Greg A Rosenfeld

1Department of Medicine, University of British Columbia, 5th Floor, Gordon and Leslie kim cương Health Care Centre, 2775 Laurel St, Vancouver, BC, V5Z 1M9, Canada


Albert Chang

1Department of Medicine, University of British Columbia, 5th Floor, Gordon and Leslie diamond Health Care Centre, 2775 Laurel St, Vancouver, BC, V5Z 1M9, Canada


Michael Poulin

2Department of Pathology, Vancouver General Hospital, 889 West 12th Avenue, Vancouver, BC, V5Z 1M9, Canada


Peter Kwan

1Department of Medicine, University of British Columbia, 5th Floor, Gordon and Leslie đá quí Health Care Centre, 2775 Laurel St, Vancouver, BC, V5Z 1M9, Canada


Eric Yoshida

1Department of Medicine, University of British Columbia, 5th Floor, Gordon và Leslie diamond Health Care Centre, 2775 Laurel St, Vancouver, BC, V5Z 1M9, Canada


1Department of Medicine, University of British Columbia, 5th Floor, Gordon and Leslie kim cương Health Care Centre, 2775 Laurel St, Vancouver, BC, V5Z 1M9, Canada
2Department of Pathology, Vancouver General Hospital, 889 West 12th Avenue, Vancouver, BC, V5Z 1M9, Canada
*
Corresponding author.

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This is an mở cửa Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Introduction

Over the last few years the use of anabolic steroids has become increasingly common amongst amateur athletes và for aesthetic purposes. As a result, the adverse events related khổng lồ their use are being seen more frequently. Methandrostenolone is an anabolic steroid which is widely available và has been used for both performance enhancement và aesthetic purposes. This drug has also been reported to cause cholestasis of the intra-hepatic bile ducts resulting in elevated aminotransferases, hyperbilirubinemia and clinical jaundice. However, to the best of our knowledge this agent has not been previously reported lớn cause pancreatitis or acute kidney injury.


Case presentation

In this paper, we report the case of a 50-year-old man of Indian descent who presented with a six week history of diffuse abdominal pain, anorexia và weight loss following an eight week cycle of methandrostenolone use. At initial presentation, his lipase level was 785 U/L, bilirubin was 922 μmol/L and creatinine was 200 U/L while his aspartate aminotransferase & alanine aminotransferase levels were only mildly elevated at 61 U/L and 56 U/L respectively. His lipase peaked on day nine at >3000 U/L whilst his creatinine màn chơi was 299 U/L. Imaging was consistent with acute pancreatitis while a liver biopsy was consistent with intra-hepatic cholestasis & a kidney biopsy revealed evidence of acute tubular necrosis.


Conclusion

Both acute pancreatitis và acute kidney injury have rarely been reported with anabolic steroid use and they have not been previously reported lớn occur in the same patient. This case demonstrates some potentially new & serious adverse consequences occurring with the use of anabolic steroids, of which physicians need khổng lồ be aware.


Introduction

Anabolic androgenic steroids (AAS) have been in widespread use amongst elite athletes lớn enhance performance for decades <1>. Major League Baseball & the National Football League have provided numerous examples of steroid use amongst their professional athletes. Several Olympic athletes have tested positive for the use of AAS or admitted to their use <2>. Meanwhile, the Vancouver 2010 Winter Olympic games saw the creation of the most sophisticated anti-doping testing laboratory to lớn date, resulting in 30 athletes testing positive & being banned from attending the games prior lớn their opening. With the knowledge of widespread steroid use has come an increased awareness of the adverse effects & sometimes serious consequences of AAS use. Nevertheless, there seems khổng lồ be an ever increasing use of these agents by recreational athletes and for aesthetic purposes. Recent estimates place AAS use in the USA and Sweden at 1% of the population and we can reasonably assume that the rates of use in Canada are similar <1>. The internet has increased the đen market availability of these drugs without prescription and consumers are frequently unaware of the risks of taking these drugs.

Methandrostenolone (Dianabol) was first introduced as an anabolic steroid by Ciba in the 1960s. Methandrostenolone was one of the AAS used khổng lồ enhance athletic performance by the former East German Olympic program <3>. This agent has numerous side effects common to anabolic androgenic steroids which include gynecomastia, acne, mood changes (aggressiveness) and testicular atrophy <4>. Stanozolol, another carbon-17-alkylated anabolic steroid, has been previously reported to cause severe cholestasis & acute renal failure in a young athlete <5>. Acute kidney injury arising from the use of anabolic steroids và vitamin supplementation in two male athletes has also been recently reported <6>.

Methandrostenolone has also been reported lớn cause cholestasis of the intra-hepatic bile ducts resulting in elevated aminotransferases, hyperbilirubinemia and clinical jaundice <7>. In this paper, we present a case of pancreatitis, cholestasis of the liver và acute kidney injury associated with the use of methandrostenolone for aesthetic purposes in a 50-year-old, non-athlete man. A brief literature đánh giá of Medline and PubMed Central, utilizing the search terms "androgenic anabolic steroids", "pancreatitis" và "methandrostenolone", failed to lớn reveal any other cases of pancreatitis arising from the use of anabolic steroids.


Case presentation

A 50-year-old man of Indian descent, known khổng lồ have mild, chronic hepatitis C, presented with a two week history of diffuse abdominal pain. Six weeks prior to lớn the onset of the pain, he had a gradual onset of anorexia và a 20 pound weight loss. Our patient noticed darkly coloured urine và pale stools beginning around the time of the onset of pain. He had not received treatment for his hepatitis C infection. He had intermittent and occasionally heavy alcohol consumption on weekends. He had also been taking methandrostenolone: 10 mg orally twice a day, five days a week for three weeks & then three times a day, five days a week for the next five weeks, for a total of eight weeks immediately prior to presentation.

When he presented, his trắng blood cell count was 9.8 giga/L (normal range 4.0-11.0 giga/L), his hemoglobin cấp độ was 172 g/L (normal range 135-170 g/L) and his platelet levels were 378 giga/L (normal range 150-400 giga/L). His lipase level was 785 U/L (normal range 0-393 U/L), gamma-glutamyltransferase (GGT) cấp độ 24 U/L (normal range 15-80 U/L), alkaline phosphatase (ALP) cấp độ 154 U/L (normal range 50-160 U"L), total bilirubin màn chơi 922 μmol/L (normal range 0-18 μmol/L), with direct bilirubin 804 μmol/L (normal range 0-5 μmol/L), alanine aminotransferase level (ALT) 56 U/L (normal range 25-80 U/L), aspartate aminotransferase (AST) cấp độ 61 U/L (normal range 10-38 U/L) & lactate dehydrogenase level 242 U/L (normal range 90-210 U/L). His international normalized ratio was 1.1 và serum albumin cấp độ was 35 g/L (normal range 34-50 g/L). He was also noted lớn have an element of acute renal failure with a serum creatinine màn chơi of 200 μmol/L (normal range 60-115 μmol/L) (Table ​(Table1).1). He had no previous history of renal disease. He was admitted khổng lồ our hospital for supportive management & further investigations.


WBCHGBBUNCRAMYLASELIPASEGGTALPBILIALTAST
Admission8.817213.2200785241549225661
Post admission Day 112.514811.9175634131337554551
Day 215810.9171381618694553
Day 310.816011.318571968101357393342
Day 411.516413.819929345241729194672
Day 516.729047417181829374867
Day 610.915319.728850461141808965267
Day 713.917024.52981411629242068045670
Day 81616124.32911855>3000161656784473
Day 914.113626.42991720>300081716606496
Day 1017.113722246841>300081515444754
Day 1117.212715206343>300091615324448
Day 1215.812112.317991594733545
Day 1316.21209.616191464472836
Day 1418.71239.415391194242738
Day 1517.31099160131454093344
Day 1620.71117.9136131223022431
Day 1714068412111362472937
Day 1818.611251201414831663237
Discharge (Day 19)13.51025.1131131301363337
At follow up(Day 38)11.813141196423723145539259
(Day 39)10.51253.91034617017128508467

A non-contrast computed tomography (CT) scan of his abdomen was performed shortly after admission which showed mild fatty infiltration of the liver. There was no evidence of inflammatory fat stranding around his pancreas or kidneys. An ultrasound of his abdomen performed 48 hours later showed mild hepatic enlargement with his liver measuring 17.1 centimet in length with a coarse, echogenic texture. There were no focal hepatic lesions or intra-hepatic duct dilatation. There was a small amount of sludge in his gallbladder but no stones. His common bile duct was of normal caliber at 2 mm in diameter. His pancreas was well seen & unremarkable. His renal parenchyma was echogenic và measured at the upper limits of normal kích cỡ which was in keeping with medical renal disease.

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Within a couple of days of admission, our patient began lớn experience worsening nausea, vomiting và abdominal pain. His serum lipase cấp độ declined over the first three days, but it later began to lớn rise & peaked on day nine at > 3000 U/L, while his ALP màn chơi also peaked on day eight at 206 U/L. His ALT và AST levels remained only mildly elevated. Our patient"s creatinine cấp độ rose to a peak of 299 μmol/L on day nine.

Serum auto-antibodies, serum protein electrophoresis và cryoglobulins were all negative. Hiv/aids antibodies were negative however, as anticipated, his hepatitis C viral RNA was qualitatively positive. His fasting serum lipid levels were low with the exception of triglycerides which were mildly elevated at 3.25 mmol/L (normal range 0.60-2.30 mmol/L). Our patient"s clinical picture was most consistent with acute pancreatitis và thus, a non-contrast (due lớn renal failure) CT scan of his abdomen was obtained on the tenth day. This showed a bulky pancreas with adjacent inflammatory fat stranding which was interpreted as consistent with pancreatitis without a focal drainable abscess. There were also no signs of chronic pancreatitis.

Our patient went on khổng lồ have a liver biopsy which revealed grade 2 portal & lobular inflammation, stage 2-3 fibrosis consistent with hepatitis C viral infection, moderately severe acute cholestasis consistent with anabolic steroid use, và mild pericellular fibrosis consistent with alcohol abuse but without evidence of steatosis or steatohepatitis (Figure ​(Figure1).1). A renal biopsy was also performed which showed acute tubular injury of uncertain etiology. His glomeruli were normal và there was evidence of desquamation of his tubular epithelial cells. Therefore, acute tubular necrosis was confirmed as the etiology of his renal failure.



Liver cholestasis due lớn methandrostenolone. Vi xử lý core liver biopsy showing bile filled canaliculi (black arrows) & bile in the hepatocytes (white arrows). As well, there are plasma cells và periportal inflammation.


With supportive therapy, our patient"s pancreatitis began lớn resolve and he was asymptomatic at the time of discharge. One month after discharge, his renal function had returned lớn normal & his amylase (46 U/L), lipase (270 U/L), GGT (17 U/L), and ALP (128 U/L) levels had all returned to lớn normal. His total bilirubin màn chơi remained mildly elevated at 50 μmol/L & his alt (84 U/L) & AST (67 U/L) levels were also mildly elevated in keeping with his chronic hepatitis C infection.


Discussion

AAS use or misuse is no longer solely by elite athletes seeking enhanced performance. Teenage boys in Sweden reported using AAS for a variety of reasons <8>, while bodybuilders, weight-lifters và prison populations have also been shown to have higher levels of misuse <9>. Our patient took AAS not for athletic performance but for aesthetic reasons. He reported wanting lớn "remain in shape" as the main reason for taking these pills. Anabolic steroids are readily available lớn the general public over the internet and at public gyms, they are easily obtained illegally, without a prescription. As a result, patients are less likely to lớn report taking AAS khổng lồ their physician and physicians are less likely khổng lồ consider the possibility of the use of AAS in the non-athlete population.

Our patient represents the first case of a patient developing pancreatitis as a result of anabolic androgenic steroid use. A recent clinical workshop reviewed the criteria necessary for reporting cases of Drug Induced Liver Injury <10>. We believe that this case report meets those criteria & we have reported on all of the necessary elements và many of the supportive elements outlined in the summary document emanating from that workshop. The usual causes of pancreatitis were excluded in our patient. He did not have any evidence of gallstones on repeated imaging studies, nor were his alkaline phosphatase or GGT significantly elevated as would be expected with obstructing gallstones. His triglyceride levels were only mildly elevated và not lớn the degree usually seen with pancreatitis. He had been hospitalized for four days before the first sign of pancreatitis & had not consumed alcohol for at least a week at that time. Given that his liver biopsy confirmed a cholestatic picture consistent with steroid use, we conclude that this was the main contributing factor in the pathogenesis of his pancreatitis. His hepatitis C may have made him more prone to liver injury from steroid use but the relatively low elevation of transaminases suggests that his hepatitis C infection was quite mild và stable. Furthermore, his liver biopsy showed a cholestatic pattern much more in keeping with steroid use than hepatitis C infection.

Our patient"s acute kidney injury is unique in that the pathology showed acute tubular necrosis (ATN). In two previous case reports with anabolic steroid use and vitamin supplementation as the cause of acute kidney injury, the biopsies showed acute interstitial nephritis <6>. In these cases, the kidney injury was attributed khổng lồ the supplementation of vitamin D with resultant hypercalcemia as the mechanism of kidney injury. Excessive vi-ta-min intake & hypercalcemia were not factors in our patient. The extremely high bilirubin level found in our patient is consistent with a previously reported case of severe cholestasis and ATN secondary to AAS use <5>. In that report, the proposed mechanism of ATN was secondary lớn severe cholestasis and the increased renal excretion of bilirubin. Two additional cases of acute kidney injury associated with the use of an over-the-counter nutritional supplement (Superdrol™) have been reported <11,12>. In the first case a kidney biopsy was not performed, while the second case reported a biopsy consistent with IgA nephropathy <12>. Whatever the exact mechanism, our patient"s history is most consistent with his AAS use as the main culprit in both his acute kidney injury & pancreatitis.


Conclusion

AAS use và misuse is being seen in an expanding population of patients because they are readily available và often perceived as safe. The side effects & risks of taking AAS are difficult khổng lồ assess in controlled trials due lớn the unethical nature of administering these drugs in the doses usually taken by patients who use them for aesthetic or athletic purposes. As a result, with the increasing use of these drugs, we can expect lớn see an increase in previously unreported adverse consequences. Although there have been previous reports of severe cholestasis và jaundice with the recreational use of anabolic steroids <13>, this is the first case report where acute pancreatitis và acute kidney injury also resulted from such recreational use. Physicians need khổng lồ be aware of the risks to their patients who consume AAS, và to consider that even with only mild elevations of aminotransferases, serious consequences such as cholestasis, acute kidney injury & pancreatitis may result.


Consent

Written informed consent was obtained from the patient for publication of this case report & any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.


Authors" contributions

GR và AC were major contributors in writing the manuscript. EY and PK analyzed và interpreted the patient data regarding the patient"s presentation and provided the clinical care of the patient. MP performed the histological examination of the liver biopsy and prepared the figure for the manuscript. All authors contributed to lớn the writing of the manuscript & approved the final version.

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