Disuse osteoporosis.

Reduction of mechanical stress on bone inhibits osteoblast-mediated bone formation and accelerates osteoclast-mediated bone resorption, and leads to what has been called disuse osteoporosis. Prolonged therapeutic bed rest, immobilization due to motor paralysis from injury of the central nervous system or peripheral nerves, application of cast to treat fractures, a common causes of disuse osteoporosis. Imaging diagnosis shows coarse trabecular pattern and thinning of cortical bones. Bone metabolism markers have been used to evaluate bone metabolism. From the viewpoint of bone metabolism, antiresorptive agents should be administered to inhibit bone resorption. Rehabilitation, including bed positioning, therapeutic exercise and electrical stimulation, should be prescribed to subject the atrophied bone to an appropriate level of mechanical stress. In spite of these aggressive and continuous treatments, most cases of disuse osteoporosis require a long time for bone to recover its bone mineral density and strength. Hence, we have to keep in mind that there are no treatments better than prophylaxis of disuse osteoporosis.

A patient with severe palindromic rheumatism and frequent episodes of pain.

A 44-year-old man began to experience episodes of joint pain with erythema in his knees, elbows, shoulders, and hands in April 1996. He was diagnosed as having palindromic rheumatism. Due to the increasing frequency and severity of these episodes, he was admitted to our hospital in May 1999. Heat therapy to the affected area produced a rapid improvement in symptoms. In addition, the continued use of physical therapy during symptom-free periods tended to reduce the frequency and severity of pain attacks. We present this case and discuss treatment options in patients with palindromic rheumatism.

Effect of beta 2-agonists on histamine-induced airway microvascular leakage in ozone-exposed guinea pigs.

beta 2-adrenergic agonists exhibit antipermeability effects in the airways. However, it is not known whether beta 2-agonists have this beneficial effect in airway mucosa that is already inflamed. We evaluated the effects of two inhaled beta 2-agonists, salbutamol and formoterol, on the histamine-induced bronchoconstriction and plasma extravasation in the airways of guinea pigs with or without ozone exposure. Total pulmonary resistance (RL) was measured before and after histamine inhalation in anesthetized animals that were pretreated with inhaled salbutamol, formoterol, or saline. Plasma extravasation in the airways was measured using Evans blue dye. In the control animals not exposed to ozone, salbutamol and formoterol each significantly reduced both the histamine-induced bronchoconstriction and the plasma extravasation in the trachea and main bronchi. In the ozone-exposed animals, the increase in RL after histamine was greater than that in control animals. Salbutamol and formoterol each significantly reduced histamine-induced bronchoconstriction, even in the ozone-exposed animals. Salbutamol did not affect the histamine-induced plasma extravasation, whereas formoterol reduced the plasma extravasation in the main bronchi, but not in the trachea, of the animals exposed to ozone. These results suggest that the anti-inflammatory properties of formoterol in inflamed airways may contribute to the beneficial effects in the treatment of airway inflammation.

Lipoxygenase product formation and cell adhesion during neutrophil-glomerular endothelial cell interaction.

Leukotriene (LT) and lipoxin (LX) levels were monitored in ionophore-stimulated coincubations of polymorphonuclear neutrophils (PMN) and microvascular kidney glomerular endothelial cells (GEN) to determine the profile of lipoxygenase (LO) products generated during cell-cell interactions and the relative contributions of transcellular pathways to LO product biosynthesis in this setting. LTB4 and LTC4 were the major products formed, as determined by reverse-phase high-performance liquid chromatography and radioimmunoassay. LTB4 and LTC4 levels were increased by 23 and 185%, respectively, in coincubations of PMN and GEN, compared with incubations of PMN alone. In contrast, LXA4 and LXB4 levels were not changed in the presence of GEN. These data suggested that GEN utilize PMN-derived LTA4 to generate LT. In keeping with this hypothesis, LT biosynthesis was enhanced if PMN were primed with human granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that augments LTA4 biosynthesis by activated PMN. The influence of LT on PMN adhesion to GEN was also assessed, since adhesion appears to be a pivotal event in recruitment of PMN in acute glomerulonephritis. Under basal conditions, LTB4 provoked low levels of adhesion via a PMN-directed CD11/CD18-dependent mechanism. The level of adhesion was markedly enhanced by prior priming of PMN with GM-CSF or activation of GEN with tumor necrosis factor-alpha (TNF). LTB4 was as potent in this regard as the complement component C5a, platelet-activating factor (PAF), and interleukin-8 (IL-8), other mediators that contribute to the entrapment of PMN in inflamed glomeruli. LTC4 also provoked PMN-GEN adhesion via a CD11/CD18-dependent mechanism, but, in contrast to LTB4, via actions with GEN. This action of LTC4 appeared to be mediated, at least in part, by induction of PAF synthesis by GEN. Interestingly, LT-induced PMN-GEN adhesion was markedly attenuated following remodeling of PMN phospholipids with 15(S)-hydroxyeicosatetraenoic acid, a product of 15-LO, which has been implicated as an anti-inflammatory eicosanoid in some experimental and human inflammatory diseases. Taken together, these results provide further evidence that 1) transcellular biosynthetic pathways may amplify the profiles of inflammatory mediators and thereby contribute to leukocyte recruitment in acute glomerulonephritis and 2) that products of the 5-LO and 15-LO pathways may exert opposing actions on PMN trafficking during glomerular inflammation in vivo.

Effects of bed rest on bone metabolism in patients with femoral neck fracture.

The effect of continuous 1 week bed rest during traction on bone metabolism were studied in patients with femoral neck fracture. Bone demineralization was assessed by measuring serum calcium (Ca), phosphorus (P), and alkaline phosphatase (AlkP) before, during, and after 1 week-bed rest with skeletal traction. In addition, 24-hour urinary excretion of calcium and phosphorus were measured. Serum Ca did not change significantly before, during, and after bed rest, whereas serum P increased after 1 week bed rest and postoperatively remained significantly elevated. Serum AlkP did not increase with bed rest, but became elevated postoperatively. Urinary Ca excretion increased from 105.8 +/- 15.2 to 138.0 +/- 15.4 mg/24h after 1 week of bed rest, and remained elevated postoperatively. In contrast, urinary P excretion initially increased 495.1 +/- 65.0 to 610.8 +/- 87.7 mg/24h, and subsequently decreased to a level significantly less than the admission level. These results suggest that 1 week bed rest for the patients with femoral neck fracture resulted in bone atrophy and demineralization.

Calcium treatment of essential hypertension in elderly patients evaluated by 24 H monitoring.

We used 24-h monitoring of blood pressure (BP) to evaluate the effect of calcium supplementation on mild to moderate essential hypertension in elderly hospitalized patients for the first time in a controlled crossover study. The mean systolic and diastolic BP over a period of 24 h declined by 13.6 mm Hg (P less than .005) and 5.0 mm Hg (P less than .05) respectively in patients whose diet was supplemented with 1 g of elemental calcium in the form of oystershell electrolysate (AA calcium). Serum ionized calcium and urinary calcium and sodium excretion increased (serum Ca2+ 0.16 +/- 0.03 mEq/L, P less than .05; FECa 0.5 +/- 0.2%, P less than .05; FENa 0.4 +/- 0.1%, P less than .05) and plasma parathyroid hormone was suppressed (12.2 +/- 2.3 pg/mL, P less than .005). These data suggest that supplementation of dietary calcium may contribute to a reduction of BP in elderly patients with essential hypertension.

Schizonodiol, Schizonol, and Schizonepetosides D and E, Monoterpenoids of Schizonepeta tenuifolia Spikes1.

Four new monoterpenoids, shizonodiol, shizonol, and shizonepetosides D and E, have been isolated from SCHIZONEPETA TENUIFOLIA spikes along with the known flavonoids, diosmetin, hesperetin, and luteolin.

Anticomplementary activity of the constituents of Eucommia ulmoides bark.

A study was made on the anticomplementary activity of the lignoid and iridoid derivatives isolated from the bark of Eucommia ulmoides as well as the enzymatic hydrolysis products of the isolated iridoid glucosides.