Acute psychotic stress is associated with decreased adiponectin serum levels.

OBJECTIVE: To determine the effect of acute psychotic stress on adipokine secretion in non-diabetic subjects. RESEARCH DESIGN AND METHODS: Adiponectin, leptin, and cortisol serum levels were determined in 39 non-diabetic patients with acute psychotic stress reaction admitted to a psychiatric ward. The clinical global impression (CGI) score was used to evaluate the level of psychotic stress. Insulin sensitivity (IS) was determined by the homeostasis model assessment (HOMA). Patients were re-assessed 2 weeks after admission. During hospitalization patients were treated for variable times with either phenothiazines or thioxanthenes. RESULTS: The mean CGI score decreased significantly with time: 5.3+/-0.8 and 2.6+/-0.8 on admission and after 2 weeks respectively (p<0.001). On admission, the mean adiponectin level was significantly lower in patients compared to normal controls: 15.3+/-8.2 mug/ml and 26+/-12.8 mug/ml, respectively (p=0.02). It increased significantly after 2 weeks to 18.2+/-10 mug/ml (p=0.003). By contrast, the leptin and cortisol levels did not change significantly. No correlation was found between the changes in individual CGI scores and adiponectin levels. However, female patients with the highest stress on admission demonstrated the lowest adiponectin levels and insulin sensitivity: p=0.002 and 0.03 respectively. CONCLUSIONS: These data suggest a link between acute psychotic stress reaction and decreased serum adiponectin levels. Further studies are recommended to determine the strength of this association.

Successful treatment of prolonged agranulocytosis caused by acute parvovirus B19 infection with intravenous immunoglobulins.

A 21-year-old previously healthy male presented with prolonged fever of 3 weeks duration and profound agranulocytosis that did not respond to treatment with granulocyte-stimulating factors. A bone marrow biopsy demonstrated an absence of myeloid lineage. Acute parvovirus B19 infection was diagnosed by the presence of both IgM and IgG anti-parvovirus antibodies. Two days treatment with intravenous immunoglobulins (IVIg) resulted in complete recovery. The role of treatment with immunoglobulins in acute and persistent parvovirus infection is discussed.

[Anticoagulant treatment in pericardial effusion--a therapeutic dilemma].

Anticoagulant treatment for acute myocardial infarction (AMI) and pericardial effusion is controversial, since the treatment might cause hemopericardium and tamponade. On the other hand, anticoagulants are strongly indicated in many situations in AMI, including: left ventricular thrombus, unstable angina, severe heart failure, deep vein thrombophlebitis, pulmonary embolism, atrial fibrillation, as part of thrombolytic treatment, and during cardiac catheterization. We describe a 70-year-old man who presented with both pericardial effusion and a left ventricular thrombus 3 weeks after an extensive, anterior wall AMI. Anticoagulants and corticosteroids were administered simultaneously under hemodynamic and echocardiographic monitoring without complications. It is our impression that anticoagulant treatment is safe in patients with pericardial effusion.

[Terbinafine-induced cholestatic liver injury].

A 43-year-old man presented with weakness, pruritus, skin rash and jaundice 2 weeks after treatment for onychomycosis with terbinafine (Lamisil) was started. Liver function tests showed combined hepatocellular and cholestatic injury. Ultrasound examination, computerized tomography and ERCP excluded extrahepatic obstruction. Serology was negative for HBV, HCV, HAV, CMV, and EBV. Liver biopsy was consistent with drug-induced cholestatic injury. Since the clinical picture did not improve when terbinafine was stopped, corticosteroids were started and resulted in complete clinical and laboratory recovery; liver function tests were normal 8 months after corticosteroids were discontinued.

Effect of exercise training on glomerular filtration rate of mice with various degrees of renal mass reduction.

We studied the effect of repeated heavy physical activity on glomerular filtration rate (GFR) in healthy, uninephrectomized and experimentally uremic mice. Exercise consisted of running uphill in the inner surface of a rotating cylinder in ideal environmental temperature. In the control groups, no extra physical activity was imposed. In sham-operated and nephrectomized mice, GFR rose significantly following training. By contrast, GFR did not change significantly in the exercised mice with experimental renal failure 24 h following the last exercise session. During the same period, no significant change was observed in GFR of any of the control groups. Following training in each experimental group, mean aortic blood pressure as well as fractional kidney weight (kidney weight/body weight) were not different from the respective controls. Our results indicate that the capacity to augment GFR by physical training is dependent upon the amount of remaining functional renal tissue.