Severe hypoglycaemia in a person with insulin autoimmune syndrome accompanied by insulin receptor anomaly type B.

AIMS: A rare case of the insulin autoimmune syndrome (IAS) accompanied by insulin receptor anomaly is reported. METHODS: Antibodies to insulin and insulin receptor were determined in the patient with severe hypoglycaemia before and after the treatment with prednisolone. RESULTS: Titers of antibody to insulin and insulin receptors were 73.0% and 41.5%, respectively. Drug-induced lymphocyte stimulation tests were all negative for the suspicious drugs. Her HLA-DR was DRB1*0403/04051. Following steroid therapy, the formation of antibodies was suppressed and alleviated her symptoms. Scatchard analysis yielded findings specific to polyclonal antibodies. CONCLUSIONS: The changes in autoantibodies resulted in alleviation of the hypoglycemic symptoms as a result of steroid therapy.     

The changes in EEG, evoked potentials and neurological recovery after global brain ischemia in dogs

Electroencephalography (EEG), evoked potentials and neurological recovery score were compared between 10 min and 15 min transient global brain ischemia in 18 dogs. The transient global brain ischemia was induced by occluding aorta, superior and inferior caval veins. The grade of EEG (1: normal approximately 5: flat) 2 hrs after ischemia was significantly lower with the 10 min ischemic group (n = 9) than with the 15 min group (n = 9) (3.7 +/- 0.5 vs 4.1 +/- 0.3, P less than 0.05). The rate of reappearance in evoked potential waves 2 hrs after ischemia was higher with the 10 min ischemic group than with the 15 min group (auditory brainstem response 5 wave: 100% vs 33%, middle latency response Pa wave: 80% vs 0%, somatosensory evoked potential N2 wave: 83% vs 78%, N3 wave: 67% vs 33%). The neurological recovery score (0: death approximately 100: normal) 7 days after ischemia was significantly higher with the 10 min group than with the 15 min group (58 +/- 34 vs 27 +/- 23, P less than 0.05). In both groups, there was a significant correlation (r = +0.85, P less than 0.01) between the total score of EEG and evoked potential waves (0: no wave appeared approximately 6: all waves appeared) 2 hours after ischemia and the neurological recovery score 7 days after ischemia. These results suggest that the neurological recovery after transient global brain ischemia would be estimated by EEG and evoked potential waves.     

Furosemide Given by Inhalation Ameliorates Acute Exacerbation of Asthma

Previous studies have suggested that inhaled furosemide may have a protective effect against a wide variety of bronchoconstrictor agents, but a therapeutic effect has not been established in acute exacerbation of asthma. The purpose of this study was to investigate whether inhaled furosemide would exhibit any therapeutic benefit in acute asthma. We conducted a double-blind, placebo-controlled, randomized study in 40 patients with acute mild or moderate exacerbation of asthma. All patients received intravenous (IV) aminophylline 250 mg for 90 min and IV hydrocortisone 100 mg at entry. After randomization, 3 patients were excluded from the final analysis. At 30 min after starting IV aminophylline, 20 patients were given inhaled furosemide 20 mg and 17 patients received normal saline as placebo-control. Both inhalations were given by a jet nebulizer. The baseline forced expiratory volume at 1 sec (FEV₁), peak expiratory flow rate (PEFR), and serum concentration of theophylline did not differ between the two groups. An increase in FEV₁ in the furosemide group by 28.2 ± 5.9% (mean ± SE) was noted at 60 min, and this was significantly higher than in the control group. PEFR at 60 min was also significantly higher in the furosemide group than in control group. We conclude that inhaled furosemide has a bronchodilator effect on mild to moderate exacerbation of asthma when it is used with IV theophylline. Inhaled furosemide may benefit certain acute asthma patients, especially those suffering complications from the adverse effects of β₂-agonists.     

Hyperthyroidism associated with papilloedema and pyramidal tract involvement

Summary In a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes [MELAS] who had normal mitochondrial enzyme activity, high doses of coenzyme Q₁₀ (CoQ) were administered. Clinical improvement with decreased serum lactate and pyruvate levels was observed. Though the mechanism of action of CoQ is not known, a trial is worthwhile in patients with MELAS.