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PubMed1995

Liver transplantation in two cases of propionic acidaemia.

Orthotopic liver transplantation (OLT) was performed in two patients with propionic acidaemia, a 7-year-old boy and a 9-year-old girl, diagnosed with a severe neonatal form with high risk of metabolic decompensation. In both cases the metabolic liver functions recovered within the 12 postoperative hours; no clinical symptoms of propionic acid toxicity, metabolic acidosis, severe hyperammonaemia, hyperglycinaemia or haematological abnormalities were observed. In both cases insulin-dependent diabetes mellitus occurred early after OLT (persisting in the boy's case). Severe post-transplantation complications were observed (acute rejection and CMV infection in both patients) which did not trigger metabolic decompensation. The boy developed chronic rejection and vanishing bile duct syndrome due to incomplete hepatic arterial thrombosis. He required permanent in-patient care with chronic hyperammonaemia and neurological sequelae involving the basal ganglia and died 15 months after OLT. The girl left hospital after 2 months and is presently leading a normal life with almost no dietary protein restriction (40 g protein per day). Urinary urea excretion and daily protein intake increased after liver transplantation. Propionyl- and tiglylglycine disappeared immediately after OLT. Urinary methylcitrate and 3-hydroxypropionate remained at concentrations corresponding to those before OLT. However, the total of all characteristic metabolites of organic acid analysis was reduced to 50-60% of the values before OLT in both patients. Propionylcarnitine was still detected at significant concentrations. Plasma odd-chain fatty acid concentrations decreased continuously after OLT only in the girl's case. Tissue of both transplanted livers showed increased odd-chain fatty acid concentrations 9 and 15 months after OLT, respectively, in both patients. We consider that at present OLT should only be performed in severe forms of propionic acidaemia.

Acidosis↗
PubMed2001

Enteric conversion after bladder-drained pancreatic transplantation; a simple and safe salvage procedure.

OBJECTIVE: To present our experience with conversion from bladder to enteric drainage after simultaneous pancreatic and renal transplants, so that new transplant centres know that it is both safe and effective. DESIGN: Retrospective study. SETTINGS: Teaching hospital, Republic of Ireland. SUBJECTS: Six patients who had simultaneous pancreatic and renal transplants for insulin-dependent diabetes and who subsequently developed complications of bladder drainage including recurrent episodes of dehydration and metabolic acidosis (n = 3), haematuria (n = 2), and urinary tract infections (n = 1). INTERVENTION: Conversion to enteric drainage. MAIN OUTCOME MEASURE: Resolution of symptoms. RESULTS: All symptoms resolved, but one patient each developed pulmonary oedema, haematuria, and prolonged ileus. All three complications resolved on conservative treatment. All patients are well with surviving grafts a mean of 40 months later (range 19-50). CONCLUSION: Conversion to enteric drainage is safe and effective in patients with refractory metabolic or urological complications of bladder drainage after simultaneous pancreatic and renal transplantation.

Adult↗
PubMed1985

Recurrent high-permeability pulmonary edema associated with diabetic ketoacidosis.

Delayed-onset pulmonary edema complicating severe diabetic ketoacidosis was observed twice in one patient. Hemodynamic measurements during the second episode showed normal transmural pulmonary capillary wedge pressure, suggesting an alteration in alveolocapillary permeability. Hyperventilation and acidosis may underlie this alteration. Vigorous fluid therapy, while decreasing oncotic pressure, may also contribute to the pulmonary edema. The two episodes in one patient suggest that pulmonary microvascular diabetic angiopathy may predispose some diabetics with severe ketoacidosis to increased-permeability pulmonary edema.

Adult↗
PubMed2004

Autonomic dysregulation as a basis of cardiovascular, endocrine, and inflammatory disturbances associated with obstructive sleep apnea and other conditions of chronic hypoxia, hypercapnia, and acidosis.

Obstructive sleep apnea has traditionally been viewed as a structural disease. A multitude of systemic endocrine and cardiovascular abnormalities have been previously attributed to the prevalence of obesity in these patients. A growing body of clinical evidence, however, points to a relationship between sleep apnea and its systemic abnormalities independent of obesity. We hypothesize that this association is based on a maladaptive autonomic response of chemoreceptors, reacting to the hypoxia, hypercapnia, and acidosis of sleep apnea. The elevated sympathetic response triggers an inflammatory cascade that results in a myriad of downstream consequences including insulin resistance, hypertension, diabetes, atherosclerosis and metabolic syndrome. The sympathetic bias and endocrine disturbances may further exacerbate sleep disturbance in a potentially pernicious cycle. Our proposal may extend to any chronic respiratory or metabolic conditions that manifest hypoxia, hypercapnia, and acidosis and elicit a maladaptive autonomic and inflammatory response.

Acidosis↗
PubMed1996

Mitochondrial gene mutations in patients with insulin-dependent diabetes mellitus in Taiwan.

We studied the prevalence of mitochondrial gene mutations in subjects with insulin-dependent diabetes mellitus (IDDM) in a Chinese population living in Taiwan. Eighty-four subjects with insulin-dependent diabetes mellitus and 105 unrelated normal controls were recruited in the present study. Both an A-to-G mutation at position 3243 and a mutation at position 8,344 of the mitochondrial DNA were screened by polymerase chain reaction-restriction fragment length polymorphism methods and confirmed by direct DNA sequence analysis. The insulin secretory response was assessed by the C-peptide response to glucagon administration. Among 84 IDDM patients, two (2.4%) subjects were found to carry the 3,243 nucleotide pair (np) mutation. There was no np 8,344 mutation in this series. Of the two subjects carrying a mitochondrial gene mutation, case 1 manifested initially as gestational diabetes mellitus. Manifestation of case 2 was consistent with MELAS, a syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes. The pancreatic beta cell reserve was reduced, as the glucagon-stimulated C-peptide response was very low in these two cases. HLA genotyping studies revealed that case 2 carried DRB1*0301-DQA1*0501-DQB*0201/ DRB1*0405-DQA1*0301-DQB1*0302, which was the most susceptible genotype to IDDM in our population. Anti-GAD65 antibody was also positive in this patient. In addition to the nuclear genes, a defective mitochondrial gene might contribute to some of the clinical cases with IDDM.

Adult↗
PubMed1997

An unusual case of mesenteric ischemia in a patient with new-onset diabetes mellitus.

The early detection of acute mesenteric ischemia is crucial for the preservation of bowel viability. The emergency physician must have a high index of suspicion to identify mesenteric ischemia when there is a paucity of physical examination findings. We discuss the case of a patient who presented to the emergency department with confusion, hyperglycemia, abdominal tenderness, and metabolic acidosis who also developed mesenteric ischemia.

Aged↗
PubMed1997

Diabetes mellitus associated with 3243 mitochondrial tRNA(Leu(UUR)) mutation: clinical features and coenzyme Q10 treatment.

Diabetes mellitus associated with mitochondrial tRNA mutation at position 3243(DM-Mt3243) is a new disease. Patients have a distinctly different picture from MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). During observations at the Saiseikai Central Hospital, the following findings were noted in DM-Mt3243 patients: DM-Mt3243 patients are diagnosed earlier with diabetes, compared to NIDDM (non-insulin dependent diabetes mellitus) controls without family history. DM-Mt3243 patients often need insulin more often than NIDDM controls without family history. Post-treatment neuropathy and insulin edema are often found in DM-Mt3243, and the two phenomena possibly have a similar pathophysiology related to mitochondrial dysfunction. Ambiguous psychiatric disorders of functional psychosis are observed frequently in DM-Mt3243. Mild headache is common in DM-Mt3243 cases. Ambiguous neuromuscular abnormalities such as sleep disturbance, paresthesia of the legs, edema of the legs, and palpitation may be symptoms associated with mitochondrial dysfunction in DM-Mt3243. Coenzyme Q may be effective in the relief of these neuromuscular symptoms.

Adult↗
PubMed1994

Mitochondrial gene defects in patients with NIDDM.

Non-insulin-dependent diabetes mellitus (NIDDM) has a strong genetic component and maternal factors have recently been implicated in disease inheritance. The mitochondrial myopathies are a group of diseases which often show maternal inheritance as a result of mtDNA defects; some patients have impaired glucose tolerance. Occasional families with maternally inherited diabetes and deafness associated with a deletion or point mutation of mtDNA have been reported. To assess the importance of mitochondrial gene defects in NIDDM, 150 unrelated diabetic subjects from Wales, UK and 68 unrelated patients with diabetes and at least one affected sibling from England, UK were studied. Southern blot analysis did not show any large mtDNA deletions or duplications. One patient had a mutation in the mitochondrial tRNAleu(UUR) gene at bp 3243. This mutation is commonly associated with the syndrome of mitochondrial encephalomyopathy, lactic acidosis and stroke like episodes (MELAS). Study of this patient and his siblings showed a distinct form of late-onset diabetes associated with nerve deafness but no clinical features of the MELAS syndrome. No diabetic subject was shown to have the mtDNA mutation at position 8344 (tRNA(lys)) which has previously been described in the syndrome of mitochondrial encephalomyopathy and red-ragged fibres (MERRF). The role of other mitochondrial gene defects in diabetes and the pathophysiological basis of glucose intolerance in patients with the MELAS mutation requires further elucidation.

Base Sequence↗
PubMed1983

Successful therapy for rhinocerebral mucormycosis with associated bilateral brain abscesses.

A case of extensive rhinocerebral mucormycosis, with associated bilateral brain abscesses, occurred in a man with diabetes. A Rhizopus sp grew from the initial nasal biopsy specimens. Successful therapy consisted of correcting metabolic acidosis, using serial computed tomographic (CT) scans to follow the progressive course of brain involvement from cerebritis to encapsulated abscesses, and performing successive biopsies to determine the adequacy of treatment. On 18-month follow-up, the patient had returned to full-time employment with minimal neurologic impairment. With CT scanning and aggressive therapy, rhinocerebral mucormycosis with bilateral brain involvement can be cured.

Adult↗
PubMed1985

Intrinsic stiffening of red blood cells as the fundamental cause of diabetic nephropathy and microangiopathy: a new hypothesis.

It is proposed that stiffened red cells can interfere with normal microvascular and glomerular function. In diabetics intrinsic stiffening of red cells is intensified during poor metabolic control when plasma osmolarity is increased. Hypoxia, acidosis, catecholamines and other changes in red cell environment also increase red cell stiffness. Exercise proteinuria may help to identify individuals with the greatest intrinsic stiffening of red cells which appears to be due to the disposition of spectrin molecules rather than to changes in the lipid bilayer. Stiffened red cells may impede blood flow in the microcirculation and stimulate an autoregulated vasodilation which increases perfusion pressure, enhancing transudation. In the absence of vasodilation, stasis will lead to vascular occlusion and localised ischaemic necrosis. If diabetic microangiopathy is caused by abnormal haemorheology then the possibility exists that the complications of diabetes might be alleviated or prevented by agents which enhance red cell flexibility and improve blood rheology.

Blood Viscosity↗
PubMed1983

The status of metformin in Canada.

During the 1970s two biguanide drugs, phenformin and metformin, were used to control hyperglycemia. Phenformin was phased out of the Canadian market because it carried an unacceptable risk of causing lactic acidosis, but metformin remains available. All documented cases of lactic acidosis associated with metformin administration, which are rare, have occurred abroad in patients who were taking the drug in spite of having contraindications to its use. The two drugs are metabolized differently, phenformin being deactivated and concentrated in the liver, and metformin being excreted rapidly, unchanged, by the kidneys. In properly selected diabetic patients therapeutic doses of metformin do not raise the blood levels of intermediary metabolites enough to induce ketoacidosis or lactic acidosis. The safety of the drug is supported by the clinical experience over about 56,000 patient-years in Canada.

Acidosis↗
PubMed1992

[MELAS associated with diabetes mellitus and point mutation in mitochondrial DNA].

Point mutation of mitochondrial DNA has been described in the blood from a MELAS patient. The 39-year-old patient developed progressive dementia, stroke-like episodes, heart conduction defect (Lown-Ganong-Levin syndrome) and cortical blindness. CT scan revealed brain atrophy and low density areas in the bilateral occipital lobes. Laboratory tests showed hyperglycemia and lactic acidosis. Muscle biopsy showed ragged red fibers on Gomori trichrome staining. He was clinically diagnosed as having MELAS and insulin-dependent diabetes mellitus. Onset of diabetes mellitus and MELAS was almost same. Family history showed his mother's brother and sisters had also insulin-dependent diabetes mellitus. We amplified the leucine (UUR) tRNA gene from the patient's blood with polymerase chain reaction (PCR) and analysed it by restriction enzyme analysis and sequencing. Genetic analysis showed A-to-G substitution at the nucleotide position 3243 in the leucine (UUR) tRNA gene. This substitution made a new restriction site Apa I. Mutant DNA coexisted with wild type DNA (heteroplasmy). It is shown that in some types of mitochondrial encephalomyopathies, especially patients of Kearns-Sayre syndrome (KSS), diabetes mellitus is often complicated. And in KSS patients insulin receptor in normal, but insulin secretion from beta cells of pancreas is decreased. In MELAS patients, however, has diabetes mellitus been reported to be rarely complicated and relationship between MELAS and diabetes mellitus is not done. As far as we know, two cases, including ours, with genetically diagnosed MELAS have been reported to have diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

Metabolic effects of dichloroacetate in patients with diabetes mellitus and hyperlipoproteinemia.

Dichloroacetate is known to reduce plasma glucose and triglycerides in diabetic and starved animals and to lower plasma lactate under various experimental conditions. To investigate its metabolic effects in man, we administered oral doses (3 to 4 g) of dichloroacetate as the sodium salt to patients with diabetes mellitus or hyperlipoproteinemia or both for six to seven days. Dichloroacetate significantly reduced fasting hyperglycemia an average of 24 per cent (P less than 0.01) from base line and produced marked, concomitant falls in plasma lactate (73 per cent; P less than 0.05 to less than 0.01) and alanine (82 per cent; P less than 0.01 to less than 0.001). In addition, it significantly decreased plasma cholesterol (22 per cent; P less than 0.01 to less than 0.001) and triglyceride (61 per cent; P less than 0.01) levels while increasing (71 per cent; P less than 0.01) plasma ketone-body concentrations. Plasma insulin, free fatty acid and glycerol levels were not affected. Serum uric acid rose, whereas excretion and renal clearance fell. Some patients experienced mild sedation, but no other laboratory or clinical evidence of adverse effects was noted during or immediately after the treatment phase.

Acetates↗
PubMed1980

Metabolic effects and pharmacokinetics of intravenously administered dichloroacetate in humans.

Dichloroacetate decreases plasma glucose, lactate, and alanine concentrations in normal and diabetic subjects, and lowers lactate concentrations and increases survival in animals with experimentally induced lactic acidosis. The relationship between these effects and plasma dichloroacetate concentrations have not been previously studied in man. Dichloroacetate (1-50 mg/kg) was infused over 30 min to 16 healthy subjects and plasma drug concentrations were followed by gas chromatography over the next 8 h. Peak plasma concentrations were linearly related to the dose (r = 0.98, p < 0.001) up to 30 mg/kg, above which 4 of 7 subjects had disproportionately high plasma drug concentrations. Nonlinear disposition was also indicated by the convex decreasing plasma elimination curves; levels declining less rapidly initially than later. At plasma concentrations below 10 micrograms/ml, elimination was monoexponential with a half-life of 32 +/- 11 min (mean +/- SD). Plasma drug clearance also decreased with doses greater than 20 mg/kg. Within 2 h of administration of the maximally effective dichloroacetate dose of 35 mg/kg, plasma lactate concentrations fell 75% below baseline and alanine fell 50% below baseline, while blood glucose was unaffected.

Acetates↗

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