presenting with a serum osmolarity >375 mOsmol/L were at greatest risk. However, in a multivariate analysis only age emerged as a significant independent predictor of mortality (P < 0.01). CONCLUSIONS: The mixed state of ketoacidosis and hyperosmolarity was observed in 30% of presentations for diabetic hyperglycaemic emergencies. Although age and degree of hyperosmolarity both influenced mortality rates, only age was found to be an independent predictor of mortality. The mortality rate for diabetic emergencies associated with ketoacidosis remained low, in keeping with other studies. By contrast, the mortality rate for diabetic emergencies associated with a hyperosmolar state remained considerably higher. This higher mortality will most likely persist because deaths associated with a hyperosmolar state were in elderly patients with significant comorbidity.

Adolescent↗
PubMed1998

[Exercises on a bicycle ergometer in a family of diabetes mellitus associated with a mutation of mitochondrial DNA].

The serum pyruvate and lactate levels were studied after exercise on a bicycle ergometer in a family of diabetes mellitus (DM) associated with a mutation at nucleotide 3243 in the mitochondrial gene. A 56-year-old Japanese woman with the mutation at a percentage of 5% in the blood had insulin-dependent DM and sensory hearing loss without muscle symptoms. Her serum lactate and pyruvate levels increased markedly during and after exercise on a bicycle ergometer. Two of her sons were found to have the same mutation at a percentage of 17% and 18%, respectively. Her 26-year-old son was found to have borderline DM after oral glucose loading, although he showed no abnormalities of the metabolism of pyruvate and lactate. Her 31-year-old son showed no abnormalities after oral glucose loading and after exercise on a bicycle ergometer. Although the same mutation causes more severe MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), little is known about whether these diabetic patients are subclinically involved with myopathy. The noninvasive ergometer exercise with determination of serum pyruvate and lactate may be useful in evaluating the severity of myopathy in these patients.

Adult↗
PubMed1978

Renal net glucose release in vivo and its contribution to blood glucose in rats.

This study describes the contribution of de novo glucose synthesis by the kidney to blood glucose homeostasis in rats. The net glucose release by the kidney in vivo was measured by an isotope-dilution method, which calculated the extent of dilution of injected [(14)C]glucose by glucose newly synthesized in the kidney. The extent of dilution was determined from the difference between the decrease of the actual blood glucose concentration and that of the radioactivity of [(14)C]glucose, after injecting [(14)C]glucose into functionally hepatectomized rats. The results indicate that the net glucose release by the kidney in vivo in normal fed rats was 0.75+/-0.13 mg/dl per min, and that its contribution to blood glucose was 25.9+/-5.0%. When unilateral nephrectomy was performed, under the same conditions, renal net glucose release was one-half of that in rats with two intact kidneys, which indicates the quantitative accuracy of the isotope-dilution method employed in this study. In rats starved for 24 h, the renal net glucose release increased to 0.99+/-0.08 mg/dl per min. Diabetic rats showed a remarkably higher renal net glucose of 2.28+/-0.33 mg/dl per min, which was 360% of the normal level. Treatment of diabetic rats with insulin, restored the renal net glucose release to the normal level. In acidotic rats, renal net glucose release was as great as 1.03+/-0.15 mg/dl per min, which suggests that the acid-base balance participates in control of renal glucose output. Measurements every 6 h throughout the day showed that glucose was supplied from the kidney at a constant rate without any circadian rhythm. These data suggest that renal gluconeogenesis is of physiological importance in the maintenance of homeostasis of blood glucose.

Acidosis↗
PubMed2006

Neonatal diabetes mellitus.

Neonatal diabetes mellitus is a rare form of insulin dependent diabetes mellitus that present within the first month of life, lasting at least two weeks and requiring insulin therapy. Intrauterine growth restriction, failure to thrive, fever, dehydration, hyperglycemia and acidosis with or without ketonuria are the clinical features of the disease. We report four cases of neonatal diabetes mellitus; two of them had a transient course.

Diabetes Mellitus, Type 1↗
PubMed1974

Treatment of diabetic coma with continuous low-dose infusion of insulin.

Thirty-eight patients in diabetic coma from four different centres were treated with a continuous low-dose intravenous infusion of insulin at an average dose of 7.2 IU/hr. All patients recovered rapidly except for one profoundly shocked patient who died. The mean fall in plasma glucose was 58% four hours after the start of insulin. Blood ketone bodies and plasma free fatty acids showed a similar response. There was no significant difference in plasma glucose response according to severity of acidosis or previous treatment with insulin. Hypokalaemia was uncommon. In the treatment of diabetic coma this technique has proved simple, safe, and effective.

Adolescent↗
PubMed1993

Antihyperglycemic action of guanidinoalkanoic acids: 3-guanidinopropionic acid ameliorates hyperglycemia in diabetic KKAy and C57BL6Job/ob mice and increases glucose disappearance in rhesus monkeys.

To evaluate the long-held concept that acidic guanidines lack glycemic effects, guanidinoalkanoic acids and the biguanide metformin (positive control) were administered to KKAy mice, a model of noninsulin-dependent diabetes. Two acidic guanidines, 3-guanidinopropionic acid (3-GPA) and guanidinoacetic acid, decreased the plasma glucose level; other compounds were ineffective. 3-GPA was more potent than even metformin. Insulin suppression tests in KKAy mice indicated that improved insulin sensitivity was the mode of action for 3-GPA. Glycemic effects in KKAy mice resulted from increased glucose disposal whereas gluconeogenesis, hepatic glycogen content and intestinal glucose absorption were unchanged. 3-GPA's glycemic effect was corroborated in two other models of noninsulin-dependent diabetes. In ob/ob mice, the compound reduced hyperglycemia, polyuria, glycosuria and hyperinsulinemia. In insulin-resistant rhesus monkeys, it increased the disappearance of i.v. glucose. The glycemic action of 3-GPA required the presence of some circulating insulin as well as hyperglycemia because the compound was ineffective in normoglycemic mice, insulinopenic Chinese hamsters and streptozotocin-diabetic rats. These data indicate that acidic guanidine derivatives can ameliorate hyperglycemia in animal models of noninsulin-dependent diabetes. Because acidic derivatives uniquely lack the propensity of guanidine compounds for inducing lactic acidosis, our finding suggests a new approach for developing improved antidiabetes compounds from this chemical class.

Animals↗
PubMed2003

[Insulin-sensitizing agents: metformin and thiazolidinedione derivatives].

Both metformin and thiazolidinedione derivatives(TZDs) improve insulin resistance, a major pathogenesis of type 2 diabetes, and decrease blood glucose levels without stimulating insulin secretion. Metformin inhibits glucose output from the liver, while TZDs increase glucose utilization in the peripheral tissues. In addition, there has been indicated that these agents ameliorate metabolic syndrome beyond glucose-level lowering. Molecular targets of these agents have recently been revealed; AMP-activated protein kinase (AMPK) for metformin and adiponectin, while PPAR gamma for TZDs which induce gene expression of adipocyte glycerol kinase and adiponectin. Insulin-sensitizing agents are clinically useful for obese diabetic patients with insulin resistance. However, periodical examinations are necessary to avoid serious adverse effects such as lactic acidosis, although rare, by metformin and liver injury by TZDs.

Adipocytes↗
PubMed1999

Changes in serum amylase, lipase and leukocyte elastase during diabetic ketoacidosis and poorly controlled diabetes.

Diabetic ketoacidosis (DKA) is frequently associated with pancreatic enzyme abnormalities. In order to determine the main factors that lead to this increase, serum total amylase (TA), pancreatic amylase (PA), lipase (L) and leukocyte elastase (LE), an early predictor of acute pancreatitis, were measured in four groups of patients on admission. Group 1 consisted of 52 patients with DKA (age: 41.9 +/- 19.2 years; blood glucose (Glc): 27.4 +/- 11.5 mmol/L; pH: 7.20 +/- 0.16; plasma bicarbonate: 10.5 +/- 6.2 mmol/L; blood urea nitrogen (BUN): 0.60 +/- 0.44 g/L; HbA(1C): 12.5% +/- 2.8%). Group 2 consisted of 90 patients with poorly controlled non-ketotic diabetes (age: 53.4 +/- 16.0; Glc: 14.3 +/- 0.6; HCO(3)(-): 26.6 +/- 3.2; BUN: 0.38 +/- 0.20; HbA(1C): 11.3 +/- 2.1). Group 3 consisted of 22 patients with well-controlled diabetes (age: 53.7 +/- 12.8; Glc: 10. 1 +/- 5.2; HCO(3)(-): 27.4 +/- 3.8; BUN: 0.36 +/- 0.19; HbA(1C): 6.8 +/- 0.8). Group 4 (controls) comprised 27 non-diabetic patients (age: 46.0 +/- 15.0; Glc: 4.9 +/- 0.5; HCO(3)(-): 28.4 +/- 2.5; BUN: 0.30 +/- 0.16; HbA(1C): 5.2 +/- 0.7) (means +/- SD). Increased enzyme activities were more frequent in group 1 (TA: 30.7; PA: 27.0; L: 36.5; LE: 73%) than in groups 2 (TA: 8.9; PA: 7.1; L: 8.9; LE: 45. 5%), 3 (TA: 13.6; PA: 9.0; L: 18.1; LE: 31.8%) and 4 (TA: 7.0; PA: 3. 0; L: 0.0; LE: 29.6%). Mean serum enzyme activities were significantly different in the 4 groups (ANOVA, P < 0.01) and were higher in group 1 than in groups 2, 3 and 4 (Student's t-test; group 1 vs 2 or 3 or 4: P < 0.001). In groups 1 + 2 + 3 + 4 (all patients), the four enzymes correlated with one another and also with Glc, BUN and HCO(3)(-) (P < 0.001). In group 1, TA correlated negatively with HCO(3)(-) (P < 0.001) and pH (P < 0.05); PA and L correlated positively with Glc and BUN (P < 0.01) and negatively with HCO(3)(-) (respectively, p < 0.01 and 0.05). PA correlated positively with pH (P < 0.01); LE correlated with Glc (P < 0.05) and BUN (P < 0.01). In conclusion, this study suggests that the serum levels of pancreatic enzymes increase with the degree of diabetic disequilibrium, and mainly correlate with metabolic factors such as hyperglycaemia, dehydration and acidosis. Increased pancreatic enzyme activities in patients with DKA, even in combination with abdominal pain, should not be diagnosed as acute pancreatitis; this could be important, particularly for younger clinicians.

Adult↗
PubMed1989

Induction of renal phosphoenolpyruvate carboxykinase mRNA: suppressive effect of glucose.

The mRNA for the important gluconeogenic enzyme phosphoenolpyruvate carboxykinase (GTP) (PEPCK; EC 4.1.1.32) is expressed in liver and kidney. In the kidney, acidosis is a unique and potent stimulus, whereas insulin, the major counterregulatory hormone of gluconeogenesis, has no effect. In this study, we find that oral glucose administration to rats rapidly decreases the abundance of renal PEPCK mRNA by 50-72%. This reduction takes place in normal euglycemic, in insulin-induced hypoglycemic, and in streptozotocin-induced hyperglycemic diabetic animals. The effect of glucose is not seen in the presence of metabolic acidosis, whether induced by NH4Cl or by prolonged fasting. Therefore, it appears that oral glucose loading is a physiological suppressor of renal PEPCK message abundance, although not in acidosis.

Acidosis↗
PubMed1984

[Differential diagnosis of the symptom of lactic acidosis in childhood].

Transitory Lactic acidemia may be found under very different conditions, eg. hyperventilation, hypoxia, strenuous muscular work, diabetic ketoacidosis, malignancies and totally parenteral alimentation. In contrast chronic, permanent lactic acidemia and lactic aciduria may point to one of several and usually severe inherited metabolic diseases of gluconeogenesis, pyruvate oxidation, the Krebs cycle or the respiratory chain. Clinical hints for a stepwise differential diagnosis are presented.

Acidosis↗
PubMed1979

[Diabetic ketoacidosis and hyperosmolar diabetic coma in childhood. Low-dose continuous intravenous infusion of insulin (author's transl)].

Continuous intravenous infusion of low doses of insulin has been successfully used since 1972 in the treatment of "diabetic coma". The achieved levels of plasma insulin satisfy the transport of glucose and the inhibition of lipolysis. We are to report upon 8 children (mean age: 8.5 years), 6 with diabetic ketoacidosis and 2 with hyperosmolar diabetic coma. Blood sugar levels of 300 mg/dl or less were reached after averagely 8 hours of therapy and an average consumption of 0.8 U insulin/kg. Sodium and potassium levels, osmolality and acid base parameters for the first 24 hours are described. Low-dose continuous intravenous insulin infusion was effective, simple and safe in all cases. The presently recommended dosage of 0.1 insulin/kg x hour is to be used flexibly (range: 0.05--0.2 U/kg x hour). The administration of bicarbonate should be cautiously used for patients with severe acidosis. Infusion of hypotonic solutions as part of the treatment of the hyperosmolar diabetic coma can be dangerous. A new therapeutic regime based on our results is proposed.

Adolescent↗
PubMed1984

The various renal manifestations of the nephropathic form of cystinosis.

Three phenotypic forms of cystinosis (nephropathic, juvenile-onset and benign adult forms) are well recognized. That not all infants and children have the classical nephropathic form with Fanconi's syndrome is illustrated by 2 of the 3 patients in this report. Case 1 had the typical nephropathic form with generalized proximal tubular dysfunction. In contrast, case 2 had transient features of Bartter's syndrome which preceded the manifestations of Fanconi's syndrome. Case 3 was more complex because he first presented with a syndrome of nephrogenic diabetes insipidus. He then developed features of Fanconi's syndrome as well as metabolic acidosis, hyponatremia and hyperkalemia. The failure of deoxycorticosteroid administration to elevate the serum concentration suggested, in retrospect, that he may also have had a form of acquired pseudohypoaldosteronism.

Aldosterone↗
PubMed2001

[Metabolic considerations in the treatment of coronary disease in diabetic patients].

Coronary heart disease represents the first cause of death in diabetic patients. The poor outcome of this ischemic disease is multifactorial. The abnormalities in myocardial energy metabolism encountered by the diabetic heart explain both the ischemic severity and the worsening of reperfusion lesions. The metabolic abnormalities in diabetic heart consist in both an impairment of glucose metabolism (diminished glucose uptake, reduced glycolysis, decreased glucose oxidation...) and an increase in fatty acid oxidation. During ischemia, glucose oxidation is reduced and anaerobic glycolysis becomes the main ATP substrate. Lactate accumulate in myocardial cells, inducing both a metabolic acidosis and an intracellular calcium overload. During reperfusion, intracellular homeostasis is restored very slowly in diabetic heart. Several therapeutic approaches are used to correct these metabolic disturbances. Glucose--insulin--potassium infusion in acute myocardial infarction leads to a significant reduction in the mortality relative risk in diabetic patients (ECLA and DIGAMI studies). The benefit is greater in diabetic patients who where non-insulin-treated prior to ischemia followed by myocardial reperfusion therapy. Others more direct pharmacological approaches improve glucose oxidation during myocardial ischaemia and myocardial reperfusion. The reference drug remains trimetazidine for which one of the fundamental mechanism of action was discovered recently. This specific metabolic, non haemodynamic approach, complete the gold-standard treatment of coronary heart disease in diabetic patients (e.g. aspirin, beta-blockers, ACE inhibitors and statins).

Coronary Disease↗
PubMed2002

[A case report of a patient with emphysematous cystitis who was cured by early cystectomy under a life threatening condition].

A 80-year-old female with insulin-dependent diabetes mellitus (IDDM) visited our hospital on November 24, 1999, because of nausea, vomiting and macrohematuria. Cystoscopy demonstrated a diffuse hyperemic mucosa and gas-filled vesicles in the submucosa. Despite treatment with antibiotics, infection was not controlled and metabolic acidosis was increased. Simple cystectomy and ureterocutaneostomy were performed. Histological examination showed whole mucosal necrosis and vacuolation with aerogenesis in the submucosa and muscle layer of the bladder. Urine and mucosal surface cultures revealed Escherichia coli infection. After operation, the general condition was improved. Thirty six cases of emphysematous cystitis have been reported in Japan including this case. Successful treatment with cystectomy under the life threatening condition was reported for the first time.

Acidosis↗
PubMed1980

[Orbito-rhino-cerebral phycomycosis (mucormycosis): report of a case].

The case of a 15 year old white man, diabetic in cetoacidosis, with a orbit-rhino-cerebral phycomycosis is reported. The illness had an acute onset and the treatment was iniciated early with Amphotericin-B and unilateral osteotomy of maxillary and ethmoidal sinus. With this treatment the patient did well with residuals of ophtalmoplegia and amaurosis on the right. Interesting investigation aspects are the occluded internal carotid on the same side of the affected orbit and the CAT-SCAN finding of moderated ventricular dilatation (two months after hospital admission). Mycology, pathophysiology, histopathology, clinical aspects, diagnosis and therapy are discussed, comparing the findings of this case with avaliable literature. An increased number of survivors can be expected with earlier recognition and more aggressive therapy. Treatment of the underlying debilitating disease, Amphotericin-B and surgical debridement of necrotic tissue, are frequently necessary such as observed in the case reported. The favorable results obtained with the proposed managment are stressed.

Acidosis↗