- Email: [email protected]
Re: Early and Late Long-term Effects of Vasectomy on Serum Testosterone, Dihydrotestosterone, Luteinizing Hormone and Follicle-Stimulating Hormone Levels
1784
LETTERS TO THE EDITOR
ask couples not to remove the condom or to wipe the cream from the penis if the condom is removed. Respectfully, Hayrettin $ahin and M. Kamuran Bircan Department of Urology Dicle University School of Medicine 21280-Diyarbakir nrkey
1. American Society of Plastic and Reconstructive Surgery: Report on autologous fat transplantation by the American Society of Plastic and Reconstructive Surgery ad hoc committee on new procedures. Chicago: American Society of Plastic and Reconstructive Surgery, 1987. 2. Alter, G. J.: Augmentation phalloplasty. Urol. Clin. N. h e r , , 22: 887, 1995. 3. Alter, G. J.: Penile enhancement. Adv. Urol., 9: 225, 1996. 4. Horton, C. E. and Horton, C. E., Jr.: Personal communication.
Reply by Authors. Much more work is needed to optimize the use of prilocaine-lidocaine cream for premature ejaculation. We focused on short-term efficacy, and acknowledge that long-term effectiveness must be examined in a rigorous protocol. The complaint of vaginal numbness highlights why a double-blind, placebo controlled protocol will be needed. Contact of the prilocaine-lidocaine cream with the vagina is brief, and this mixture of local anesthetics is generally documented to require 5 to 20 minutes for maximal effect on mucous membranes.l While it is conceivable that some women may experience numbness even during intercourse, many may not. Therefore, it appears more logical to allow couples to decide for themselves whether use of a condom during intercourse is necessary.
Reply by Authors. We agree that penile enhancement should not be condemned only because complications exist, unless the complication rate is excessive. Presently, this statistic remains unknown. Mthough, as stated, . . some surgeons are obtaining good results and high patient satisfaction rates," references 2 and 3 in the Letter provide no objective evidence to support the efficacy of penile enhancement. No series has reported mean values for preoperative and postoperative length or girth after penile enhancement, although Bondil and Delmas were able to increase the flaccid length by 1.6 cm. in cadavers.' In addition, no validated questionnaire has been devised to assess patient satisfaction. We believe that men with normal phallic dimensions should not undergo a procedure that remains unproved, even in the hands of competent and ethical practitioners. To some extent the controversy is about the legitimacy of aesthetic surgery as a treatment for men with feelings of inadequacy related to penile length, when mostly they have normal penile dimensions." 3 However, we recognize that merely telling a patient that penile length is normal does not address the cultural and psychological factors influencing the perception of penile length.
1. Koren, G.: Eutectic Mixture of Local Anesthetics: A Breakthrough in Skin Anesthesia. New York Marcel Dekker, pp. 24-25, 1995.
RE: COMPLICATIONS OF PENILE LENGTHENING AND AUGMENTATION SEEN AT 1 REFERRAL CENTER
Y.
H. Wessells, T.F. Lue and J . W. McAninch
J. Urol., 155: 1617-1620, 1996 To the Editor. Many similar patients have presented to me for reconstruction after unfavorable penile lengthening and augmentation surgery. Most of these operations were performed by 1of several surgeons using a large V-Y advancement flap associated with suspensory ligament release. These surgeons also usually injected autologous fat. This large V-Y advancement flap can cause severe deformities, including unsightly scars, an unnatural proximal, hairbearing penile hump and scrota1 dog-ears. By design, the proximal penile skin and dartos fascia are often almost completely circumcised, thereby injuring the distally based blood supply of the flap with the risk of poor wound healing. Fortunately, most surgeons who perform penile lengthening now use either a much smaller V-Y advancement flap, a linear incision or a double Z-plasty. Autologous fat injections cause complications of fat resorption, nodules and penile asymmetry, so that many surgeons now increase girth with dermal fat grafts.' Having performed reconstruction in many cases of penile enhancement with poor results, I agree that reconstruction can be hazardous. These men frequently have had multiple scar revisions or recurrent fat injections, causing further fibrosis and damage to the vascular supply and lymphatics. Combining V-Y advancement flap reversal with aggressive removal of fat deformities can cause skin loss and prolonged edema. Understanding anatomy and plastic surgical principles is imperative. Staged operations are often necessary to obtain optimal results safely. Penile augmentation procedures are new and not standardized. Markedly different techniques are performed but are falsely classified as being similar. Since there have been no well designed, peer controlled articles, the authors are justified in classifying these operations as investigational. However, some surgeons are obtaining good results and high patient satisfaction As with any new operation, improvements in design and technique will decrease the complication rate. Penile enhancement should not be condemned because of complications but poorly designed operations should cease. The purpose of penile enhancement, as in all aesthetic surgery, is to improve patient self-esteem. This operation is justified if it is performed effectively with a reasonably low complication rate. Respectfully, Gary ,I. Alter Department of Plastic Surgery IJC1.A School of Medicine 43.5 North Bedfbrd Drioe. Suite 300 Hruerly Hills. California 90210
1. Bondil, P. and Delmas, V.: Is the section of the suspensory ligament of penis really efficient for penile lengthening: preliminary results of an anatomical study. Int. J. Impotence Res., suppl. 1, 7: 32, 1995. 2. Schonfeld,W. A. and Beebe, G. W.: Normal growth and variation in the male genitalia from birth to maturity. J. Urol., 48: 759, 1942. 3. Wessells, H., Lue, T. F. and McAninch, J. W.: Penile length in the flaccid and erect states: guidelines for penile augmentation. J. Urol., 156 995, 1996.
RE: EARLY AND LATE LONG-TERM EFFECTS OF VASECTOMY ON SERUM TESTOSTERONE, DIHYDROTESTOSTERONE,LUTEINIZING HORMONE AND FOLLICLE-STIMULATINGHORMONE LEVELS Z.-N. Mo, X. Huang, S.-C. Zhang and J.-R. Yang
J. Urol., 154: 2065-2069, 1995 To the Editor. The authors carefully investigated long-term effects of vasectomy on serum androgen levels in men. There was a significant increase in dihydrotestosterone levels in men undergoing vasectomy compared to controls. Control subjects did not differ from patients with respect to age, demographic data, exogenous toxins, such as alcohol and smoke, marital and educational status or sexual activity. However, authors cannot state why vasectomy alone should influence the conversion rate of testosterone to dihydrotestosterone. A major parameter, namely fertility status of men, was not considered for matching patients and controls, and this might have biased the results. Patients seeking vasectomy usually had successfully finished family planning and were expected to have a t least 1 child. While marital status was comparable, no information was given on proved fatherhood or history of infertility in either group. Contraceptive trials have shown different susceptibilities to exogenous hormonal treatment, for example testosterone esters, in men of different racial groups as well as in different individuals.1.2 If fertility resulting from normal hormonal regulation of spermatogenesis reflects a normal endocrine equilibrium, one may speculate that infertile men might have a different hormonal equilibrium, possibly influencing endogenous serum androgen levels. Thus, the difference in dyhy-
1785
LETTERS TO THE EDITOR drotestosterone levels reported may be overestimated in the vasectomy group if infertile men belong to the controls investigated. Respectfully, Sabine KZiesch, Stephan Roth and Lothar Hertle Klinik und Poliklinik fur Urologie Westfalische Wilhelms-Universitat Munster Albert-Schweitzer-Str.33, 0-48129 Miinster Germany
1.0
h
1. Contraceptive efficacy of testosterone-induced azoospermia in normal men. World Health Organization Task Force on methods for the regulation of male fertility. Lancet, 336: 955, 1990. 2. Behre, H. M., Baus, S., Kliesch, S., Keck, C., Simoni, M. and Nieschlag, E.: Potential of testosterone buciclate for male contraception: endocrine differences between responders and nonresponders. J. Clin. Endocr. Metab., 8 0 2394, 1995.
Reply by Authors. Many potential confounding factors may influence sex hormone levels and the only way to lessen their influence is to control these factors as much as possible. Kliesch et a1 raise some important questions about fertility status as a potential confounding factor that might bias results. We did not know how many children the subjects had but if a potential match was infertility the patient was considered ineligible for the study as were those with prostatitis. This question should have been addressed in the section on study subjects in our article. We regret our error and appreciate the comments by Kliesch et al.
RE: PROSTATE CANCER MORTALITY IN PATIENTS SURVIVING MORE THAN 10 YEARS AFTER DIAGNOSIS J . Hugosson, G . Aus, C. Bergdahl and S. Bergdahl
J. Urol., 164: 2115-2117, 1995 To the Editor. In this study a high prostate cancer specific mortality rate of 62% was reported in patients surviving longer than 10 years after diagnosis. The authors concluded that i t seems hard to justify deferred treatment to patients with localized prostate cancer and with a long expected survival. This statement could be agreeable if the data presented were correct. Several methodological problems in this study might invalidate the conclusions of the authors, some of which have already been noted by Chodak.1 However, a main criticism regards the determination of cause of death. Since most prostate cancer patients are elderly they may often die of other diseases, and it is well recognized that crude figures for total deaths in a population diagnosed as having prostate cancer are a n overestimate of deaths from the cancer. There are 2 approaches to consider and to correct for the contribution of deaths from other causes. Relative survival rates are calculated by using the observed survival in the studied patient population and dividing that number by the expected survival of a n age matched population in the same region. With this method the actual cause of death is not determined in each patient. For cause specific survival rates the cause of death for each patient studied is determined. Medical records or death certificates can be used to determine cause of death. Since 1952 all causes of deaths in Sweden on issued death certificates are coded and registered in the Causes of Death Register. The causes of death are divided into direct or contributory (associated with but not causing death). In the official data on causes of death due to cancer only cancer coded as a direct cause of death is reported as a cancer death.2 To study these different methods of estimating prostate cancer survival and mortality, the relative and cause specific survival rates were estimated using data from the Causes of Death Register in 6,514 prostate cancer cases diagnosed in northern Sweden between 1971 and 1987 (see figure). The cause specific survival rate was calculated with prostate cancer as either the direct cause of death ( 0 )or, when prostate cancer was mentioned on the death certificate (X), as a direct or contributory cause of death (called pooled analysis by Hugosson et al). The figure obtained shows clearly that the relative and cause specific ( 0 )survivals are almost equal, while the pooled cause specific survival (X) provides a significantly h e r survival rate and consequently more deaths from prostate cancer. Hugosson et a1 used death certificates and classified patients as
RSR o CSRl x CSR2 A
0.0'
0
"
"
I
'
"
5
"
10
"
"
' 15
Years Relative (RSR)and cause specific (CSR)survival rates for prostate cancer in northern Sweden diagnosed between 1971 and 1987. Cause specific survival rate used data taken directly from Cause of Death Register, and was calculated with prostate cancer only as direct cause of death (1, O), or combining direct and associated cause of death (2, X).
having died of prostate cancer when prostate cancer was coded as a direct or contributory cause of death. This classification is not correct and causes a large overestimation of prostate cancer mortality (see figure). If the figures of Hugosson et al are correct, 75 to 80% of all patients diagnosed between 1960 and 1979 in Giiteborg would have died of prostate cancer, which is a mortality rate that most of us would find unrealistically high. The authors justify the pooling of causes of death with their previous survey of medical records and death certificates. This subjective determination of cause of death is difficult to reproduce and also unnecessary, since valid and good registry data are available in the population registries and Cause of Death Register. The authors calculated the mean survival of this select group of prostate cancer patients to be 15 years. Furthermore, they also stated that the remaining life expectancy of this group was only 12 years based on available population data, which implicates that having prostate cancer prolongs remaining life expectancy if one survives for at least 10 years after diagnosis. However, since mean age after 10 years of survival in this study was 78 years and remaining life expectancy for a Swedish man of this age is 7 years? this indicates that total life expectancy from diagnosis is 17 and not 12 years due to the selection criteria using only patients who survived for at least 10 years. Therefore, the conclusion by the authors that relative survival is unsuitable when calculating prostate cancer survival is not supported by the data presented. On the contrary, we found that relative and cause specific survivals with data from the Cause of Death Register are compatible (see figure). We suggest that the authors recalculate their data with a correct method of determining cause of death. Otherwise, their report is of limited value and might even be misleading. The Swedish registries are of good quality and good scientific research can be based on them. However, it is of utmost importance that data be analyzed in a correct manner, otherwise more confusion than clarity would be added to our effort to understand the natural history of prostate cancer. Respectfully, Henrik Griinberg, Jan-Erik Damber, Lena Damber and Hdkan Jonsson Departments of Oncology and Urology Umed Uniuersitet Umed, Sweden 1. Chodak, G. W.: What to expect from prostate cancer. J. Urol., 154: 2132,1995. 2. Causes of Death 1991 in Sweden. Official Statistics of Sweden. National Central Bureau of Statistics. Stockholm: Statistics Sweden, 1993.
LETTERS TO THE EDITOR
ask couples not to remove the condom or to wipe the cream from the penis if the condom is removed. Respectfully, Hayrettin $ahin and M. Kamuran Bircan Department of Urology Dicle University School of Medicine 21280-Diyarbakir nrkey
1. American Society of Plastic and Reconstructive Surgery: Report on autologous fat transplantation by the American Society of Plastic and Reconstructive Surgery ad hoc committee on new procedures. Chicago: American Society of Plastic and Reconstructive Surgery, 1987. 2. Alter, G. J.: Augmentation phalloplasty. Urol. Clin. N. h e r , , 22: 887, 1995. 3. Alter, G. J.: Penile enhancement. Adv. Urol., 9: 225, 1996. 4. Horton, C. E. and Horton, C. E., Jr.: Personal communication.
Reply by Authors. Much more work is needed to optimize the use of prilocaine-lidocaine cream for premature ejaculation. We focused on short-term efficacy, and acknowledge that long-term effectiveness must be examined in a rigorous protocol. The complaint of vaginal numbness highlights why a double-blind, placebo controlled protocol will be needed. Contact of the prilocaine-lidocaine cream with the vagina is brief, and this mixture of local anesthetics is generally documented to require 5 to 20 minutes for maximal effect on mucous membranes.l While it is conceivable that some women may experience numbness even during intercourse, many may not. Therefore, it appears more logical to allow couples to decide for themselves whether use of a condom during intercourse is necessary.
Reply by Authors. We agree that penile enhancement should not be condemned only because complications exist, unless the complication rate is excessive. Presently, this statistic remains unknown. Mthough, as stated, . . some surgeons are obtaining good results and high patient satisfaction rates," references 2 and 3 in the Letter provide no objective evidence to support the efficacy of penile enhancement. No series has reported mean values for preoperative and postoperative length or girth after penile enhancement, although Bondil and Delmas were able to increase the flaccid length by 1.6 cm. in cadavers.' In addition, no validated questionnaire has been devised to assess patient satisfaction. We believe that men with normal phallic dimensions should not undergo a procedure that remains unproved, even in the hands of competent and ethical practitioners. To some extent the controversy is about the legitimacy of aesthetic surgery as a treatment for men with feelings of inadequacy related to penile length, when mostly they have normal penile dimensions." 3 However, we recognize that merely telling a patient that penile length is normal does not address the cultural and psychological factors influencing the perception of penile length.
1. Koren, G.: Eutectic Mixture of Local Anesthetics: A Breakthrough in Skin Anesthesia. New York Marcel Dekker, pp. 24-25, 1995.
RE: COMPLICATIONS OF PENILE LENGTHENING AND AUGMENTATION SEEN AT 1 REFERRAL CENTER
Y.
H. Wessells, T.F. Lue and J . W. McAninch
J. Urol., 155: 1617-1620, 1996 To the Editor. Many similar patients have presented to me for reconstruction after unfavorable penile lengthening and augmentation surgery. Most of these operations were performed by 1of several surgeons using a large V-Y advancement flap associated with suspensory ligament release. These surgeons also usually injected autologous fat. This large V-Y advancement flap can cause severe deformities, including unsightly scars, an unnatural proximal, hairbearing penile hump and scrota1 dog-ears. By design, the proximal penile skin and dartos fascia are often almost completely circumcised, thereby injuring the distally based blood supply of the flap with the risk of poor wound healing. Fortunately, most surgeons who perform penile lengthening now use either a much smaller V-Y advancement flap, a linear incision or a double Z-plasty. Autologous fat injections cause complications of fat resorption, nodules and penile asymmetry, so that many surgeons now increase girth with dermal fat grafts.' Having performed reconstruction in many cases of penile enhancement with poor results, I agree that reconstruction can be hazardous. These men frequently have had multiple scar revisions or recurrent fat injections, causing further fibrosis and damage to the vascular supply and lymphatics. Combining V-Y advancement flap reversal with aggressive removal of fat deformities can cause skin loss and prolonged edema. Understanding anatomy and plastic surgical principles is imperative. Staged operations are often necessary to obtain optimal results safely. Penile augmentation procedures are new and not standardized. Markedly different techniques are performed but are falsely classified as being similar. Since there have been no well designed, peer controlled articles, the authors are justified in classifying these operations as investigational. However, some surgeons are obtaining good results and high patient satisfaction As with any new operation, improvements in design and technique will decrease the complication rate. Penile enhancement should not be condemned because of complications but poorly designed operations should cease. The purpose of penile enhancement, as in all aesthetic surgery, is to improve patient self-esteem. This operation is justified if it is performed effectively with a reasonably low complication rate. Respectfully, Gary ,I. Alter Department of Plastic Surgery IJC1.A School of Medicine 43.5 North Bedfbrd Drioe. Suite 300 Hruerly Hills. California 90210
1. Bondil, P. and Delmas, V.: Is the section of the suspensory ligament of penis really efficient for penile lengthening: preliminary results of an anatomical study. Int. J. Impotence Res., suppl. 1, 7: 32, 1995. 2. Schonfeld,W. A. and Beebe, G. W.: Normal growth and variation in the male genitalia from birth to maturity. J. Urol., 48: 759, 1942. 3. Wessells, H., Lue, T. F. and McAninch, J. W.: Penile length in the flaccid and erect states: guidelines for penile augmentation. J. Urol., 156 995, 1996.
RE: EARLY AND LATE LONG-TERM EFFECTS OF VASECTOMY ON SERUM TESTOSTERONE, DIHYDROTESTOSTERONE,LUTEINIZING HORMONE AND FOLLICLE-STIMULATINGHORMONE LEVELS Z.-N. Mo, X. Huang, S.-C. Zhang and J.-R. Yang
J. Urol., 154: 2065-2069, 1995 To the Editor. The authors carefully investigated long-term effects of vasectomy on serum androgen levels in men. There was a significant increase in dihydrotestosterone levels in men undergoing vasectomy compared to controls. Control subjects did not differ from patients with respect to age, demographic data, exogenous toxins, such as alcohol and smoke, marital and educational status or sexual activity. However, authors cannot state why vasectomy alone should influence the conversion rate of testosterone to dihydrotestosterone. A major parameter, namely fertility status of men, was not considered for matching patients and controls, and this might have biased the results. Patients seeking vasectomy usually had successfully finished family planning and were expected to have a t least 1 child. While marital status was comparable, no information was given on proved fatherhood or history of infertility in either group. Contraceptive trials have shown different susceptibilities to exogenous hormonal treatment, for example testosterone esters, in men of different racial groups as well as in different individuals.1.2 If fertility resulting from normal hormonal regulation of spermatogenesis reflects a normal endocrine equilibrium, one may speculate that infertile men might have a different hormonal equilibrium, possibly influencing endogenous serum androgen levels. Thus, the difference in dyhy-
1785
LETTERS TO THE EDITOR drotestosterone levels reported may be overestimated in the vasectomy group if infertile men belong to the controls investigated. Respectfully, Sabine KZiesch, Stephan Roth and Lothar Hertle Klinik und Poliklinik fur Urologie Westfalische Wilhelms-Universitat Munster Albert-Schweitzer-Str.33, 0-48129 Miinster Germany
1.0
h
1. Contraceptive efficacy of testosterone-induced azoospermia in normal men. World Health Organization Task Force on methods for the regulation of male fertility. Lancet, 336: 955, 1990. 2. Behre, H. M., Baus, S., Kliesch, S., Keck, C., Simoni, M. and Nieschlag, E.: Potential of testosterone buciclate for male contraception: endocrine differences between responders and nonresponders. J. Clin. Endocr. Metab., 8 0 2394, 1995.
Reply by Authors. Many potential confounding factors may influence sex hormone levels and the only way to lessen their influence is to control these factors as much as possible. Kliesch et a1 raise some important questions about fertility status as a potential confounding factor that might bias results. We did not know how many children the subjects had but if a potential match was infertility the patient was considered ineligible for the study as were those with prostatitis. This question should have been addressed in the section on study subjects in our article. We regret our error and appreciate the comments by Kliesch et al.
RE: PROSTATE CANCER MORTALITY IN PATIENTS SURVIVING MORE THAN 10 YEARS AFTER DIAGNOSIS J . Hugosson, G . Aus, C. Bergdahl and S. Bergdahl
J. Urol., 164: 2115-2117, 1995 To the Editor. In this study a high prostate cancer specific mortality rate of 62% was reported in patients surviving longer than 10 years after diagnosis. The authors concluded that i t seems hard to justify deferred treatment to patients with localized prostate cancer and with a long expected survival. This statement could be agreeable if the data presented were correct. Several methodological problems in this study might invalidate the conclusions of the authors, some of which have already been noted by Chodak.1 However, a main criticism regards the determination of cause of death. Since most prostate cancer patients are elderly they may often die of other diseases, and it is well recognized that crude figures for total deaths in a population diagnosed as having prostate cancer are a n overestimate of deaths from the cancer. There are 2 approaches to consider and to correct for the contribution of deaths from other causes. Relative survival rates are calculated by using the observed survival in the studied patient population and dividing that number by the expected survival of a n age matched population in the same region. With this method the actual cause of death is not determined in each patient. For cause specific survival rates the cause of death for each patient studied is determined. Medical records or death certificates can be used to determine cause of death. Since 1952 all causes of deaths in Sweden on issued death certificates are coded and registered in the Causes of Death Register. The causes of death are divided into direct or contributory (associated with but not causing death). In the official data on causes of death due to cancer only cancer coded as a direct cause of death is reported as a cancer death.2 To study these different methods of estimating prostate cancer survival and mortality, the relative and cause specific survival rates were estimated using data from the Causes of Death Register in 6,514 prostate cancer cases diagnosed in northern Sweden between 1971 and 1987 (see figure). The cause specific survival rate was calculated with prostate cancer as either the direct cause of death ( 0 )or, when prostate cancer was mentioned on the death certificate (X), as a direct or contributory cause of death (called pooled analysis by Hugosson et al). The figure obtained shows clearly that the relative and cause specific ( 0 )survivals are almost equal, while the pooled cause specific survival (X) provides a significantly h e r survival rate and consequently more deaths from prostate cancer. Hugosson et a1 used death certificates and classified patients as
RSR o CSRl x CSR2 A
0.0'
0
"
"
I
'
"
5
"
10
"
"
' 15
Years Relative (RSR)and cause specific (CSR)survival rates for prostate cancer in northern Sweden diagnosed between 1971 and 1987. Cause specific survival rate used data taken directly from Cause of Death Register, and was calculated with prostate cancer only as direct cause of death (1, O), or combining direct and associated cause of death (2, X).
having died of prostate cancer when prostate cancer was coded as a direct or contributory cause of death. This classification is not correct and causes a large overestimation of prostate cancer mortality (see figure). If the figures of Hugosson et al are correct, 75 to 80% of all patients diagnosed between 1960 and 1979 in Giiteborg would have died of prostate cancer, which is a mortality rate that most of us would find unrealistically high. The authors justify the pooling of causes of death with their previous survey of medical records and death certificates. This subjective determination of cause of death is difficult to reproduce and also unnecessary, since valid and good registry data are available in the population registries and Cause of Death Register. The authors calculated the mean survival of this select group of prostate cancer patients to be 15 years. Furthermore, they also stated that the remaining life expectancy of this group was only 12 years based on available population data, which implicates that having prostate cancer prolongs remaining life expectancy if one survives for at least 10 years after diagnosis. However, since mean age after 10 years of survival in this study was 78 years and remaining life expectancy for a Swedish man of this age is 7 years? this indicates that total life expectancy from diagnosis is 17 and not 12 years due to the selection criteria using only patients who survived for at least 10 years. Therefore, the conclusion by the authors that relative survival is unsuitable when calculating prostate cancer survival is not supported by the data presented. On the contrary, we found that relative and cause specific survivals with data from the Cause of Death Register are compatible (see figure). We suggest that the authors recalculate their data with a correct method of determining cause of death. Otherwise, their report is of limited value and might even be misleading. The Swedish registries are of good quality and good scientific research can be based on them. However, it is of utmost importance that data be analyzed in a correct manner, otherwise more confusion than clarity would be added to our effort to understand the natural history of prostate cancer. Respectfully, Henrik Griinberg, Jan-Erik Damber, Lena Damber and Hdkan Jonsson Departments of Oncology and Urology Umed Uniuersitet Umed, Sweden 1. Chodak, G. W.: What to expect from prostate cancer. J. Urol., 154: 2132,1995. 2. Causes of Death 1991 in Sweden. Official Statistics of Sweden. National Central Bureau of Statistics. Stockholm: Statistics Sweden, 1993.