Development of silent gastric carcinoid in a type 1 diabetic patient with primer hypothyreosis

2007 ◽  
Vol 148 (35) ◽  
pp. 1667-1671 ◽  
Author(s):  
Anikó Somogyi ◽  
Éva Ruzicska ◽  
Timea Varga ◽  
Károly Rácz ◽  
Géza Nagy
Keyword(s):  
Diabetic Patient ◽  
Chromogranin A ◽  
Gastric Carcinoid

Az 1-es típusú cukorbetegség gyakran társul egyéb autoimmun kórképekkel. A parietalis sejtellenes antitestek (PCA), melyek az 1-es típusú cukorbetegek mintegy 20%-ában megtalálhatók, autoimmun gastritis és anaemia perniciosa jelenlétére figyelmeztetnek. A PCA-k a gyomor-H + /K + ATP-ázt károsítják, és hypo-/achlorhydriát, hypergastrinaemiát okozhatnak. Ennek következtében az enterochromaffin-szerű (ECL) sejtek hyper-/dysplasiaja alakulhat ki, mely carcinoid gyomortumor kialakulására hajlamosít. Az ECL-sejtek hyperplasiájából fejlődő gyomorcarcinoidok az autoimmun gastritises vagy anaemia perniciosában szenvedő betegek 4–9%-ában alakulnak ki. A 29 éves, 6 éve 1-es típusú diabéteszben szenvedő, 8 éves kora óta primer hypothyreosis miatt pajzsmirigyhormon-szubsztitúcióban részesülő nőbetegünknél gyomorpanaszok miatt felső panendoszkópia és biopsziás vizsgálat történt. Az endoszkópia többszörös kicsi polipokat mutatott a fundus területén nonantral hypergastrinaemiás (A-típusú) atrophiás gastritissel. A parietalis sejtantitest-vizsgálat pozitív volt, a szérum-chromogranin-A koncentrációja (CgA) 289,7 ng/ml (norm: 98 ng/ml alatt), a TSH-szint 9,93 mIU/L volt. A szövettani vizsgálat carcinoid tumort igazolt. Octreotidterápiát követően parciális gastrectomiát végeztek. Műtét után a szérum-chromogranin-A-szint normalizálódott. A nonatral, többszörös polipok néma neuroendocrin tumort takarhatnak, melyek rendszerint lassan növekvő, benignus viselkedésű endokrin daganatok, de magas malignitású endokrin karcinómák is lehetnek. A specifikus szérum- vagy szöveti chromogranin-A (CgA) és egyéb endokrin tumorra utaló markerek mérésének elérhetővé válásával e tumorok könnyen felismerhetők lehetnek a klinikus számára.

Autoimmune hepatitis, autoimmune gastritis, and gastric carcinoid in a type 1 diabetic patient

2000 ◽  
Vol 14 (2) ◽  
pp. 116-120 ◽  
Author(s):  
Christophe E.M De Block ◽  
Ivo H De Leeuw ◽  
Paul A Pelckmans ◽  
Peter P Michielsen ◽  
Johannes J.P.M Bogers ◽  
...  
Keyword(s):  
Diabetic Patient ◽  
Autoimmune Hepatitis ◽  
Autoimmune Gastritis ◽  
Gastric Carcinoid

scholarly journals PTU-159 Variable Utility Of Chromogranin A Assays In The Diagnosis Of Gastric Carcinoid Type 1

Gut ◽  
2014 ◽  
Vol 63 (Suppl 1) ◽  
pp. A108.2-A108
Author(s):  
RE Rossi ◽  
NG Martin ◽  
J Garcia-Hernandez ◽  
D Mandair ◽  
M Mullan ◽  
...  
Keyword(s):  
Chromogranin A ◽  
Gastric Carcinoid

scholarly journals Clinical symptoms, hormone profiles, treatment, and prognosis in patients with gastric carcinoids

Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 223-228 ◽  
Author(s):  
D Granberg ◽  
E Wilander ◽  
M Stridsberg ◽  
G Granerus ◽  
B Skogseid ◽  
...  
Keyword(s):  
Liver Metastasis ◽  
Chromogranin A ◽  
Clinical Symptoms ◽  
Chronic Atrophic Gastritis ◽  
Gastric Carcinoid ◽  
Interferon Α ◽  
Gastric Carcinoids ◽  
Type 3

Background—Type 1 gastric carcinoids are associated with hypergastrinaemia and chronic atrophic gastritis, type 2 occur in patients with multiple endocrine neoplasia type 1 combined with Zollinger-Ellison syndrome, and type 3 lack any relation to hypergastrinaemia. Type 1 tumours are usually benign whereas type 3 are highly malignant.Aims—To identify possible tumour markers in patients with gastric carcinoids.Patients/method—Nine patients with type 1, one with type 2, and five with type 3 were evaluated with regard to symptoms, hormone profile, and prognosis.Results—Plasma chromogranin A was increased in all patients but was higher (p<0.01) in those with type 3 than those with type 1 carcinoids. All patients with type 3 carcinoids died from metastatic disease, but none of the type 1 patients died as a result of their tumours. One type 1 patient with a solitary liver metastasis received interferon α and octreotide treatment. Nine months later, the metastasis was no longer detectable. She is still alive eight years after diagnosis, without recurrent disease. This represents the only reported case of foregut carcinoid with an unresectable liver metastasis that seems to be have been cured by biotherapy.Conclusions—Plasma chromogranin A appears to be a valuable tumour marker for all types of gastric carcinoid. Combination therapy with interferon α and octreotide may be beneficial in patients with metastasising type 1 gastric carcinoids.

scholarly journals Robotic pancreas transplantation in a type 1 diabetic patient with morbid obesity

Medicine ◽  
2017 ◽  
Vol 96 (6) ◽  
pp. e5847 ◽  
Author(s):  
Chun Chieh Yeh ◽  
Mario Spaggiari ◽  
Ivo Tzvetanov ◽  
José Oberholzer
Keyword(s):  
Morbid Obesity ◽  
Diabetic Patient ◽  
Pancreas Transplantation

scholarly journals The post-translational processing of chromogranin A in the pancreatic islet: involvement of the eukaryote subtilisin PC2

1994 ◽  
Vol 298 (3) ◽  
pp. 521-528 ◽  
Author(s):  
S D Arden ◽  
N G Rutherford ◽  
P C Guest ◽  
W J Curry ◽  
E M Bailyes ◽  
...  
Keyword(s):  
Secretory Granule ◽  
Pancreatic Islet ◽  
Pancreatic Beta Cells ◽  
Chromogranin A ◽  
Time Course ◽  
Deae Cellulose ◽  
Neuroendocrine Cells ◽  
Time Period ◽  
Sds Page

The post-translational processing of chromogranin A (CGA) and the nature of the enzyme(s) involved were investigated in rat pancreatic islet and insulinoma tissue. Pulse-chase radiolabelling experiments using sequence-specific antisera showed that the 98 kDa (determined by SDS/PAGE) precursor was processed to an N-terminal 21 kDa peptide, a C-terminal 14 kDa peptide and a 45 kDa centrally located peptide with a rapid time course (t1/2 approx. 30 min) after an initial delay of 30-60 min. The 45 kDa peptide was, in turn, converted partially into a 5 kDa peptide with pancreastatin immunoreactivity and a 3 kDa peptide with WE-14 immunoreactivity over a longer time period. Incubation of bovine CGA with rat insulinoma secretory-granule lysate produced peptides of 18, 16 and 40 kDa via intermediates of 65 and 55 kDa. N-terminal sequence analysis indicated that cleavage occurred at the conserved paired basic sites Lys114-Arg115 and Lys330-Arg331, suggesting that cleavage of the equivalent sites (Lys129-Arg130 and Lys357-Arg358) in the rat molecule produced the initial post-translational products observed in intact pancreatic beta-cells. The enzyme activity responsible for the cleavage of bovine CGA co-chromatographed on DEAE-cellulose with the type-2 proinsulin endopeptidase and with PC2 immunoreactivity. The type-1 enzyme (PC1/3) appeared inactive towards CGA. The requirement for Ca2+ ions and an acidic pH for conversion was consistent with the involvement of a member of the eukaryote subtilisin family, and the composition of the released peptides in pulse-chase and secretion studies suggested that conversion occurred in the secretory-granule compartment. The overall catalytic rate as well as the relative susceptibilities of the Lys114-Arg115 and Lys330-Arg331 sites to cleavage were affected by pH, suggesting that the ionic environment of the processing compartment may play a role in the differential processing of CGA which is evident in various neuroendocrine cells.

scholarly journals GH replacement causing acute hyperglycaemia and ketonuria in a type 1 diabetic patient

2013 ◽  
Vol 2013 ◽  
Author(s):  
Dominic Cavlan ◽  
Shanti Vijayaraghavan ◽  
Susan Gelding ◽  
William Drake
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Type 1 Diabetes ◽  
Fatty Acid ◽  
Diabetic Patient ◽  
Acid Cycle ◽  
Gh Replacement ◽  
Glucose Fatty Acid Cycle ◽  
Gh Excess

Summary A state of insulin resistance is common to the clinical conditions of both chronic growth hormone (GH) deficiency and GH excess (acromegaly). GH has a physiological role in glucose metabolism in the acute settings of fast and exercise and is the only anabolic hormone secreted in the fasting state. We report the case of a patient in whom knowledge of this aspect of GH physiology was vital to her care. A woman with well-controlled type 1 diabetes mellitus who developed hypopituitarism following the birth of her first child required GH replacement therapy. Hours after the first dose, she developed a rapid metabolic deterioration and awoke with hyperglycaemia and ketonuria. She adjusted her insulin dose accordingly, but the pattern was repeated with each subsequent increase in her dose. Acute GH-induced lipolysis results in an abundance of free fatty acids (FFA); these directly inhibit glucose uptake into muscle, and this can lead to hyperglycaemia. This glucose–fatty acid cycle was first described by Randle et al. in 1963; it is a nutrient-mediated fine control that allows oxidative muscle to switch between glucose and fatty acids as fuel, depending on their availability. We describe the mechanism in detail. Learning points There is a complex interplay between GH and insulin resistance: chronically, both GH excess and deficiency lead to insulin resistance, but there is also an acute mechanism that is less well appreciated by clinicians. GH activates hormone-sensitive lipase to release FFA into the circulation; these may inhibit the uptake of glucose leading to hyperglycaemia and ketosis in the type 1 diabetic patient. The Randle cycle, or glucose–fatty acid cycle, outlines the mechanism for this acute relationship. Monitoring the adequacy of GH replacement in patients with type 1 diabetes is difficult, with IGF1 an unreliable marker.

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