CASEA 49-year-old woman (previous history of childhood asthma, no medication) presented to the emergency department with nausea and vomiting that had occurred for 5 days and slurred speech for 1 day prior to presentation. The patient denied use of alcohol and illicit drugs. Physical examination revealed her blood pressure to be 125/70 mmHg; she had no postural drop and had a regular pulse of 72 beats/min. She had no fever and no signs of contracted extracellular fluid volume. Results of further physical and neurological examination were unremarkable and revealed no goiter, pigmentation, or vitiligo. Her laboratory results are shown in Table 1. Additional diagnostic tests included chest x-ray, abdominal ultrasound, and brain computed tomography, none of which revealed abnormalities. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) 3 was suspected. However, fluid restriction (500 mL/day) did not lead to increased serum sodium. DISCUSSIONBecause of the lack of response to therapy for SIADH, the diagnosis was reconsidered and hypothyroidism and/or adrenal insufficiency were suspected, especially because serum glucose was also low. Serum thyroidstimulating hormone was 63 mU/L (reference interval 0.4 -4.0 mU/L) with free thyroxine of 5 pmol/L (reference interval 9 -24 pmol/L; to convert pmol/L of free thyroxine to ng/dL, divide by 13). Random cortisol was 151 nmol/L (reference interval 150 -700 nmol/L; to convert nmol/L of cortisol to g/L, divide by 0.0157), and a stimulation test with the 1-24 fragment of adrenocorticotropic hormone (ACTH) showed a baseline cortisol of 56 nmol/L, which increased only to 57 nmol/L (normal response Ͼ500 nmol/L). Plasma ACTH was 1124 ng/L (reference interval 7-50 ng/L; to convert ng/L of ACTH to pmol/L, multiply by 0.220). These results confirmed the presence of both primary adrenal insufficiency and primary hypothyroidism. Antibodies against the adrenal cortex, thyroid peroxidase, parietal cells, and intrinsic factor were present, establishing the diagnosis of autoimmune polyglandular syndrome type 2. Intravenous hydrocortisone was administered (bolus 100 mg followed by 200 mg/24 h), which corrected serum sodium (Fig. 1). After a sodium concentration within the reference interval was achieved, the patient was switched to oral hydrocortisone (10 -5-5 mg daily) and L-thyroxine (50 g).This case has 2 salient features. First, it illustrates the diagnostic challenges of severe hyponatremia with high urine sodium and osmolality. Second, it illustrates quite strikingly how atypical the presentation of adrenal insufficiency can be. APPROACH TO A PATIENT WITH SEVERE HYPONATREMIAWhen a clinician is confronted with a case of hyponatremia, the first question should be whether it is acute or chronic (1 ).In acute hyponatremia the most important risk to address is cerebral edema, because brain cells have too little time to adapt to cell swelling. Conversely, when chronic hyponatremia is treated too fast, the risk is osmotic demyelination (brain cells have adapted and are exposed ...
Patients with diabetes mellitus (DM), type 1 and type 2, have an increased risk of coronary heart disease as a result of accelerated atherosclerosis. Dyslipidemia, often found in these patients, plays an important role in this process. This study investigates the efficacy and safety of lipid-lowering therapy with pravastatin, a 3-HMG-Coenzym A reductase inhibitor in hypercholesterolemic type-1 and type-2 diabetic patients. Of 49 patients (22 type-1 DM and 27 type-2 DM), 24 patients were treated with pravastatin, 20 mg/day, and 25 patients with placebo. After 24 weeks, total cholesterol (TC) was decreased by 22.2%, low-density lipoprotein (LDL) cholesterol by 25.8% and triglycerides (TG) by 13.6%. Pravastatin treatment did not induce a significant change in high-density (HDL) cholesterol levels. No differences in effects of pravastatin treatment on serum lipids and lipoproteins were found with respect to the diabetes type. No serious side effects occurred and pravastatin treatment did not cause any deterioration in glycemia control. The data suggest that pravastatin is effective and safe in the treatment of dyslipidemia in both type-1 and type-2 diabetic patients.
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