Normal metabolism of apolipoprotein B100-containing lipoproteins despite qualitative abnormalities in type 1 diabetic men.

AIMS/HYPOTHESIS: Type 1 diabetic subjects are at increased risk of cardiovascular disease and exhibit multiple qualitative abnormalities of apolipoprotein (apo) B100-containing lipoproteins. This stable isotope kinetic experiment was designed to study whether these abnormalities are associated with changes in the synthesis and fractional catabolic rates of VLDL-, IDL- and LDL-apoB100. METHODS: Using a bolus followed by a 16-h constant infusion of 13C-leucine, we performed a kinetic study in eight men with type 1 diabetes treated with a continuous subcutaneous insulin infusion administered by an external pump and in seven healthy men, in the fed state. RESULTS: The mean HbA1c level in the type 1 diabetic patients was 8.00+/-1.48%. Plasma triglyceride, and total, LDL and HDL cholesterol levels were similar in patients and control subjects. VLDL were less triglyceride rich in type 1 diabetic patients than in control subjects (VLDL triglyceride : apoB 6.91+/-0.81 vs 8.29+/-1.24 mmol/g, p=0.05). Conversely, the IDL and LDL of the type 1 diabetic patients contained relatively higher levels of triglycerides (IDL triglycerides : apoB 2.16+/-0.36 vs 1.57+/-0.30 mmol/g, p<0.01; LDL triglycerides : apoB 0.27+/-0.06 vs 0.16+/-0.04 mmol/g, p<0.05). The apoB100 pool size, production and fractional catabolic rates in the two groups of subjects were similar for all lipoprotein fractions. CONCLUSIONS/INTERPRETATION: Despite qualitative abnormalities, especially abnormalities of triglyceride content, the metabolism of apoB100-containing lipoproteins is not altered in type 1 diabetic men with fair glycaemic control with continuous subcutaneous insulin infusion. The high risk of atherosclerosis in these patients cannot be explained by kinetic abnormalities of apoB100-containing lipoproteins.

Intravenous methylprednisolone pulse therapy in the treatment of Graves' ophthalmopathy.

Graves' ophthalmopathy (GO) is a specific immune-mediated disorder, whose treatment is sometimes difficult. In order to investigate the efficacy of intravenous methylprednisolone (MP) pulse therapy in GO, we studied eight patients with GO, followed up for at least 6 months by clinical patient self-assessment, ophthalmological examination and orbital computed tomography (OCT). A 12.5 mg/kg dose of MP was administered intravenously over a 10 hour period, once every month. Three to six MP pulse administrations were performed in each patient. All patients were outpatients. A 0.5 mg/kg/day oral prednisone dose was given to each patient as interpulse therapy. Clinical assessment of MP pulse therapy showed a good response in 87.5% and no response in 12.5% of patients. The treatment was rapidly efficient, mostly on patient self-assessment, soft tissue inflammation, ophthalmoplegia, corneal involvement, visual acuity and extraocular muscle enlargement on OCT. Post-treatment ophthalmic index was significantly improved (6.75 +/- 3.06 vs. 2.5 +/- 1.41: p < 0.05). MP pulse therapy had less effect on proptosis (22.94 +/- 2.32 mm vs. 21.56 +/- 2.22 mm: p < 0.05). No adverse effects were noted with MP pulse therapy. Patients showed no relapse of eye involvement during a mean follow up of 31.8 months (2-77 months). In conclusion, our results suggest that intravenous MP pulse therapy is a good immunosuppressive therapy for GO. Moreover, in comparison with the previous studies, the MP dose used in our present study appears to be optimal with high efficacy. MP pulse therapy represents a safe and efficient treatment in GO, which can easily be performed in outpatients.

[Factitious hyperchloremia disclosing bromide poisoning. 4 cases]. / Hyperchlorémie factice révélatrice d'intoxication par le brome. 4 observations.

BACKGROUND: When routine blood chemistry shows elevated chloride alone, another anion (bromide, iodine, fluoride) may be involved. CASE REPORTS: Hyperchloremia and decreased anion gap was observed in four patients. Chloremia ranged from 134 to 174 mmol/l at initial blood tests. Careful history taking led to the discovery of long-term use of calcium bromogalacto-glucomate. Specific assay with inductively coupled plasma mass spectrometry (ICPMS) confirmed the presence of bromide in the blood. Chloridemia returned to normal levels after discontinuing use of bromine. DISCUSSION: Bromism is not a common diagnosis. Risks include neurological and psychiatric disorders due to bromide diffusion through the blood-brain barrier. Clinical manifestations have been described including skin lesions, digestive intolerance, and fever. Bromide is contained in certain prescription drugs. Patients should be warned against the adverse effects of overuse.

[Primary hyperparathyroidism and pregnancy]. / Hyperparathyroïdie primaire et grossesse.

We report a case of primary Hyperparathyroidism (HPT) occuring in a 36 year old woman, during pregnancy. This woman received medical therapy to the delivery, then underwent parathyroidectomy in post-partum. Primary HPT during pregnancy is associated with increased risk of fetal loss, neonatal and maternal morbidity. Neonatal hypocalcemia is due to transient hypoparathyroidism consequent to abnormal suppression of fetal parathyroid hormone secretion by maternal hypercalcemia. Maternal hypercalcemia may be masked by hypoalbuminemia during pregnancy and often leads to aspecific symptoms which will differ the diagnosis. The recommanded treatment is parathyroidectomy which should preferably be performed during the second trimester of pregnancy; the efficacity of medical treatment is poor and transient.

[Food-dependent Cushing syndrome: a new entity of organic hypercorticism]. / Le syndrome de Cushing alimentaire: une nouvelle entité d'hypercorticisme organique.

Diagnosis of Cushing's syndrome is quite difficult in endocrinology. Spontaneous Cushing's syndrome is usually divided into two subgroups, one which is dependent on corticotropin (ACTH) and another one which is not. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic corticotropin-releasing hormone (CRH) syndrome; these ACTH-dependent Cushing's syndrome have usually diffusely enlarged adrenal glands. In the second class are cortisol producing unilateral adrenocortical adenomas or carcinomas, and the recent Cushing's syndrome with food dependent periodic hormonogenesis. This food dependent Cushing's syndrome is an ACTH-independent Cushing's syndrome with multinodular enlargement of both adrenal glands. Pathogenesis is an aberrant adrenal sensitivity to physiologic secretion of gastric inhibitory peptide (GIP). Ectopic expression of GIP receptors on adrenal cells involve pathologic food induced cortisol secretion. Food dependent Cushing's syndrome is a new cause of Cushing's syndrome. Food induced cortisol secretion may have to be explored in the ACTH-independent Cushing's syndrome.

[Evolution of bronchial hyperreactivity during post-exercise asthma]. / Evolution de l'hyperréactivité bronchique au cours de l'asthme post-exercice.

The occurrence of a late reaction following exercise induced asthma is questionable and its relationship with the non specific bronchial hyperreactivity is poorly known. In this study, nine patients (age 15-21 years) underwent an exercise challenge in order to (a) determine the incidence of immediate and late phase reaction and (b) analyse the modifications of non specific bronchial hyperreactivity. Study design was a follow; day-3: determination of bronchial responsiveness to metacholine; day 0: control day with FEV1 measurements every hour for 11 hours; day 1: exercise challenge followed by a careful observation of change in FEV1; day 2: new determination of bronchial responsiveness to metacholine. An immediate exercise induced bronchial obstruction was observed in 5 patients. A late phase reaction (6th hour) with a fall of FEV1 equal to or more than 20% has been demonstrated in two patients. For the former, the change in FEV1 did not differ from the value of the control day. For the second, the FEV1 changed spontaneously during the control day so that decreases of FEV1 during control and challenge days were parallel. Thus, no late phase reaction were observed (F = 0.46; ns). There was no modification of bronchial responsiveness to metacholine (pre-exercise: 1,784 +/- 1,970 [SD]; post-exercise 1,827 +/- 2,231 micrograms [SD]). The lack of true late phase reaction when the post-exercise change in FEV1 is compared to the one of a control day and the absence of modification of non specific bronchial hyperreactivity weaken the hypothesis of an inflammatory mechanism of exercise induced asthma.