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

Over a period of 4 years, 20 patients suffering from severe forms of psoriasis (erythrodermic, sub-erythrodermic, resistant generalized forms and/or forms associated with acute arthropathy) were treated with 96 h of continuous i.v. infusion of somatostatin (Stilamin, Serono) diluted in D5W at 250 micrograms/h. In addition to the usual blood chemistry parameters, circadian levels of growth hormone (GH) and epidermal growth factor (EGF) were measured before, during, and after therapy. Approximately 2-3 weeks after termination of therapy, erythrodermic and suberythrodermic symptoms had disappeared. In some patients, a few lesions of psoriasis vulgaris remained, although they were much less severe. Remission of acute arthropathy was impressive. Blood chemistry parameters were unchanged after therapy. Circadian levels of GH and EGF, normal before therapy, were significantly decreased after therapy. The infusion was well-tolerated. Infusion rates of greater than 250 micrograms/h caused only some complaints of abdominal pain, nausea, and vomiting. During the 4 years, erythrodermic symptoms reappeared only in seven patients, three of whom were also arthropathic. After 6-8 months, they underwent a second course of somatostatin therapy with good results. The other patients are still able to control their disease with tar-based products alone or with low-dose 8-methoxypsoralen + UVA (PUVA) or UV therapy. The arthropathic patients control their symptoms with periodic low-dose nonsteroidal antiinflammatory drug therapy.
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PMID:Treatment of severe psoriasis with somatostatin: four years of experience. 290 Jun 24

In 59 patients suffering from chronic psoriasis, we tested the therapeutic effects of yohimbine and colchicine. It is well known that yohimbine, an alpha 2-adrenoceptor-blocking agent, reduces the secretion of insulin and the platelet factors. 85% of our psoriatic patients showed decreased values for somatostatin, in association with hyperinsulinemia (88%) and low platelet counts. Successful therapy with yohimbine resulted in the normalization of the pathological blood levels.
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PMID:[Somatostatin deficiency, hyperinsulinism and thrombocyte aggregation in psoriasis]. 290 97

In previous investigations we observed an increase of growth hormone (HGH) in the blood serum of patients suffering from various clinical forms of psoriasis. The skin lesions disappeared in about 70% when treated systemically with somatostatin and/or bromocriptine, which are inhibitors of HGH secretion. These findings suggested a post mortem investigation of the pituitary glands of 10 patients who had suffered from psoriasis or psoriatic arthritis. Using histochemical and immunochemical methods, we investigated the distribution of cells producing HGH, PRL, LH or FSH. In all 10 pituitary glands we found hyperplasia of the HGH cells, whereas cells producing LH, TSH, FSH and PRL had a normal distribution. The pituitary glands of controls showed no accumulation or hyperplasia of HGH cells.
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PMID:[Hyperplasia of growth hormone-producing cells in the hypophysis in psoriasis. Study of 10 patients]. 353 Oct 93

First report on nine patients suffering from psoriasis who were treated with somatostatin or bromocriptin or both. These are inhibitors of HGH. The therapeutical effect on skin lesions and psoriatic alterations to joints is described.
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PMID:Psoriasis and human growth hormone: aetiology and therapy. 611 17

In 22 of 26 patients suffering from psoriasis the drip infusion therapy with Somatostatin, an inhibitor of the human growth hormone (HGH), leads to complete or partial remission of skin lesions. Fast reduction of joint pains in arthropathic psoriasis could be observed in four of four patients. The repeated measurement of HGH blood level showed a decrease of HGH in five cases following the Somatostatin therapy combined with the clinical remission.
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PMID:Treatment of psoriasis with somatostatin. 613 48

Somatostatin treatment was administered to 20 psoriatic patients according to the following protocol: Continuous infusion (250 micrograms/h) for at least 2 days followed either by short infusions (1 h) at 8 A.M. and 8 P.M. (12 cases) or by repeating the initial 2-day infusion (eight patients). Before treatment (day 0) and on day 6, biopsy specimens were taken for routine examination (12 patients) and for ultrastructure (seven patients). In vitro immunological studies were carried out on peripheral blood lymphocytes (six patients) on day 0 and day 8. In two patients, somatostatin was stopped because of serious side effects. Thus, clinical results were evaluated in 18 patients, on day 30. In ten of them no improvement whatsoever occurred, two had a partial clearing and an almost complete remission was achieved in six others. Ultrastructural studies showed, on day 6, enlargement of the intercellular spaces with deposits of granular material of glucidic composition, associated with features of cellular damage. Percentages of T and B cells were unmodified but a significant depression of mitogenic stimulation by PHA and ConA was clearly observed on day 8. Even if somatostatin treatment may have a beneficial effect in some patients it seems much less valid than other well-known therapies for psoriasis.
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PMID:Somatostatin treatment of psoriasis. 613 49

Peptide T, the HIV envelope-derived fragment Ala-Ser-Thr-Thr-Thr-Asn-Tyr-Thr, has already been used to successfully treat psoriatic patients without major side-effects. The underlying reason for the positive effect is, however, at present unknown. In the following minireview, we summarize today's knowledge regarding peptide T's interaction with other chemical messenger molecules, such as somatostatin, vasoactive intestinal polypeptide (VIP) and epidermal growth factor (EGF), within the human skin, and, finally, speculate about their relationship to each other. In summary, we believe that the clearance effect of peptide T on psoriasis will open up new avenues with regard to the concept of the pathogenesis of as well as the clinical attendance to this disease.
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PMID:Speculations around the mechanism behind the action of peptide T in the healing of psoriasis: a minireview. 790 47

Peptide T has been shown to be an effective treatment in psoriasis. The mechanism through which peptide T works in psoriasis is at present unknown. Furthermore, a clearance of psoriasis has also been registered using the inhibitory peptide somatostatin. These observations all focus on the fact that peptide T, somatostatin, and/or other peptides, might provide a clue to understanding the etiology and pathogenesis of psoriasis. Therefore, the effect of peptide T administration on somatostatin containing cutaneous cell populations was investigated. Ten psoriatic patients were treated with peptide T (D-Ala-peptide T amide; 2 mg/day i.v.) for 28 days. Serial biopsies were obtained from the psoriatic lesions before, once weekly during and 4 weeks after discontinuation of the peptide T treatment. An indirect immunofluorescence procedure was performed using a polyclonal antiserum against somatostatin. Clinically, most of the patients responded successfully to the treatment. Immunohistochemical investigations of the serial biopsies revealed the appearance of extensive changes in the number of dermal somatostatin immunoreactive dendritic cells. We believe that peptide T may stimulate the local synthesis and/or release of somatostatin, or proliferation and/or migration of certain dendritic cell populations in psoriatic lesions during healing. Since the benefits of peptide T treatment of psoriatic patients parallel earlier investigations using somatostatin infusions, it is likely that somatostatin given exogenously or synthesized/released endogenously plays a vital role in inducing the healing process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatostatin immunoreactive cells in lesional psoriatic human skin during peptide T treatment. 791 13

The concept of neuro-immuno-cutaneous system (NICS) means narrow interrelations between nervous system, immunity and skin. Indeed, there are numerous cellular contacts between nerve fibers, cutaneous cells and immune cells; cutaneous cells can synthesize neuromediators and they express receptors to these molecules; neuromediators are able to modulate functions of cutaneous and/or immune cells. Using confocal or electron microscopy, connexions between nerve fibers and cutaneous cells have been observed. In the skin, nerve fibers may secrete neuromediators: substance P, vaso-active intestinal peptide (VIP), somatostatin, calcitonin-gene related peptide (CGRP), gastrin-releasing peptide (GRP), neuropeptide Y, peptide histidine-isoleucine (PHI), neurotensin, neurokinins A et B, bradykinin, acetylcholine, catecholamines, endorphins and enkephalins. Neurohormones such as prolactin, melano-stimulating hormone (MSH) or adreno-corticotrophic hormone (ACTH) are also expressed in the skin. Neuromediators and neurohormones are also secreted by cutaneous cells and these cells express receptors. Functions of epidermal or dermal cells are modulated by these substances. Immune cells transiently present in the skin (macrophages, lymphocytes...) are modulated by neuromediators through receptors. In the course of skin diseases, especially inflammatory diseases, the NICS is destabilized. Psoriasis and atopic dermatitis are good examples. This phenomenon might be due to inflammation but is also responsible for induction and maintenance of the inflammation.
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PMID:[Neuro-immuno-cutaneous system (NICS)]. 915 66

Neuropeptides (NP) are a heterogeneous group of proteins functioning as neurotransmitters, neuromodulators and neurohormones. More than fifty of these molecules have been described, and some have been detected in human skin through immunochemistry and radioimmunoassay. In this article we attempt to study the role played by some of these substances such as substance P (SP), calcitonin gene related peptide (CGRP), neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), somatostatin (S), and neurotensin (N). Several NP induce inflammatory response with edema and erythema. They can also induce the release of histamine by mastocytes, regulate cutaneous blood flow, and participate in sweat regulation and nociception. They also exert their action over several cells that participate in immunity, acting as mitotic, and chemotactic factors, inhibiting or stimulating inflammatory mechanisms. Specific NP have their receptors on epidermal cells. We will also try to study certain diseases in which NP play an important role in inducing or alleviating lesions, such as psoriasis, atopic eczema, alopecia areata, vitiligo, nodular prurigo, aquagenic pruritus, hypertrophic scars and other entities.
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PMID:[Role of neuropeptides in dermatology]. 927 66


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