Heart Failure Due to Anabolic-Androgenic Steroids Abuse: A Case Report - Juniper Publishers

 Juniper Publishers- Open Access Journal of Case Studies

Heart Failure Due to Anabolic-Androgenic Steroids Abuse: A Case Report

Authored by Badr Eslam R

Abstract

Anabolic-androgenic steroids (AAS, prominent examples include Nandrolone, Clenbuterol and Stanozolol) act as valuable treatment options for people presenting with hypogonadism and stimulate erythropoiesis in bone marrow failures [1]. However, a growing number of people misuse AAS in order to obtain a muscular body shape and enhance their physical performance. The use of anabolic steroids has increased rapidly in the last few years, not only being used by bodybuilders, but also casual fitness enthusiasts [2].

We report the case of a 25-year-old man, who suffered from heart failure as a result of massive use of anabolic steroids over only three months. Initially blood samples and echocardiography parameters were collected. A biopsy was taken by which myocarditis could be excluded. Heart failure was assessed using cardiac MRI. Medical treatment with Valsartan/Sacubitril was implemented and regular check-ups were performed. After four months ejection fraction returned to normal levels.

To conclude, physicians and athletes should be aware of the possible serious acute and long-term side effects of AAS consumption. Moreover Valsartan/Sacubitril seems to be effective in treating heart failure due to AAS abuse. However, further clinical trials are required to verify these effects.

Keywords:Heart failure; AAS; Sacubitril/Valsartan

Abbreviations: AAS: Anabolic-Androgenic Steroids; ALAT (GPT): Alanine Aminotransferase (Glutamate-Pyruvate Transaminase); ASAT (GOT): Aspartate Amino Transferase (Glutamic Oxaloacetic Transaminase); Gamma-GT: Gamma-Glutamyl Transferase; bpm: Beats per Minute; NT-proBNP: N-Terminal pro B-type Natriuretic Peptide; LVEF: left Ventricular Ejection Fraction; HF: Heart Failure; CPET: Cardiopulmonary Exercise Testing

Introduction and Background

Anabolic-androgenic steroids (AAS) not only have a therapeutic use, but are also used by athletes to improve their physical performance [1]. The last few years the abuse of AAS has increased, as they are used by high-level sportsmen and also casual fitness enthusiasts [2]. The substances used include the male hormone testosterone and its synthetic derivates. The illicitly use of AAS often results in blood concentrations more than 100 times the physiological blood levels. In supraphysiological dosages AAS cause numerous side effects that involve most organ systems. However, the most severe side effects pertain to the cardiovascular system and may cause hypertension, sudden cardiac death, intracoronary thrombi, atrial and ventricular arrhythmias and cardiomyopathy [3].

Case Presentation

This is a case report of a 25-year-old man who presented with progressive dyspnea and orthopnea as well as tachycardia (heart rate: 180bpm). The patient had a history of anabolic steroid abuse over the past 3 months with testosterone.

Initial work up

Laboratory assessment showed an elevated NT-proBNP level (1030pg/mL) as well as elevated liver enzymes (ALAT (GPT): 112U/L; ASAT (GOT): 35U/L; Gamma-GT: 79U/L). Echocardiography showed severe left ventricular dilatation, highly impaired left ventricular systolic function as well as a slow flow of the left ventricle without thrombus. The patient underwent coronary angiography to exclude stenosis of the coronary arteries. At the same time a biopsy of the left ventricle was taken, which excluded myocarditis. His clinical condition deteriorated rapidly requiring intubation within hours after first presentation, two days after initial onset of symptoms. Cardiac magnetic resonance imaging revealed a left ventricular ejection fraction (LVEF) of 28% (Table 1).

Diagnosis and management

The patient was admitted to the ICU with cardiogenic shock. A diagnosis of dilated cardiomyopathy resulting in cardiorespiratory insufficiency associated with anabolic steroids was made after ruling out other causes of non-ischemic dilated cardiomyopathy. Sacubitril/ Valsartan was given in an initial dose of 24mg/26mg and titrated up to a maximum dose of 97mg/103mg. At the time of discharge the patient was provided with a LifeVest (ZOLL, Cologne, Germany).

Follow-up

The follow up visit one month after initial presentation showed an increase of LVEF from initially 28% to 32.7%. The left ventricle was still significantly enlarged. Due to close follow up and constant therapy optimization a LVEF of 62% (reference range: 55-70%) could be achieved 4 months later, obviating the need for carrying a LifeVest. The patient resumed his training 3 times per week. Cardiopulmonary exercise testing (CPET) was performed 9 months after establishing the diagnosis to exclude cardiac limitation at exertion. The test showed a VO2 max of 3147ml/min (96% of predicted peak oxygen uptake value) and a VE/VCO2 (ventilatory equivalent of carbon dioxide) slope of 21.38, which was within the normal range. The patient could now resume with his normal training routine.

Discussion and Conclusion

Sacubitril/ Valsartan seem to be an effective and good therapy for heart failure due to anabolic-androgenic steroid abuse and contribute to the improvement of the left ventricular ejection fraction rapidly.

Cardiopulmonary exercise testing (CPET) presents a complete assessment of exercise concerning the pulmonary, cardiovascular, muscular and cellular oxidative systems [4]. The application of CPET in the management of patients with heart failure (HF) is valuable to make activity recommendations, quantify the response to therapy and exclude cardiac limitation at exertion. Especially powerful in evaluating risk in HF are indices of ventilatory inefficiency, such as peak VO2 and VE/VCO2 slope [5]. The spread of anabolic androgenic steroids abuse among athlete’s worldwide calls for Physicians to caution users about the serious risk of possible long-term cardiac complications linked with AAS (Figure 1 & 2).

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Heineke-Mikulicz Strictureplasty: Alternative Treatment Approach for Hepaticojejunostomy Strictures - Juniper Publishers

 Juniper Publishers- Open Access Journal of Case Studies

Heineke-Mikulicz Strictureplasty: Alternative Treatment Approach for Hepaticojejunostomy Strictures

Authored by Mohamad Rakka

Abstract

A 63-year-old man underwent an uneventful pancreaticoduodenectomy (whipple procedure) for an adenocarcinoma of the head of the pancreas. He presented 7 months later with progressive jaundice. Blood chemistry tests revealed high bilirubin level and elevated Gamma-glutamyl transferase (GGT), alkaline phosphatase. Ultrasound examination of abdomen showed dilated intrahepatic bile ducts. The magnetic resonance cholangiopancreatography (MRCP) detected a stricture at the hepaticojejunostomy (HJ) anastomosis with a stone in the common hepatic duct just above the biliary-enteric anastomosis with dilated intrahepatic bile ducts. Thus, surgery was suggested and to proceed with Heineke-Mikulicz strictureplasty.

Keywords: Pancreaticoduodenectomy; Hepaticojejunostomy; Stricture; Whipple; Heineke-Mikulicz

Introduction

Pancreaticoduodenectomy (PD) is a major surgical abdominal operation performed to treat several periampullary benign and malignant diseases and it carries high risk for postoperative complications.

One of the complications associated with PD is hepaticojejunostomy (HJ) stricture. Concerning PD for both benign and malignant diseases the median time to stricture formation is 13 months and it can manifest 1 month and up to 9 years after PD [1]. Its incidence varies widely across the literature and it ranges from 4% to 10% [2]. House et al. [3] reported an incidence of 2.6% and it was similar in benign and malignant disease [1]. However, Kim and colleagues reported a higher rate (24%) [3].

Multiple risk factors predispose to the HJ stricture formation after PD and they include: preoperative and postoperative percutaneous biliary drainage, ischemia resulting from iatrogenic causes or patient comorbidities, multiple repair of recurrent stricture, HJ leak secondary to infectious/inflammatory processes, recurrent malignant disease, small or fragile bile duct wall, and gastric or enteric reflux into biliary tree [1,2,4,5].

Most commonly HJ stricture manifests as recurrent cholangitis and/or obstructive jaundice [6]. These clinical presentations should be evaluated and treated as early as possible to prevent the progression to secondary biliary cirrhosis.

Case Presentation

A 63-year-old man underwent an uneventful pancreaticoduodenectomy (whipple procedure) for an adenocarcinoma of the head of the pancreas. He presented 7 months later with progressive jaundice. Blood chemistry tests revealed high bilirubin level (Total: 3, Direct: 2) and elevated GGT, alkaline phosphatase. Ultrasound examination of abdomen showed dilated intrahepatic bile ducts.

The magnetic resonance cholangiopancreatography (MRCP) detected a stricture at the HJ anastomosis with a stone in the common hepatic duct just above the biliary-enteric anastomosis with dilated intrahepatic bile ducts as seen in Figure 1.

A percutaneous Transhepatic Cholangiography (PTC) confirmed the presence of stricture and the impacted stone at the biliary-enteric anastomosis as seen in Figure 2.

A guide was inserted and successfully crossed the anastomosis into the jejunum. Unfortunately, the balloon dilatation of the stricture was unsuccessful. Attempted endoscopic intervention (Rendez-vous technique) failed to demonstrate the biliary-enteric anastomosis due to the limited length of the available endoscope (Figure 3).

Thus, surgery was suggested, and we decided to proceed with Heineke-Mikulicz strictureplasty. Exploration revealed dense and fibrotic adhesions. A meticulous adhesiolysis was done. A stone was palpated in the common hepatic duct that was approximately 2cm in length as seen in Figure 4.

A longitudinal incision of 3cm was made in the anastomotic line (Figure 5 & 6) and the stone was successfully extracted. The biliary duct was then irrigated using sterile water and good biliary drainage was achieved. The incision was closed in a transverse fashion using an absorbable 4-0 polyglactin interrupted simple sutures as seen in Figure 7(A&B)

The post operation course was uneventful, the patient was discharged on the fifth post-operative day in a good condition.

The patient was followed up clinically, biochemically and radiologically for a total of 12 months. He was completely asymptomatic with a normal serum bilirubin, liver enzymes and nondilated biliary tree.

Discussion

Diagnosis of HJ stricture is based on clinical, laboratory and radiological findings. Biliary obstruction should be confirmed by abdominal ultrasonography, multidetector computed tomography, and/or magnetic resonance cholangiography. Furthermore, direct visualization of the stricture is also one of the diagnostic clues. This can be accomplished by ERCP or percutaneous transhepatic cholangiography (PTC) which also can play a therapeutic role [6].

In addition, ERCP and PTC allow biliary biopsy using cytobrushing or clam shell in order to rule out recurrent malignant disease as a cause of HJ stricture [7]. Nonsurgical methods and surgical revision of the HJ are both considered in the management of the HJ stricture.

The interventional techniques including both percutaneous (PTC) and endoscopic routes (ERCP) are commonly used in the management of HJ stricture through balloon dilatation and insertion of one or more stents.

Although high success rate of endoscopic management of biliary stricture is reported by many studies [8], the endoscopic cannulation of the HJ after PD remain a challenge secondary to the anatomy changes [9]. Concerning the percutaneous techniques, House et al. [1] reported that 90% of all patients were treated successfully using the percutaneous biliary approach.

Although minimally invasive treatment is best option for HJ stricture after PD, it has the disadvantage of restenosis on longterm follow-up [10]. Thus, surgical redo of HJ should be considered especially when interventional methods failed in several attempts. In addition, several interventional attempts result in fibrosis at the anastomosis which makes surgery more difficult [11]. Therefore, early surgical revision is recommended [6].

Recently, Heineke-Mikulicz strictureplasty was included in the management of HJ stricture. Its concept based on longitudinal incision with transverse closure of the stricture was introduced in the 1970s as a therapy for tubercular strictures in the GI tract and in the 1980s for Crohn’s strictures [12,13], and later on in urethroplasty and pyloric stenosis repair [14,15].

This technique is beneficial as it provides a simple, time effective method that makes it a good alternative for redo HJ. It has although some limitations. Long thin strictures are for example not candidate for such procedure. Moreover, in order to perform this surgical concept, appropriate length of the remnant common hepatic duct of =/ >1cm as well as sufficient diameter of the newly formed anastomosis of >1cm are needed [16].

Heineke-Mikulicz strictureplasty has a disadvantage is that when applied on fibrotic tissue due to chronic inflammation associated with cholangitis it may predispose to restenosis or biliary leakage; yet this disadvantage is also proved in redo HJ [16].

Our case was presented for jaundice after 7 months of PD and was diagnosed with HJ stricture along with stone formation. A percutaneous transhepatic intervention was carried out but was unsuccessful due to the presence of the stone near the anastomosis. Endoscopic access also failed due to technical difficulty (short endoscope). Then, surgery was suggested. After reviewing the literature and the available surgical options, Heineke-Mikulicz strictureplasty was decided. Clinical follow up, along with laboratory testing and imaging for 12 months were uneventful.

In conclusion, Heineke-Mikulicz strictureplasty is one of the promising procedures that can be easily done in case of HJ stricture after PD, with good postoperative prognosis. It is useful as an alternative for redo HJ and refractory cases to interventional techniques. Our case is the second in the literature after a similar one that was released in Turkey in July 2012. This makes additional studies required to achieve a definitive conclusion.

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