Clinical Application of the Knowledge Base: Valid and Timely Diagnosis
Targeted treatment of ASIH must begin with a valid diagnosis. That is, one which is informed by the distinct characteristics of this unique form of hypogonadism. Brower (2009) has provided an operational definition for diagnosis of ASIH: ‘To confirm the physiological basis of dependence (on AAS), just ask the patient how he feels when he stops use.’ This physiologically based ‘withdrawal syndrome’ is characterized primarily by sexual dysfunction, e.g. poor libido and ED, and depressed mood–the ‘hallmarks’ of HPT shutdown. (Kaskin & Kleben, 1989; Hochberg et al, 2009; Tan & Scally, 2009; Brower, 2009; Rhanema et al, 2014)
Thus, when these symptoms are present in a confirmed past or current AAS user, a diagnosis of ASIH can be made with confidence.
Regarding the physical exam for hypogonadism, Salenave et al (2012) have reported that this exam is ‘usually normal if hypogonadism is of recent onset. Diminished facial, body hair and muscle mass, fine facial wrinkles, gynecomastia, and hypotrophic testes are observed in long-standing and complete AHH.’ Rhanema et al (2014) state that these symptoms should be noted ‘if observed’. Obviously, if observed in addition to the hallmark ASIH symptoms, these symptoms should also be treated. However, the absence of these additional side effects, which vary with length of AAS use and completeness of testicular shutdown, should neither discourage nor delay an initial diagnosis of ASIH. Acknowledgement of AAS use, and what have been described by experts as its hallmark symptoms of sexual and mood dysregulation, have been well documented.
The benefit of this disease-specific approach to diagnosing ASIH is two-fold: First, it would promote immediate medical intervention to relieve suffering and its potentially harmful sequellae which can include depression severe enough to trigger resumption of use or even suicidality. (Brower, 2009). Secondly, it would support the timely intervention needed to limit continuing damage to the HPT system as patients undergo vithdrawal, and to begin reversal of existing damage caused by AAS. To delay medical intervention by requiring lengthy, expensive and arguably superfluous diagnostic procedures which would not change a physician’s treatment decision in any case, risks what has been characterized as ‘hormonal collapse” (Turek, 2013).
This has been described as anything from persistent, longterm AAS induced hypogonadism to permanent testicular shutdown, irreversible (primary) hypogonadism. (Borogowda, et al, 2001; Rhanema et al, 2014)
In order to prevent this outcome of failure to treat in a timely manner, a number of experts have recommended immediate intervention, cautioning that intervention must not only be timely and symptom focused, but must also continue until symptoms indicate adequate restoration of HPT. (Brower, 2009; Hochberg, 2003; Rahnema et al, 2014)
The Role of Labs in Diagnosis and Treatment
It is important to recognize that patients who may still be using, or have recently used AAS will have testosterone levels, which are not valid indicators for clinical decision making, as these will be predictably high. Requiring patients to wait until their current high levels of testosterone fell to hypogonadal levels, per labs, before treating them, would cause them needless suffering, since years of being on supraphysiologic testosterone, whether prescribed or self-administered (i.e., illegal), predictably results in hypogonadism when these are removed. (Jarow & Lipschultz, 1990; Kanayama et al, 2009; Brower, 2009; Talih et al, 2007; Spratt, 2012; Hochberg, 2003). Clearly, requiring patients to go this ‘cold turkey’ route can not only cause unnecessary suffering, but can also be physiologically harmful and psychologically dangerous, as indicated earlier.
A ‘more rational approach” recommended by a number of experts, is immediate substitution of physiological testosterone to relieve symptoms and support cessation, tapering the dose as HPT function is restored, and/or provision of medications to relieve symptoms, e.g., gynecomastia (tamoxifen), restore fertility (hCG), and encourage restoration of HPT, with the understanding that these medications warrant continuation for as long as they are required. That is, until symptoms indicate adequate restoration of HPT. (Zitzmann & Nieschlag, 2000; Hochberg et al, 2003; Talih et al, 2007; Spratt, 2012; Rahnema et al, 2014).
While lab values may not be valid or reliable diagnostic indicators of AAS related hypogonadism, they are, however, important guides for subsequent treatment. For example, after treatment has begun, persistence of symptoms, despite ‘normal’ testosterone levels, could indicate inadequate medications/doses, or severely damaged HPT, requiring adjustments in the treatment. Too high lab values during treatment can indicate either use of illegal steroids and ancillary drugs, or too-early lab draws when patients do not understand the importance of timely draws, indicating the need for patient counseling.
In summary, in addition to individualizing the treatment of hypogonadism, which is already a complex undertaking (Morgentaler et al, 2012), it is important for clinicians to recognize the need to tailor diagnosis and treatment of ASIH which, because of its unique pharmacodynamics, presents predictably unique challenges. Hopefully, the foregoing discussion of the current ASIH literature can provide some guidelines to help clinicians adapt their diagnosis and treatment of this condition, which is considered one of the most intractable of all substance abuse.