Intrathecal somatostatin in terminally ill patients. A report of two cases

Meynadier, J.; Chrubasik, J.; Dubar, M.; Wünsch, Erich

doi:10.1016/0304-3959(85)90224-6

Cited by 76 publications

(16 citation statements)

References 14 publications

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“…Most patients showed subjective improvement, especially a decrease in pain, which improvement might be caused by the analgetic effect of somatostatin (analogues) (Chrubasik et al, 1984;Meynadier et al, 1985). The observed slight steatorrhea is a consequence of the inhibitory effect of somatostatin (analogue) treatment on exocrine pancreatic and gastrointestinal function (Reichlin, 1983a,b).…”

Section: Discussionmentioning

confidence: 99%

Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects

Klijn

Hoff²,

Planting³

et al. 1990

Br J Cancer

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Summary Somatostatin analogues can suppress the secretion of some gastrointestinal hormones and growth factors involved in the growth regulation of gastrointestinal cancers and can inhibit the growth of experimental pancreatic tumours. Therefore, in a phase II study 34 patients with metastatic pancreatic (n = 14), colorectal (n = 16) and gastric cancer (n = 4) were treated with three daily subcutaneous injections of 100-200 lAg of the somatostatin analogue Sandostatin . All patients had an extensive tumour load and 13 were pretreated with chemotherapy. Before Sandostatin treatment the patients with pancreatic cancer showed a higher mean plasma concentration of GH (P<0.05) and a lower concentration of 'total' somatomedin-C (P < 0.005) compared with patients with colorectal cancer; there was no significant difference betwen these two groups in plasma levels of directly assayable somatomedin-C, EGF/TGF-a, insulin and prolactin. Within 3 days after start of treatment, somatomedin-C levels initially decreased (without a change in basal plasma GH levels), but returned to pretreatment levels within 4-13 weeks. Plasma insulin levels also were suppressed but only during the first 3-5 days of treatment. Plasma EGF-TGF-a levels increased significantly at day 5 of treatment only in the pancreatic cancer patients. Twenty-seven per ceht of the patients showed stable disease for 3-9 months, but most patients experienced subjective improvement in the absence of serious side-effects. However, the overall survival remained disappointing, emphasising the need for better treatment regimens.

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Section: Discussionmentioning

confidence: 99%

Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects

Klijn

Hoff²,

Planting³

et al. 1990

Br J Cancer

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“…Third, intrathecally applied SOM inhibits motor reflexes in response to noxious stimuli and reduces c-Fos expression and mechanical hyperalgesia in neuropathic pain model (Mollenholt et al, 1988;Tsai et al, 2002). Finally, SOM has been shown to be analgesic when given systemically to patients with cluster headache, or when given intrathecally to patients with cancer pain or postoperative pain (Sicuteri et al, 1984;Chrubasik et al, 1985;Meynadier et al, 1985;Penn et al, 1992;Paice et al, 1996). Collectively, these findings suggest that SOM plays a significant role in the transmission of nociceptive information.…”

Section: Introductionmentioning

confidence: 92%

Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats

Jung

Lee

et al. 2008

Korean J Physiol Pharmacol

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Somatostatin (SOM) is a widely distributed peptide in the central nervous system and exerts a variety of hormonal and neural actions. Although SOM is assumed to play an important role in spinal nociceptive processing, its exact function remains unclear. In fact, earlier pharmacological studies have provided results that support either a facilitatory or inhibitory role for SOM in nociception. In the current study, the effects of SOM were investigated using anesthetized cats. Specifically, the responses of rostrally projecting spinal dorsal horn neurons (RPSDH neurons) to different kinds of noxious stimuli (i.e., heat, mechanical and cold stimuli) and to the Aδ -and C-fiber activation of the sciatic nerve were studied. Iontophoretically applied SOM suppressed the responses of RPSDH neurons to noxious heat and mechanical stimuli as well as to C-fiber activation. Conversely, it enhanced these responses to noxious cold stimulus and Aδ -fiber activation. In addition, SOM suppressed glutamate-evoked activities of RPSDH neurons. The effects of SOM were blocked by the SOM receptor antagonist cyclo-SOM. These findings suggest that SOM has a dual effect on the activities of RPSDH neurons; that is, facilitation and inhibition, depending on the modality of pain signaled through them and its action site.

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“…First, SRIF is localized in a subset of small-diameter dorsal root ganglion (DRG) cells (Hökfelt et al, 1975). Second, activation of SRIF receptors results in inhibition of both nociceptive behaviors in animals (Eschalier et al, 1991;Chapman and Dickenson, 1992;Corsi et al, 1997;Carlton et al, 2001) (but see Hitosugi et al, 1999;Kamei et al, 1999) and acute and chronic pain in humans Meynadier et al, 1985;Plourde et al, 1993;Taura et al, 1994;Paice et al, 1996). Third, SRIF inhibits dorsal horn neuronal activity (Randic and Miletic, 1978;Miletic and Randic, 1982;Murase et al, 1982;Sandkuhler et al, 1990).…”

Section: Abstract: Primary Afferent; Nociception; Inhibitory Peptidementioning

confidence: 99%

Tonic Control of Peripheral Cutaneous Nociceptors by Somatostatin Receptors

Carlton

Zhou

et al. 2001

J. Neurosci.

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The peptide somatostatin [somatotropin release-inhibiting factor (SRIF)] is widely distributed in the body and exerts a variety of hormonal and neural actions. Several lines of evidence indicate that SRIF is important in nociceptive processing: (1) it is localized in a subset of small-diameter dorsal root ganglion cells; (2) activation of SRIF receptors results in inhibition of both nociceptive behaviors in animals and acute and chronic pain in humans; (3) SRIF inhibits dorsal horn neuronal activity; and (4) SRIF reduces responses of joint mechanoreceptors to noxious rotation of the knee joint. The goal of the present study is to show that cutaneous nociceptors are under the tonic inhibitory control of SRIF. This is accomplished using behavioral and electrophysiological paradigms. In a dose-dependent manner, intraplantar injection of the SRIF receptor antagonist cyclosomatostatin (c-SOM) results in nociceptive behaviors in normal animals and enhancement of nociceptive behaviors in formalin-injected animals, and these actions can be blocked when c-SOM is coapplied with three different SRIF agonists. Furthermore, intraplantar injection of SRIF antiserum also results in nociceptive behaviors. Electrophysiological recordings using an in vitro glabrous skin-nerve preparation show increased nociceptor activity in response to c-SOM, and this increase is blocked by the same three SRIF agonists. Parallel behavioral and electrophysiological studies using the opioid antagonist naloxone demonstrate that endogenous opioids do not maintain a tonic inhibitory control over peripheral nociceptors, nor does opioid receptor antagonism influence peripheral SRIF effects on nociceptors. These findings demonstrate that SRIF receptors maintain a tonic inhibitory control over peripheral nociceptors, and this may contribute to mechanisms that control the excitability of these terminals.

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Intrathecal somatostatin in terminally ill patients. A report of two cases

Cited by 76 publications

References 14 publications

Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects

Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects

Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats

Tonic Control of Peripheral Cutaneous Nociceptors by Somatostatin Receptors

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