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What to Do if the PSA Starts Rising after Radiation
After radiation (either external beam or seeds) the PSA should slowly decline and may not reach a low point or nadir for 12 - 18 months. Sometimes it will bounce up slightly for no apparent reason. If however the PSA starts rising again and consistently on two or more readings is rising then you have to assume the patient still has active cancer. Read the literature review about salvage options here or the protocol for radioactive seeds after external beam therapy (RTOG 0526 here). There are generally three scenarios:

1. if the PSA is rising slowly (not doubling within a 12 month interval) then often no treatment is necessary
2. if the PSA is rising quickly (doubling in less than 12 months) and [particularly if the tumor with high Gleason (7 or more) and if the PSA never fell below 1 or 1.5, then hormone therapy (e.g. Lupron) will often be given. Sometimes it is worthwhile to repeat a bone scan or prostascint scan prior to making a decision
3. if the PSA is clearly rising and the scans are all negative, some doctors will re-biopsy the gland if there is an apparent local failure (meaning in the gland and nowhere else) consider treating the gland further (more radiation, e.g. seeds if they originally had only external) or surgery (radical prostatectomy after full course radiation has a high complication rate) or cryosurgery (also somewhat experimental.) (See NCCN guidelines.)
There is good evidence that the risk to the patient form a PSA relapse is much higher if the PSA rises quickly e.g. doubles in less than 3 months, (see study), particularly if the original Gleason Score was high like 8 - 10, (see study.)

Another good discussion of which patients to place on hormone therapy (androgen deprivation, i.e. Lupron +/- Casodex) is noted in the study below, note that if the PSA is not rising quickly (i.e. not doubling within 12 months) patients do well without starting Lupron (see figure 1.) If the PSA rises quickly then need Lupron (see figure 2.) if the PSA never got lower than 1.5 they do poorly (figure 3) and if the Gleason was higher than 6 the do poorly (figure 4.) A similar study from SKM showed that if the rise in PSA is slow (i.e. doubling time grater than 12 months) then the risk of developing metastases is small (see graph.)    A recent study suggested drinking pomegranate juice (go here.)

Validation of a treatment policy for patients with prostate specific antigen failure after three-dimensional conformal prostate radiation therapy
Wayne H. Pinover
Department of Radiation Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania
Eligible patients included 248 men with T1-T3N0M0 prostate carcinoma who demonstrated PSA failure (according to the American Society for Therapeutic Radiology and Oncology definition) after completing definitive 3DCRT alone or with androgen deprivation (AD) therapy between May 1989 and November 1997. The primary endpoint evaluated was freedom from distant metastasis (FDM). The secondary endpoints evaluated included cause specific survival (CSS) and overall survival (OS). The variables evaluated in the multivariate analyses (MVA) included initial PSA, Gleason score, T classification, dose, PSA nadir, time to PSA failure, PSA doubling time (PSADT), initial use of AD therapy, and the use of AD therapy upon PSA failure.

RESULTS
The 5-year FDM, CSS, and OS rates for the entire group were 76%, 92%, and 76%, respectively. It was found that four variables were independent predictors of FDM: Gleason score, PSA nadir, PSADT, and the use of AD on PSA failure. One hundred forty-eight men demonstrated a PSADT < 12 months. AD therapy was started in 59 men, and 89 men refused AD therapy and were observed. The use of AD therapy was associated with a significant improvement in the 5-year FDM rate (57% vs. 78%). In the group of men with PSADT < 12 months, the median time to distant failure was significantly longer in the men who received AD therapy (6 months vs. 25 months).

Of the 100 men with a PSADT > 12 months, 89 men were observed, and 11 men received AD therapy. There was no improvement in the 5-year FDM rate with the use of AD therapy compared with observation (88% vs. 92%, respectively).

CONCLUSIONS
The current results validate the use of PSADT as an indicator of patients who may be observed expectantly or treated with AD therapy for PSA failure after 3DCRT. Prospective trials are needed to define further the optimal treatment for these patients. Our results support the use of AD therapy in men with a PSADT of < 12 months and observation in men with a longer PSADT. MVA also demonstrated the predictive value of the PSA nadir and Gleason score for patients with distant recurrence. Therefore, for the subgroup of men with a PSADT of > 12 months, the use of AD therapy may be considered for those with a PSA nadir of > 1.5 ng/mL, especially if they demonstrate a biopsy Gleason score of 7-10. We were not able to demonstrate the outcomes in each subgroup depicted in the algorithm due to small patient numbers. However, the results of our MVA support taking into account the PSA nadir and the Gleason score in addition to the PSADT when considering treatment for patients who demonstrate PSA failure. Finally, the morbidity of long-term AD therapy itself must be considered, because this treatment is not without risks. Side effects of hormone use include hot flashes, weight gain, fatigue, bone and muscle loss, and sexual dysfunction as well as cost. The benefits of early hormone use (increased time to the development of distant metastases) must be weighed against the risks (impotence, osteoporosis, muscle loss and weight gain). Cancer 2003;97:1127-33.