Steroid induced acute renal failure

The use of Anabolic Androgenic Steroids (AAS) has been linked to causing myocardial infarction, sudden cardiac death, ventricular fibrillation with exercise, atrial fibrillation, cardiac tamponade, and development of dilated cardiomyopathy [5]. AAS like other endogenous steroids influence left ventricular hypertrophic response through the androgen receptor. Androgen receptors are found on skeletal muscle and also on cardiac myocytes. They cause alterations in heart structure, including left ventricular hypertrophy, dilation which can cause impaired contraction and relaxation [6]. Anabolic steroids can induce an unfavorable enlargement and thickening of the left ventricle, which loses its diastolic properties with the mass increase [7]. AAS can also cause hypertension, dyslipidemia, and impaired fasting glucose [8]. The effect of anabolic androgenic steroids on the cardiovascular system has been well described in the literature; however, the knowledge of these effects amongst amateur sports participants is poor [9].  A qualitative, cross-sectional, observational study using an anonymous online questionnaire completed by amateur sports participants enrolled in competitive sports teams at an Irish university demonstrated that one-third of respondents personally knew someone that uses anabolic steroids, however 59% of participants were never advised about their health effects [9]. The majority (59%) of respondents obtained their nutritional advice from Internet sites or friends and only 26% of respondents knew about the blood pressure and cholesterol effects of anabolic steroid use [9].

Although alcohol consumption is included as one of the elements for assessing causality in the Roussel Uclaf Causality Assessment Method (RUCAM) causality instrument (17,18), there is no evidence to suggest that chronic alcohol consumption is a risk factor for all-cause DILI. However, heavy alcohol consumption is a risk factor for causing DILI owing to certain compounds such as APAP, methotrexate, and isoniazid. The package insert recommends that individuals with substantial alcohol consumption should not take duloxetine, although there are no published data to show that alcoholism increases the risk of duloxetine hepatotoxicity.

Treatment for Steroid Induced Glaucoma

If possible the corticosteroid treatment should be discontinued, and typically the lowering of IOP tends to mirror the initial response of IOP increase, . within one to four weeks, or for rapid onset, it will fade away in a few days. In a very small proportion of patients, usually those with long term steroid use or family history of glaucoma, the IOP will not fall after cessation of steroid use.

Otherwise management of the elevated IOP is similar to the standard treatment for POAG. Eyedrops to lower IOP are effective such as beta-blockers and carbonic anhydrase inhibitors. Prostaglandins are also effective although not recommended for patients who have uveitis or cystoid macular oedema.

In terms of surgery, in some cases a trabeculectomy may be required.

If steroids are still required, the general guideline is for doctors to try and prescribe the weakest dosage for the shortest possible time required to achieve their objectives, and to switch from delivery to the eye to a systemic exposure to the medication.

Before starting any corticosteroid treatment, especially if the patient has any of the risk factors above, a baseline IOP should be measured and the patient assessed for their risk of developing glaucoma. They should then be checked for any increase in IOP by an eye doctor on a regular basis, . every two weeks for the first month and monthly for three months, then every three months thereafter.

Acute lung injury is a syndrome with a diagnostic criteria base on hypoxaemia and a classical radiological appearance, with acute respiratory distress syndrome at the severe end of the disease spectrum. Its incidence is common, it is likely to exist outside the intensive care setting and therefore is a condition relevant to all clinicians. Genetically predisposed individuals are subject to environmental triggers which can be intra or extrapulmonary in nature. An inflammatory response causes damage to alveolar epithelial cells and vasculature, impairing gas exchange and can lead to multiple organ failure. Management centres around supportive care and treating the cause, but evidence supports use of low tidal volume ventilatory settings and conservative intravenous fluid strategies. Long term outcomes are related to neuromuscular, cognitive and psychological issues rather than pulmonary, and rehabilitation during recovery needs to focus on this.

Steroid induced acute renal failure

steroid induced acute renal failure

Acute lung injury is a syndrome with a diagnostic criteria base on hypoxaemia and a classical radiological appearance, with acute respiratory distress syndrome at the severe end of the disease spectrum. Its incidence is common, it is likely to exist outside the intensive care setting and therefore is a condition relevant to all clinicians. Genetically predisposed individuals are subject to environmental triggers which can be intra or extrapulmonary in nature. An inflammatory response causes damage to alveolar epithelial cells and vasculature, impairing gas exchange and can lead to multiple organ failure. Management centres around supportive care and treating the cause, but evidence supports use of low tidal volume ventilatory settings and conservative intravenous fluid strategies. Long term outcomes are related to neuromuscular, cognitive and psychological issues rather than pulmonary, and rehabilitation during recovery needs to focus on this.

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