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At least 1,549 records · Page 86Linked to original sources
PubMed1996

The T-C(8356) mitochondrial DNA mutation in a Japanese family.

A rare point mutation at nucleotide position 8356 in the transfer RNA gene in mitochondrial DNA was found in a Japanese family. Our proband had migraine and dementia associated with lactic acidosis in addition to myoclonic epilepsy with ataxia and ragged-red fibres in a muscle biopsy specimen consistent with the clinical characteristics of myoclonic epilepsy with ragged-red fibres (MERRF). His mother, who had the same point mutation, also had migraine but without myoclonus or ataxia. His aunt, who had the same point mutation and migraine, developed diabetes mellitus, encephalomyopathy and several stroke-like episodes associated with lactic acidosis (MELAS). This is the third family with the rare mutation seen in American and Italian families. The mutation may not be specific to Caucasians, and is probably closely related to the MERRF/MELAS overlap syndrome.

Adult↗
PubMed1981

Treatment of ketoacidosis and diabetic coma by continuous intravenous administration of water, glucose, regular insulin and electrolytes.

The therapeutical scheme prescribed for the treatment of ketoacidosis and diabetic coma before the 1970s is quite stereotyped and inflexible in regard to the routes of administration and doses of insulin, as well as the management of dehydration and metabolic acidosis. This paper reports the experience of the Endocrinology Service of the General Hospital of the "La Raza" Medical Center for over 10 years. 35 patients with diabetic ketoacidosis were included in a treatment by continuous intravenous administration of glucose, water, insulin and potassium. These patients were programmed in a 12 hour study. The dose of insulin was estimated at a ratio of 1 IU per 1 gm of excess glucose over 2.0 gm/l. The amount of glucose administered was in ratio to the caloric requirements per kilo of bodyweight of the individual patient. The volume of water was administered on the basis of the degree of dehydration estimated. The potassium was prescribed at a ratio of 20 mEq/l of solution, or more if necessary. The patient's recovery was observed during a period of from 7 to 10 hours, with improvement of the hyperglycemia, dehydration and metabolic acidosis. The method has allowed us to observe the diabetic patient's rapid recovery when he has been in ketoacidosis or coma, without complications such as hypoglycemia. No mortality was observed.

Diabetic Coma↗
PubMed1997

Screening of patients with maternally transmitted diabetes for mitochondrial gene mutations in the tRNA[Leu(UUR)] region.

To investigate the prevalence and clinical characteristics of diabetes mellitus caused by mitochondrial gene mutations in the tRNA[Leu(UUR)] region, a known 'hot spot' for pathogenic mutations, we screened 440 diabetic patients with diabetic mothers for 11 mitochondrial gene mutations reported in mitochondrial neuromuscular disorders; nucleotide pairs (np) 3250, 3251, 3252, 3254, 3256, 3260, 3271, 3291, 3302 and 3303 in addition to an A to G transition at np 3243. The dot-blot hybridization method using 32P-labelled sequence-specific oligonucleotides as probes was used. One subject carrying a T to C transition at np 3271 and seven carrying the A to G transition at np 3243 were identified, while none of the other diabetic patients screened had these mutations in the tRNA[Leu(UUR)] region. The patient with the 3271 mutation, a 39-year-old male, had excellent glycaemic control with diet alone and had neither hearing impairment nor symptoms suggesting mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Thus, among patients with maternally transmitted diabetes, the prevalence of the 3271 mutation was approximately one-seventh that of the 3243 mutation, and other mutations are even more rare in the mitochondrial tRNA[Leu(UUR)] region.

Adult↗
PubMed2003

Massive ischemic intestinal necrosis at the onset of diabetes mellitus with ketoacidosis in a three-year-old girl.

A previously healthy 3-year-old girl had severe diabetic ketoacidosis complicated by hypovolemic shock. When her abdominal pain and acidosis failed to improve despite vigorous fluid resuscitation and insulin therapy, further investigation found an intestinal perforation. At laparotomy, gangrenous bowel was found, requiring an extensive enterectomy from the distal jejunum to the transverse colon; less than 90 cm of viable small intestine remained. The child survived a complicated postoperative course and currently is thriving on a normal diet.

Child, Preschool↗
PubMed2000

Mitochondrial DNA disorders.

UNLABELLED: Over 100 pathogenic point mutations and 200 deletions, insertions, and rearrangements have been identified since the first mitochondrial DNA mutations were described in 1988. About 60% of the point mutations affect mitochondrial tRNAs, 35% affect polypeptide subunits of the respiratory chain, and 5% affect mitochondrial ribosomal RNAs. The clinical phenotypes of mitochondrial tRNA disease span the spectrum of all known oxidative phosphorylation disorders and include MELAS, MERRF, Leigh syndrome, PEO, deafness, diabetes, sideroblastic anemia, myoclonus, skeletal myopathy, cardiomyopathy, and renal tubular acidosis. Mutations in respiratory chain proteins encoded by mtDNA result in phenotypes ranging from exercise intolerance to blindness, ataxia, dystonia, dementia, and Leigh syndrome. CONCLUSION: The primary disorders of oxidative phosphorylation are commonly associated with a delayed age of onset, organ selectivity, and an episodic, progressive course. Organ-specific, non-ATP related functions of mitochondria are discussed as important considerations in evaluating the pathogenesis of mitochondrial disease.

DNA, Mitochondrial↗
PubMed2006

Use of base in the treatment of acute severe organic acidosis by nephrologists and critical care physicians: results of an online survey.

BACKGROUND: Acute severe metabolic acidosis associated with lactic acidosis or ketoacidosis can have severe detrimental effects on organ function, and might contribute to mortality. A general consensus exists that elimination of the cause of the acidosis is essential for treatment, but there is controversy concerning the use of base for the treatment of these disorders. Some physicians advocate administration of base when the acidosis is severe to prevent a decrease in cardiac output, whereas others oppose administration of base even when the acidosis is severe given the potential compromise of cardiac function. Nephrologists and critical care specialists are often the physicians developing recommendations for the treatment of severe acid-base disorders. METHODS: A short online survey of 20 questions was developed to assess the approach to the treatment of acute metabolic acidosis of program directors of fellowship programs and experts from the specialties of critical care and nephrology. RESULTS: Although there was variability among individual physicians from both specialties, a larger percentage of nephrologists than critical care physicians queried recommended administration of base for the treatment of lactic acidosis (86% vs 67%) and ketoacidosis (60% vs 28%). Also, critical care physicians in general used a lower level of blood pH when deciding when to initiate treatment. Of the physicians who gave base, most utilized sodium bicarbonate as the form of base given. CONCLUSIONS: The results of this survey indicate that the decisions whether to use base for the treatment of acute severe metabolic acidosis, and under which circumstances, vary among physicians, and indicate the need for further studies to develop evidence-based guidelines for therapy.

Acidosis↗
PubMed1996

Risk factors for ifosfamide nephrotoxicity in children.

BACKGROUND: Risk factors for long-term nephrotoxicity after ifosfamide for childhood cancers are not fully known. We have studied patient-related and treatment-related risk factors for chronic ifosfamide nephrotoxicity. METHODS: A group of 23 children who had received ifosfamide at age 2.1-16.2 years (median 6.9) for various cancers were assessed for nephrotoxicity, at 1-28 (2) months after the end of treatment, by renal function testing, laboratory values, and a grading score (none, mild, moderate, severe). No patient had received cisplatin or undergone nephrectomy. 13 children were reassessed at 10-26 (23) months; eight had died and two were not evaluable. The median total ifosfamide dose was 100.8 (9.0-160.4) g/m2 over a median of 15 courses every 3 weeks as a 48-72 h continuous intravenous infusion (in 22 cases), with mesna and hydration. FINDINGS: Glomerular filtration rate was below normal in ten (45%) of 22 evaluable children; their rate was 61-85 mL/min per 1.73 m2. Proximal tubular toxicity led to hypophosphataemic rickets and/or renal tubular acidosis in six children, and distal tubular toxicity caused nephrogenic diabetes insipidus in one. Of the risk factors analysed by multiple regression, only total ifosfamide dose was associated with proximal tubular toxicity. Only two of ten evaluable patients who received under 100 g/m2 developed moderate nephrotoxicity, whereas six of ten who received over this dose had moderate or severe nephrotoxicity. INTERPRETATION: High total ifosfamide dose was the only risk factor we identified. Although inter-patient variability was high, cumulative doses of 100 g/m2 or higher should be avoided in children with cancer.

Adolescent↗
PubMed1988

Disturbances in acid-base metabolism. Recognition in the office setting.

Determination of the appropriateness of the compensatory response is essential in evaluation of any acid-base disturbance. Adequate compensation supports the presence of a single acid-base event. Inadequate compensation may indicate that a second primary acid-base event is present or, in some circumstances, that time has been inadequate for maximal physiologic compensation. When acid-base disturbances are mixed, treatment of one disorder may unmask the full pH-altering potential of the second disorder. Close monitoring of patients at risk for the development of acid-base disorders permits detection of problems at a time when intervention may prevent serious complications. Relatively inexpensive and easy-to-use chemical analytic systems to assist early diagnosis are now present in many office-based laboratories.

Acid-Base Imbalance↗
PubMed1980

The kidney in health and disease: XVIII: lactic acidosis and the elevated anion gap (II).

This concluding article of a two-part discussion deals with clinical presentations and management of the basic types of lactic acidosis - with and without appaent hypoxia - and the various complicating conditions that may coexist with them. Although symptomatic treatment is essential, cure can be effected only by seeking and treating the underlying cause of the electrolyte derangement.

Acidosis↗
PubMed2006

Metformin-associated lactic acidosis precipitated by acute renal failure.

Metformin-associated lactic acidosis (MALA) is a rare but serious clinical entity. It is almost always seen in patients with a serious underlying medical disorder, most often a degree of renal impairment or other factors that are known to predispose to the lactic acidosis. We report a case of MALA in which acute renal failure resulting from hypovolemia secondary to acute gastroenteritis likely precipitated the condition. Early recognition of this condition and initiation of treatment are important. Bicarbonate hemodialysis is the treatment of choice.

Acidosis, Lactic↗
PubMed1984

Chronic mountain sickness at an elevation of 2,000 meters.

A resident living at Lake Tahoe, Calif, at an elevation of 2,000 meters, had fatigue, edema, and erythrocythemia. Hematocrit was 63 percent, and arterial blood gas values revealed hypoxemia and respiratory acidosis. Results of pulmonary function tests, sleep study, and thyroid function all were normal. Erythrocytosis, cor pulmonale, and respiratory acidosis resolved after the patient moved to sea level. This patient suffered from chronic mountain sickness. Her symptoms resolved with relief of hypoxia.

Acidosis, Respiratory↗
PubMed1996

Acute renal failure and the MELAS syndrome, a mitochondrial encephalomyopathy.

Melas (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) is one of a group of heterogeneous yet clinically distinct syndromes ascribed to a defect in mitochondrial function. Here, the case of a patient diagnosed with the MELAS syndrome who subsequently developed acute renal failure is reported. Although no clear renal insult was evident at the time, the clinical picture was consistent with the diagnosis of acute tubular necrosis. The patient's renal function subsequently returned to baseline. This article reviews the literature concerning renal involvement in the mitochondrial encephalomyopathies, including MELAS, and proposes a mechanism by which patients suffering from mitochondrial disorders may be more susceptible to renal hypoxic injury and acute renal failure.

Acidosis, Lactic↗