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PubMed1973

Ketosis.

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Acidosis↗
PubMed1996

Acute necrotizing pancreatitis, lactic acidosis and prolonged hypoglycemia in a hemodialysed patient--a logical but unfortunately fatal combination.

A hemodialysed patient with abdominal pain, severe lactic acidosis and prolonged hypoglycemia is described. The diagnosis of acute necrotizing pancreatitis was delayed and the patient died from both systemic and peripancreatic complications of the acute pancreatitis. The article deals with the problem of diagnosing acute pancreatitis in an end-stage renal failure (ESRF) patient; on the possible surgical options open to the physician in the management of acute pancreatitis and on a pathophysiological explanation behind both the lactic acidosis and hypoglycemia in this patient.

Acidosis, Lactic↗
PubMedDate not supplied

The outcome of diabetic pregnancies: a prospective study.

In a large prospective study of pregnancy the perinatal mortality rate was 141/1000 births for diabetic gestations in which the onset of labour was spontaneous, 33/1000 for diabetic gestations in which labour was induced or the infant delivered by Caesarean section and 34/1000 for the non-diabetics. Forty per cent of the perinatal mortality excess in the diabetics was due to the consequences of maternal vascular lesions, i.e. large placental infarcts and marked retardation of placental growth. Seventeen per cent of the perinatal mortality excess was related to maternal acidosis or to insulin shock, 12% to severe congenital anomalies, 12% to the complications of Caesarean sections and the remainder to other disorders. Mothers with diabetes mellitus had more than twice the frequency of atheromata, fibrinoid change and thrombi in decidual arteries as non-diabetic mothers. Histological grading revealed that overweight newborns of diabetic mothers had immature lungs by comparison with the lungs of normally grown infants of diabetic mothers and infants of non-diabetic mothers. Low IQ values and an excess of neurological abnormalities in children of diabetic mothers who were ketotic during pregnancy were found to be due to amniotic fluid bacterial infections and their complications rather than to the maternal ketosis.

Birth Weight↗
PubMed2005

Intensive care treatment of severe mixed metabolic acidosis.

We report a case of severe metabolic acidosis associated with acute renal failure and septicaemia following treatment with maximal therapeutic doses of metformin and diclofenac. On the second day of intensive care the patient deteriorated with respiratory insufficiency and abdominal pain during continuous renal replacement therapy. A laparoscopy revealed a perforated cholecystitis with abscess formation. The patient regained renal function and recovered. Intake of diclofenac 5 days before this episode could have been the main cause of renal insufficiency and metabolic acidosis in this patient and could also have delayed surgical treatment by masking early clinical signs of perforated cholecystitis. The renal failure may also have caused metformin and lactate to accumulate, contributing to the mixed pattern of metabolic acidosis. This case report describes a mixed organic and non-organic metabolic acidosis associated with acute renal failure, presumably resulting from a combination of drugs and diseases often found in the elderly - metformin for diabetes mellitus and a non-steroidal anti-inflammatory drug for cholecystolithiasis. Acid-base balance and electrolyte changes were rapidly normalized by continuous renal replacement therapy.

Abdominal Abscess↗
PubMed1990

Biguanide-induced lactic acidosis.

Phenformin-induced lactic acidosis has been thought to be rare in India due to a high carbohydrate intake, use of suboptimal doses of phenformin and a lesser prevalence of alcoholism, as compared to Western countries. We studied the blood lactate levels of 31 non-insulin dependent diabetics (Group A) before and after treatment with phenformin, 75 mg/day for 4 weeks. Blood lactate rose significantly after treatment (mean +/- SEM 16.6 +/- 1.2 mg/dl to 30.7 +/- 2.2; p less than 0.01). Seven patients from this group had blood lactic acid level greater than 72 mg/dl. Six of these patients were restudied off treatment and after 4 weeks of phenformin therapy. The arterial blood pH, pCO2, pO2 and bicarbonate remained unchanged on treatment although a significant rise in blood lactic acid was reconfirmed in these 6 patients. Another group of 12 patients on phenformin for more than six months had significantly lower blood lactate levels as compared to group A (mean +/- SEM 20.2 +/- 1.8 mg/dl vs 30.7 +/- 2.2 mg/dl; p less than 0.01) indicating the possibility of a process of adaptation on prolonged treatment. This possibility was confirmed by a serial follow-up study of 11 patients for a 6 month period on phenformin therapy. A case of biguanide-induced lactic acidosis diagnosed and treated by us is described.

Acidosis, Lactic↗
PubMed1999

MELAS with prominent white matter gliosis and atrophy of the cerebellar granular layer: a clinical, genetic, and pathological study.

This report concerns an autopsy case of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with unusual neuropathological findings. The patient was a Japanese woman who was 21 years old at the time of death. Her mother is a patient with genetically confirmed MELAS. Her clinical manifestations included convulsions and lactic acidosis in the latter half of the first decade of life, followed by deafness, dementia, muscle weakness in the lower extremities, slight ataxia in the upper and lower extremities, and diabetes mellitus. Muscle biopsy revealed ragged-red fibers, and genetic study showed a point mutation at nucleotide pair 3243 in mitochondrial DNA. She died of lactic acidosis. In the clinical course, she did not develop stroke-like episodes. The neuropathological examination revealed not only minute to small necrotic foci in the cerebral cortex, amygdala, hippocampus, and cerebellum, but also prominent white matter gliosis in the central nervous system and cerebellar cortical degeneration of granular cell type. Our neuropathological findings, including prominent white matter gliosis of the central nervous system and cerebellar cortical degeneration of granular cell type, may indicate morphologically widespread cellular dysfunction, not restricted to either neuronal or vascular derangement, in the brain pathology of MELAS.

Adult↗
PubMed1973

Renal response to acid load after phenformin.

Normally the kidneys respond to an acid load by increased ammonia production. In six patients with adult-type diabetes this response was reduced by a mean 50% after a therapeutic dose of phenformin. The reduced ability to compensate for acid loads may be one factor leading to metabolic acidosis and lactoacidosis sometimes associated with phenformin therapy.

Adult↗
PubMed1992

Biguanides and NIDDM.

The main biguanides, metformin and phenformin, were introduced in 1957 as oral glucose-lowering agents to treat non-insulin-dependent diabetes mellitus (NIDDM). Phenformin was withdrawn in many countries because of an association with lactic acidosis, but metformin does not have the same risk if appropriately prescribed. Metformin is now widely used as a monotherapy and in combination with a sulfonylurea. Unlike sulfonylureas, metformin is not bound to plasma proteins, is not metabolized, and is eliminated rapidly by the kidney. The glucose-lowering effect occurs without stimulation of insulin secretion and results mainly from increased glucose utilization. The presence of insulin is required, and enhancement of insulin action at the postreceptor level occurs in peripheral tissues such as muscle. In peripheral tissues metformin increases insulin-mediated glucose uptake and oxidative metabolism. Metformin also increases glucose utilization by the intestine, primarily via nonoxidative metabolism. The extra lactate produced is largely extracted by the liver and serves as a substrate to sustain gluconeogenesis. This limits the extent to which metformin reduces hepatic glucose production but provides a safeguard against excessive glucose lowering. Because metformin does not cause clinical hypoglycemia, it is actually an antihyperglycemic drug. It does not cause weight gain, it helps combat hypertriglyceridemia, and it has been ascribed some vasoprotective properties. Metformin offers a useful treatment for insulin-resistant overweight NIDDM patients.

Adipose Tissue↗