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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Contraction of fibrous capsules is the most common complication of augmentation mammaplasty using silicone implants. This contraction occurs unpredictably with all kinds of implants, and despite various surgical maneuvers to prevent it. Current clinical practices are reviewed. Wound healing around silicone breast implants is similar to that elsewhere in the body. Acute inflammation is followed by collagen synthesis. Breast capsules contain contractile fibroblasts like those found in other contracting scars. Silicones implanted into tissue undergo some detectable changes that at present cannot be related to capsular contraction. The possible roles of physical and chemical characteristics of the silicone implants are discussed. Steroids are widely used to prevent contraction, but much debate exists over whether or not they actually work. Other possible drug treatments are discussed, based on current research.
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PMID:Capsular contraction around silicone mammary prostheses. 42 Apr 88

The frequency and causes of joint stiffness are reviewed. The most sophisticated repair may be for naught if the joints stiffen. Treatment of the established condition leaves much to be desired. Since mobility cannot be maintained during many postoperative periods and during the treatment of many conditions, any aid to prophylaxis is desirable especially if the side effects are negligible. Steroids have been chosen because of their influence on collagen metabolism and because much is known of their toxicity and side effects. The drug was first given into the knee joints of rats where it was found effective in preventing joint stiffness in joints immobilized three weeks. In view of the animal success, fourteen patients with thenar pedicles have had a single dose of triamcinolone injected into the peri-articular tissues of their proximal interphalangeal joints at the time of construction of the pedicle. Follow up observation shows all patients to have complete proximal interphalangeal joint extension and flexion to 95 degrees. Side effects were minimal.
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PMID:Some results using triamcinolone on immobilized joints. 73 58

Alcoholic hepatitis is the precursor of cirrhosis. Susceptibility is independent of amount and duration of ethanol intake or of diet. Centrilobular hyalin, the key morphologic abnormality, sensitizes lymphocytes to secrete factors which may account (in part) for necrosis, liver cell destruction, increased collagen synthesis and development of cirrhosis. Diagnosis may be facilitated by detection of alcoholic hyalin antigen (AHAg) and antibody (AHAb) in serum of patients with alcoholic hepatitis. Treatment requires abstinence. Steroids have not reduced mortality rates. Measures to improve immunologic reactivity may be helpful. Persons unable to abstain should be enrolled in a surveillance group.
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PMID:Alcoholic hepatitis. 77 53

The abuse of anabolic-androgenic steroids by athletes has recently been associated with the development of myocardial infarction and stroke. Because platelets play a pathogenic role in these disorders, the authors hypothesized that androgenic steroid abuse among weight lifters was associated with increased platelet aggregation as measured in vitro. Twenty-eight study participants were recruited. Twelve denied current androgen use. However, 8 of these 12 tested positive for urinary androgens. Nonsignificant trends toward increased platelet counts and increased platelet aggregation to adenosine diphosphate were noted when androgen users were compared to nonusers. However, when stratified by age, older (greater than 22 years) androgen users required lower concentrations of collagen to produce 50% aggregation of test platelets than did younger (less than or equal to 22 years) androgen users (1.47 versus 3.35 micrograms/ml; p = .01). Further subgroup analysis revealed nonsignificant trends toward increased adenosine diphosphate-induced aggregability and nonsignificant trends in the platelet count in older weight lifters. Subsequent studies using collagen threshold aggregometry revealed no age-dependent effect in 17 other men (aged 18 to 46 years) not specifically selected for activity (r = .17). This study suggests an association between androgen use, age, and increased platelet sensitivity to collagen in weight lifters and may be helpful in explaining recent thrombotic disease in androgen users. It additionally calls into question the validity of subjective reporting when assessing androgen use among weight lifters.
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PMID:Androgenic-anabolic steroid abuse and platelet aggregation: a pilot study in weight lifters. 153 13

We studied the clinico-pathological correlation of collagen disease-related pulmonary lesions to examine the pathological and radiological features of collagen lung, and the effect of steroid therapy. Ten open lung biopsy cases were examined; 4 male, and 6 female. The mean age was 55 years old. Seven cases developed pulmonary shadows after the diagnosis of collagen disease, and 3 cases showed pulmonary shadow prior to diagnosis. Pathologically, 6 cases proved to be bronchiolitis obliterans organizing pneumonia (BOOP), 3 cases were chronic interstitial pneumonia (UIP), and 1 case was acute interstitial pneumonia. All cases had inflammatory thickening of the interstitium involving the pleura, bronchial wall, and perivascular connective tissue. Half of the cases had bronchiolar inflammatory lesions. Radiologically BOOP cases showed either localized ground glass shadows, or diffuse reticulonodular shadows predominantly in the lower lung fields with shrinkage of affected areas. UIP cases showed reticulonodular shadows, and active UIP cases showed overlapping ground glass shadows. Steroids were administered in cases of BOOP and active UIP, and all cases showed improvement. We consider that open lung biopsy is of use in the diagnosis of some cases and in assessing whether steroid therapy is indicated.
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PMID:[Clinico-pathological study of collagen-related pulmonary lesions in cases of open lung biopsy]. 160 60

Anabolic steroids have attained a prominent, albeit highly controversial, position among ergogenic aids for power athletes. Adverse effects of these compounds are well documented, but their popularity persists. One of their possible side effects which has received little attention is abnormal form and function of connective tissue in steroid-abusing athletes. Scientific and medical literature addressing this concern is scant and is generally limited to observed effects in animals. Anabolic steroid use paralleled with exercise may lead to dysplasia of collagen fibrils, which can decrease the tensile strength of tendon. Changes in tendon's crimp morphology have been shown to occur, as well, which may alter the rupturing strain of tendon and the normal biomechanics of the extremities. Given the megadoses of steroids taken by some athletes and the large forces incurred by power-trained musculature, the integrity of tendinous tissue in these athletes may be at significant risk of compromise if steroids do, in fact, exert a destructive effect. Additional investigation in the area reviewed here is warranted before anabolic steroids can be decisively implicated in human connective tissue disruption. It is recommended, however, that consideration be given to including potential tissue alterations among the side effects of steroid abuse.
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PMID:Anabolic steroid-induced tendon pathology: a review of the literature. 199 2

The sequence of events within the ovary during the process of ovulation discussed in this review is schematically represented in Fig. 1. It is obvious that LH, perhaps with some contribution from FSH, is the normal physiological trigger for the ovulatory sequence of events, and it appears from the available information that the effects of LH are mainly mediated via adenylate cyclase and increased cAMP levels. The cAMP in turn, via cAMP-dependent protein kinase, influences at least three distinct steps in the ovulatory process which seem to be of crucial importance, namely 1) the stimulation of steroidogenesis; 2) the stimulation of cyclooxygenase/lipooxygenase leading to increased prostaglandin/leukotriene synthesis; and 3) the stimulation of plasminogen activator which catalyzes the conversion of plasminogen to plasmin. A fourth crucial step in the ovulatory mechanism is the LH-induced increase in latent collagenase, but it remains to be determined if this step is mediated via cAMP. Concomitant with the increase in latent collagenase, there also appears to be an LH-dependent increase in collagenase inhibitors. The latent collagenase is then activated, and it appears that leukotrienes and prostaglandins, as well as plasmin, may be involved in this process. The active collagenase causes a digestion of the collagen in the follicle wall, and plasmin, as well as possibly other proteolytic enzymes such as proteoglycanases, may cause a further dissociation of the follicular wall. These processes of digestion of collagen and dissociation of the collagen fibers result in an opening in the follicular wall with the formation of the stigma and rupture. While the weakening of the follicular wall takes place throughout the entire wall, rupture remains for the most part a localized process at the apex of the follicle. This localization of the rupture may be explained on the basis of mechanical factors operating when the follicle wall thins and weakens. While it is clear that prostaglandins and leukotrienes can influence smooth muscle by causing contractions and that these compounds can cause vascular changes such as increased permeability, vasodilation, and vasoconstriction, it is not clear what the exact role of these latter processes are in ovulation. It appears that progesterone and not estrogen play an important role in the mechanism of LH-induced follicular rupture, but the locus of action of progesterone and its mechanism of action remains to be determined.(ABSTRACT TRUNCATED AT 400 WORDS)
Steroids 1989 Nov
PMID:Mechanism of mammalian ovulation. 255 97

A meshwork of collagen over the apical region of the follicle must be breached to permit the ovum to escape. We propose that specific collagenase activity is responsible for collagen breakdown in this region. Immature rats are primed with pregnant mare serum gonadotropin (PMSG), followed at 48 h by hCG. At 8 h after hCG, collagenase activity, measured in extracts of ovarian tissue, is elevated about five-fold. Ovulation follows at 10-12 h. Ovaries from PMSG-primed rats are dissected at 48 h, placed in a perfusion apparatus, and perfused with luteinizing hormone and 3-isobutyl-1-methyl xanthine. The ovulations induced by this treatment can be blocked to the extent of 70% with a synthetic collagenase inhibitor. The activation of procollagenase is believed to involve plasminogen activator and plasmin. In support of this, we find that tranexamic acid at 1 mM inhibits ovulation about 70%. The inhibitor must be added within 3-4 h of LH to be effective. A specific plasmin inhibitor, D-Val-Phe-Lys-chloromethyl ketone, is similarly effective.
Steroids 1989 Nov
PMID:Connective tissue breakdown in ovulation. 255 98

The first case of collagenous colitis in a child with protracted watery diarrhoea and abdominal pain is reported. Small bowel investigations and the macroscopic appearances were normal, but histological examination of the colon showed collagenous colitis. Steroids temporarily relieved the diarrhoea and induced transient dissolution of the subepithelial collagen band.
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PMID:Diarrhoea caused by collagenous colitis. 277 20

Uninephrectomized rats maintained on 0.9% NaCl as drinking fluid and infused for 8 weeks with aldosterone 0.75 micrograms/h via subcutaneous osmotic minipumps respond with hypertension, cardiac hypertrophy, and both interstitial and perivascular cardiac fibrosis. Similar animals injected with desoxycorticosterone (20 mg/week), or the glucocorticoid antagonist RU 486 (2 mg/day) show interstitial cardiac fibrosis to a lesser degree than animals injected with aldosterone, and show perivascular fibrosis to a greater degree. These findings suggest that glucocorticoid antagonist activity may play a role in exacerbating perivascular collagen deposition in response to chronic mineralocorticoid and salt imbalance.
Steroids 1995 Jan
PMID:Adrenal steroids and cardiac fibrosis. 779 98


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