Osteoporotic stress fractures in anorexia nervosa: etiology, diagnosis, and review of four cases.

Anorexia nervosa (AN) is a chronic eating disorder characterized by self-imposed semi-starvation that affects 1% of adolescent females. AN predisposes to osteoporosis through hypothalamic dysfunction, which may lead to elevated cortisol as well as diminished estrogen and progesterone. The osteoporosis associated with AN affects both trabecular and cortical bone and increases the risk of osseous fracture. Fractures in this population may go unrecognized, because planar X-rays may be nondiagnostic for 6 weeks or more. Four women with AN ranging in ages from 22 to 34 with skeletal pain and nondiagnostic roentgenographs are described. Stress fractures in these patients were subsequently identified by bone scan. Although moderate exercise in patients with AN-associated osteoporosis may be beneficial, strenuous exercise can be detrimental, with its potential risk of stress fractures and exacerbation of the underlying neurohormonal abnormalities. This risk for fracture may persist well after improvement in the patient's AN.

A prenylflavone, artonin E, as arachidonate 5-lipoxygenase inhibitor.

Several naturally occurring prenylflavones were tested for their inhibitory actions on arachidonate 5-lipoxygenase purified from porcine leukocytes. Of the compounds tested, artonin E (5'-hydroxymorusin) exhibited the most potent inhibition on arachidonate 5-lipoxygenase (IC50 = 0.36 microM). Arachidonate 12-lipoxygenase purified from porcine leukocytes and human platelets, 15-lipoxygenase from rabbit reticulocytes and fatty acid cyclooxygenase from bovine vesicular glands were inhibited by the compound only at higher concentrations (IC50 = 2.3, 11, 5.2 and 2.5 microM, respectively).

The prevalence of peripheral neuropathy in patients with anorexia nervosa.

A prospective, controlled study was conducted to determine the prevalence of peripheral neuropathy (PN) in patients with anorexia nervosa (AN). Fifty-one patients (49 females, 2 males) between the ages of 12 and 47 (means = 22.5) who met the criteria for AN of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, were randomly selected from an inpatient eating disorders unit during 15 months. Fifty healthy volunteers (41 females, 9 males) between the ages of 17 and 50 (means = 26.5) served as controls. After a neurologic history, all patients were evaluated by physical examination and standardized electrodiagnostic testing. Chi-square contingency testing was used to assess data. Four study group patients (8%) had electrodiagnostic evidence of a sensorimotor PN compared with none in the control group. This is approaching statistical significance (p = 0.13). Three of four patients with AN for at least ten years were among those with PN. The prevalence of subjective symptoms among the study group (65%) as compared to the control group (4%) was of marked significance (p = 5.62 x 10(-10]. In addition, three anorexic patients were found to have an isolated peroneal nerve palsy. We conclude that PN is a notable complication of AN, particularly in long-standing cases. The PN is most likely a product of chronic malnutrition rather than a specific nutrient deficiency. Patients with AN also appear to be at increased risk for developing localized compression neuropathies secondary to subcutaneous tissue loss.

Effects of heparin and aminoguanidine on anaphylatoxin activity in the guinea-pig.

Heparin inhibited the bronchoconstrictor and pressor responses to histamine and anaphylatoxin. However, anaphylatoxin-induced hypotension, in contrast to that induced by histamine, was resistant to heparin inhibition. Aminoguanidine alone had no effect upon histamine or anaphylatoxin but it abolished the heparin-induced inhibition. It is therefore concluded that histamine mediates the bronchiolar and pressor but not the hypotensive effects of anaphylatoxin. Furthermore, anaphylatoxin causes the release of heparin to modulate the bronchiolar effects of extra-pulmonary histamine.

Interaction between chloroquine and indomethacin in airways smooth muscle in vivo.

The indomethacin-induced enhancement of airways smooth muscle contractility to histamine reported earlier in vitro has now been demonstrated in conscious guinea-pigs. Chloroquine, an anti-malarial drug with phospholipase A2 inhibitory activity, antagonized histamine and also reversed the indomethacin-induced enhancement. These observations indicate that histamine-induced bronchospasm in vivo is modulated by the arachidonate system and that chloroquine-type phospholipase A2 inhibitors may ameliorate such bronchospasm. These findings also explain the observed clinical benefits of chloroquine in chronic asthmatics.

The anti-inflammatory effect of a crude aqueous extract of the root bark of "Ficus elastica" in the rat.

An investigation has been carried out to determine whether the aqueous extract of Ficus elastica is active as an anti-inflammatory agent in the carrageenin-induced oedema and adjuvant-induced arthritis in the rat. This investigation was prompted by the fact that practitioners of herbal medicine in West Africa use the plant for the treatment of muscle and joint pain. The results of the investigation clearly indicated that orally administered Ficus elastica extract markedly inhibited the experimentally induced inflammation in the two test models. This effect of Ficus elastica was very similar to that of indomethacin. Thus in the carrageenin-induced oedema Ficus elastica (2-10 mg/kg) and indomethacin (1-5 mg/kg) produced inhibition of the magnitude of 5.41-68.92% and 27.03-69.26%, respectively. Similarly, both the extract of Ficus elastica and indomethacin inhibited the primary as well as the secondary lesions of adjuvant arthritis in the rat. The extract used in this study was coloured buff and there is considerable evidence that flavonoids of plant origin possess anti-inflammatory activity. Therefore it may be concluded that the anti-inflammatory activity of the extract of Ficus elastica was probably due to the presence of a pigment of the flavonoid class. Further studies are in progress to elucidate the chemical characteristics of this active principle.

The nature of adrenergic mechanisms involved in anaphylatoxin activity in the guinea-pig.

1. Evidence is presented to elucidate the nature of the adrenergic mechanisms involved in responses of the guinea-pig to anaphylatoxin (AT).2. Investigation by means of adrenalectomy, adrenergic neurone blockade, alpha- and beta- adrenoceptor blockade and exclusion of autonomic reflexes, revealed that the adrenergic mechanisms provoked included catecholamine release from the adrenal medulla, sympathetic reflex activity, stimulation of adrenergic neurones and alpha- and beta-adrenoceptor activity.3. The cardiovascular effects of AT, mediated by histamine release, were largely attributable to adrenal medullary and adrenergic neuronal mechanisms. These mechanisms also exerted a restraint on the predominantly histamine mediated bronchoconstrictor effect of AT.4. The cardiovascular effects of AT activity, not attributable to histamine release, were also probably associated with catecholamine release. However, the bronchoconstrictor component of this AT activity was not significantly affected by guanethidine, and it would, therefore, appear that neuronal bronchodilator mechanisms did not exert a restraint upon this aspect of AT activity.5. These findings are generally compatible with previous work showing that adrenergic mechanisms operate during AT-induced responses. In contrast to previous reports, however, the adrenergic activity was predominantly associated with the effects of released histamine.