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PubMed2006

Detection of low levels of the mitochondrial tRNALeu(UUR) 3243A>G mutation in blood derived from patients with diabetes.

BACKGROUND: Mutations in the human mitochondrial genome have been suspected to play a significant role in the etiological development of mitochondrial diabetes. Detection of the 3243A>G mutation in the mitochondrial transfer RNALeu(UUR) gene (MTTL1), especially at low heteroplasmy levels, is highly desirable since it facilitates the diagnosis and subsequent management of the disease. The proportions of mutant mitochondrial DNA (mtDNA) can vary between tissues and are usually significantly higher in muscle than in blood, but muscle biopsies from patients with diabetes are rarely available. METHODS: Here, we describe a technique that can not only determine the presence of MTTL1 3243A>G, but can also estimate the percentage of mutant DNA. The technique is based on the use of the WAVE system for the high-performance liquid chromatography (HPLC)-mediated analysis of mutation-specific restriction fragments derived from mutant PCR amplicons. PCR amplicon restriction fragment analysis by HPLC (PARFAH) can also be used for the detection of other mutations. RESULTS: This PARFAH analytical approach led to the discovery of the 3243A>G mutation in blood samples from a series of patients who had initially been reported to lack the mutation, even though matrilineal relatives had been shown to harbor the mutation associated with maternally inherited diabetes and deafness (MIDD) or mitochondrial myopathy encephalopathy lactic acidosis stroke-like episodes (MELAS) phenotypes. We have established that the PARFAH method can reliably detect as little as 1% mutant DNA in a sample, which would normally be missed by commonly used gel electrophoresis or sequencing methods. CONCLUSIONS: The PARFAH method not only provides a sensitive, high-throughput, and cost-effective strategy for the detection of low levels of mtDNA mutations in peripheral tissues, but also facilitates the estimation of the percentage of mutant DNA in the sample. The fact that samples can be readily obtained from peripheral tissues in many cases will avoid the need for invasive muscle biopsies. Our ability to detect low levels of mtDNA mutations in blood samples of carriers will allow us to reassess the prevalence of the MTTL1 3243A>G mutation in patients with diabetes.

Adolescent↗
PubMed1994

[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy].

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1994

The high prevalence of the diabetic patients with a mutation in the mitochondrial gene in Japan.

Recently, an A to G transition at position 3243 in transfer ribonucleic acidLeu(UUR) [the 3243 base-pair (bp) mutation] originally found in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes has been identified in patients with diabetes and deafness. To determine the prevalence of the diabetic patients with this mutation in Japan, we screened 550 randomly selected cohorts of diabetic patients without prior information about clinical features such as type of diabetes, family history of diabetes, age of onset, and mode of therapy. We have identified 5 patients with this mutation, suggesting that approximately 0.9% of diabetic patients have the 3243 bp mutation. However, there were no subjects with this mutation in 250 controls with normal glucose tolerance. The percentage of mutant DNA in whole mitochondrial DNA did not correlate to the degree of symptoms. We conclude that the 3243 bp mutation in the mitochondrial gene plays an important part as a cause of diabetes in Japan.

Adolescent↗
PubMed1983

Hyperkalaemia in patients in hospital.

Significant hyperkalaemia occurred in 406 out of 29 063 patients admitted to a major Scottish teaching hospital in one year (1.4%). Mortality was higher in these patients than in control patients and was strongly correlated with the severity of the hyperkalaemia. Overall seven deaths were directly due to hyperkalaemia (out of 58 deaths among patients with hyperkalaemia). Factors contributing to a poor prognosis were severity and speed of onset of hyperkalaemia and the presence of appreciable renal impairment. Patients with hyperkalaemia were older and more likely to be male; this trend was present in all diagnostic subcategories. Genitourinary disease, gastrointestinal disease, and cancer were significantly more common among the patients with hyperkalaemia than the controls. Hyperkalaemia due to drug treatment was invariably mild and non-fatal, whereas genitourinary disease was often associated with moderate to severe hyperkalaemia, which in two cases proved fatal. Use of electrocardiographic monitoring was rare, and although the treatment of hyperkalaemia was effective, it was often used when not required. Hyperkalaemia is a potential hazard in diabetic ketoacidosis, and use of potassium supplements should be carefully monitored during correction of the acidosis.

Diabetic Ketoacidosis↗
PubMed2000

[Severe lactic acidosis due to metformin therapy in a patient with contra-indications for metformin].

A 52-year-old woman with a medical history of diabetes mellitus type 2, chronic alcoholism and liver function disorders was hospitalized because of complaints of haematemesis, abdominal complaints and dyspnoea. This was due to a severe lactic acidosis caused by acute alcohol intoxication and the use of metformin. With bicarbonate infusion and haemofiltration, the lactic acidosis disappeared, but she developed a distributive shock with multiple organ failure and died 23 days after admission. Lactic acidosis is a rare but serious adverse effect of metformin. Almost all patients described had contraindications to the drug, like renal failure, liver disease, alcohol abuse, and intercurrent conditions causing hypoxia or ischaemia. It is important to be aware of the circumstances in which metformin should not be prescribed.

Acidosis, Lactic↗
PubMedDate not supplied

Unusual renal involvement during diabetic ketoacidosis (DKA) in a newly diagnosed type I diabetic child.

A 10-year-old boy, in a precomatose state, was admitted to our Endocrine Unit for diabetic ketoacidosis. It took unusually long to reequilibrate the acidosis despite a bicarbonate drip. On the 4th day the patient suddenly complained of an acute abdominal pain associated with macrohematuria and oliguria; ankle edema was evident. No radio-opaque image was detected along the urinary tract. An intravenous pyelogram (IVP) showed an almost totally silent left kidney. Ten days later a control IVP showed complete normality of both kidneys. We postulated that the serious and protracted dehydration might have resulted in the formation of a blood clot along the renal tract and that the rehydration may have subsequently removed it.

Acute Kidney Injury↗
PubMed1969

Cerebral syndromes of diabetes mellitus.

Three labile diabetic patients had recurring episodes of altered sensorium. Each had severe cerebrovascular disease with superimposed metabolic derangements, including ketoacidosis, hyperglycemia without ketosis, mild uremia, and possibly cerebral edema. Two of the patients were examined postmortem. Severe leptomeningeal scarring, basal ganglial calcification and destruction of small intracerebral vessels without evidence of large vessel atherosclerosis were found unexpectedly in one patient, a rare occurrence in this country although recently reported from Europe. The other patient had large vessel atherosclerosis only. The clinical expression of the vascular disease was modified by concurrent abnormalities and reflected the sum total of the complexities which coexisted. The pathophysiology of the unconscious state necessarily depends on the inciting factors. Ketoacidotic coma is associated with depressed cerebral oxygen consumption. Spinal fluid pH is usually maintained during ketosis but is sometimes lowered inadvertently during bicarbonate therapy, with resultant coma. Other variables influencing the clinical expression, with or without ketosis, would include, among others, blood viscosity alterations, rapid decrements in blood sugar, and existing degrees of lactic acidosis. The increasing life-span of the juvenile diabetics, favorably influenced by improved management and recently by hemodialysis, may uncover vascular complications heretofore rarely seen and create additional diagnostic and therapeutic enigmas.

Adult↗
PubMedDate not supplied

Ketoalkalosis as a result of triple derangement of acid-base equilibrium in a diabetic patient.

A diabetic patient presented with weight loss, ketosis, and hyperventilation, thus mimicking the clinical picture of diabetic ketoacidosis. Laboratory investigations revealed alkalemia and a pattern consistent with a triple derangement of acid-base equilibrium: respiratory alkalosis, metabolic acidosis and metabolic alkalosis. High cortisol level suggested a genesis of ketosis different from diabetes mellitus. The patient died suddenly from acute gastrointestinal bleeding. Autopsy showed a carcinoma of the head of the pancreas with secondary portal hypertension and rupture of varices. Pulmonary micrometastases were demonstrated. It is suggested that stress hormones were the main cause of the 'ketoalkalotic' pattern observed.

Aged↗
PubMed2006

["Ghost peak" in gas chromatography in a delirious woman with severe metabolic acidosis. Intoxication with an unknown substance?].

HISTORY AND CLINICAL FINDINGS: A 31-year-old female with known type 1 diabetes mellitus was referred because of symptomatic hyperglycemia. On admission she was delirious and impressed with marked Kussmaul breathing. All other vital signs were normal. INVESTIGATIONS: Blood serum glucose concentration was 26.4 mmol/l. Arterial blood gas analysis revealed massive metabolic acidosis (pH 6.80) with an elevated anion gap (21 mmol/l) and a marginally increased osmolar gap (21,5 mOsm/l). TREATMENT AND COURSE: Despite normalization of the serum glucose and acidemia after administration of normal saline, insulin and bicarbonate, the delirium persisted, and the possibility of an additional intoxication had to be considered. Serum headspace analysis for intoxication with solvents (gas chromatography) finally detected a "ghost peak", which could not be assigned to any established substance. The same peak was, however, found in a healthy subject's serum and was found to be a "toluene peak". Toluene is contained as "contaminator" in gels in blood collection tubes. The patient gradually regained consciousness and "merely" suffered from diabetic ketoacidosis associated with cocaine use. CONCLUSION: The differential diagnosis of high anion gap metabolic acidosis includes among other reasons intoxications with different kinds of solvents. When looking for solvents in the serum when poisoning is suspected (headspace analysis), only blood collection tubes without gel (EDTA plasma) should be used, because all gels contain solvents (in this case toluene).

Acid-Base Equilibrium↗
PubMed1995

Point mutation of the mitochondrial tRNA(Leu) gene (A 3243 G) in maternally inherited hypertrophic cardiomyopathy, diabetes mellitus, renal failure, and sensorineural deafness.

The A 3243 G mutation of the mitochondrial tRNA(Leu) gene was found to segregate with maternally inherited diabetes mellitus, sensorineural deafness, hypertrophic cardiomyopathy, or renal failure in a large pedigree of 35 affected members in four generations. Presenting symptoms almost consistently involved deafness and recurrent attacks of migraine-like headaches, but the clinical course of the disease varied within and across generations. The A 3243 G mutation has been previously reported in association with the mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode syndrome (MELAS) and with diabetes mellitus and deafness. To our knowledge, however, hypertrophic cardiomyopathy is not a common feature in people with the A 3243 G mutation and renal failure has not been hitherto reported in association with this mutation. The present observation gives additional support to the variable clinical expression of mtDNA mutations in humans.

Adenine↗
PubMed2002

Quality of prereferral care in patients with chronic renal insufficiency.

BACKGROUND: Appropriate care in chronic renal insufficiency (CRI) includes blood pressure and diabetes control, as well as the investigation and management of anemia, acidosis, and bone disease. There is a lack of data on the control of these parameters at the time of referral to a nephrologist. Similarly, early referral has been emphasized in the literature, yet very little published has examined current referral patterns. METHODS: A single-center retrospective/prospective review of all new outpatient referrals to nephrologists in Halifax, Canada, in 1998 and 1999 was conducted to identify patients with CRI (serum creatinine > 1.6 mg/dL [141 micromol/L] for men or >1.2 mg/dL [106 micromol/L] for women). Quality of prereferral care was based on data from the initial clinic visit. RESULTS: Of 1,050 charts reviewed, 411 patients met the study criteria. Twenty-six percent of patients had diabetes mellitus, 18% were referred with a calculated glomerular filtration rate less than 15 mL/min, and blood pressure was optimally controlled (<130 mm Hg systolic and <80 mm Hg diastolic) in only 24%. Only 44% of patients were administered an angiotensin-converting enzyme inhibitor. Patients were administered an average of 1.9 antihypertensive agents. Significant anemia (hemoglobin < 10 g/dL) was present in 21%, and appropriate investigations were performed in only 35% of these patients. Calcium levels less than 8.6 mg/dL (2.15 mmol/L) were found in 19% of patients, and only 14% of these patients were started on calcium supplement therapy. Phosphate levels greater than 5.0 mg/dL (1.6 mmol/L) were seen in 20% of patients, and 14% of these patients were on phosphate-binder therapy. Parathyroid hormone levels were more than five times normal values in 18% of patients, and 25% of patients had bicarbonate levels less than 23 mmol/L. CONCLUSIONS: A significant proportion of patients referred with CRI receive inadequate prereferral care. Continuing education programs and referral guidelines must not only emphasize the importance of early referral, but also address the related consequences of CRI to delay the progression of renal disease and avoid complications.

Acidosis↗
PubMed2004

The CORE Diabetes Model: Projecting long-term clinical outcomes, costs and cost-effectiveness of interventions in diabetes mellitus (types 1 and 2) to support clinical and reimbursement decision-making.

OBJECTIVES: We have developed an Internet-based, interactive computer model to determine the long-term health outcomes and economic consequences of implementing different treatment policies or interventions in type 1 and type 2 diabetes mellitus. The model projects outcomes for populations, taking into account baseline cohort characteristics and past history of complications, current and future diabetes management and concomitant medications, screening strategies and changes in physiological parameters over time. The development of complications, life expectancy, quality-adjusted life expectancy and total costs within populations can be calculated. METHODS: The model is based on a series of sub-models that simulate important complications of diabetes (cardiovascular disease, eye disease, hypoglycaemia, nephropathy, neuropathy, foot ulcer, amputation, stroke, ketoacidosis, lactic acidosis and mortality). Each sub-model is a Markov model using Monte Carlo simulation incorporating time, state, time-in state, and diabetes type-dependent probabilities derived from published sources. Analyses can be performed on cohorts with type 1 or type 2 diabetes. Cohorts, defined in terms of age, gender, baseline risk factors and pre-existing complications, can be modified or new cohorts defined by the user. Economic and clinical data in the model can be edited, thus ensuring adaptability by allowing the inclusion of new data as they become available; creation of country- or provider-specific versions of the model; and allowing the investigation of new hypotheses. CONCLUSIONS: The CORE Diabetes Model allows the calculation of long-term outcomes, based on the best data currently available. Diabetes management strategies can be compared in different patient populations in a variety of realistic clinical settings, allowing the identification of efficient diabetes management strategies.

Adult↗
PubMedDate not supplied

[Diabetic nephropathy: oral anti-diabetic agents or insulin?].

Diabetic nephropathy is a microvascular complication, as well as retinopathy and neuropathy of type 1 and type 2 diabetes mellitus. The pathogenesis directly correlates with hyperglycemia. The direct glucose toxicity, hypercoagulability, oxidative stress and endothelial dysfunctions play a role. Strict glycemic control with HbA1c levels <7% for 10 yrs is associated with a 25% microvascular end point reduction. Patients underwent pancreas transplantation, and after 10 yrs the present nephropathy and functional and structural abnormalities have regressed. Diabetic nephropathy alters the pharmacokinetic profile of almost all oral anti-diabetic agents, as well as insulin metabolism; therefore, it is imperative to determine creatinine clearance. Renal failure requires insulin therapy. Incipient diabetic nephropathy allows very limited indications to oral anti-diabetic agents because of the altered pharmacokinetic profile and side effects (hypoglycemia with secretagogues agents, lactic-acidosis with metformin and other biguanides, and hydric retention and weight gain with thiazolidinediones). Moreover, oral anti-diabetic agents reduce the percentage of HbA1c by no more than 1.5%. Insulin therapy is preferred, with a dose reduction when creatinine clearance is <60 mL/m. To control better the post-prandial glycemic peak, it is useful to use bolus insulin analogues at each meal and basal intermediate-acting insulin at bedtime to mimic the natural insulin patterns as far as possible.

Clinical Trials as Topic↗