Am Fam Physician. 1998 Feb 15;57(4):685-92. Testicular masses. Junnila J1, Lassen P.
Family physicians often must evaluate patients with testicular pain or masses. The incidental finding of a scrotal mass may also require evaluation. Patients may seek evaluation of a scrotal mass as an incidental finding. An accurate history combined with a complete examination of the male external genitalia will help indicate a preliminary diagnosis and proper treatment. Family physicians must keep in mind the emergency or “must not miss” diagnoses associated with testicular masses, including testicular torsion, epididymitis, acute orchitis, strangulated hernia and testicular cancer. Referral to a urologist should be made immediately if one of these diagnoses is suspected. Benign causes of scrotal masses, including hydrocele, varicocele and spermatocele, may be diagnosed and managed easily in the primary care office.
Postgrad Med. 1995 Oct;98(4):151-3, 156-8. Chronic testicular pain. A workup and treatment guide for the primary care physician Baum N1, Defidio L.
Chronic pain syndromes are encountered in every medical practice, and workup can be costly and frustrating. Patients with chronic testicular pain were once referred early to urologists but are now being seen and successfully treated in primary care offices. Referral is usually reserved for diagnosis of questionable testicular masses and for surgery. Antibiotic therapy, often combined with a nonsteroidal anti-inflammatory drug, may be useful–in some cases even when infection has not been identified. Spermatic cord block and transcutaneous electrical nerve stimulation may help relieve pain, although it often recurs. Antidepressants sometimes relieve pain and alleviate the psychogenic symptoms that may accompany it. Many patients benefit from a program at a multidisciplinary pain-management clinic and should complete one before opiate therapy is prescribed. When all conservative efforts have failed and testicular pain continues to diminish the patient’s quality of life, orchiectomy may have to be considered. In general, however, we recommend that surgery be undertaken only when a pathologic condition is found and not for pain relief alone.
Oxygen toxicity is an inherent challenge to aerobic life, including spermatozoa, the cells responsible for propagation of the species. How this toxicity affects the spermatozoan in its interactions with the ovum is still unknown.
Aust Fam Physician. 1993 Aug;22(8):1357-9, 1362, 1365. Chronic testicular pain. Hayden LJ1.
The cause of chronic testicular pain is often difficult to define. Careful examination of the inguino-scrotal region is useful. Chronic orchalgia is a diagnosis of exclusion for which a multidisciplinary approach may be rewarding.
Neuwinger, J., Behre, H.M. and Nieschlag, E. (1990) External quality control in the andrology laboratory: an experimental multicenter trial. Fertil. Steril., 54, 308–314
Purpose: Results from an external quality control programme for semen analysis carried out in Spain are analysed.
Methods: Quality control materials were distributed and the following seminal parameters were determined: concentration, total motility, progressive motility, rapid progressive motility, morphology and sperm vitality. The between-laboratories coefficients of variation were assessed on different types of quality control material.
Results: The majority of participating laboratories utilised manual versus computer-assisted semen analysis methods. Some between-laboratories coefficients of variation ranges were: 20.8–33.8% for concentration (semen pool suspension); 13.9–19.2% for total motility (videotapes); 54.2–70.2% for sperm morphology (strict criteria using stained smears); and 9.8–41.1% for sperm vitality (stained smears). There was an inverse relation between mean percentage of sperm and coefficients of variation between laboratories for sperm motility, morphology and vitality.
Conclusions: These data highlight the urgent need for improvement in the overall quality of andrology testing.
Keywords: External quality control, semen analysis, sperm concentration, sperm morphology, sperm motility
The effects of alcohol (2.5 and 3.5 g/kg) on luteinizing hormone (LH) and testosterone were studied in adult male macaque monkeys under both basal and naloxone-stimulated conditions
The effects of alcohol (2.5 and 3.5 g/kg) on luteinizing hormone (LH) and testosterone were studied in adult male macaque monkeys under both basal and naloxone-stimulated conditions. Integrated plasma samples were collected at 30-min intervals for 90 min before nasogastric intubation of alcohol (2.5 and 3.5 g/kg) or a sucrose control solution, isocalorically equivalent to 2.5 g/kg of alcohol. Under basal (non-naloxone-stimulated) conditions, alcohol (2.5 or 3.5 g/kg) did not change LH levels significantly from prealcohol control levels. When basal testosterone levels were normal (600-1300 ng/dl), alcohol significantly suppressed testosterone levels in a dose-dependent manner. Testosterone levels decreased by 52% (P less than .05) within 30 min after a 3.5 g/kg dose of alcohol. As average blood alcohol levels increased to 400 mg/dl and above, testosterone levels fell monotonically and remained over 70% below base-line levels (P less than .01). After administration of 2.5 g/kg alcohol, testosterone levels were significantly suppressed within 90 min (P less than .05) and remained 52 to 63% below control levels (P less than .02-.05) as average blood alcohol levels increased to 300 mg/dl. However, when basal testosterone levels were abnormally low (100-200 ng/dl), alcohol had no effect on testosterone or LH. Naloxone stimulation was used to circumvent the high incidence of abnormally low testosterone levels observed. Naloxone (0.5 mg/kg i.v.) administration 90 min after alcohol (2.5 and 3.5 g/kg) or sucrose control administration significantly increased LH levels in comparison to base line (P less than .02-.001). LH reached peak values within 60 min after naloxone administration. A significant increase in testosterone (P less than .001) was observed 90 min after naloxone administration as LH levels began to decline. Alcohol (2.5 and 3.5 g/kg) did not attenuate or delay naloxone-stimulated increases in LH and testosterone in comparison to sucrose control conditions
The effects of acute and chronic alcohol administration on serum testosterone and luteinizing hormone (LH) levels were examined in the male rat.
The effects of acute and chronic alcohol administration on serum testosterone and luteinizing hormone (LH) levels were examined in the male rat. Chronic alcohol administration resulted in depressed serum testosterone and LH levels when alcohol-fed rats were compared with rats maintained, ad libitum, on rat chow and water. However, neither testosterone nor LH levels were significantly lower in alcohol-treated rats when comparisons were made to pair-fed control animals, indicating that the nutritional deficits imposed by the chronic alcohol-feeding regimen contributed heavily to the observed reductions in the two hormones. To avoid the problems associated with a chronic drug delivery model, we injected rats with a single acute injection of alcohol. LH levels dropped significantly within 2 hours after the injection of a 2.5 g/kg dose of alcohol and remained depressed, at a level between 25 and 30% of control values, from 2 to 4 hours. By 6 hours after the injection, LH levels had returned to base-line levels. Testosterone levels were also reduced by alcohol, but this drop was not significant until at least 3 hours after the injection. Testosterone levels did not return to control levels throughout the 6-hour course of the experiment. Dose-response determinations revealed that alcohol produced a biphasic effect on serum testosterone and LH: low doses of alcohol significantly increased testosterone and LH, whereas high doses decreased the levels of both hormones. The results of these studies suggest that the ability of alcohol to depress serum testosterone levels, and thus produce symptoms of hypogonadism in the male of several species, is due to a primary effect of alcohol on the hypothalamic-pituitary aspect of the hypothalamic-pituitary-gonadal axis.