References: AVASCULAR NECROSIS Volume 4 Issue 2

AVASCULAR NECROSIS

21. AUTHOR	Wang-K-Z, Mao-L-Z, Hu-C-G.
INSTITUTION	Second Teaching Hospital, Xi'an Medical University.
TITLE	(Experimental study on mechanism of steroid-induced avascular necrosis of femoral head).
SOURCE	Chung-Hua-Wai-Ko-Tsa-Chih 1994 Sep, VOL: 32 (9), P: 515-7, ISSN: 0529-5815.
ABSTRACT	The authors adopted an animal model to observe the pathogenic mechanism of steroid-induced avascular necrosis of the femoral head. Sixty-four white rabbits were divided into two groups: hydrocortisone acetate (8 mg/kg) was hypodermically given to 48 experimental animals and 0.32 mg/kg of normal saline to 16 rabbits for control. Two groups of animals were fed and kept in the same condition. The results showed that application of the steroid drug could produce fat degeneration and necrosis of osteocytes and fat embolism in the small blood vessels of the femoral head. The abnormal hypertrophied fat cells in the bone marrow compressed small veins in the femoral head resulting in blood stasis of the capillaries, thus growth and regeneration of the capillary were inhibited. Author.

22. AUTHOR	Pfeiffer-M, Griss-P.
INSTITUTION	Klinik fur Orthopadie Philipps-Universitat, Marburg.
TITLE	(Craniocerebral trauma and aseptic osteonecrosis. Steroid-induced sequelae after therapy of brain edema). TT Schadel-Hirn-Trauma und aseptische Osteonekrose. Steroidbedingte Folgezustande nach Hirnodemtherapie.
SOURCE	Unfallchirurg 1992 Jun, VOL: 95 (6), P: 284-7, ISSN: 0177-5537.
ABSTRACT	In this publication we present three cases of avascular osteonecrosis (AON) of the femoral head and the talus in adolescent and young adult patients following short-term, high-dose steroid therapy for cerebral trauma. All patients were proven to be free of other risk factors for AON. The latency period between the steroid therapy and the occurrence of AON ranged from 12 to 60 months; steroid therapy lasted for 12 to 16 days with a total dosage equivalent to 2370-7180 mg prednisolone. Our case reports are added to a review of the literature with 14 similar cases reported receiving short-term, high- dose steroid therapy; 2 of them were also after brain trauma. To the best of our knowledge, 1 of our cases shows the longest latency period ever described after such therapy, and all our cases had a shorter therapy time than reported by other authors who have mentioned brain trauma patients. Additionally, bilateral necrosis of the talus due to short-term, high-dose steroid therapy has also not previously been described. Whereas AON is quite common after long- term steroid therapy (e.g., for immunosuppression and rheumatic disorders), our cases prove that serious complications can occur even after a short period of emergency steroid therapy in cerebral trauma, a possibility that is generally unknown. The minimal dosage and the maximum time steroids can be applied to exclude the risk of AON has not yet been determined, although we do recognize that steroids are useful for the prevention of brain edema.(ABSTRACT TRUNCATED AT 250 WORDS) Author.
23. AUTHOR	Hurel-S-J, Kendall-Taylor-P.
INSTITUTION	Endocrine Unit, Royal Victoria Infirmary, Newcastle-upon-Tyne, UK.
TITLE	Avascular necrosis secondary to postoperative steroid therapy.
SOURCE	Br-J-Neurosurg 1997 Aug, VOL: 11 (4), P: 356-8, ISSN: 0268-8697.
ABSTRACT	Hypothalamic and pituitary tumours may present with vague symptoms owing to excess or lack of hormone production, including diabetes insipidus. Corticosteroids are commonly employed to limit cerebral oedema and at much lower doses to treat secondary hypocorticalism. Continuation of steroids at inappropriately high doses predisposes to the development of avascular necrosis as in the case we describe in a young woman of 34 years. This is a potentially preventable crippling disorder. When prescribing steroids the lowest effective dose should be used. Author.

24. AUTHOR	Foley-Nolan-D, Daly-C, Barry-C, Woods-A, Neligan-M, Coughlan-R-J.
INSTITUTION	Department of Rheumatology and Physical Medicine, Mater Misericordiae Hospital, Dublin.
TITLE	Avascular necrosis of the femoral head post heart-transplantation and steroid dosage.
SOURCE	Ir-Med-J 1992 Dec, VOL: 85 (4), P: 138-9, ISSN: 0332-3102.
ABSTRACT	Avascular necrosis (avn) post heart-transplantation has been considered to be due to the high doses of steroids used to immunosuppress these patients in attempting to prevent transplant rejection. This study shows that avascular necrosis occurs even when low dose steroids regimes are used and demonstrates no significant correlation between steroid dosage and the development of avn. Patients with symptomatic avn benefit from early diagnosis and management of their condition in that the need for total joint arthroplasty can be prevented in many cases. Author.

25. AUTHOR	Tang-S-C, Chan-K-C, Chow-S-P.
TITLE	Osteonecrosis of femoral head after topical steroid therapy.
SOURCE	J-R-Coll-Surg-Edinb 1986 Oct, VOL: 31 (5), P: 321-3, ISSN: 0035-8835.

26. AUTHOR	McLean-C-J, Lobo-R-F, Brazier-D-J.
TITLE	Cataracts, glaucoma, and femoral avascular necrosis caused by topical corticosteroid ointment (letter).
SOURCE	Lancet 1995 Feb 4, VOL: 345 (8945), P: 330, ISSN: 0140-6736.

27. AUTHOR	Felson-D-T, Anderson-J-J.
INSTITUTION	Boston University Multipurpose Arthritis Center, Massachusetts.
TITLE	Across-study evaluation of association between steroid dose and bolus steroids and avascular necrosis of bone.
SOURCE	Lancet 1987 Apr 18, VOL: 1 (8538), P: 902-6, ISSN: 0140-6736.
ABSTRACT	Studies investigating steroid dose and avascular necrosis of bone (AVN) have found either a weak association or none at all. This quantitative review of published studies has evaluated the effects of steroid dose and bolus steroids on the risk of AVN. 22 papers with sufficient information for analysis were identified. The mean steroid dose for the cohort was plotted against the percentage in whom AVN developed. Total dose was divided into non-bolus (oral) and bolus dose, and doses 1, 3, 6, and 12 months after beginning steroids were tested separately for their association with AVN risk. There was a strong correlation between daily total dose and AVN rate (r = 0.61-0.80). Oral dose was strongly correlated with AVN rate (r = 0.70-0.86), but bolus dose was not associated with AVN risk. This strong association between AVN and steroid dose contrasts with the weak relations found in case-control studies from individual centres in which cases and controls received similar steroid regimens and therefore did not differ greatly in steroid dose. The method of deriving a single exposure level per study and comparing the amount of exposure across studies may be useful in assessing whether a drug's toxicity is dose dependent. Author.

28. AUTHOR	Chang-C-C, Greenspan-A, Gershwin-M-E.
INSTITUTION	Division of Rheumatology, Allergy, and Clinical Immunology, University of California, Davis.
TITLE	Osteonecrosis: current perspectives on pathogenesis and treatment.
SOURCE	Semin-Arthritis-Rheum 1993 Aug, VOL: 23 (1), P: 47-69, ISSN: 0049-0172 222 Refs.
ABSTRACT	Nontraumatic osteonecrosis results from impairment of circulation to the affected bone. The femoral head is affected most frequently. The underlying cause for the circulatory defect in osteonecrosis varies and may involve both local and systemic changes. Steroid use, alcohol consumption, pancreatitis, and lipid disorders appear to lead to bone death either by development of fat emboli in the microcirculature surrounding the affected bone or by fatty infiltration of the marrow. Decompression syndrome results from the presence of gaseous emboli in the microcirculature. In Legg-Calve-Perthes disease other associated features are present such as short stature, suboptimal growth velocity, and/or hormonal imbalances, and it is likely that osteonecrosis may be secondary to systemic abnormalities, although specific factors have not been identified. Other frequently suggested pathogenic factors that play a role in the development of osteonecrosis include increased intraosseous pressures, the presence of cytotoxic cellular factors, intravascular coagulation, venous stasis, and the hyperviscosity syndrome. Some investigators have attempted, without success, to find a common etiology for all cases of osteonecrosis. In addition, patients have developed osteonecrosis without any known risk factors; this syndrome has been coined idiopathic avascular necrosis. In advanced stages of femoral head osteonecrosis, total hip arthroplasty appears to be the best therapeutic modality, particularly in older individuals. Author.


29. AUTHOR	Jacobs-B.
TITLE	Alcoholism-induced bone necrosis.
SOURCE	N-Y-State-J-Med 1992 Aug, VOL: 92 (8), P: 334-8, ISSN: 0028-7628.
ABSTRACT	A total of 164 patients with alcoholism-induced osteonecrosis were seen over a 22-year period, from 1962 to 1984. Twenty-three percent of patients were female and 30.5% were black. The average duration of alcohol abuse was 9.5 years, ranging from 8 to 20 years. The presence of femoral head necrosis was diagnosed in patients aged 21-67 years; 28% of patients were under 40 years of age and 76% were under 50 years. Bilateral hip necrosis was present in 44.5% of patients and, within three years of the diagnosis of FHN, the presence of multifocal necrosis became evident in 23 cases at sites away from the hip (shoulders and knees). Hyperlipidemia was found in 38.4% of cases, involving both cholesterol and triglycerides. Serum amylase was elevated in 33 patients; liver dysfunction was present in 50; hepatomegaly was found in 32; and biopsy-confirmed cirrhosis was present in 22 cases. Hyperuricemia was found in 22 patients, some of whom had received steroids. Disabling hip pain was the first manifestation of disability related to alcohol abuse in 158 patients, most of whom required total hip joint replacement. This study supports the hypothesis that alcoholism-induced bone necrosis is caused by fat embolism linked to co-existent hyperlipidemia. The treatment of hyperlipidemia by dietary means or lipotropic medication and the cessation of alcohol abuse is advised. Multi-center studies employing such treatment should provide evidence of its effect on the evolution of necrosis as well as the incidence of bilateral hip femoral head necrosis and multifocal lesions. Author.

30. AUTHOR	Orlic-D, Jovanovic-S, Anticevic-D, Zecevic-J.
INSTITUTION	Department of Orthopaedic Surgery, Faculty of Medicine, University of Zagreb, Yugoslavia.
TITLE	Frequency of idiopathic aseptic necrosis in medically treated alcoholics.
SOURCE	Int-Orthop 1990, VOL: 14 (4), P: 383-6, ISSN: 0341-2695.
ABSTRACT	The occurrence of idopathic aseptic necrosis of bone in multiple sites has been studied in persons who have had medical treatment for excessive consumption of alcohol. The incidence was 5.3% in 1157 such persons and there were 92 different sites in 62 patients. There were 82 lesions affecting the femoral head, 46 in the left hip and 36 in the right. In 10, it was present in the head of the humerus. Multiple foci were found in 6.1% of patients with the disease. In 2 men and 2 women both femoral heads and both humeral heads were affected. In 2 men the necrosis was present in both humeral heads and the head of the right femur. Author.

31. AUTHOR	Summers-R-W, Switz-D-M, Sessions-J-T-Jr, Becktel-J-M, Best-W-R, Kern- F-Jr, Singleton-J-W.
INSTITUTION	Divisions of Gastroenterology, University of Iowa Medical Center, Iowa City.
TITLE	National Cooperative Crohn's Disease Study: results of drug treatment.
SOURCE	Gastroenterology 1979 Oct, VOL: 77 (4 Pt 2), P: 847-69, ISSN: 0016-5085.
ABSTRACT	The response of active and quiescent Crohn's disease to prednisone, sulfasalazine, or azathioprine has been studied in 569 patients in a placebo-controlled, randomized, multicenter cooperative trial. The response of active symptomatic disease to prednisone or sulfasalazine was significantly better than to placebo. Response to azathioprine was better than to placebo, but the difference did not reach conventional levels of statistical significance. Patients with colonic involvement were especially responsive to sulfasalazine, and those with small bowel involvement were especially responsive to prednisone. Patients' drug therapy immediately before entry to the study significantly affected subsequent response. For patients with quiescent disease, none of the drugs was superior to placebo in prophylaxis against flare-up or recurrence. There is less than a 5% risk that a clinically significant prophylactic effect of any of the drug regimens was missed. Author.

32. AUTHOR	Eliakim-R, Rachmilewitz-D.
INSTITUTION	Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel.
TITLE	Assessing disease activity in Crohn's disease--are we there yet? (comment).
SOURCE	Eur-J-Gastroenterol-Hepatol 1997 Oct, VOL: 9 (10), P: 929-30, ISSN: 0954-691X. CM Comment on: Eur-J-Gastroenterol-Hepatol 1997 Oct; 9(10):939-44.
ABSTRACT	Many attempts have been made over recent years to assess accurately disease activity in Crohn's disease. We review some of these attempts, giving particular emphasis to the combination of serum levels of proinflammatory cytokines (interleukin-6, tumour necrosis factor alpha, recombinant interleukin-2 and acid alpha-1- glycoprotein). Author.