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PubMedDate not supplied

Kearns-Sayre syndrome. A case report.

Kearns-Sayre syndrome (KSS) is a mitochondrial disorder. There is a large-scale mitochondrial DNA (mtDNA) deletion in most of the case. In this article, a case of KSS who has progressive external ophthalmoplegia (PEO), retinitis pigmentosa (RP), complete heart block, encephalopathy attacks, type-1 diabetes mellitus, ragged-red fiber (RRF) and lactic acidosis is presented and discussed in light of the literature available on this subjects. Diagnosis is confirmed by determination of mtDNA deletion.

Acidosis, Lactic↗
PubMed1985

Ketone body production and disposal in diabetic ketosis. A comparison with fasting ketosis.

This work compares the metabolism of total ketone bodies in 13 insulin-deprived, type I diabetic subjects and 26 control subjects fasted for 15 h to 23 days, with the two groups showing a similar range of ketone body levels (1-12 mM). Ketone turnover rate was measured using a primed, constant infusion of either 14C-acetoacetate or 14C-beta-hydroxybutyrate, both tracers yielding comparable results. The major conclusions of this study are the following: the kinetics of ketone bodies are comparable in the two groups within the range of concentrations tested. The hyperketonemia of fasting and diabetes is primarily caused by an increased production of ketone bodies, but the phenomenon is amplified by a progressive limitation in the ability of tissues to remove ketones from blood as the concentration rises. The inverse relationship between the metabolic clearance and the plasma levels of ketones, which underlies this process, represents a general characteristic of ketone body metabolism that applies to both types of ketosis. A maximal metabolic disposal rate of about 2.3 mmol/min/1.73 m2 is attained in both groups at concentrations of 10-12 mM, which correspond to the highest ketone body levels encountered during prolonged fasting. Thus, up to these levels, there is no evidence for the existence of a ketone body removal defect specific to diabetes.

3-Hydroxybutyric Acid↗
PubMed1976

Light-chain nephropathy. Renal tubular dysfunction associated with light-chain proteinuria.

We observed idiopathic light-chain proteinuria in a patient with multiple abnormalities of proximal-tubule transport mechanisms (Fanconi syndrome), nephrogenic diabetes insipidus, and distal renal tubular acidosis. Seventeen of the 19 urinary amino acid levels measured were elevated. Uric acid and phosphate clearances were greater than 60 per cent and 50 per cent, respectively, of the simultaneous inulin clearance. When water deprivation was coupled with vasopressin administration, the maximum urinary concentration observed was 384 mOsm per kilogram of water. During ammonium-chloride loading, the level of hydrogen-ion concentration in the urine remained less than 100 times that in the blood. Kappa light-chain excretion was 149 mg per 24 hours. It appears that the concurrence of proximal tubular dysfunction, distal tubular dysfunction and light-chain proteinuria represents a distinct syndrome, which we call "combined light-chain nephropathy." Available evidence indicates that excessive light-chain production with subsequent filtration, reabsorption and catabolism, causes the complex tubular dysfunctions observed.

Acidosis, Renal Tubular↗
PubMed1987

[Physiopathological approach to pathological hyperlactatemia in the diabetic patient. Value of blood metformin].

Type B lactic acidosis, or pathological hyperlactatemia (PHL), is defined by an arterial lactate level greater than 5 mmol X l-1. It is a known and severe complication of diabetes mellitus treated with biguanide hypoglycaemic agents, particularly phenformin which was taken off the French pharmaceutical market in 1977. Metformin, which remains the only biguanide hypoglycaemic agent currently prescribed in France, may also lead to this complication. However it does so less frequently and mostly in the diabetic presenting with renal failure. A few well studied cases showed that PHL could be correlated with excessive metformin blood levels, i.e. a toxic mechanism. In order to find out whether this toxic mechanism was the real cause of PHL in diabetics treated with metformin, a systematic study of metformin blood levels was carried out in 20 such patients. They had all been admitted to a critical care unit presenting with PHL. The results of this study led us to distinguish between two groups of patients. The seven patients of the first group had high metformin blood levels (4.3 to 65.8 micrograms X l-1). In these, renal excretion or extrarenal dialysis lowered or normalized their hyperlactatemia, and six of the seven recovered from PHL. In the second group, with thirteen patients, metformin blood levels were within the normal therapeutic range (0.225 to 3 micrograms X l-1) for seven patients and close to zero for the other six. This second group received the same treatment as the first one. Only three patients recovered, the others all died.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1988

Bone mineral metabolism in human type 1 (insulin dependent) diabetes mellitus.

Decreased bone mineral content has been observed in several studies of type 1 (insulin-dependent) diabetics in comparison with age and sex matched control subjects. In type 2 diabetics contradictory results have been obtained, probably related to varying degrees of body overweight in the patients investigated. The decrease in bone mineral content in type 1 diabetics was most pronounced in patients with childhood or adolescent onset of the disease, with ceased beta-cell function, with high insulin dosage, and poor glucose regulation. In a subgroup of patients having all these "risk factors" bone mineral content was decreased some 20%, as compared with patients without any "risk factors", and/or with sex and age matched controls. Bone mineral homeostasis was characterized by increased urinary excretions of bone minerals (calcium, phosphate and magnesium) related to the degree of hyperglycaemia and insulin dosage, by decreased serum concentrations of ionized calcium and magnesium, by increased to normal serum concentrations of phosphate, by a low-normal serum concentration of parathyroid hormone, and by a low-normal serum concentration of 1,25-dihydroxyvitamin D. This indicates a state of functional hypoparathyroidism in type 1 diabetics. Several mechanisms may thus contribute to diabetic osteopenia: Proneness to metabolic acidosis, hypocalcaemia, insulin deficiency and perhaps also hypomagnesaemia and hypoparathyroidism.

Adult↗
PubMed1991

[Level of calcitonin in blood serum of children with insulin dependent diabetes].

Calcitonin concentration (CT) was measured in 52 children with insulin-dependent diabetes (IDDM). All the patients studied were divided into three groups. The first group consisted of children with freshly diagnosed diabetes remaining in the condition of ketonemic acidosis. The second group was composed of children with the well controlled diabetes during the first two years od duration of the disease. The third group included the patients with poorly controlled diabetes of the duration longer than ten years having the accompanying vascular complications. The control values were determined in children without metabolic disturbances of either diabetic or other origin. CT concentration was significantly elevated both in the patients of the first group and those of the third group. In the second group the concentration of this hormone was close to normal. It is known that calcitonin participates in the homeostasis of calcium and is an important regulator of insulin secretion. The results obtained suggest that calcitonin may play a role both in the pathogenesis of diabetes and in developing of diabetic osteopenia.

Adolescent↗