Advances in the treatment of depression in older adults

Depressive symptoms in older adults are common, but the minority of elderly meet criteria for major depressive disorder. This has led to confusion regarding the recognition of diagnosis, approach to treatment, and monitoring of outcomes in this needy population. Few depressed older adults are willing to seek treatment from psychiatrists or mental health specialists. Treatment approaches to the depressive spectrum of disorders in late life, which encompasses major and minor depressive disorder, dysthymic disorder, and mood disorders related to medical conditions, must include evidence-based algorithms that can be delivered in a variety of health care settings. Several recent multisite trials have advanced the use of collaborative care models and the systematic stepwise approach to the treatment of depression and anxiety states in older adults. This offers the ability to provide effective treatment of depression for older adults, consistent with current guidelines, in primary care and specialized health care settings.     

Short-term niflumic-acid-induced acute renal failure in children

Several reports emphasize the adverse effects of non-steroidalanti-inflammatory drugs (NSAIDs) on renal function. We haveobserved over the last 10 years seven cases of acute renal failure(ARF) due to immune interstitial nephritis in children. A recommendedoral or rectal dose of niflumic acid was prescribed for ear-nose-throatdisorders, Length of exposure was 1–5 days. Clinical symptoms (oedema, oliguria or anuria) appeared between3 and 6 days. Three patients had previously received the drug.Hypersensitivity signs (fever, skin rash, eosinophilia, and/orincreased IgE) were present in all cases, leukocyturia in fivecases, and haematuria in six cases. Renal biopsy showed interstitiallesions with lymphocyte, eosinophil, and plasma cell infiltrateswithout tubular cell necrosis. Glomeruli were normal on light-microscopy,except in one patient. Electron-microscopy showed extensivepodocyte fusion in two patients, who had clinical and laboratoryevidence of nephrotic syndrome (NS). ARF rapidly disappeared after NSAID withdrawal, except in twopatients whose renal failure was irreversible despite methylprednisolonebolus. ARF is very rare in children treated with niflumic acid.When ARF occurs, different pathophysiological mechanisms areinvolved but the most common is immunological.     

Mediators of pulmonary injury induced by inhalation of bacterial endotoxin

The purpose of this study has been to further define the pathophysiologic aspects of lung injury caused by the inhalation of endotoxin (LPS) using the morphometric approach to identify mediators that influence distal lung structure and function. Hamsters were divided into 3 groups 24 h prior to low dose LPS inhalation exposure (4 micrograms/m3 for 5 h): (1) pretreated with cobra venom factor to deplete complement in vivo, (2) pretreated with indomethacin to block prostaglandin production, and (3) untreated control group. Both pretreatments abolished LPS-induced decreases in lung volume as well as increases in capillary PMN and platelets seen in untreated control animals. Neither pretreatment had any effect on the LPS-induced decreases of other capillary leukocytes. Similarly, both methods of pretreatment failed to block increases in cellular interstitium of distal capillary septa induced with LPS alone. LPS provoked changes in capillary endothelium, especially seen as an increase in numerical density of endothelial pinocytotic vesicles. Decomplementation failed to alter this increase, but indomethacin pretreatment blocked the effect. Neither treatment had any effect on their size. Low dose LPS inhalation also altered pulmonary capillary permeability to a 125I-BSA probe, which was found in significantly greater amounts in LPS-exposed lungs than in those of saline aerosol control lungs, but was not present in the air space as evidenced by negligible counts in bronchoalveolar lavages. It is evident that endotoxin on the epithelial side of the air-blood barrier leads to changes on the other side of that barrier.(ABSTRACT TRUNCATED AT 250 WORDS)