Detection of unrecognised nocturnal hypoglycaemia in insulin-treated diabetics.

Cortisol to creatinine ratios in overnight urine samples, urinary glucose excretion, and plasma glucose concentrations were determined in 43 diabetic inpatients. All initially had normal cortisol to creatinine ratios (less than 55 x 10(-6)) and were initially treated by increasing their long-acting insulin component. Nine patients in whom this ratio became raised then had their long-acting insulin component reduced until their fasting plasma glucose concentration was 4-7 mol/l (72-126 mg/100 ml). The 34 patients who had never had a raised ratio were treated by increasing their long-acting insulin component until their fasting plasma glucose concentration was in the range 4-7 mmol/l. All the raised cortisol to creatinine ratios were clearly separate from the other values. A mean reduction in total insulin dose of 23% and in long-acting insulin dose of 53% was achieved, abolishing presumptive nocturnal hypoglycaemia by reducing the ratio to normal and dramatically improving diabetic control. Although there was no definite evidence that the patients who had raised cortisol to creatinine ratios had suffered from nocturnal hypoglycemia, these results strongly support the view that a raised ratio indicates an otherwise unrecognised episode of this condition.     

Transient ischemic attacks and stroke.

Transient ischemic attacks (TIAs) constitute the most specific and powerful warnings of impending stroke. They are defined as brief, focal neurological events of sudden onset. Their proper recognition and treatment rank second only to the modification of risk factors in importance for stroke prevention. Carotid endarterectomy, although widely used to treat TIAs, remains unproven; randomized clinical trials are attempting to define its role. Anticoagulant therapy appears worth while for suspected cardiac embolism and possibly for disabling TIAs. Acetylsalicylic acid is the only agent that has been found to be effective in controlled trials, but questions persist about its dosage, its efficacy in women and its use after stroke. Another platelet inhibitor, ticlopidine hydrochloride, is being investigated and may prove to be an effective alternative.     

Severe hypoglycaemia due to combined use of parenteral nutrition and renal dialysis.

A 24-year-old woman who had sustained serious injuries in a road traffic accident required renal dialysis daily and was fed intravenously with a solution containing 25% dextrose. Subsequently insulin had to be added to the parenteral fluid to maintain blood glucose concentrations at physiological values. On one occasion parenteral feeding was continued until dialysis was started; she became comatose and the plasma glucose concentration was found to be less than 1 mmol/l (18 mg/100 ml). She responded rapidly to a 50 ml intravenous bolus of 50% dextrose. When parenteral feeding and dialysis are used simultaneously glucose passes across the semi-permeable membrane from the blood to the dialysate so that hypoglycaemia may occur. Insulin added to the parenteral fluid further decreases blood glucose concentrations. Stopping parenteral feeding 30-45 minutes before dialysis is started eliminates this danger of hypoglycaemia.     

Alpha-delta sleep in a patient with nocturnal panic attacks

Sleep and Biological Rhythms - We report here on our finding of an alpha-delta sleep in a 40-year-old-female patient suffering from panic attacks, including nocturnal panic attacks, who complained...     

Transient glucose intolerance during attacks of thyrotoxic periodic paralysis

In a 19-year-old Japanese male (case 1) with thyrotoxic periodic paralysis (TPP), an increase of plasma glucose concentration together with abnormally high levels of serum immunoreactive insulin (IRI) was observed preceding a spontaneous attack of paralysis. Therefore, the plasma glucose, glucagon, epinephrine, norepinephrine, serum IRI, growth hormone and cortisol levels, and the erythrocyte insulin receptors were measured in case 1 and a 40-year-old Japanese male (case 2) with TPP during attacks of paralysis induced by prolonged glucose loading. In case 1, the serum IRI concentration was elevated to the extraordinarily high level of 655.0 microU/ml at the beginning of paralysis, and at that time, the plasma glucose concentration was 147 mg/dl. However, when paralysis was not induced by a similar glucose loading during methimazole treatment, the serum IRI and plasma glucose levels at the corresponding time after glucose loading were 20.9 microU/ml and 87 mg/dl, respectively. Furthermore, the affinity of the erythrocyte insulin receptors was decreased during the attack. In case 2, plasma glucose and serum IRI concentrations were increased in accordance with the initiation of paralysis although the blood levels of hormones counteracting insulin were not significantly changed. These findings suggest that there is something interacting with the normal action of the insulin in the early phase of paralysis.     

Transient neonatal hyperthyrotrophinaemia: a serum abnormality due to transplacentally acquired antibody to thyroid stimulating hormone.

In a screening programme for neonatal hypothyroidism an otherwise healthy female infant was found to have a high concentration of thyroid stimulating hormone in a filter paper blood spot and in serum. A high concentration was also found in the maternal serum. Mother and baby were both biochemically euthyroid with normal serum thyroxine concentrations. The apparently high concentration of thyroid stimulating hormone in the mother was due to the presence of an IgG antibody that bound to human but not bovine thyroid stimulating hormone. Maternal serum inhibited the action of human thyroid stimulating hormone in an in vitro bioassay for the hormone. It is suggested that the baby acquired the antibody transplacentally, especially as the concentration of thyroid stimulating hormone subsequently fell. It is concluded that maternal serum should be assayed for thyroid stimulating hormone when a neonate is found to have a high concentration of the hormone and a normal concentration of thyroxine to establish the incidence of this finding and to avoid inappropriate replacement treatment.