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Biomedical subjects

J J Fallon

Publications and source records attributed to J J Fallon.

9 recordsLinked to original sources
PubMed1999

Chronic glucocorticoid therapy-induced osteoporosis in patients with obstructive lung disease.

Long-term glucocorticoid (GC) therapy has been instrumental in decreasing morbidity and mortality in a variety of chronic inflammatory diseases, including persistent asthma. Long-term GC therapy is also widely prescribed for COPD. One of the important and often unrecognized side effects of chronic GC therapy is secondary osteoporosis. The risk of GC-induced bone loss is roughly correlated with daily dose, duration, and total cumulative lifetime dose of GC treatment. Oral prednisone increases the risk of bone loss and fracture. High doses of inhaled GCs may also increase the risk of osteopenia/osteoporosis, but the risk appears to be less than that associated with oral GCs. Hormone replacement therapy, oral and parenteral bisphosphonates, supplemental calcium and vitamin D, calcitonin, and fluoride compounds have been used, experimentally, in the management of GC-induced bone loss. Asthma and COPD specialists are key prescribers of oral and inhaled steroids and are likely to encounter patients with significant bone loss. Despite known risk factors and the availability of reliable diagnostic tools to recognize bone loss, the opportunity to slow, reverse, and treat bone loss is often missed. We present a review of the current literature regarding the incidence, treatment, and prevention of osteopenia/osteoporosis secondary to chronic GC therapy in adult asthma and COPD patients. Guidelines are presented regarding the identification of patients at risk for developing GC-induced secondary bone loss, and therapeutic alternatives are discussed.

Administration, Inhalation↗
PubMed1987

Immunogenicity of malondialdehyde-modified low density lipoproteins. Studies with monoclonal antibodies.

Malondialdehyde (MDA)-modified low density lipoprotein (LDL) can stimulate the accumulation of cholesteryl esters in cultured macrophages through its interaction with specific scavenger receptors. It has been speculated that such interaction occurs in vivo thus contributing to the formation of foam cells within atherosclerotic lesions. This report describes the development of new tools in the form of a specific assay for MDA-LDL to investigate this hypothesis. We have immunized BALB/c mice with malondialdehyde mouse low density lipoproteins and antibodies against malondialdehyde human low density lipoproteins were generated. Monoclonal antibodies were produced using hybridoma techniques and one particular clone (EB 7-3) was expanded for further studies. The immunoreactivity of several antigens was tested using antibody EB 7-3 in an enzyme-linked immunosorbent assay (ELISA). In a typical assay malondialdehyde human LDL (with at least 40% of lysines modified) was coated (2 micrograms/ml, 100 microliter) in 96-well microtiter plates. Antibody plus one of several antigens were then added and the interaction between the antibody and coated antigen was measured using alkaline phosphatase-conjugated affinity purified goat anti-mouse immunoglobulin. The binding of antibody EB 7-3 to wells coated with malondialdehyde-LDL was competitively inhibited by malondialdehyde-LDL added in solution, with half maximal inhibition occurring at 150 +/- 80 ng/ml. In addition, the ability of malondialdehyde-LDL to inhibit this interaction was proportional to the degree of modification: the more lysines were modified the more did malondialdehyde-LDL inhibit the binding of antibody EB 7-3 to coated malondialdehyde-LDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1984

Euthyroid sick syndrome. Association with urosepsis in an elderly man.

A 91-year-old man with chronic incontinence managed by indwelling catheter was hospitalized for investigation of fever, hypotension, and cloudy urine. Dopamine was administered to maintain adequate blood pressure, and cefazolin and tobramycin were given for presumed urosepsis. Persistent bradycardia suggested hypothyroidism, but laboratory data were consistent with euthyroid sick syndrome. Thyroid values returned to normal with correction of the sepsis and improvement in nutrition. Exogenous thyroid was not necessary. The case reported here demonstrates that proper assessment of thyroid function in an acutely or chronically ill elderly patient requires attention to the factors that can influence thyroid values--such as non-thyroidal illness like sepsis, poor nutritional status, and use of medication like dopamine--as well as careful correlation of results of thyroid function studies with clinical findings. Euthyroid sick syndrome resolves with correction of the underlying disease and improvement in nutrition. In addition, the total thyroxine (T4) value in this condition is a good predictor of risk of death.

Aged↗