Long-term Steroid Therapy in Chronic Intractable Asthma

Rees, H.A.; Williams, D. A.

doi:10.1136/bmj.1.5292.1575

Cited by 40 publications

(9 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Estimation of the prevalence of osteoporosis in these patients, given by the proportion of patients with fractures, indicates that the prevalence ranged from 20 to 70%. [2.3] Similar prevalences of fractures have been reported in patients requiring long term high-dose corticosteroid therapy.l4-6] In other studies, however, the prevalence of bone fractures in patients receiving long term high-dose corticosteroid therapy has been found to be similar to the incidence seen in healthy individuals.l7· 8 ] It is commonly held that corticosteroids deplete bone preferentially in the axial skeleton. The fact that bone loss in trabecular bone occurs more rapidly and markedly than loss in cortical bone results in a greater likelihood of fractures in bones with a higher proportion of trabecular bone, such as the vertebrae and ribs.l 9 ] Recent studies, however, suggest that corticosteroid-induced osteoporosis is a generalised process causing bone loss at various sites.l IO ] Prospective studies have suggested that there is an initial phase of very rapid bone loss, followed by slower continued bone loss.…”

Section: Pathophysiologymentioning

confidence: 70%

Corticosteroid-Induced Bone Loss

Picado

Luengo

1996

Drug Safety

View full text Add to dashboard Cite

Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Bone loss occurs soon after corticosteroid therapy is initiated and results from a complex mechanism involving osteoblastic suppression and increased bone resorption. There are a number of factors that may increase the risk of corticosteroid-induced osteoporosis [smoking, excessive alcohol (ethanol) consumption, amenorrhoea, relative immobilisation, chronic obstructive pulmonary disease, inflammatory bowel disease, hypogonadism in men, organ transplantation]. The initial assessment of patients about to start taking corticosteroids should include measurement of spinal bone density, urinary calcium level and plasma calcifediol (25-hydroxycholecalciferol) level; serum testosterone levels should also be measured when hypogonadism is suspected. Many different drugs have been used to prevent osteoporosis in patients receiving long-term corticosteroid therapy, including thiazide diuretics, cholecalciferol (vitamin D) metabolites, bisphosphonates, calcitonin, fluoride, estrogens, anabolic steroids and progesterone. At present, however, published studies have failed to demonstrate a reduction in the rate of fracture using different preventive pharmacological therapies in patients being treated with corticosteroids on a continuous basis. Among the drugs studied, bisphosphonates (pamidronic acid and etidronic acid) and calcitonin appear to be effective in increasing bone density. Cholecalciferol preparations have been reported to be effective in some, but not all, studies. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma. Patients should take as much physical activity as possible, maintain an adequate daily intake of calcium (1000 mg/day0 and cholecalciferol (400 to 800 U/day), stop smoking and avoid excessive alcohol intake. It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. A thiazide diuretic should be considered if hypercalciuria is present (urinary calcium excretion in excess of 4 mg/kg/day). High-risk patients and those with established osteoporosis should be treated with bisphosphonates (cyclical etidronic acid or intravenous pamidronic acid), nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.

show abstract

Section: Pathophysiologymentioning

confidence: 70%

Corticosteroid-Induced Bone Loss

Picado

Luengo

1996

Drug Safety

View full text Add to dashboard Cite

show abstract

“…Thus Pearson, Bayliss, and Smellie (1961) and Livingstone and Davies (1961) showed that longterm steroid treatment of severe chronic asthma in 36 and 71 cases for periods of up to five years was effective in the majority of cases. Rees and Williams (1962) reported the results of treatment of 317 cases for an average period of two and a half years with approximately similar results: 96 of these cases received corticotrophin as well as adrenal steroids. Walsh and Grant (1966) treated 273 patients with chronic asthma for periods of 1 to 10 years, using regular intermittent treatment in 180 adults and 17 children with equally good results.…”

Section: Discussionmentioning

confidence: 87%

Long-term corticosteroid treatment of asthma.

Maunsell¹,

Pearson²,

Livingstone³

1968

BMJ

View full text Add to dashboard Cite

This report deals with 170 hospital patients suffering from severe bronchial asthma treated with long-term steroids. The first admissions to this survey were in April 1952 and the last in April 1962. The periods of observation ranged from 2 to 13 years. The patients were seen weekly or monthly at first and then at gradually longer intervals, with the exception of five who were followed-up by postal questionary at least twice each year. One patient was lost. All were under the care of two of us (J. L. L. and R. S. B. P.), and only those whose treatment with long-term corticosteroids was initiated by us are included in this study. Assessments were made by one of us (K. M.), who had access to all records and interviewed the patients individually.In defining asthma we used the functional criterion of attacks of dyspnoea due to widespread airways obstruction which alternated with more or less normal breathing ; more severe cases had evidence of obstruction between attacks. These fluctuations in respiratory function were measured by simple physiological tests when the patients visited hospital. The major factors known to precipitate attacks, acting singly or in combination, were allergic or infective. Other conditions which played a major or minor part included emotional disturbances and nasal abnormalities-polypi, infected antra (24). In some cases there was no clue to the cause, and they were labelled " idiopathic " or non-specific. All patients with chronic bronchitis who developed attacks of wheezing as a secondary phenomenon were excluded.Patients who were thought to need steroid treatment were usually admitted to hospital for investigation. Many were subject to recurrent attacks of status asthmaticus, and treatment was often begun after emergency admission for this condition.The assessment of severity was based mainly on the length of time lost from work and the response to treatment, as follows:Group 5.-Unable to work for six months during the previous year because of asthma (32 patients Each patient was issued with a steroid card and instructed on no account to stop taking steroids without consulting his doctor. The latter was advised to double or treble the dose of steroids temporarily at the onset of infection or if asthma appeared to be deteriorating: after a few days the increased dose was brought back over 7 to 10 days to the maintenance level. Many patients learnt to do this for themselves, thereby preventing severe recurrences. Antibiotics were given concurrently if infection developed. The doctor was advised to arrange admission to hospital in the event of a relapse which was not responding to increased steroid treatment after 24 hours.The main drugs used were prednisone or prednisolone given in 5-mg. and 1-mg. tablets, labelled as such to avoid errors by the patient when adjusting the dose. Methylprednisolone and triamcinolone, as well as betamethasone, were given in a few cases. Patients treated with corticotrophin only were not included, but one patient received it once or twice weekly in addition t...

show abstract

“…Moreover the well-recognized tendency to bleeding brought about by salicylates is not a feature of 'steroid ulcers' (Scott et al, 1961) In view of all the possible discrepancies in estimating ulcer incidence, it is perhaps surprising that (apart from a few reports in the early days of steroid therapy) it is now generally agreed that steroids do not increase the tendency to ulcer in conditions other than rheumatoid disease. An ulcer incidence of the order of 2%Y over variable periods has been found in cases of asthma (Rees & Williams, 1962), ulcerative colitis (Truelove & Witts, 1955;Palmer & Kirsner, 1959) and chronic skin disease (Spiro & Milles, 1960).…”

Section: Corticosteroidsmentioning

confidence: 99%

Gastric ulcer and the anti-arthritic drugs

Emmanuel¹,

Montgomery²

1971

Postgraduate Medical Journal

View full text Add to dashboard Cite

Summary Sixteen cases are described of gastric ulcer in patients receiving anti-arthritic drugs. Half of the ulcers were in the antrum or on the greater curve. Ten patients were under treatment with indomethacin and/or prednisone, seven of them receiving both drugs. The ulcers healed readily when the drugs were withdrawn, and in the case of prednisone a continued daily dose of 10 mg or less did not prevent healing. All the patients with haemorrhage were taking aspirin, with or without other drugs. The literature is reviewed, and it is suggested that the increased incidence of peptic ulcer in patients receiving anti-arthritic drugs is confined to gastric ulcer. There is suggestive evidence of an increased susceptibility to antral ulcer in severe rheumatoid disease, which may largely account for the ‘steroid ulcer’. Indomethacin is potentially ulcerogenic, and its combined use with steroids may be inadvisable. Apart from its tendency to produce haemorrhagic erosions, the role of aspirin in the aetiology of chronic ulcer remains doubtful. No serious ill-effects have been reported in the use of ibuprofen or Distalgesic in ulcer subjects.

show abstract

Long-term Steroid Therapy in Chronic Intractable Asthma

Cited by 40 publications

References 13 publications

Corticosteroid-Induced Bone Loss

Corticosteroid-Induced Bone Loss

Long-term corticosteroid treatment of asthma.

Gastric ulcer and the anti-arthritic drugs

Contact Info

Product

Resources

About