Chlamydia and erectile dysfunction: What's the link? Some people who have chlamydia also experience erectile dysfunction (ED), which involves problems getting or maintaining an erection. Chlamydia can infect the prostate gland, leading to prostatitis, pain, and ED. In this article, learn more about the link between this common infection and ED, and treatments for both. Read now
The initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
Urinary infections are more common in people with poorly controlled diabetes and can cause discomfort for women during intercourse and for men during urination and ejaculation. These generally are temporary complications, but they can recur. Sexual activity should be stopped during treatment of urinary tract and yeast infections, which also are relatively common in people with diabetes.
If this treatment approach fails, it is useful, however frustrating, to start again from the beginning. Reassess the history to ensure that nothing was missed originally. Obtain labs and perform a PCDU. This will give the objective information that you might need in order to make a diagnosis of a known etiology for ED and to provide the patient reassurance that your evaluation has been thorough.
Sexuality and erection are controlled by multiple areas of the human brain including the hypothalamus, the limbic system, and the cerebral cortex. Stimulatory or inhibitory messages are relayed to the spinal erection centers to facilitate or inhibit erection (5). Two mechanisms have been proposed to explain the inhibition of erection in psychogenic dysfunction: direct inhibition of the spinal erection center by the brain as an exaggeration of the normal suprasacral inhibition and excessive sympathetic outflow or elevated peripheral catecholamine levels, which may increase penile smooth muscle tone and prevent the relaxation necessary for erection (8). Animal studies demonstrate that the stimulation of sympathetic nerves or systemic infusion of epinephrine causes detumescence of the erect penis (6,7). Clinically, higher levels of serum norepinephrine have been reported in patients with psychogenic ED than in normal controls or patients with vasculogenic ED (9).
ED is common among patients with cardiovascular diseases (CVD). Sexual problems usually precede the onset of CVD, and should, therefore, be considered as a risk factor for cardiac events. Similarly, patients with preexisting CVD are at increased risk of experiencing ED. Therefore, ED and CVD might be considered as two different clinical manifestations of the same systemic disease.19
Patients should continue testosterone therapy only if there is improvement in the symptoms of hypogonadism and should be monitored regularly. You will need periodic blood tests for testosterone levels and blood tests to monitor your blood count and PSA. Testosterone therapy has health risks, and thus doctors should closely monitor its use. Testosterone therapy can worsen sleep apnea and congestive heart failure.
Sildenafil is available as oral tablets at doses of 25 mg, 50 mg, and 100 mg. Patients should take sildenafil approximately one hour before sexual activity. In some men, the onset of action of the drug may be as early as 11-20 minutes. It's best for men to take sildenafil on an empty stomach for best results since absorption and effectiveness of sildenafil can be diminished if it is taken shortly after a meal, particularly a meal that is high in fat. Sildenafil and the other PDE5 inhibitors don't cause an immediate erection. Sexual stimulation is necessary for these medications to work.
Aging, liver and kidney problems, and concurrent use of certain medications (such as erythromycin [an antibiotic] and protease inhibitors for HIV) slows the metabolism (breakdown) of sildenafil. Slowed breakdown allows sildenafil to accumulate in the body and potentially may increase the risk of side effects. Therefore, in men over 65 years of age, in men with significant kidney and liver disease, and in men who also are taking medications called protease inhibitors, the doctor will initiate sildenafil at a lower dose (25 mg) to avoid accumulation of sildenafil in the body. A protease inhibitor ritonavir (Norvir) is especially potent in increasing the accumulation of sildenafil, thus men who are taking Norvir should not take sildenafil doses higher than 25 mg and at a frequency of no greater than once in 48 hours. Other medications that may affect the level of sildenafil include erythromycin and ketoconazole.
As recently as two decades ago, doctors tended to blame erectile dysfunction on psychological problems or, with older men, on the normal aging process. Today, the pendulum of medical opinion has swung away from both notions. While arousal takes longer as a man ages, chronic erectile dysfunction warrants medical attention. Moreover, the difficulty is often not psychological in origin. Today, urologists believe that physical factors underlie the majority of cases of persistent erectile dysfunction in men over age 50.
Hormonal disorders, such as low testosterone, may contribute to ED. Another possible hormonal cause of ED is increased production of prolactin, a hormone produced by the pituitary gland. Additionally, an abnormally high or low thyroid hormone level can result in ED. Young men who use steroids to help build muscle mass are also at a higher risk for ED.
Penile implants: This treatment involves permanent implantation of flexible rods or similar devices into the penis. Simple versions have the disadvantage of giving the user a permanent erection. The latest (and most expensive) device consists of inflatable rods activated by a tiny pump and switch in the scrotum. Squeezing the scrotum stiffens the penis, whether the person is aroused or not. The penis itself remains flaccid, however, so the diameter and length are usually less than a natural erection, and hardness is lacking, although it's sufficient for intercourse.
ED has been for long time considered a problem mainly related to psychological conditions and distress. Accordingly, until phosphodiesterase type 5 inhibitors (PDE5i) were introduced, psychoanalysis and cognitive-behavioural therapy were the only option for ED. In the last few decades, ED has been recognized as a clinical consequence of several different organic diseases and the importance of vascular health in erectile function has been so emphasized that ED is now considered not only the result of vascular impairment, but also a harbinger of forthcoming cardiovascular (CV) events (17). Despite the increasing attention of research towards organic mechanisms and conditions leading to ED, it is now known that considering this symptom as entirely due to organic disorders, is as imprecise as considering it only secondary to psychological conditions. In fact, this pathogenetic dichotomy is now obsolete (1,18,19), because it is now known that ED is a multidimensional disorder deriving from the interaction of different components related to organic conditions, relational context and psychological status (20,21). Even when only one of these components is involved in the initial development of erectile impairment, eventually the other ones will appear, thus further worsening ED (21-23). The multidimensional nature of ED is still not fully accepted by health care professionals when dealing with young patients. In fact, complaints of ED in young men is often underestimated and attributed to transient and self-limiting psychological conditions, such as performance anxiety. Young patients are often reassured without any further medical investigations, including physical exam. However, organic disorders, as well as relational and psychological or psychiatric conditions, can be meaningful in determining ED in younger men. In a population of subjects seeking medical care at the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, the first tertile of age (n=1,873 subjects) represents younger subjects (18–44 years). Pathogenetic components of ED in our sample are investigated by the Structured Interview on Erectile Dysfunction (SIEDY), a structured interview including 13 questions, whose answers, organized in a Likert scale, provide three scales, one for the organic subdomain [(SIEDY Scale 1); (22)], one for the relational subdomain [(SIEDY Scale 2); (23)] and one for the intrapsychic subdomain [(SIEDY Scale 3); (21)]. According to these scale scores, organic, relational and intrapsychic conditions are all significant risk factors for ED in younger patients of our population (Figure 2).
ED is easily and successfully treated! If your sex drive is unaffected, but you experience problems achieving or sustaining erection for a period of four to five weeks, you may have ED. Talk to your doctor immediately. Don’t delay—erectile dysfunction doesn’t “just go away!” Additionally, ED could be a sign of a serious, even life-threatening complication, such as congestive heart failure or kidney disease. Ignoring your ED because it’s embarrassing could jeopardize your health.