Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment procedure with 121 in-patients suffering from respiratory obstruction is described following a short review of the etiology and pathogenesis of bronchial asthma, and the consequences for treatment resulting therefrom. While patients with chronic bronchitis caused by an emphysema of the lungs were treated primarily with antibiotics, synthetic corticotrophin (Synacthen, Synacthen Depot) and/or cortisone were prescribed in the treatment of 3/4 of the cases involving asthmatics and patients with chronic asthmatoid bronchitis caused by an emphysema. In severe cases ACTH was combined with cortisone. As a result of corticotrophin's direct effect on the bronchial muscles and the mast cells, along with its stimulation of the adrenal cortex, treatment with ACTH has the advantage over the classic cortisone treatment of retaining the functional ability of the adrenal cortex and reducing the amount of cortisone needed. No ACTH-caused side effects were reported. Included are tables containing guidelines for therapy suitable in private practice.
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PMID:[Bronchial asthma. Pathogenetic assumptions - therapeutic guidelines - the significance of synthetic corticotrophin (ACTH) in its treatment (author's transl)]. 17 68

The authors have tested the effectiveness of ACTH 1-17, administered in a single dose of 100 micrograms intramuscularly at 07(00) for 10 consecutive days, in 10 male patients suffering from chronic obstructive bronchitis with different ventilatory impairment. The subjects performed every 4 h (02(00), 06(00), 10(00), 14(00), 18(00), 22(00] for 14 consecutive days (3 days of wash-out and 10 days of treatment) spirometric tests with recording of 8 ventilatory parameters and of oral temperature. The day before and after treatment plasma cortisol levels were also determined 6 times a day. After the period of treatment 4 subjects improved, 4 remained stationary and 2 worsened as concerns the ventilatory functions, while 7 perceived a better general condition. The normal circadian synchronization of the respiratory function of the group, with acrophase in the afternoon, was maintained and the temperature rhythm was not influenced. The circadian rhythm of plasma cortisol showed a significant mesor reduction after treatment with a slight advance in acrophase indicating a partial inhibition of the hypothalamo-hypophyseal axis. The success of treatment was independent of the severity of the ventilatory impairment and the subjects showed different patterns of response both quantitatively (probably related to the dosage) and temporally (immediate or delayed). Hyperpigmentation of the skin owing to the intrinsic melanotropic activity of the peptide occurred in 2 subjects. As a side effect, weight increase was apparent in 3 subjects.
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PMID:ACTH 1-17 effects in chronic obstructive bronchitis. 609 Dec 43

Leukemia inhibitory factor (LIF) exhibits multiple biological activities in various tissues, and we have shown that LIF activates POMC gene transcription in response to immune signals. As higher serum levels of LIF have been reported in septicemia, we measured LIF values in biological fluids by RIA. Immunoreactive LIF was detected in 303 of 428 human serum samples. Circulating LIF detection rates were 69% in acute inflammatory diseases, 83% in chronic inflammatory diseases, 61% in noninflammatory diseases, and 90% in cancer patients. Serum concentrations of human LIF was higher in patients with inflammatory disease than in noninflammatory disease (0.80 +/- 0.10 vs. 0.53 +/- 0.02 ng/mL; P < 0.05) or in cancer patients (0.44 +/- 0.06; P < 0.05). Higher serum human LIF levels were found in septicemia (0.78 +/- 0.14 ng/mL), pneumonia (0.80 +/- 0.10 ng/mL), acute bronchitis (0.88 +/- 0.09 ng/mL), other infections (1.01 +/- 0.17 ng/mL), and systemic lupus erythematosus (SLE; 0.79 +/- 0.06 ng/mL). In 7 septicemia patients, Gram-negative infection was associated with higher LIF levels (1.06 +/- 0.16 ng/mL) than was Gram-positive infection (0.58 +/- 0.14 ng/mL). In patients with acute inflammatory disease, serum LIF levels decreased within several days after hospitalization. To test circulating mouse (m) LIF changes in response to inflammatory stress, lipopolysaccharide (LPS) was injected ip to mice. LPS increased serum mLIF values concordantly with ACTH levels. After i.p. injection of 80 microg LPS, serum mLIF increased by 144% (P < 0.05), 173% (P < 0.05), and 134% at 30, 90, and 120 min respectively. In vitro, however, LPS did not increase ACTH and mLIF secretion from dispersed mouse primary pituitary cells. These results suggest that LIF is an important participant in the pathogenesis of the acute inflammatory response. The elevated serum LIF levels observed in inflammation do not appear to originate from the pituitary.
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PMID:Measurement of leukemia inhibitory factor in biological fluids by radioimmunoassay. 954 56