1. Testicular torsion

Each testicle hangs from a spermatic cord consisting of arteries, veins, and nerves. If the cord twists (usually spontaneously), bloodflow is cut off, causing severe pain. Go to an ER for an ultrasound—you’ll lose the testicle if the condition goes untreated for longer than four hours. A surgeon will untwist the cord and sew each testicle to the inside of your scrotum to prevent future torsion.

2. Varicoceles

All veins contain valves to keep blood flowing in one direction, but sometimes the valves malfunction. If that happens in your scrotum, the veins will swell with blood, sometimes producing pain and a heavy sensation. While there’s no immediate danger from varicoceles, the resulting increase in temperature can cause a decrease in semen quality and testosterone production. Talk to your doctor about having the problem veins tied off to correct the leaky valves.

3. Epididymitis

Bacteria can inflame the epididymis, the gland on top of each testicle that collects sperm and transports it to the vas deferens. The resulting pain is hard to distinguish from that caused by torsion, so go to an ER for an ultrasound, says Larry Lipshultz, M.D., a Men’s Health advisor and the chief of male reproductive medicine at Baylor College of Medicine. Antibiotics will fight the infection, and anti-inflammatories will ease the pain.

Source: Carolyn Kylstra, Men’s Health via MSN Health

Treatment of localized prostate cancer is controversial because, for some, this disease will not progress during their life time, and treatment may incur serious and long-lasting side effects. An increasingly popular option is active surveillance, or deferring treatment until evidence of disease progression.

To investigate outcomes of patients treated with active surveillance, Pär Stattin, M.D., of the Department of Surgical and Perioperative Science at Umea University, and colleagues conducted an observational study of 6849 patients in the National Prostate Cancer Register of Sweden with localized prostate cancer who were 70 years old or younger. The patients had low or intermediate risk of prostate cancer progression and were treated with active surveillance or watchful waiting; or radical prostatectomy or radiation therapy from 1997 through December 2002.

In this cohort, 2021 patients received surveillance, 3399 received radical prostatectomy, and 1429 received radiation therapy. After a median follow-up of 8.2 years, there were 413 deaths in the surveillance group; 286 in the radical prostatectomy group, and 1429 patients in the radiation therapy group. The researchers found a much higher percentage of death from competing causes in the surveillance group (19.2%, compared with 6.8% in the prostatectomy group and 10.9% in the radiation therapy group), suggesting that patients with a shorter life expectancy were more often selected for surveillance than surgery or radiation therapy.

This observational study found that the risk of calculated cumulative prostate cancer-specific death was lower among patients in the prostatectomy group than those in the surveillance group. However, the difference in absolute risk between the groups was modest, at 1.2%, after 10 years of follow-up.

The authors conclude that surveillance is the best strategy for many patients with low-risk prostate cancer. “With a 10-year prostate cancer-specific mortality of less than 3% for patients with low-risk prostate cancer on surveillance, this strategy appears to be suitable for many of these men,” they write.

In an accompanying editorial, Siu-Long Yao and Grace Lu-Yao of The Cancer Institute of New Jersey write that perhaps the most remarkable result of this and other recent studies is that survival among most patients with localized disease managed conservatively is now similar to that of control subjects of similar ages.

Indeed, most men will die of another disease, and a prostate cancer diagnosis should act as a wake-up call for men to take charge of their healthcare and take better care of themselves. However, the authors write that a significant challenge is that, “A bevy of cancer research has demonstrated that cancer patients are particularly receptive to health-care advice after diagnosis, although older men, like those with prostate cancer, appear to be less receptive to change.”

Source: Kristine Crane, Journal of the National Cancer Institute

There is already evidence to suggest that soy beans contain natural chemicals that mimic the effect of female sex hormones.

Soy contains genistein, known to interact with the ‘receptor’ molecules on cells designed to respond to oestrogens.

A new study by Ren-Shan Ge of the Wenzhou Medical College in China found that genistein could interfere with the production of vital enzymes involved in producing sperm.

“Following ingestion, soy isoflavones are known to reach the reproductive organs. Thus, excessive exposure to agents that exhibit oestrogenic activity may affect male reproductive tract developments and functions,” the Independent quoted the researchers as saying.

“With regard to this concern, it has been estimated the genistein and daidzein can reach high concentrations in infants who consume large amounts of soy-based products,” they added.

The concentrations of genistein used in the study are roughly equivalent to the levels that can build up in the human body following a diet rich in soy products.

However, Professor Ieuan Hughes of the University of Cambridge said that a comprehensive inquiry into the oestrogenic chemicals found in soy and other food has failed to find any adverse effects on male reproductive health.

“I suspect the genistein effect is of little relevance to male human health… there was no evidence that soy products had adverse effects on male reproductive health, either via testis function or any other mechanism such as androgen [male hormone] action,” he said.

The study has been published in the Asian Journal of Andrology.

Results of a study published online ahead of print in the journal Diabetes Care, conducted by University at Buffalo endocrinologists, showed that 40 percent of obese participants involved in the Hypogonadism in Males (HIM) study had lower-than-normal testosterone readings.

The percentage rose to 50 percent among obese men with diabetes. Results also revealed that as body mass index (BMI) — a relationship of weight–to-height — increased, testosterone levels fell.

“The effect of diabetes on lowering testosterone levels was similar to that of a weight gain of approximately 20 pounds,” says Sandeep Dhindsa, MD, an endocrinology specialist in the UB Department of Medicine and first author on the study.

“In view of the fact that almost one-third of the U.S. is obese, these observations have profound pathophysiological, clinical, epidemiological and public health implications.”

This is the largest analysis of the association between obesity and low testosterone, and the first to compare prevalence of low testosterone with obesity and diabetes separately and together. The study shows that obesity and diabetes may exert independent influences on testosterone concentrations.

“We published a report in 2004 on the high prevalence of low testosterone levels in men with type 2 diabetes, and multiple studies all over the world have confirmed the association of low testosterone with diabetes,” Dhindsa notes.

“The Endocrine Society now recommends that all men with type 2 diabetes should have their testosterone levels measured. Our new study shows that obese men also have a very high prevalence of low testosterone levels, so physicians should consider screening obese non-diabetic men, as well, for low testosterone.”

The HIM study was funded by Solvay Pharmaceuticals Inc., and was conducted from November 2003 to February 2004 in 95 primary care practices throughout the U.S. The study involved 2,165 men 45 years or older who provided blood samples for analysis of testosterone concentrations.

UB researchers excluded participants from the full study who had no BMI data or were on certain drugs that can affect testosterone levels, providing a study population of 1,849 men — 398 with diabetes and 1,451 non-diabetics.

“With the rising prevalence of obesity in the U.S. and the rest of the world,” says Paresh Dandona, MD, head of the Division of Endocrinology, Diabetes and Metabolism at UB and Kaleida Health, and senior author of the study, “it is imperative that the prevalence of low testosterone levels in obese men be defined. In addition, the magnitude of the contribution of obesity to subnormal testosterone needs to be quantified.

“We hypothesized that obese men are more likely to have low testosterone than non-obese men, and that we would find more low testosterone levels in men with diabetes than in men without diabetes, both obese and non-obese.”

Results confirmed these hypotheses, showing a 40 percent higher prevalence of low testosterone in obese men compared to the non-obese participants. Men with diabetes, whether obese or not, showed lower levels of testosterone than non-diabetic men across all weight categories. Testosterone levels decreased significantly in both diabetic and non-diabetic men as BMI increased.

“In view of the increasing prevalence of obesity, even in younger populations, it would be important to conduct a similar study in the men at the prime of their reproductive years,” he says.

UB endocrinologists published a study in Diabetes Care in 2008 showing that more than 50 percent of men between 18 and 35 years old with type 2 diabetes had lower than normal testosterone levels.

“In view of the high rates of subnormal testosterone in patients with obesity or diabetes,

testosterone concentrations should be measured regularly in these populations, especially when these conditions occur together,” says Dandona.

Contributors to this study from UB, in addition to Dhindsa and Dandona, are Donald E. Mager, PharmD, PhD, Husam Ghanim, PhD, and Ajay Chaudhuri, MD. Cecilia L. McWhirter and Michael G. Miller, PharmD, both from Solvay Pharmaceuticals Inc., also contributed to the study.

This was an unfunded analysis of HIM data. Dandona and Dhindsa are supported by grants from The American Diabetes Association and Dandona’s work also is supported by the NIH.

The University at Buffalo is a premier research-intensive public university, a flagship institution in the State University of New York system and its largest and most comprehensive campus. UB’s more than 28,000 students pursue their academic interests through more than 300 undergraduate, graduate and professional degree programs. Founded in 1846, the University at Buffalo is a member of the Association of American Universities.

Source: Lois Baker, University at Buffalo via EurekAlert

The health of the prostate has long been considered dependent on the level of the male hormones collectively known as androgens however, it is now recognized that estrogens and their metabolites (estrogen broken down by chemical processes in the body) play a role in its normal growth as well as in prostate cancer.

“The aim of our study was to evaluate the use of estrogen metabolites, as a marker for prostate cancer risk,” says Ourania Kosti, PhD, at Georgetown Lombardi Comprehensive Cancer Center.

For the study, the researchers measured estrogens and their metabolites in the urine collected from 77 men with prostate cancer, 77 healthy controls and 37 men that underwent biopsy and but were diagnosed cancer-free.

The relative amounts of the 15 estrogens and estrogen metabolites in the urine of prostate cancer cases were similar to that of non-cancer patients with the exception of the estrogen metabolite 4-OHE1.

“This particular estrogen metabolite appeared to be more abundant among men diagnosed with prostate cancer,” explains Kosti.

Kosti says her team also observed that the estrogen metabolites considered as ‘harmful’ estrogens in breast cancer (16-KE2 and 17-epiE3) are secreted in higher amounts among those without prostate cancer and in lower amounts in those with prostate cancer.

“This suggests that these particular estrogens may have a protective role against prostate cancer development,” explains Kosti. “It is possible that different tissues respond to estrogens different ways, therefore the potential role of 16-KE2 and 17-epiE3 in prostate cancer prevention and management should be further explored.”

Source: Karen Mallet, Georgetown University Medical Center via EurekAlert

Published today in the revered New England Journal of Medicine, the study details how a young man suffered a cardiac arrest but survived thanks to the work of the ambulance paramedics. An investigation at Sahlgrenska University Hospital led to the discovery of not only a new disorder but also how a defect in the protein glycogenin can lead to an energy crisis in the muscle cells.

This protein’s job is to initiate the build-up of glycogen that constitutes the muscle cells’ carbohydrate reserves. The glycogenin starts the actual process by building up a short chain of around ten sugar molecules, which can then be turned into glycogen with the help of other enzymes. During strong muscular work the sugar molecules in the glycogen are used to create energy.

“The disorder is characterised by an inability to form the initial chain of sugar molecules,” says Anders Oldfors, who headed up the research team and is a professor at the Sahlgrenska Academy and consultant at Sahlgrenska University Hospital. “This leads to a shortage of glycogen and an energy crisis in the muscle cells that can result in cardiac arrest.”

The study also reveals how muscle cells that have a severe congenital defect can adjust and find other ways of sourcing energy, though it may not be sufficient in all situations.

“We’re hoping that our continued research in the field will provide answers to how the change in the glycogenin causes an inability to start accumulating carbohydrates in the muscle cells,” says Oldfors.

Clinically, the discovery means that this disorder must be considered as a diagnosis when investigating heart problems. For patients, a correct diagnosis means that there is preventative treatment available, though no cure is on the horizon at present. As the cause of the disorder is a genetic defect, it is hoped that in the future patients can be given a customised treatment, or gene therapy, for it.

“But we don’t yet know how common this disorder is,” says Oldfors. “This is something that the future will hold now that we are in a position to make the correct diagnosis.”

Cardiac Arrest

Cardiac arrest occurs when the blood suddenly stops pumping out of the heart. This leads to unconsciousness, and the breathing stops on account of an inadequate supply of blood. It is one of the most common causes of death and accounts for 11-18 per cent of all deaths in Sweden. Many old people are affected, with the trigger frequently being a heart attack. Cardiac arrest is very rare in young people and is generally caused by some form of hereditary heart muscle disorder. Cardio-pulmonary resuscitation and defibrillation can save patients who have suffered cardiac arrest. Preventative treatment takes the form of medication, and a surgically inserted defibrillator can also be used as protection. According to the Swedish Resuscitation Council 300-400 people a year are revived after cardiac arrest outside hospital and roughly 1,000-1,500 people in hospital.

Source: Anders Oldfors, University of Gothenburg via EurekAlert

According to the findings of the Phase 1-2 study, MDV3100 not only shrank patients’ tumors, but also reduced serum levels of the tumor marker prostate-specific antigen (PSA), stabilized disease that had spread to soft tissues and the bone, and reduced the number of circulating tumor cells in the blood.

“We were encouraged to see antitumor activity in men whose disease had spread to other parts of the body after either becoming resistant to previous hormone treatments or progressing following chemotherapy,” said the study’s lead author Howard Scher, MD, Chief of the Genitourinary Oncology Service at Memorial Sloan-Kettering. “These findings strengthen the drug’s potential to change the outlook for a group of patients who currently have limited effective treatment options from which to choose.”

According to the research, MDV3100 slows tumor growth and induces tumor cells to die in men with CRPC, or hormone-refractory disease, which depends on male hormones to grow, but is unresponsive or becomes resistant to standard therapies used to lower or block those hormones. MDV3100 works by blocking testosterone from binding to the androgen (male hormone) receptor, stopping the movement of the androgen receptor to the nucleus of prostate cancer cells, preventing the receptor from binding to DNA, and inducing cancer cell death, even when the expression of the androgen receptor is elevated.

“This study validates what our preclinical studies have suggested: that sustained androgen receptor signaling drives CRPC and that a substantial number of CRPC tumors that progress despite multiple hormone and chemotherapy treatments remain dependent on androgen receptor signaling for growth,” said study co-author, Charles Sawyers, MD, Chair of Memorial Sloan-Kettering’s Human Oncology and Pathogenesis Program and a Howard Hughes Medical Institute investigator.

The drug was co-invented by Dr. Sawyers and Michael Jung, PhD, Professor of Chemistry at the University of California, Los Angeles. Their research originally demonstrated that CRPC cells have increased expression of the androgen receptor and that elevated expression of this receptor may contribute to disease progression due to a developed resistance to hormone treatment. Their collaboration led to the discovery of a number of nonsteroidal, small molecule antiandrogen compounds, including MDV3100.

In the current study, 140 patients were treated with doses of MDV3100 ranging from 30 to 600 mg daily. PET imaging, bones scans, and blood tests were used to assess the antitumor effects of the drug, which were observed at all dosages. Investigators reported declines in PSA of at least 50 percent in more than half of the patients and tumor regressions in 22 percent of the patients. Overall, two-thirds of patients had partial remissions or stable disease in tumors that had spread to soft tissue or bone.

The findings also showed that the number of circulating tumor cells fell in 49 percent of patients, and 91 percent of patients who initiated therapy with favorable counts retained favorable counts during treatment. This is important because previous research shows that changes in circulating tumor cell counts after treatment were more predictive of survival than were changes in PSA, with favorable post-treatment counts associated with a 21-month median survival.

The drug was generally well tolerated, with nausea, constipation, diarrhea, and anorexia being the most common mild side effects reported. The most frequently reported Grade 3 side effect at higher doses was fatigue. The researchers determined that the maximum tolerated dose for sustained treatment was 240 mg daily.

Based on the positive results of the current study, a multinational randomized Phase 3 clinical trial has begun to examine MDV3100 versus a placebo for the treatment of men with advanced prostate cancer who were previously treated with chemotherapy. Information about patient eligibility and enrollment can be obtained by visiting www.affirmtrial.com or by calling the AFFIRM study’s toll free hotline at 888-782-3256.

Source: Jeanne D’Agostino, Memorial Sloan-Kettering Cancer Center

The recently discovered retrovirus, xenotropic murine leukemia virus-related virus (XMRV), has been identified in some prostate cancer patients. In light of conflicting data concerning XMRV, standardized diagnostic testing is important to identify patients in which XMRV is present and to determine whether it plays a role in the incidence of prostate cancer. An article published in the April issue of Urology® is a step in this direction as researchers from Emory University report the successful development of an experimental clinical test for XMRV.

“We cannot as a scientific community begin to answer the basic questions of XMRV transmission, frequency in the population, association with disease, etc. until we can effectively test for infection,” according to lead investigator John A. Petros, MD, Associate Professor of Urology, Emory University School of Medicine and Veterans Administration Hospital.

Dr. Petros and co-investigators adapted technology developed in the HIV arena (neutralizing antibody assay) and have developed a serum test that can identify patients who have previously been infected with the virus. This assay has been rigorously confirmed by two independent labs and two independent technologies (PCR and FISH), thus confidence in the accuracy of the test is high.

The mode of transmission of the virus is unknown. No method is available to screen either blood or tissue donors for infection and no data are available regarding whether the virus can be transmitted by blood transfusion or tissue transplantation. Dr. Petros comments, “The public deserves to know if the next blood transfusion or organ donation will give them XMRV retrovirus, an infection which lasts for life, and could possibly be related to prostate cancer. The failure to develop accurate tests for this virus is a serious public health oversight.”

Although the assay used in the present report involved the inhibition of infection of target cells by viral-like particles with the XMRV envelope protein expressed on their surface, results also suggest that more standard serologic tests for antibodies against specific viral antigens can be developed in the future.

The authors conclude that “our report adds to the growing body of evidence that XMRV is indeed a novel gamma-retrovirus capable of infecting humans and that at least some patients with prostate cancer have been infected with XMRV. We have reported serologic evidence of infection and that the serology correlated with tissue-based assays. The concordance of 3 independent methods of detecting infection added confidence to the assertion that this recently discovered virus is real and possibly related to human disease. Robust clinical assays are needed to detect XMRV infection, and much work remains to be done in determining whether XMRV is indeed an oncogenic virus or simply an associated epiphenomenon.”

Source: Sarah Kane, Elsevier Health Sciences

Research focusing on the number of children a man has have pointed to male fertility’s potential associated with risk for prostate cancer. However, studies on the topic have generated conflicting results: some have found that men with children had a higher risk than childless men; some have found that men with fewer children had a higher risk than men with more children; still others failed to identify any association between the number of children fathered and a man’s risk for prostate cancer.

Because the number of children a man has may not accurately reflect his ability to cause a pregnancy, Thomas Walsh, MD, MS, of the University of Washington in Seattle and his colleagues designed a more accurate study to evaluate the association between male infertility and prostate cancer. They studied the risk for prostate cancer in a group of 22,562 men evaluated for infertility from 1967 to 1998 in 15 California infertility centers. The incidence of prostate cancer in these men was compared with the incidence in a sample of men in the general population who were of similar ages and from similar geographic locations.

The researchers identified 168 cases of prostate cancer that developed in men who were evaluated for infertility. That number not significantly different from the expected rate (185 cases), suggesting that overall, men evaluated for infertility were not at a higher risk of being diagnosed with any type of prostate cancer compared with men in the general population. However, men who were evaluated and found to be infertile were 2.6 times more likely to be diagnosed with high grade prostate cancer than men who were evaluated but were found not to be infertile.

The authors say if these results are confirmed in other studies, it may be appropriate for infertile men to be considered for early prostate cancer screening, given their elevated risk for aggressive disease. They add that the results should stimulate research on possible common biological pathways underlying infertility and prostate cancer.

Source: David Sampson, American Cancer Society

The drug, minocycline, likely will improve on the current treatment regimens of HIV-infected patients if used in combination with a standard drug cocktail known as HAART (Highly Active Antiretroviral Therapy), according to research published now online and appearing in print April 15 in The Journal of Infectious Diseases. “The powerful advantage to using minocycline is that the virus appears less able to develop drug resistance because minocycline targets cellular pathways not viral proteins,” says Janice Clements, Ph.D., Mary Wallace Stanton Professor of Faculty Affairs, vice dean for faculty, and professor of molecular and comparative pathobiology at the Johns Hopkins University School of Medicine.

“The big challenge clinicians deal with now in this country when treating HIV patients is keeping the virus locked in a dormant state,” Clements adds. “While HAART is really effective in keeping down active replication, minocycline is another arm of defense against the virus.”

Unlike the drugs used in HAART which target the virus, minocycline homes in on, and adjusts T cells, major immune system agents and targets of HIV infection. According to Clements, minocycline reduces the ability of T cells to activate and proliferate, both steps crucial to HIV production and progression toward full blown AIDS.

If taken daily for life, HAART usually can protect people from becoming ill, but it’s not a cure. The HIV virus is kept at a low level but isn’t ever entirely purged; it stays quietly hidden in some immune cells. If a person stops HAART or misses a dose, the virus can reactivate out of those immune cells and begin to spread.

The idea for using minocycline as an adjunct to HAART resulted when the Hopkins team learned of research by others on rheumatoid arthritis patients showing the anti-inflammatory effects of minocycline on T cells. The Hopkins group connected the dots between that study with previous research of their own showing that minocycline treatment had multiple beneficial effects in monkeys infected with SIV, the primate version of HIV. In monkeys treated with minocycline, the virus load in the cerebrospinal fluid, the viral RNA in the brain and the severity of central nervous system disease were significantly decreased. The drug was also shown to affect T cell activation and proliferation.

“Since minocycline reduced T cell activation, you might think it would have impaired the immune systems in the macaques, which are very similar to humans, but we didn’t see any deleterious effect,” says Gregory Szeto, a graduate student in the Department of Cellular and Molecular Medicine working in the Retrovirus Laboratory at Hopkins.
“This drug strikes a good balance and is ideal for HIV because it targets very specific aspects of immune activation.”

The success with the animal model prompted the team to study in test tubes whether minocycline treatment affected latency in human T cells infected with HIV. Using cells from HIV-infected humans on HAART, the team isolated the “resting” immune cells and treated half of them with minocycline. Then they counted how many virus particles were reactivated, finding completely undetectable levels in the treated cells versus detectable levels in the untreated cells.

“Minocycline reduces the capability of the virus to emerge from resting infected T cells,” Szeto explains. “It prevents the virus from escaping in the one in a million cells in which it lays dormant in a person on HAART, and since it prevents virus activation it should maintain the level of viral latency or even lower it. That’s the goal: Sustaining a latent non-infectious state.”

The team used molecular markers to discover that minocycline very selectively interrupts certain specific signaling pathways critical for T cell activation. However, the antibiotic doesn’t completely obliterate T cells or diminish their ability to respond to other infections or diseases, which is crucial for individuals with HIV.

“HIV requires T cell activation for efficient replication and reactivation of latent virus,” Clement says, “so our new understanding about minocyline’s effects on a T cell could help us to find even more drugs that target its signaling pathways.”

The research was supported by grants from the National Institutes of Health.

Authors of the paper, in addition to Clements and Szeto, are Angela K. Brice, Sheila A. Barber and Robert F. Siliciano, all of Johns Hopkins. Also, Hung-Chih Yang of National Taiwan University Hospital.

Source: Maryalice Yakutchik, Johns Hopkins Medical Institutions