editorial comment

1
system disorders. Overview of physical and behavioral ho- meostasis. JAMA, 267: 1244, 1992 4. Sternberg, A. M., Chrousos, G. P., Wilder, R. L. et al: The stress response and the regulation of inflammatory disease. Ann Intern Med, 117: 854, 1992 5. Basbaum, A. I. and Levine, J. D.: The contribution of the nervous system to inflammation and inflammatory disease. Can J Physiol Pharmacol, 69: 647, 1991 6. Affleck, G., Urrows, S., Tennen, H. et al: A dual pathway model of daily stressor effects on rheumatoid arthritis. Ann Behav Med, 19: 161, 1997 7. Schmid-Ott, G., Jacobs, R., Jager, B. et al: Stress-induced endo- crine and immunological changes in psoriasis patients and healthy controls. A preliminary study. Psychother Psychosom, 67: 37, 1998 8. Cottone, M.: Stress and physical activity: are they risk factors for IBD? Ital J Gastroenterol Hepatol, 30: 252, 1998 9. Spanos, C., Pang, X., Ligris, K. et al: Stress-induced bladder mast cell activation: implications for interstitial cystitis. J Urol, 157: 669, 1997 10. Theoharides, T. C., Spanos, C. P., Pang, X. et al: Stress-induced intracranial mast cell degranulation. A corticotropin releasing hormone-mediated effect. Endocrinology, 136: 5745, 1995 11. Singh, L. K., Pang, X., Alexacos, N. et al: Acute immobilization stress triggers skin mast cell degranulation via corticotropin releasing hormone, neurotensin, and substance P: a link to neurogenic skin disorders. Brain Behav Immun, 13: 225, 1999 12. Simon, L. J., Landis, J. R., Erickson, D. R. et al: The Interstitial Cystitis Data Base Study: concepts and preliminary baseline descriptive statistics. Urology, suppl., 49: 64, 1997 13. Kirschbaum, C., Pirke, K. M. and Hellhammer, D. H.: Prelimi- nary evidence for reduced cortisol responsivity to psychological stress in women using oral contraceptive medication. Psycho- neuroendocrinology, 20: 509, 1995 14. Matthews, K. A., Caggiula, A. R., McAllister, C. G. et al: Sym- pathetic reactivity to acute stress and immune response in women. Psychosom Med, 57: 564, 1995 15. Pang, X., Cotreau-Bibbo, M. M., Sant, G. R. et al: Bladder mast cell expression of high affinity oestrogen receptors in patients with interstitial cystitis. Br J Urol, 75: 154, 1995 16. Saab, P. G., Matthews, K. A., Stoney, C. M. et al: Premenopausal and postmenopausal women differ in their cardiovascular and neuroendocrine responses to behavioral stressors. Psycho- physiology, 26: 270, 1989 17. Dyer, F. N.: The Stroop phenomenon and its use in the study of perceptual, cognitive, and response processes. Mem Cognit, 1: 106, 1973 18. Cohen, S., Kamarck, T. and Mermelstein, R.: A global measure of perceived stress. J Health Soc Behav, 24: 385, 1983 19. Spielberger, C. D., Gorsuch, R. L., Lushene, R. E. et al: The State-Trait Anxiety Inventory (Form Y). Palo Alto: Consulting Psychologists Press, 1970 20. Sutherland, H. J., Lockwood, G. A. and Cunningham, A. J.: A simple, rapid method for assessing psychological distress in cancer patients: evidence of validity for linear analog scales. J Psychosoc Oncol, 7: 31, 1989 21. Wilkie, D., Lovejoy, N., Dodd, M. et al: Cancer pain intensity measurement: concurrent validity of three tools—finger dyna- mometer, pain intensity number scale, visual analogue scale. Hosp J, 6: 1, 1990 22. Hohenfeller, M., Nunes, L., Schmidt, R. A. et al: Interstitial cystitis: increased sympathetic innervation and related neu- ropeptide synthesis. J Urol, 147: 587, 1992 23. Lundeberg, T., Liedberg, H., Nordling, L. et al: Interstitial cys- titis: correlation with nerve fibres, mast cells and histamine. Br J Urol, 71: 427, 1993 24. Stein, P. C., Torri, A. and Parsons, C. L.: Elevated urinary norepinephrine in interstitial cystitis. Urology, 53: 1140, 1999 25. Janig, W., Levine, J. D. and Michaelis, M.: Interactions of sym- pathetic and primary afferent neurons following nerve injury and tissue trauma. Prog Brain Res, 113: 161, 1996 26. Letourneau, R., Pang, X., Sant, G. R. et al: Intragranular acti- vation of bladder mast cells and their association with nerve processes in interstitial cystitis. Br J Urol, 77: 41, 1996 27. Theoharides, T. C. and Sant, G. R.: The mast cell as a neuroim- munoendocrine effector in interstitial cystitis. In: Interstitial Cystitis. Edited by G. R. Sant. Philadelphia: Lippincott-Raven, chapt. 12, pp. 101–108, 1997 28. Keller, J. T., Dimlich, R. V., Zuccarello, M. et al: Influence of the sympathetic nervous system as well as trigeminal sensory fibres on rat dural mast cells. Cephalalgia, 11: 215, 1991 29. Levine, J. D., Coderre, T. J., Helms, C. et al: Beta 2-adrenergic mechanisms in experimental arthritis. Proc Natl Acad Sci USA, 85: 4553, 1988 30. Sternberg, E. M.: Hyperimmune fatigue syndromes: diseases of the stress response? J Rheumatol, 20: 418, 1993 31. Webster, E. L., Torpy, D. J., Elenkov, I. J. et al: Corticotropin- releasing hormone and inflammation. Ann N Y Acad Sci, 840: 21, 1988 32. Castagliuolo, I., LaMont, J. T., Qiu, B. et al: Acute stress causes mucin release from rat colon: role of corticotropin releasing factor and mast cells. Am J Physiol, 271: G884, 1996 33. Hsieh, J.-C., Stahle-Backdahl, M., Hagermark, O. et al: Trau- matic nociceptive pain activates the hypothalamus and the periaquedeuctal gray: a positron emission tomography study. Pain, 64: 303, 1996 34. Manuck, S. B., Kasprowicz, A. L., Monroe, S. M. et al: Psycho- physiologic reactivity as a dimension of individual differences. In: Handbook of Research Methods in Cardiovascular Behav- ioral Medicine. Edited by N. Schneiderman, S. M. Weiss and P. G. Kaufmann. New York: Plenum Press, chapt. 23, pp. 365–382, 1989 EDITORIAL COMMENTS The authors designed a laboratory study to confirm objectively what many patients with interstitial cystitis and clinicians have long suspected, that is stress increases interstitial cystitis symptoms. Patients and controls were exposed to standard laboratory stress situations, and then pain and urgency scores were measured as well as physiological and psychological stress responses. The interstitial cystitis and control groups had similar physiological and psycholog- ical stress responses. However, the 2 groups had different bladder responses to stress. Controls had no change in pain or urgency with stress but patients with interstitial cystitis had increased pain and urgency during and after stress. The study makes an important contribution by demonstrating objectively that psychological stress increases interstitial cystitis symptoms. Also, this noninvasive laboratory test would be useful in future studies to define the mechanisms by which stress increases interstitial cystitis symptoms. The authors suggest several possible mechanisms. For example, stress involves the secretion of cortico- tropin releasing hormone, which is a potent activator of mast cell degranulation. Sympathetic nervous system activity may also induce mast cell degranulation. Stress also involves the release of norepi- nephrine, which may potentiate inflammation pain by inducing pros- taglandin release. These mechanisms may be tested by measuring urine and serum mediators. For example, to evaluate the role of mast cell degranulation one would measure urinary histamine and tryptase in patients and controls at baseline, during and after the laboratory stress test. After defining the mechanisms new interven- tions may be developed to block the stress induced exacerbation of interstitial cystitis symptoms. Deborah Erickson Department of Urology Milton S. Hershey Medical Center Hershey, Pennsylvania The authors confirm by a laboratory study what we all know from our medical practices, that is stress tends to intensify the symptom- atic expression of most diseases. Nowhere does this truism apply more than to interstitial cystitis. Their argument would have been strengthened if there had been an interstitial cystitis group with a nonstressful task to perform to serve as active controls. My impres- sion is that many healthy individuals have urinary frequency when in a stressful situation. A study similar to that of the authors may be modified to demonstrate the role that stress and sympathetic activity have in voiding behavior in the normal and diseased states. Since in many ways interstitial cystitis is an exaggeration of the symptoms universally experienced by persons with a full bladder, such infor- mation would prove useful. Philip M. Hanno 657 Augusta Ct. Berwyn, Pennsylvania STRESS AND SYMPTOMATOLOGY IN INTERSTITIAL CYSTITIS 1269

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system disorders. Overview of physical and behavioral ho-meostasis. JAMA, 267: 1244, 1992

4. Sternberg, A. M., Chrousos, G. P., Wilder, R. L. et al: The stressresponse and the regulation of inflammatory disease. AnnIntern Med, 117: 854, 1992

5. Basbaum, A. I. and Levine, J. D.: The contribution of the nervoussystem to inflammation and inflammatory disease. CanJ Physiol Pharmacol, 69: 647, 1991

6. Affleck, G., Urrows, S., Tennen, H. et al: A dual pathway modelof daily stressor effects on rheumatoid arthritis. Ann BehavMed, 19: 161, 1997

7. Schmid-Ott, G., Jacobs, R., Jager, B. et al: Stress-induced endo-crine and immunological changes in psoriasis patients andhealthy controls. A preliminary study. Psychother Psychosom,67: 37, 1998

8. Cottone, M.: Stress and physical activity: are they risk factors forIBD? Ital J Gastroenterol Hepatol, 30: 252, 1998

9. Spanos, C., Pang, X., Ligris, K. et al: Stress-induced bladdermast cell activation: implications for interstitial cystitis.J Urol, 157: 669, 1997

10. Theoharides, T. C., Spanos, C. P., Pang, X. et al: Stress-inducedintracranial mast cell degranulation. A corticotropin releasinghormone-mediated effect. Endocrinology, 136: 5745, 1995

11. Singh, L. K., Pang, X., Alexacos, N. et al: Acute immobilizationstress triggers skin mast cell degranulation via corticotropinreleasing hormone, neurotensin, and substance P: a link toneurogenic skin disorders. Brain Behav Immun, 13: 225, 1999

12. Simon, L. J., Landis, J. R., Erickson, D. R. et al: The InterstitialCystitis Data Base Study: concepts and preliminary baselinedescriptive statistics. Urology, suppl., 49: 64, 1997

13. Kirschbaum, C., Pirke, K. M. and Hellhammer, D. H.: Prelimi-nary evidence for reduced cortisol responsivity to psychologicalstress in women using oral contraceptive medication. Psycho-neuroendocrinology, 20: 509, 1995

14. Matthews, K. A., Caggiula, A. R., McAllister, C. G. et al: Sym-pathetic reactivity to acute stress and immune response inwomen. Psychosom Med, 57: 564, 1995

15. Pang, X., Cotreau-Bibbo, M. M., Sant, G. R. et al: Bladder mastcell expression of high affinity oestrogen receptors in patientswith interstitial cystitis. Br J Urol, 75: 154, 1995

16. Saab, P. G., Matthews, K. A., Stoney, C. M. et al: Premenopausaland postmenopausal women differ in their cardiovascular andneuroendocrine responses to behavioral stressors. Psycho-physiology, 26: 270, 1989

17. Dyer, F. N.: The Stroop phenomenon and its use in the study ofperceptual, cognitive, and response processes. Mem Cognit, 1:106, 1973

18. Cohen, S., Kamarck, T. and Mermelstein, R.: A global measure ofperceived stress. J Health Soc Behav, 24: 385, 1983

19. Spielberger, C. D., Gorsuch, R. L., Lushene, R. E. et al: TheState-Trait Anxiety Inventory (Form Y). Palo Alto: ConsultingPsychologists Press, 1970

20. Sutherland, H. J., Lockwood, G. A. and Cunningham, A. J.: Asimple, rapid method for assessing psychological distress incancer patients: evidence of validity for linear analog scales.J Psychosoc Oncol, 7: 31, 1989

21. Wilkie, D., Lovejoy, N., Dodd, M. et al: Cancer pain intensitymeasurement: concurrent validity of three tools—finger dyna-mometer, pain intensity number scale, visual analogue scale.Hosp J, 6: 1, 1990

22. Hohenfeller, M., Nunes, L., Schmidt, R. A. et al: Interstitialcystitis: increased sympathetic innervation and related neu-ropeptide synthesis. J Urol, 147: 587, 1992

23. Lundeberg, T., Liedberg, H., Nordling, L. et al: Interstitial cys-titis: correlation with nerve fibres, mast cells and histamine.Br J Urol, 71: 427, 1993

24. Stein, P. C., Torri, A. and Parsons, C. L.: Elevated urinarynorepinephrine in interstitial cystitis. Urology, 53: 1140, 1999

25. Janig, W., Levine, J. D. and Michaelis, M.: Interactions of sym-pathetic and primary afferent neurons following nerve injuryand tissue trauma. Prog Brain Res, 113: 161, 1996

26. Letourneau, R., Pang, X., Sant, G. R. et al: Intragranular acti-vation of bladder mast cells and their association with nerveprocesses in interstitial cystitis. Br J Urol, 77: 41, 1996

27. Theoharides, T. C. and Sant, G. R.: The mast cell as a neuroim-munoendocrine effector in interstitial cystitis. In: InterstitialCystitis. Edited by G. R. Sant. Philadelphia: Lippincott-Raven,chapt. 12, pp. 101–108, 1997

28. Keller, J. T., Dimlich, R. V., Zuccarello, M. et al: Influence of thesympathetic nervous system as well as trigeminal sensoryfibres on rat dural mast cells. Cephalalgia, 11: 215, 1991

29. Levine, J. D., Coderre, T. J., Helms, C. et al: Beta 2-adrenergicmechanisms in experimental arthritis. Proc Natl Acad SciUSA, 85: 4553, 1988

30. Sternberg, E. M.: Hyperimmune fatigue syndromes: diseases ofthe stress response? J Rheumatol, 20: 418, 1993

31. Webster, E. L., Torpy, D. J., Elenkov, I. J. et al: Corticotropin-releasing hormone and inflammation. Ann N Y Acad Sci, 840:21, 1988

32. Castagliuolo, I., LaMont, J. T., Qiu, B. et al: Acute stress causesmucin release from rat colon: role of corticotropin releasingfactor and mast cells. Am J Physiol, 271: G884, 1996

33. Hsieh, J.-C., Stahle-Backdahl, M., Hagermark, O. et al: Trau-matic nociceptive pain activates the hypothalamus and theperiaquedeuctal gray: a positron emission tomography study.Pain, 64: 303, 1996

34. Manuck, S. B., Kasprowicz, A. L., Monroe, S. M. et al: Psycho-physiologic reactivity as a dimension of individual differences.In: Handbook of Research Methods in Cardiovascular Behav-ioral Medicine. Edited by N. Schneiderman, S. M. Weiss andP. G. Kaufmann. New York: Plenum Press, chapt. 23, pp.365–382, 1989

EDITORIAL COMMENTS

The authors designed a laboratory study to confirm objectivelywhat many patients with interstitial cystitis and clinicians have longsuspected, that is stress increases interstitial cystitis symptoms.Patients and controls were exposed to standard laboratory stresssituations, and then pain and urgency scores were measured as wellas physiological and psychological stress responses. The interstitialcystitis and control groups had similar physiological and psycholog-ical stress responses. However, the 2 groups had different bladderresponses to stress. Controls had no change in pain or urgency withstress but patients with interstitial cystitis had increased pain andurgency during and after stress.

The study makes an important contribution by demonstratingobjectively that psychological stress increases interstitial cystitissymptoms. Also, this noninvasive laboratory test would be useful infuture studies to define the mechanisms by which stress increasesinterstitial cystitis symptoms. The authors suggest several possiblemechanisms. For example, stress involves the secretion of cortico-tropin releasing hormone, which is a potent activator of mast celldegranulation. Sympathetic nervous system activity may also inducemast cell degranulation. Stress also involves the release of norepi-nephrine, which may potentiate inflammation pain by inducing pros-taglandin release. These mechanisms may be tested by measuringurine and serum mediators. For example, to evaluate the role of mastcell degranulation one would measure urinary histamine andtryptase in patients and controls at baseline, during and after thelaboratory stress test. After defining the mechanisms new interven-tions may be developed to block the stress induced exacerbation ofinterstitial cystitis symptoms.

Deborah EricksonDepartment of UrologyMilton S. Hershey Medical CenterHershey, Pennsylvania

The authors confirm by a laboratory study what we all know fromour medical practices, that is stress tends to intensify the symptom-atic expression of most diseases. Nowhere does this truism applymore than to interstitial cystitis. Their argument would have beenstrengthened if there had been an interstitial cystitis group with anonstressful task to perform to serve as active controls. My impres-sion is that many healthy individuals have urinary frequency whenin a stressful situation. A study similar to that of the authors may bemodified to demonstrate the role that stress and sympathetic activityhave in voiding behavior in the normal and diseased states. Since inmany ways interstitial cystitis is an exaggeration of the symptomsuniversally experienced by persons with a full bladder, such infor-mation would prove useful.

Philip M. Hanno657 Augusta Ct.Berwyn, Pennsylvania

STRESS AND SYMPTOMATOLOGY IN INTERSTITIAL CYSTITIS 1269