scholarly journals A case of nonislet cell tumor hypoglycemia associated with malignant mesothelioma requiring a multifaceted approach for optimal glycemic control

2021 ◽  
Vol 9 (10) ◽  
Author(s):  
Mariko Ono ◽  
Yuki Maeda ◽  
Nobuyuki Koyama ◽  
Terumasa Nagase ◽  
Yoshiya Katsura ◽  
...  
Keyword(s):  
Glycemic Control ◽  
Malignant Mesothelioma ◽  
Cell Tumor ◽  
Multifaceted Approach ◽  
Tumor Hypoglycemia

scholarly journals A Rapid Method for Analyzing Serum Pro-Insulin-Like Growth Factor-II in Patients with Non-Islet Cell Tumor Hypoglycemia

2005 ◽  
Vol 90 (7) ◽  
pp. 3819-3823 ◽  
Author(s):  
Farideh Miraki-Moud ◽  
Ashley B. Grossman ◽  
Michael Besser ◽  
John P. Monson ◽  
Cecilia Camacho-Hübner
Keyword(s):  
Growth Factor ◽  
Rapid Method ◽  
Islet Cell ◽  
Islet Cell Tumor ◽  
Cell Tumor ◽  
Insulin Like Growth Factor ◽  
Factor Ii ◽  
Tumor Hypoglycemia

Non-Islet Cell Tumor Hypoglycemia Associated with Uterine Leiomyomata

2011 ◽  
Vol 17 (4) ◽  
pp. e109-e112 ◽  
Author(s):  
Albert Ndzengue ◽  
Zwege Deribe ◽  
Richard Rafal ◽  
Maximo Mora ◽  
Schiller Desgrottes ◽  
...  
Keyword(s):  
Islet Cell ◽  
Islet Cell Tumor ◽  
Cell Tumor ◽  
Uterine Leiomyomata ◽  
Tumor Hypoglycemia

A Case of Non-islet Cell Tumor Hypoglycemia

2006 ◽  
Vol 21 (1) ◽  
pp. 74 ◽  
Author(s):  
Yun-Tae Chae ◽  
Il-Jun Hwang ◽  
Kyung-Hee Ryu ◽  
Eun-Hyang Ko ◽  
Jung-Im Rue ◽  
...  
Keyword(s):  
Islet Cell ◽  
Islet Cell Tumor ◽  
Cell Tumor ◽  
Tumor Hypoglycemia

scholarly journals Bioactive insulin-like growth factors as a possible molecular target for non-islet cell tumor hypoglycemia

2015 ◽  
Vol 26 ◽  
pp. vii95
Author(s):  
Takashi Setoyama ◽  
Shin'ichi Miyamoto ◽  
Takahiro Horimatsu ◽  
Taro Funakoshi ◽  
Miutsuhiro Nikaido ◽  
...  
Keyword(s):  
Growth Factors ◽  
Islet Cell ◽  
Islet Cell Tumor ◽  
Molecular Target ◽  
Cell Tumor ◽  
Tumor Hypoglycemia ◽  
Insulin Like Growth Factors

Serum acid-labile subunit levels in 31 patients with non-islet cell tumor hypoglycemia

1998 ◽  
Vol 8 (4) ◽  
pp. 339
Author(s):  
N Hizuka ◽  
I Fukuda ◽  
K Takano ◽  
Y Ishikawa ◽  
K Asakawa-Yasumoto ◽  
...  
Keyword(s):  
Islet Cell ◽  
Islet Cell Tumor ◽  
Cell Tumor ◽  
Acid Labile Subunit ◽  
Tumor Hypoglycemia ◽  
Acid Labile

Solitary Fibrous Tumor Associated With Non-Islet Cell Tumor Hypoglycemia

2007 ◽  
Vol 84 (1) ◽  
pp. 292-294 ◽  
Author(s):  
Kotaro Kameyama ◽  
Norihito Okumura ◽  
Yujiro Kokado ◽  
Kentaroh Miyoshi ◽  
Tomoaki Matsuoka ◽  
...  
Keyword(s):  
Solitary Fibrous Tumor ◽  
Islet Cell ◽  
Islet Cell Tumor ◽  
Cell Tumor ◽  
Fibrous Tumor ◽  
Tumor Hypoglycemia

scholarly journals An Adrenocortical Carcinoma Associated with Non-Islet Cell Tumor Hypoglycemia and Aberrant ACTH Production

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
M. D. S. A. Dilrukshi ◽  
A. W. Wickramarachchi ◽  
D. D. K. Abeyaratne ◽  
Brian Shine ◽  
Bahram Jafar-Mohammadi ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Cushing’S Syndrome ◽  
Adrenocortical Carcinoma ◽  
Islet Cell ◽  
Islet Cell Tumor ◽  
Severe Hypoglycemia ◽  
Cushing's Syndrome ◽  
Cell Tumor ◽  
Adrenocortical Carcinomas ◽  
Tumor Hypoglycemia

Introduction. Adrenocortical carcinomas (ACCs) are infrequently reported to present with severe hypoglycemia syndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by tumor cells. Adrenocorticotropic hormone- (ACTH) independent hypercortisolism is the norm of hormonally active ACCs, but aberrant ACTH production by tumor cells can theoretically cause ACTH-dependent hypercortisolism. The purpose of this report was to present a case of an ACC manifested with the co-occurrence of two extremely rare presentations. Case Description. We present a rare case of a 43-year-old male patient admitted with recurrent episodes of severe non-ketotic and non-insulin-mediated hypoglycemia due to IGF-II mediated disease and ACTH-dependent Cushing’s syndrome. He was diagnosed with a diffusely disseminated adrenocortical carcinoma with immunohistochemistry of tumor cells showing focal ACTH immunostain positivity. Conclusion. Non-islet cell tumor hypoglycemia and ACTH-dependent Cushing’s syndrome are extremely rare presentations of an ACC, and co-occurrence of these entities in a single patient is never reported in the literature.

scholarly journals Hypoglycemia from IGF2 Overexpression Associated with Activation of Fetal Promoters and Loss of Imprinting in a Metastatic Hemangiopericytoma

2009 ◽  
Vol 30 (4) ◽  
pp. 413-413
Author(s):  
Elizabeth A. Lawson ◽  
Xun Zhang ◽  
Jonathan T. Crocker ◽  
Wei-Lien Wang ◽  
Anne Klibanski
Keyword(s):  
Control Region ◽  
Islet Cell ◽  
Islet Cell Tumor ◽  
Major Change ◽  
Metastatic Tumor ◽  
Cell Tumor ◽  
Rt Pcr ◽  
Loss Of Imprinting ◽  
Promoter Usage ◽  
Tumor Hypoglycemia

ABSTRACT Context The mechanism of IGF2 overexpression in non-islet-cell tumor hypoglycemia is not understood. Objective We investigated the imprinting control and promoter usage for IGF2 expression to identify a mechanism for increased IGF-II production in non-islet-cell tumor hypoglycemia. Patient and Methods A patient with metastatic hemangiopericytoma was studied. Tissue from the original hemangiopericytoma, metastatic tumor, and uninvolved liver was analyzed for IGF-II immunohistochemistry. IGF2, a paternally imprinted gene, shares a control region with maternally imprinted H19, a putative tumor suppressor. IGF-II and H19 mRNA expression was compared in metastatic tumor and uninvolved liver by quantitative RT-PCR. Imprinting of IGF2/H19 genes and IGF2 promoter usage in metastatic tumor was investigated by RT-PCR and sequence analysis, and the methylation pattern in the IGF2/H19 imprinting control region was analyzed. Results IGF-II protein expression was increased in metastatic tumor vs. uninvolved liver and original tumor. In the metastatic tumor, IGF-II mRNA was increased 60-fold, but H19 mRNA was comparable to uninvolved liver; loss of imprinting of IGF2, but not H19, was identified; no major change in methylation of the IGF2/H19 imprinting control regions was observed; and transcripts from four different IGF2 promoters were detected, compared to two in uninvolved liver. Conclusions IGF-2 overexpression, newly acquired in the metastatic tumor, was associated with loss of IGF2 gene imprinting and different promoter usage. The imprinting control mechanism governing the IGF2/H19 locus was intact, as evidenced by normal levels of H19, maintenance of H19 imprinting, and no major change in methylation of the imprinting control regions.

scholarly journals Nonislet Cell Tumor Hypoglycemia

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Johnson Thomas ◽  
Salini C. Kumar
Keyword(s):  
Glucose Utilization ◽  
Cell Tumor ◽  
Gi Tract ◽  
Normal Range ◽  
Mesenchymal Tumors ◽  
Hypoglycemia Unawareness ◽  
Factor Ii ◽  
Carcinoma Of Esophagus ◽  
Poorly Differentiated ◽  
Tumor Hypoglycemia

Nonislet cell tumor hypoglycemia (NICTH) is a rare cause of hypoglycemia. It is characterized by increased glucose utilization by tissues mediated by a tumor resulting in hypoglycemia. NICTH is usually seen in large mesenchymal tumors including tumors involving the GI tract. Here we will discuss a case, its pathophysiology, and recent advances in the management of NICTH. Our patient was diagnosed with poorly differentiated squamous cell carcinoma of esophagus. He continued to be hypoglycemic even after starting continuous tube feeds and D5W. General workup for hypoglycemia was negative and insulin-like growth factor II (IGF II) was in the normal range. Hypoglycemia secondary to “big” IGF II was considered, and patient was started on steroids. His hypoglycemia resolved within a day of treatment with steroids. Initially patient had hypoglycemia unawareness, which he regained after maintaining euglycemia for 48 hours.

Sign in / Sign up

Export Citation Format

Share Document