TEMPERATURE MEASUREMENT IN BREAST DISEASE.
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Anabolic androgenic steroids (AAS) are used illicitly at high doses by bodybuilders. The misuse of these drugs is associated with serious adverse effects to the liver, including cellular adenomas and adenocarcinomas. We report two very different cases of adult male bodybuilders who developed hepatocellular adenomas following AAS abuse. The first patient was asymptomatic but had two large liver lesions which were detected by ultrasound studies after routine medical examination. The second patient was admitted to our hospital with acute renal failure and ultrasound (US) studies showed mild hepatomegaly with several very close hyperecogenic nodules in liver, concordant with adenomas at first diagnosis. In both cases the patients have evolved favourably and the tumours have shown a tendency to regress after the withdrawal of AAS. The cases presented here are rare but may well be suggestive of the natural course of AAS induced hepatocellular adenomas. In conclusion, sportsmen taking AAS should be considered as a group at risk of developing hepatic sex hormone related tumours. Consequently, they should be carefully and periodically monitored with US studies. In any case, despite the size of the tumours detected in these two cases, the possibility of spontaneous tumour regression must also be taken in account.
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This series presents further evidence for an association between reticulosis of the intestine and steatorrhoea. Although some patients have a definite past history of gluten enteropathy, it seems likely that in certain patients the reticulosis itself is the primary cause of the steatorrhoea.
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We documented airway occlusion during sleep and an abnormally high supraglottic resistance while awake in a 54-yr-old woman who had developed physical changes and the syndrome of obstructive sleep apnea while being administered exogenous androgens. When the androgens were withdrawn, the patient's physical changes, symptoms, sleep study, and supraglottic resistance all returned to normal. A rechallenge with androgen produced symptoms of obstructive sleep apnea that abated upon withdrawal of the hormone. Previous reports have favored a role of androgens in the pathogenesis of sleep apnea. Our report provides direct evidence for this role. Structural and functional measurements indicate that androgens exert a permissive or necessary action on the structural configuration of the oropharynx that predisposes to obstruction during sleep. Development of the obstructive sleep apnea syndrome must be considered a possible side effect of androgen therapy.
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Rupture of the triceps mechanism is an uncommon injury that has been recognized with increasing frequency in recent years. It has been proposed that such injuries commonly accompany fractures of the radial head and must be actively evaluated in the presence of such a fracture. We present a unique case of isolated rupture of the triceps tendon in an athlete who was lifting weights. This case was complicated by a history of olecranon bursitis that had been treated with numerous local steroid injections, as well as a history of anabolic steroid abuse. Both systemic steroids and local injections may predispose tendons to rupture. Triceps tendon ruptures may result in uniformly good to excellent results if recognized and treated surgically. This case also serves as a reminder of the risks of treating inflamed tissues with local steroid injections, especially in strength athletes who place high demands on their musculoskeletal structures. Finally, this case documents a second case of triceps mechanism rupture in an athlete who has abused anabolic steroids. A study by Hunter et al. suggests that oral steroid abuse may be associated with detrimental effects on the mechanical properties of connective tissue, demonstrating another negative effect of anabolic steroid use in athletes.
Forty-eight male rats were randomly separated into four groups: a control group, a group treated with anabolic steroids, a group treated with daily exercise, and a group treated with both steroids and exercise. At 6 weeks, biomechanical, ultrastructural, and biochemical testing was performed on the Achilles tendons of half of the rats in each group. The remaining rats continued in the experimental protocol, but steroid administration was discontinued. Similar testing was then performed on the remaining rats at 12 weeks. Testing showed anabolic steroids produced a stiffer tendon that absorbs less energy and fails with less elongation; tendon strength was unaffected. Effects were entirely reversible on discontinuation of the steroids. Light microscopic analysis revealed no changes in the appearance of the fibrils. No change in fibril diameter or shape was noted on electron microscopic analysis. Biochemical testing revealed no change in qualitative immunofluorescence staining with Type III collagen or fibronectin. Abuse of anabolic steroids is a widespread problem among competitive athletes; consequently, complications after their use are seen with increasing frequency. Knowledge of the effects of these drugs on tendon and the musculotendinous unit may prove helpful in counseling athletes who use anabolic steroids.
The glomerular ultrafiltration rate varies as a function of age and sex. To further elucidate the basis for the sexual difference, an androgen [Deca-Durabolin (DECA)] was administered to female ovariectomized rats, and glomerular hemodynamics were evaluated by renal micropuncture after 6 and 16 weeks of therapy. Results were compared to those in control ovariectomized female rats injected with vehicle. Therapy did not produce significant differences in body weight, but kidney size was modestly increased in DECA-treated rats at 6 weeks (0.68 +/- 0.03 vs. 0.86 +/- 0.03 g wet weight; P less than 0.05); at 16 weeks major differences in renal size were documented (0.69 +/- 0.03 vs. 1.18 +/- 0.05 g wet weight; P less than 0.01). The increase in size was primarily due to tubular hypertrophy, with more modest increases in glomerular size. After 6 weeks of therapy, the single nephron glomerular filtration rate (SNGFR) was increased in DECA-treated ovariectomized rats (24.8 +/- 1.0 vs. 32.9 +/- 1.1 nl/min; P less than 0.01). Whole kidney glomerular filtration rate also rose in proportion to increases in kidney size. The greater SNGFR was attributed to higher rates of nephron plasma flow and a numerical increase in the glomerular ultrafiltration coefficient. However, after 16 weeks of androgen therapy, in spite of marked renal hypertrophy, SNGFR did not further rise in proportion to renal size, and the rate of nephron plasma flow and the glomerular ultrafiltration coefficient actually fell relative to those in control untreated rats. Light microscopic evaluation of renal tissue revealed no abnormalities in DECA-treated rats. Thus, 6-week androgen therapy to ovariectomized female rats increased both glomerular ultrafiltration rates and renal size. However, with prolonged administration a glomerular dysfunction may have ensued whereby glomerular ultrafiltration was dissociated from increases in renal size.
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