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At least 703 records · Page 39Linked to original sources
PubMed1997

[Distal tubular acidosis in a patient with insulin dependent diabetes mellitus--selected pathophysiologic, diagnostic and therapeutic aspects].

This case report describes a 42 years old male patients with distal tubular renal acidosis in whom the symptomatology of this disorder was markedly changed by the presence of concomitant endocrine and exocrine insufficiency of the pancreas. Pathophysiological, diagnostic and therapeutic aspects of coexistence of these two type of pathology are stressed.

Acidosis, Renal Tubular↗
PubMed1993

Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and diabetes mellitus: molecular genetic analysis and family study.

Two MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) patients with diabetes mellitus (DM), and their family members are described clinically and genetically. The probands have the following features in common; normal early development, short stature, deterioration of intellectual ability, convulsions, cardiac conduction defect, sensorineural hearing loss, cortical blindness, and hemiparesis. Biochemical tests showed high levels of lactate and pyruvate in the blood and cerebrospinal fluid. Muscle biopsy showed ragged-red fibers. Molecular genetic analysis of both patients revealed that they had an A-to-G substitution at nucleotide position 3243 of the mitochondrial DNA in a heteroplasmic fashion. From these clinical and molecular genetic data they were diagnosed as having MELAS. In addition, fasting blood glucose levels were also high and they were diagnosed as having insulin-dependent DM. Some of the maternal family members in both cases also had insulin-dependent DM and several clinical symptoms of MELAS. DM and clinical features of MELAS were transmitted exclusively in the maternal line. In these cases, DM and MELAS might be a clinical manifestation of the same metabolic defect.

Adolescent↗
PubMed2004

Effects of acidosis on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin-induced diabetic rats.

We have investigated the effects of acute acidosis on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin (STZ)-induced diabetic rat. Shortening and intracellular Ca2+ were measured in electrically stimulated myocytes superfused with either normal Tyrode solution pH adjusted to either 7.4 (control solution) or 6.4 (acid solution). Experiments were performed at 35-36 degrees C. At 8-12 weeks after treatment, the rats that received STZ had lower body and heart weights compared to controls, and blood glucose was characteristically increased. Contractile defects in myocytes from diabetic rat were characterized by prolonged time to peak shortening. Superfusion of myocytes from control and diabetic rats with acid solution caused a significant reduction in the amplitude of shortening; however, the magnitude of the response was not altered by STZ treatment. Acid solution also caused significant and quantitatively similar reductions in the amplitude of Ca2+ transients in myocytes from control and diabetic rats. Effects of acute acidosis on amplitude of myocyte contraction and Ca2+ transient were not significantly altered by STZ treatment. Altered myofilament sensitivity to Ca2+ and altered mechanisms of sarcoplasmic reticulum Ca2+ transport might partly underlie the acidosis-evoked reduction in amplitude of shortening in myocytes from control and STZ-induced diabetic rat.

Animals↗
PubMed1984

Metabolic alkalosis in diabetic ketosis: a case report.

A mixed metabolic alkalosis and metabolic acidosis, resulting in an alkalemic state, occurred in a hyperlipemic patient with previously diagnosed non insulin dependent diabetes. The metabolic alkalosis, due to large loss of gastric HCl, was more severe than the diabetic acidosis and resulted in an alkaline blood pH. Initially the metabolic acidosis was due to ketoacidosis and coexistent lactic acidosis. During the improvement of the alkalemic and hyperglycemic state, lactic acidosis disappeared but a paradoxical rise of plasma NEFA and ketone body concentrations supervened so that the high anion gap metabolic acidosis was virtually unchanged. The rise of plasma NEFA was probably related to the marked removal of plasma triglycerides, by insulin activation of lipoprotein lipase, and consequent saturation of the pathways of fatty acid incorporation into adipose tissue.

Adult↗
PubMed1983

[Renal manifestations of Sjögren's syndrome. Review of the literature starting with a case].

Sjögren syndrome, characterized by lymphocytic proliferation and drying up of exocrine secretions ("sicca syndrome") due to glandular destruction, is well known for it's ocular and salivary localizations. However, other glandular epithelia (bronchial, vaginal . . .) or parenchyma (such as the kidney) may be involved. Damage to the kidney is rarely prominent; it is usually discovered late in the course of the disease. Moreover the renal manifestations are multiple and variably associated: diabetes insipidus, tubular acidosis, Fanconi syndrome, tubular and interstitial nephritis, and glomerulonephritis.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Diabetes and abdominal surgery: the mutual risks.

The patient with diabetes represents to the surgeon a particular challenge in the management of acute abdominal problems. In addition to their ongoing and potential metabolic problems, diabetics have specific difficulty in their ability to handle infections and heal wounds. The present report reviews the general principles in the peri-operative management of diabetics and discusses the implications in the diabetic of several specific clinical problems. In view of the known accelerated atherosclerosis associated with diabetes, the risks of anesthesia and surgery must be assessed in the context of the coronary, cerebral, visceral, and peripheral vascular status. Infections in diabetics (potential or established) must be treated aggressively and promptly. Acidosis in the diabetic with abdominal pain must be considered both a metabolic problem and a possible secondary manifestation of an intra-abdominal process. In view of these challenges, the need for careful, anticipatory management of the diabetic patient facing major abdominal surgery is clear.

Abdomen↗
PubMed2006

Metabolic emergencies in diabetes.

Hypoglycaemia is the commonest metabolic abnormality faced by diabetic patients on hypoglycaemic therapy including insulin. Diabetic keto-acidosis (DKA) requires prompt diagnosis and all patients arriving emergency with dehydration, shock, coma, severe respiratory difficulty and evidence of any major illness should be tested for capillary blood glucose (CBG) and urinary ketones urgently not to miss DKA. Hyperosmolar non-ketotic state complicates elderly type 2 diabetes with intercurrent infections (respiratory tract infection is commonest) characterised by severe dehydration, severe hyperglycaemia and absence of acidosis and vomiting. Lactic acidosis is extremely rare; may be compounded with comorbidities like tissue hypoxia, septic shock, heart failure--metformin usage inadvertently may precipitate the condition.

Acidosis, Lactic↗
PubMed1964

OBSERVATIONS ON THE ETIOLOGY AND THERAPY OF "BRITTLE" DIABETES.

Salient aspects of prolonged metabolic studies on seven excessively labile diabetic patients and a review of the literature concerning causation and therapy of brittle diabetes are presented. Brittleness is redefined as "a syndrome of excessive insulin-sensitivity and ketosis-proneness manifested by extreme and unexplainable short-term and long-term fluctuations in the parameters of the disease". Evidence on the causation of hyperlability points to dysfunction of plasma-protein transport and of hepatic and peripheral tissue metabolism of insulin. No objectively demonstrable complete and lasting stabilization was possible by means of any antidiabetic or adjunctive therapeutic measures. However, achievement of quantitative improvement in the accuracy of regulation of diabetes and moderation in deviations from the acceptable range of parameters were feasible. To this end, therapy recommended for everyday use incorporates the following principles found to be most helpful in following the oscillations of the disease on the research ward: flexibility in the plan of therapy; accuracy, especially in timing of therapeutic events; and employment of an insulin program best suited to the patient's needs and comfort.

Acidosis↗
PubMed2001

Metformin-associated lactic acidosis in a low risk patient.

Metformin is an oral hypoglycemic agent belonging to the class of biguanides that are commonly used in the treatment of type II diabetes mellitus. Lactic acidosis is a rare but severe adverse reaction that occurs primarily in patients with contraindications such as renal failure. The case of a 71-year-old woman with type II diabetes, in whom severe metformin-associated lactic acidosis was precipitated by acute renal failure in the absence of pre-existing chronic renal failure or other absolute contraindications to biguanide use, is presented. Aggressive correction of the acidosis and prolonged dialysis resulted in a favourable outcome despite severe acidosis. The present case report shows that metformin-associated lactic acidosis can occur in patients without pre-existing renal insufficiency. Metformin should be temporarily stopped when acute renal failure occurs or is anticipated.

Acidosis, Lactic↗
PubMed2006

Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus.

BACKGROUND: Metformin is an oral anti-hyperglycemic agent used in the treatment of type 2 diabetes mellitus. The results of the UK Prospective Diabetes Study indicate that metformin treatment is associated with a reduction in total mortality compared to other anti-hyperglycemic treatments. Metformin, however, is thought to increase the risk of lactic acidosis, and is considered to be contraindicated in many chronic hypoxemic conditions that may be associated with lactic acidosis, such as cardiovascular, renal, hepatic and pulmonary disease, and advancing age. OBJECTIVES: To assess the incidence of fatal and nonfatal lactic acidosis with metformin use compared to placebo and other glucose-lowering treatments in patients with type 2 diabetes mellitus. A secondary objective was to evaluate the blood lactate levels for those on metformin treatment compared to placebo or non-metformin therapies. SEARCH STRATEGY: A search was performed of The Cochrane Library (up to 8/2005), MEDLINE (up to 8/2005), EMBASE (up to 11/2000), OLD MEDLINE, and REACTIONS (up to 8/2005), in order to identify all studies of metformin treatment from 1966 to August 2005. The Cumulated Index Medicus was used to search relevant articles from 1959 to 1965. The search was augmented by scanning references of identified articles, and by contacting principal investigators. Date of latest search: August 2005. SELECTION CRITERIA: Prospective trials in patients with type 2 diabetes that lasted longer than one month were included if they evaluated metformin, alone or in combination with other treatments, compared to placebo or any other glucose-lowering therapy. Observational cohort studies of metformin treatment lasting greater than one month were also included. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials to be included, assessed study quality and extracted data. The incidence of fatal and nonfatal lactic acidosis was recorded as cases per patient-years, for metformin treatment and for placebo or other treatments. The upper limit for the true incidence of cases in the metformin and non-metformin groups were calculated using Poisson statistics. In a second analysis lactate levels were measured as a net change from baseline or as mean treatment values (basal and stimulated by food or exercise) for treatment and comparison groups. The pooled results were recorded as a weighted mean difference (WMD) in mmol/L, using the fixed effect model for continuous data. MAIN RESULTS: Pooled data from 206 comparative trials and cohort studies revealed no cases of fatal or nonfatal lactic acidosis in 47,846 patient-years of metformin use or in 38,221 patients-years in the non-metformin group. Using Poisson statistics with 95% confidence intervals the upper limit for the true incidence of metformin-associated lactic acidosis was 6.3 cases per 100,000 patient-years, and the upper limit for the true incidence of lactic acidosis in the non-metformin group was 7.8 cases per 100,000 patient-years. There was no difference in lactate levels, either as mean treatment levels or as a net change from baseline, for metformin compared to placebo or other non-biguanide therapies. The mean lactate levels were slightly lower for metformin treatment compared to phenformin (WMD -0.75 mmol/L, 95% CI -0.86 to -0.15). AUTHORS' CONCLUSIONS: There is no evidence from prospective comparative trials or from observational cohort studies that metformin is associated with an increased risk of lactic acidosis, or with increased levels of lactate, compared to other anti-hyperglycemic treatments if prescribed under the study conditions.

Acidosis, Lactic↗
PubMed2001

Contraindications to metformin therapy in patients with Type 2 diabetes--a population-based study of adherence to prescribing guidelines.

AIMS: To define the number of people in Tayside, Scotland (population 349 303) with Type 2 diabetes who use metformin, the incidence of contraindications to its continued use in these people and the proportion that discontinued metformin treatment following the development of a contraindication. METHODS: Retrospective cohort study of the incidence of contraindications to metformin in all patients with Type 2 diabetes using metformin from January 1993 to June 1995. The contraindications of acute myocardial infarction, cardiac failure, renal impairment and chronic liver disease were identified by: the regional diabetes information system, biochemistry database and hospital admissions database and a database of all encashed community prescriptions. RESULTS: One thousand eight hundred and forty seven subjects (26.3% of those with Type 2 diabetes) redeemed prescriptions for metformin. Of these, 3.5% were admitted with an acute myocardial infarction (71 episodes); 4.2% were admitted with cardiac failure (114 episodes); 21.0% received metformin and loop diuretics for cardiac failure concurrently; 4.8% developed renal impairment; and 2.8% developed chronic liver disease. The development of contraindications rarely resulted in discontinuation of metformin, for example only 17.5% and 25% stopped metformin after admission with acute myocardial infarction and development of renal impairment, respectively. In total, 24.5% of subjects receiving metformin, 6.4% of all people with Type 2 diabetes, had contraindications to its use. There was one episode of lactic acidosis in 4600 patient years. CONCLUSIONS: This population-based study shows that 24.5% of patients prescribed metformin have contraindications to its use. Development of contraindications rarely results in discontinuation of metformin therapy. Despite this, lactic acidosis remains rare. Diabet. Med. 18, 483-488 (2001)

Cohort Studies↗
PubMed2002

A conceptual approach to the patient with metabolic acidosis. Application to a patient with diabetic ketoacidosis.

We shall illustrate that management of patients with an acid-base disorder could be improved if the acid-base analysis was based on a better understanding of basic concepts of physiology. Three concepts of acid-base physiology and their clinical implications are emphasized in a patient with diabetic ketoacidosis. First, when an acid is produced from neutral precursors in the body, there is a net increase in the number of hydrogen ions (H(+)) and new anions. The corollary is that H(+) will be removed when the accompanying anion is metabolized to a neutral end-product or is excreted in the urine with H(+) or ammonium (NH(4)(+)). Second, buffering of H(+) is beneficial if H(+) are removed by bicarbonate rather than being able to bind to proteins. This latter function depends on having a low tissue PCO(2), due to a combination of hyperventilation plus an adequate blood flow rate to vital organs. Third, the kidneys add new bicarbonate to the body when NH(4)(+) is excreted with chloride ions.

Acid-Base Equilibrium↗