Yoshihisa Hanayama | PubMed Health

PubMed2006

Steroid pulse therapy impaired endothelial function while increasing plasma high molecule adiponectin concentration in patients with IgA nephropathy.

BACKGROUND: Decreased plasma adiponectin is associated with impaired endothelial function and, thereby, increased risk for cardiovascular events. Glucocorticoid (GC) affects vascular endothelial cells either favourably or harmfully depending upon the dosages and duration. We examined the effect of GC pulse therapy on vascular endothelial function. METHODS: Fourteen young patients with IgA nephropathy were evaluated for flow-mediated vasodilation (FMD), plasma levels of adiponectin both in high molecular weight (HMW adiponectin) form and in single molecular form (total adiponectin), hepatocyte growth factor (HGF), asymmetric dimethylarginine (ADMA), and high-sensitive C-reactive protein, before and after a course of GC pulse therapy. RESULTS: GC pulse therapy significantly decreased FMD (from 7.2 +/- 2.6 to 5.7 +/- 2.5%, P < 0.01). Meanwhile, plasma adiponectin levels were significantly augmented (total adiponectin: from 10.2 +/- 4.0 to 12.1 +/- 6.3 microg/ml, P < 0.05; HMW: from 6.5 +/- 3.2 to 7.7 +/- 3.3 microg/ml, P < 0.05). In parallel, elevated concentrations of serum HGF (from 0.28 +/- 0.12 to 0.63 +/- 0.38 ng/ml, P < 0.01) and plasma ADMA (from 0.45 +/- 0.07 to 0.53 +/- 0.04 nmol/ml, P < 0.05) were observed. CONCLUSIONS: GC pulse therapy impaired endothelial function while increasing plasma adiponectin levels, which may in turn restore the endothelial function in patients with IgA nephropathy.

Adiponectin↗

PubMed2004

[A case of tuberculous pyometrium concurrent with tuberculous pleurisy].

An 84-year-old woman began to have low fever below 38 degrees C with slight lassitude from June 19, 2002. Despite oral administration of Clarithromycin for 3 days, the fever did not subside and the lassitude increased, so she was admitted to our department. While inflammatory findings were noticed, the cause was not identified by blood and imaging examinations (thoracoabdominal CT, etc.). Although her tuberculin reaction was positive, symptoms indicative of pulmonary tuberculosis were absent. Administration of Cefotiam and Imipenem Cilastatin sodium was ineffective. Pyometra was diagnosed. After drainage, the uterine cavity was washed every day. On the basis of culture of fluid retained a few colonies of Gram-negative bacteria were isolated, but were not identified, Cefpirome was administered, whereupon the fever subsided gradually, but mild inflammatory findings remained. Even after discharge on July 24, the retention increased, so drainage and washing were done repeatedly. However, mild inflammatory findings persisted. She began to have a fever from September 17 and was readmitted. After admission, administration of Flomoxef sodium was started, but no improvement was seen. A small amount of hydrothorax appeared on the left. Thoracocentesis yielded a bloody, slightly turbid exudative. Acid-fast staining and Mycobacterium tuberculosis specific PCR of pleural effusion were negative, but adenosindeaminase was 87.4 U/l. Therefore, a diagnosis of tuberculous pleurisy was made. DNA/PCR of tubercle bacilli in the fluid retained in the uterus was positive, and re-retention was prevented by administration of anti-tuberculosis drugs. These findings suggest a strong possibility of tubercle bacillus having been the causative bacteria. Particularly in the case of the elderly, it appears important that pyometra be included in differential diagnosis as the cause of fever even without gynecological symptoms and that tubercle bacillus be considered the causative bacterium.

Aged↗