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)

A 60-year-old male patient was admitted due to protracted systemic pruritus and erythema for 3 years without an obvious dermatologic cause, which exacerbated in the past 3 months, along with weight loss and diarrhoea. He had significant fasting hyperglycemia and dramatically elevated serum glucagon level in biochemical examination. Elevated chromogranin A (CgA) and neuron-specific enolase (NSE) levels were also manifested, whereas carbohydrate antigen 19-9 (CA-199) and carcinoembryonic antigen (CEA) were unremarkable. His skin presented with necrolytic migratory erythema (NME), anemia and other morphologies. Both ultrasound and computed tomography imaging revealed a space-occupying lesion in the distal pancreas and inferior vena caval thrombosis. Preoperative preparations included parenteral nutrition support, somatostatin analog treatment and inferior vena cava filter placement. Then, the patient had performed distal pancreatectomy with splenectomy with regional lymph node dissection to achieve primary R0/R1 resection. Pathology indicated a neuroendocrine tumor in distal pancreas, with spleen involved and regional lymph nodes metastases. Immunohistochemistry revealed that neuroendocrine tumor areas were diffusely positive for SSR2, SSR5, SYN and CgA. Postoperatively, skin symptoms disappear and cured without reoccurrence and blood glucose levels returned to the normal range. The postoperative surveillance was indicated after surgery for their high relapse rate and malignant behavior.
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PMID:Glucagonoma syndrome: report of one case. 2813 36

Necrolytic migratory erythema (NME) is a rare skin disorder that is a cutaneous manifestation of the glucagonoma syndrome. It presents with annular eruptions of migrating erythematous papules and plaques with superficial epidermal necrosis, central flaccid bullae, and crusted erosions located primarily in the intertriginous areas. Treatment with the long-acting somatostatin analog Octreotide is a potential therapy to help ameliorate skin symptoms. We present a case of a patient with a 1-year history of a pancreatic glucagonoma that developed an ulcerated, plaque-like, weeping rash over multiple areas of their body despite current treatment with Octreotide and stable pancreatic tumor staging. The patient had a similar rash when initially diagnosed with a glucagonoma, and it quickly improved after Octreotide treatment. Clinical examination and biopsy were consistent with necrolytic migratory erythema due to an underlying glucagonoma. This rare case adds to our understanding of the clinical presentation of NME, as well as highlights the relapsing and remitting course, even if the underlying pancreatic tumor is stable and the patient is undergoing treatment.
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PMID:A review of cutaneous manifestations within glucagonoma syndrome: necrolytic migratory erythema. 2945 Aug 80

A 70-year-old man reported progressive weight loss, fatigue and a generalised rash. The rash was consistent with necrolytic migratory erythema, further investigations were performed and the patient was diagnosed with a mass in the tail of the pancreas, in keeping with a localised glucagonoma. Somatostatin analogue therapy was started for symptom control, leading to complete resolution of the skin rash and an improvement in constitutional symptoms. Subsequently, the pancreatic lesion was excised, and pathology assessment confirmed the diagnosis of well-differentiated neuroendocrine tumour with high expression of glucagon compatible with glucagonoma.
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PMID:Resolution of necrolytic migratory erythema with somatostatin analogue in a patient diagnosed with pancreatic glucagonoma. 3140 68

Modulation of nociception and inflammation by sulfide in rheumatoid arthritis and activation of transient receptor potential ankyrin 1 (TRPA1) ion channels by sulfide compounds are well documented. The present study aims to investigate TRPA1-mediated effects of sulfide donor GYY4137 in K/BxN serum-transfer arthritis, a rodent model of rheumatoid arthritis. TRPA1 and somatostatin sst4 receptor wild-type (WT) and knockout mice underwent K/BxN serum transfer and were treated daily with GYY4137. Functional and biochemical signs of inflammation were recorded, together with histological characterization. These included detection of hind paw mechanical hyperalgesia by dynamic plantar esthesiometry, hind paw volume by plethysmometry, and upside-down hanging time to failure. Hind paw erythema, edema, and passive movement range of tibiotarsal joints were scored. Somatostatin release from sensory nerve endings of TRPA1 wild-type and knockout mice in response to polysulfide was detected by radioimmunoassay. Polysulfide formation from GYY4137 was uncovered by cold cyanolysis. GYY4137 aggravated mechanical hyperalgesia in TRPA1 knockout mice but ameliorated it in wild-type ones. Arthritis score was lowered by GYY4137 in TRPA1 wild-type animals. Increased myeloperoxidase activity, plasma extravasation, and subcutaneous MIP-2 levels of hind paws were detected in TRPA1 knockout mice upon GYY4137 treatment. Genetic lack of sst4 receptors did not alter mechanical hyperalgesia, edema formation, hanging performance, arthritis score, plasma extravasation, or myeloperoxidase activity. TRPA1 WT animals exhibited smaller cartilage destruction upon GYY4137 administration. Sodium polysulfide caused TRPA1-dependent somatostatin release from murine nerve endings. Sulfide released from GYY4137 is readily converted into polysulfide by hypochlorite. Polysulfide potently activates human TRPA1 receptors expressed in Chinese hamster ovary (CHO) cells. According to our data, the protective effect of GYY4137 is mediated by TRPA1, while detrimental actions are independent of the ion channel in the K/BxN serum-transfer arthritis model in mice. At acidic pH in inflamed tissue sulfide is released from GYY4137 and reacts with neutrophil-derived hypochlorite. Resulting polysulfide might be responsible for TRPA1-mediated antinociceptive and anti-inflammatory as well as TRPA1-independent pro-inflammatory effects.
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PMID:TRPA1 Ion Channel Determines Beneficial and Detrimental Effects of GYY4137 in Murine Serum-Transfer Arthritis. 3155 76

Glucagonoma, a rare neuroendocrine tumor of the pancreas, which is often misdiagnosed because of non-characteristic clinical manifestations. In addition, the treatment has not been well established for this disease so far. We here report a case of glucagonoma previous misdiagnosed as recurrent erythema. In this case, necrolytic migratory erythema was the main clinical manifestation, and he received surgical resection after admission although with liver metastasis. Postoperative pathological results showed that the heterogeneity of proliferative index in primary (Ki-67: 5~10%) and metastatic (Ki-67: 25~30%) tumors were obviously observed. One month postoperatively, abdominal CT and MRI showed multiple liver metastasis (type III) again. Interestingly, the skin rash was obviously improved after treatment with somatostatin combined with chemotherapy (octreotide, temozolomide and capecitabine). Subsequently, the patient received transarterial embolization (TAE). Up to now, no progression was noted for liver metastasis. Due to its rarity, clinical diagnosis is challenging; thus, further understanding of the disease by clinicians is helpful for early diagnosis and treatment, so as to improve the prognosis of patients.
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PMID:Application of Somatostatin, Chemotherapy Combined with TAE in Heterogeneous Glucagonoma Presented with Necrolytic Migratory Erythema. 3192 Mar 26

Glucagonoma is a hormonally active rare pancreatic neuroendocrine tumour causing an excess of glucagon. This is a narrative review based on a multidisciplinary approach of the tumour. Typically associated dermatosis is necrolytic migratory erythema (NME) which is most frequently seen at disease onset. Insulin-dependent diabetes mellitus, depression, diarrhoea, deep vein thrombosis are also identified, as parts of so-called 'D' syndrome. Early diagnosis is life saving due to potential aggressive profile and high risk of liver metastasis. NME as paraneoplastic syndrome may be present for months and even years until adequate recognition and therapy; it is remitted after successful pancreatic surgery. Thus the level of practitioners' awareness is essential. If surgery is not curative, debulking techniques may improve the clinical aspects and even the outcome in association with other procedures such as embolization of hepatic metastasis; ablation of radiofrequency type; medical therapy including chemotherapy, targeted therapy with mTOR inhibitors such as everolimus, PRRT (peptide receptor radiotherapy), and somatostatin analogues (including combinations of medical treatments). Increased awareness of the condition involves multidisciplinary practitioners.
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PMID:Glucagonoma: From skin lesions to the neuroendocrine component (Review). 3290 95


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