Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin peptide analogs have revolutionized the medical treatment of patients with acromegaly. More recent deep intramuscular depot preparations have further improved control, with consistent suppression of growth hormone secretion and optimal lowering of insulin-like growth factor-1. Effective control of growth hormone should, with long-term use, reduce morbidity and mortality from acromegaly and has been shown to result in partial involution of the pituitary adenoma in the majority of treated patients. The currently available depot formulations allow for an injection frequency of 14 days (lanreotide LA 30mg) to 28 days (octreotide LAR 20mg) according to the manufacturers' recommendations. In clinical practice, dose titration by evaluating a growth hormone day profile prior to the next injection can extend the interval between injection (to 6 or even 8 weeks in certain individuals). This is especially true for octreotide LAR, which also has increased flexibility regarding dosage with a 10 and 30mg preparation. The annual 'drug cost' is broadly similar between the two formulations though the additional expenditure on nurse time and clinic visits incurred by an increased injection frequency is a significant consideration. Decreased injection frequency improves acceptability for the patient without a loss in treatment efficacy. A subjective return of typical acromegalic symptoms, such as sweating and headache, also seem to be useful in predicting the timing of the next injection. Other formulations and doses of lanreotide are currently being evaluated, but more interestingly, newer analogs with greater efficacy at the type 5 somatostatin receptor subtype, and pan-receptor analogs, are being developed. These peptides, in conjunction with the likely availability of a growth hormone receptor blocking agent (pegvisomant), will further expand the medical therapy options for patients with acromegaly.
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PMID:Optimizing somatostatin analog therapy in acromegaly: long-acting formulations. 1579 7

The clinical characteristics of 84 patients with pituitary tumour who had troublesome headache were investigated. The patients presented with chronic (46%) and episodic (30%) migraine, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT; 5%), cluster headache (4%), hemicrania continua (1%) and primary stabbing headache (27%). It was not possible to classify the headache according to International Headache Society diagnostic criteria in six cases (7%). Cavernous sinus invasion was present in the minority of presentations (21%), but was present in two of three patients with cluster headache. SUNCT-like headache was only seen in patients with acromegaly and prolactinoma. Hypophysectomy improved headache in 49% and exacerbated headache in 15% of cases. Somatostatin analogues improved acromegaly-associated headache in 64% of cases, although rebound headache was described in three patients. Dopamine agonists improved headache in 25% and exacerbated headache in 21% of cases. In certain cases, severe exacerbations in headache were observed with dopamine agonists. Headache appears to be a significant problem in pituitary disease and is associated with a range of headache phenotypes. The presenting phenotype is likely to be governed by a combination of factors, including tumour activity, relationship to the cavernous sinus and patient predisposition to headache. A proposed modification of the current classification of pituitary-associated headache is given.
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PMID:The clinical characteristics of headache in patients with pituitary tumours. 1588 39

Somatostatin is a neuromodulator in the central nervous system and is involved in the regulation of metabolic and neuroendocrine functions. Recent experimental and clinical findings point to a role for somatostatin in the central processing of nociception. We studied the effects of somatostatin receptor modulation in the posterior hypothalamic area (PH) of the rat on dural nociceptive input. Somatostatin (10 microg/microl) and the somatostatin antagonist cyclo-somatostatin (50 microg/microl) were microinjected into the PH and the effects on responses of neurons in the trigeminal subnucleus caudalis studied. Injection of somatostatin (n=11) did not affect A- and C-fibre responses to dural electrical stimulation, nor was spontaneous activity altered (P>0.05). Injection of cyclo-somatostatin (n=10) into the PH reduced A-(-35.5+/-5.8%) and C-fibre (-43.1+/-7.5%) responses to dural stimulation and resulted in decreased spontaneous activity (-38.1+/-7.3%, P<0.05). Responses to facial thermal stimulation were decreased by 51.2+/-5.8% (n=5). Control injections had no significant effect (n=9). Blockade of somatostatin receptors in the PH has an anti-nociceptive effect on dural and facial input, probably mediated via GABAergic mechanisms. As somatostatin is also involved in hypothalamic regulation of metabolic, neuroendocrine and autonomic functions, somatostatin receptor mechanisms in the PH may play a role in the pathophysiology of primary headache disorders, such as migraine or cluster headache.
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PMID:Inhibition of nociceptive dural input in the trigeminal nucleus caudalis by somatostatin receptor blockade in the posterior hypothalamus. 1604 93

The aim of the present study was to verify cerebrospinal fluid (CSF) levels of glial cell line-derived neurotrophic factor (GDNF) and somatostatin, both measured by sensitive immunoassay, in: 16 chronic migraine (CM) patients, 15 patients with an antecedent history of migraine without aura diagnosed as having probable chronic migraine (PCM) and probable analgesic-abuse headache (PAAH), 20 patients affected by primary fibromyalgia syndrome (PFMS), and 20 control subjects. Significantly lower levels of GDNF and somatostatin were found in the CSF of both CM and PCM + PAAH patients compared with controls (GDNF =P < 0.001, P < 0.002; somatostatin = P < 0.002, P < 0.0003), without significant difference between the two groups. PFMS patients, with and without analgesic abuse, also had significantly lower levels of both somatostatin and GDNF (P < 0.0002, P < 0.001), which did not differ from those of CM and PCM + PAAH patients. A significant positive correlation emerged between CSF values of GDNF and those of somatostatin in CM (r = 0.70, P < 0.02), PCM + PAAH (r = 0.78, P < 0.004), and PFMS patients (r = 0.68, P < 0.008). Based on experimental findings, it can be postulated that reduced CSF levels of GDNF and somatostatin in both CM and PCM + PAAH patients can contribute to sustained central sensitization underlying chronic head pain. The abuse of simple or combination analgesics does not seem to influence the biochemical changes investigated, which appear to be more strictly related to the chronic pain state, as demonstrated also for fibromyalgia.
Cephalalgia 2006 Apr
PMID:Glial cell line-derived neurotrophic factor and somatostatin levels in cerebrospinal fluid of patients affected by chronic migraine and fibromyalgia. 1655 41

The history of the scientific ideas and events that led to the discovery of sumatriptan is outlined with personal reminiscences about individuals who influenced the approach. The development of sumatriptan revolutionized the acute treatment of migraine and led to the availability of a number of other triptans. The anti-migraine effects of all the triptans are mediated via 5-HT(1B), and possibly 5-HT(1D) receptors, which transduce their effects via G; proteins. This suggests that agonists at other G(i) protein-coupled receptor types appropriately located (eg, somatostatin sst(2), adenosine A(1)) should be examined for their effects on the trigeminovascular system, Studies on such receptor targets may provide insight into a novel approach towards the design of new anti-migraine drugs.
Headache 2007 Apr
PMID:The discovery of a new drug class for the acute treatment of migraine. 1742 4

Herein we report a rare case of a pituitary metastasis from a neuroendocrine tumour mimicking an adenoma. Moreover, starting from this unusual case, the relevant literature concerning the diagnosis and management of patients with metastasis at pituitary level is reviewed. A 69-year-old woman was admitted to our Unit for severe headache, diplopia, and critical visual field impairment. MRI showed a large pituitary mass compressing the optic chiasm and infiltrating the cavernous sinus. Trans-sphenoidal biopsy revealed a pituitary metastasis from a neuroendocrine tumour, in line with the multiple liver lesions that were already considered metastases from an ileal primary neuroendocrine tumour. In vitro receptor characterisation of both pituitary and liver tissues by immunohistochemistry showed a heterogeneous somatostatin receptor subtype pattern, with a predominant expression of sst(2) within the pituitary lesion. However, the liver metastasis receptor profile was completely different from the pituitary. Octreotide LAR was administered first, followed by receptor radiometabolic therapy with radiolabelled somatostatin analogues ((90)Y-DOTATOC and (177)Lu-DOTATATE). After 16 months, MRI showed a significant shrinkage of the sellar mass. Moreover, disappearance of diplopia and visual defects, together with a considerable improvement in quality of life were gradually recorded. To our knowledge, this is the first case of combined treatment using "cold" and radiolabelled octreotide in a pituitary metastasis from a neuroendocrine tumour.
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PMID:Treatment of a pituitary metastasis from a neuroendocrine tumour: case report and literature review. 1745 1

Juvenile cystinosis was diagnosed in a patient who presented with severe headache attacks and photophobia. Treatment with oral cysteamine and topical cysteamine eye drops was started. One-and-a-half years later, he developed unilateral gynecomastia and elevated prolactin and growth hormone levels. A pituitary macroprolactinoma was discovered and successfully treated with the dopamine agonist cabergoline. Increased serum growth hormone levels were attributed to enhanced growth hormone production by the prolactinoma and somatostatin inhibition by cysteamine. Although the occurrence of prolactinoma in this patient could be a simple coincidence, it might also be a rare yet unrecognised complication of cystinosis.
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PMID:Growth hormone producing prolactinoma in juvenile cystinosis: a simple coincidence? 1763 22

Neuroendocrine tumor metastases to the pituitary gland are very rare. There are few case reports of carcinoid tumor metastases to the pituitary, but no cases of pancreatic neuroendocrine pituitary metastases have been reported. In this report we present a 55-year-old female with a sellar mass, ophthalmoplegia and headaches initially thought to represent an invasive null cell pituitary adenoma. However a histological (trans-sphenoidal and liver biopsies) and systemic investigation proved it to be a metastasis of an undiagnosed pancreatic neuroendocrine tumor. Our patient was unique in respect to the location of the metastasis and the uncharacteristically high proliferative index of her tumor. She received conventional therapy consisting of Sandostatin, chemotherapy and radiotherapy as well as labeled somatostatin following an avid uptake on octreotide scanning. Despite a radiological improvement the patient suffered progressive clinical deterioration and died.
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PMID:Metastatic pancreatic neuroendocrine tumor presenting as a pituitary space occupying lesion: a case report. 1763 85

Pituitary tumors come to clinical attention due to endocrine dysfunction, distortion of local structures surrounding the pituitary fossa, or as an incidental finding during neuroimaging for headache. Explanations for pituitary tumor-associated headache include stretching of the dura mater and invasion of pain-producing structures within the cavernous sinus. However, small functional pituitary lesions may present with severe headache without cavernous sinus invasion or suprasellar extension. Prolactinomas and growth hormone-secreting tumors have a high prevalence of rare headache phenotypes with or without autonomic features, suggesting that biochemical abnormalities within the hypothalamo-pituitary axis may play a role in headache. Somatostatin analogues may be highly effective at aborting headache associated with functionally active pituitary lesions, particularly in the case of acromegaly. A proposed mechanism for this is inhibition of nociceptive peptides. This article summarizes the clinical features, pathophysiology, and potential treatment approaches to pituitary tumor-associated headache.
Curr Pain Headache Rep 2008 Jan
PMID:Chronic headache and pituitary tumors. 1841 28

Surgery is the first-line treatment of patients with clinically non-functioning pituitary adenomas (NFAs). Because of lack of clinical syndrome these tumours are diagnosed with a variable delay, when patients suffer from compression symptoms (hypopituitarism, headache and visual field defects) due to the extension of the tumour outside the pituitary fossa. Surgery is followed by residual tumour tissue in most patients. In these cases, radiotherapy is generally used to prevent tumour regrowth. However, NFA cell membranes, in analogy with GH- and PRL-secreting adenomas, express somatostatin and dopamine receptors. Treatment with somatostatin analogues (SSA) and dopamine agonists (DA) induced some beneficial effects on visual field defects and was also followed by tumour shrinkage in a minority of cases. DA seem to be more effective on tumour shrinkage than SSA. More recently, a combination treatment with both SSA and DA have been tested in a few patients with interesting results. Lack of randomized, placebo-controlled trials prevents any conclusion on the efficacy of these drugs. By contrast, use of gonatotrophin-releasing hormone analogues has been abandoned.
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PMID:Medical therapy for clinically non-functioning pituitary adenomas. 1878 Jul 96


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