Suppressive mechanisms of alveolar macrophages in interstitial lung diseases: role of soluble factors and cell-to-cell contact.

Alveolar macrophages (AMs) from patients with interstitial lung diseases, such as sarcoidosis and idiopathic pulmonary fibrosis, suppress the phytohaemagglutinin (PHA) stimulation of autologous peripheral lymphocytes. The aim of this study was to determine whether the suppressive effect of alveolar macrophages of patients with interstitial lung disease is due, not only to the secretion of soluble factors prostaglandin E2 (PGE2), interleukin-1 (IL-1) but is also correlated to a direct effect of AMs on the expression of IL-2 receptors (IL-2R: CD25) and on the induction of IL-2 activity. We studied 26 subjects, 8 with sarcoidosis, 7 with idiopathic pulmonary fibrosis, and 11 controls. Alveolar macrophages of sarcoid and idiopathic pulmonary fibrosis patients suppressed proliferation of autologous peripheral lymphocytes by 68 +/- 14% and 53 +/- 4.5%, respectively, compared to enhancement of 19 +/- 11% in three controls and suppression of 25 +/- 11% in the other six controls; the difference between subjects with interstitial lung disease and controls was significant. As already reported, the alveolar macrophages of sarcoid patients secreted large amounts of IL-1 (184 +/- 59 U.ml-1) whereas the alveolar macrophages from idiopathic pulmonary fibrosis patients secreted large amounts of PGE2 (3.6 +/- 2 ng.ml-1 x 10(-5) cells) compared with 23 +/- 19 U.ml-1 IL-1 and 0.34 +/- 0.15 ng.ml-1 x 10(-5) cells respectively, of controls. Suppression by supernatants recovered from lipopolysaccharide (LPS) stimulated alveolar macrophages can only partially explain the high suppressive effect of alveolar macrophages of interstitial lung diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyperphosphataemia and hypocalcaemia induced by hypertonic phosphate enema--an experimental study and review of the literature.

1. The study objective was to determine the hyperphosphataemic and hypocalcaemic effect of hypertonic phosphate enema. The study was conducted in a department of Internal Medicine at a University Medical Center. 2. Fourteen patients were studied. Patients' mean age (+/- s.d.) was 78.5 +/- 9 years. The creatinine clearance was 48.2 +/- 17.4 ml min-1 (mean +/- s.d.). 3. 500 ml (approx. 7 ml kg-1) of Fleet enema (FE - Na2HPO4.7H2O 224 mmol l-1 and NaH2PO4.H2O 1160 mmol l-1) were administered to each patient. Blood was drawn before FE administration and 1/2, 1, 3, 5, 12 and 24 h thereafter. Serum was analysed for levels of inorganic phosphorus and for calcium. 4. The serum inorganic phosphorus level rose from 1.01 +/- 0.3 mmol l-1 to 1.4 +/- 0.5 mmol l-1 (P = 0.001) 1 h after FE was administered. Serum calcium decreased from 2.32 +/- 0.12 mmol l-1 to 2.12 +/- 0.1 mmol l-1 (P less than 0.001) 12 h after FE was administered. 5. We conclude that FE carries a potential risk for acutely ill elderly patients. To avoid untoward effects due to hyperphosphataemia and hypocalcaemia, the phosphate load must be adjusted to the patient's renal function, i.e. enema volume is to be lowered when phosphate concentration is high, so that if renal function is compromised the amount of phosphate absorbed does not exceed renal excretion capacity.

Septic complications following endoscopic retrograde cholangiopancreatography: the experience in Tel Aviv Medical Center.

At the Tel-Aviv Medical Center, five of 720 (0.69%) patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) subsequently developed septicaemia. One of these patients (0.14%) died as a direct result and three other septicaemic patients died from other complications. The most important risk factor associated with infectious complications was obstructive jaundice. Retrospective analysis of our data revealed that no cases of septicaemia developed in patients given prophylactic antibiotics, whereas 4.3% of patients who received no prophylactics developed infectious complications. Prophylactic antibiotics are therefore recommended for patients undergoing ERCP who have biliary obstruction.

Pregnancy and Cushing's syndrome: example of endocrine interaction.

Pregnancy rarely occurs in women with Cushing's syndrome, and when it does, fetal mortality and morbidity are very high. We describe a 30-year-old woman who was found to have severe Cushing's syndrome in the 22nd week of her first pregnancy, after a year of unsuccessful attempts to conceive. The patient had the majority of the symptoms and signs characteristic of the syndrome. Laboratory examinations revealed hypokalemia of 2.7 mEq/l, serum cortisol 39.5 micrograms/dl without diurnal variation, free urinary cortisol 1,850 to 3,500 micrograms/24 h, 17-hydroxycorticosteroids (OHCS) 52.5 mg/24 h, 17-ketosteroids (KS) 12 mg/24 h, and ACTH 29 pg/ml. No suppression was observed upon dexamethasone administration (2 and 8 mg). Ultrasound examination of the adrenal glands revealed a left adrenal tumor with a diameter of 4.2 cm. An adrenocortical adenoma was successfully excised in the 24th week of pregnancy. During the 37th week of pregnancy, she delivered a normal baby girl. Postoperatively, the patient was put on maintenance therapy. One year after delivery, mother and child are in perfect health.