Intractable Fasting Hypoglycemia as a Manifestation of Hepatocellular Carcinoma

Forde, Justin; Ewelukwa, Ofor; Brar, Tony; Cabrera, Roniel

doi:10.1155/2017/7465025

Cited by 7 publications

(12 citation statements)

References 20 publications

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“…High glucose use in patients with decreased gluconeogenesis plays an important role in the pathophysiology of hypoglycemia in non-islet cell malignancies such as HCC. This type of NICTH (type A) is observed in late-stage HCC when the tumoral burden is high and hepatic destruction is extensive [7]. In such cases, insulin and C-peptide levels are found to be low [8].…”

Section: Discussionmentioning

confidence: 99%

A Case of Hepatocellular Carcinoma Diagnosed with Resistant Hypoglycemia

Albayrak¹,

Duman²,

Ayvaz³

2022

OJGas

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Background: There are many causes of the etiology of hypoglycemia. Hypoglycemia is very rare in individuals without diabetes. Although it can accompany islet cell malignancies such as insulinoma, it is much less common in solid organ tumors such as hepatocellular carcinoma as a component of paraneoplastic syndrome. Case Presentation: We present a 58-year-old male patient with no additional disease, who was examined for resistant hypoglycemia and was diagnosed as having hepatocellular carcinoma radiologically for the first time. Insulin level measured when serum glucose was 44 mg/dl: 0.4 µU/mL, c-peptide level: 0.355 ng/mL detected. Viral serology was found to be positive for HbsAg. In dynamic magnetic resonance imaging, showing continuity in segments 6 -7 and 8 in the right lobe, and also partially towards 5, heterogeneous hyperintense in T2 A's, diffusion-limiting, heterogeneous contrast enhancement in postcontrast series, cystic-necrotic in the center. The alpha-fetoprotein level was 60,500 ng/mL. Conclusion: Paraneoplastic hypoglycemia due to underlying malignancies should be considered in patients presenting with hypoglycemia.

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Section: Discussionmentioning

confidence: 99%

A Case of Hepatocellular Carcinoma Diagnosed with Resistant Hypoglycemia

Albayrak¹,

Duman²,

Ayvaz³

2022

OJGas

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“…IGF-2 might be falsely normal in our patient because the sample was collected after the first dose of prednisolone was administered, which was able to inhibit the production of IGF-2[ 22 ]. In addition, serum IGF-2 levels in NICTH are often not elevated partially because most “big IGF-2” are not measured by common commercially available assay[ 16 , 23 , 24 ]. It has also been found by a few case reports that the levels of serum IGF-2 were decreased or normal in contrast to an increased pro-IGF-2 in NICTH[ 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

Non-islet cell tumor hypoglycemia as an initial presentation of hepatocellular carcinoma coupled with end-stage liver cirrhosis: A case report and review of literature

Douli

Suarez

et al. 2020

WJH

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BACKGROUND Non-islet cell tumor hypoglycemia (NICTH) is a rare cause of persistent hypoglycemia seen in patients with hepatocellular carcinoma (HCC). It is likely to be underdiagnosed especially in the patients with poor hepatic function and malnutrition. Herein, we report a rare case of NICTH as the initial presentation of HCC in a patient with chronic hypoglycemia due to end-stage liver cirrhosis. CASE SUMMARY A 62-year-old male with chronic fasting hypoglycemia secondary to end-stage hepatitis C-related cirrhosis, presented with altered mental status and dizziness. He was found to have severe hypoglycemia refractory to glucose supplements. Imaging studies and biopsy discovered well differentiated HCC without metastasis. Further evaluation showed low insulin, C-peptide and beta-hydroxybutyrate along with a high insulin-like growth factor-2/insulin-like growth factor ratio, consistent with the diagnosis of NICTH. As patient was not a candidate for surgical resection or chemotherapy, he was started on prednisolone with some improvements in the glucose homeostasis, but soon decompensated after a superimposed hospital acquired pneumonia. CONCLUSION NICTH can occur as the sole initial presentation of HCC and is often difficult to correct without tumor removal. Clinicians should maintain high clinical suspicion for early recognition of paraneoplastic NICTH in patients at risk for HCC, even those with chronic fasting hypoglycemia in the setting of severe hepatic failure and malnutrition.

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“…Type A is characterized by an increased consumption of glucose by tumor in malnourished patients with low glycogen deposits and defective gluconeogenesis. This type of NICTH is observed in late-stage HCC when the tumoral burden is high and hepatic destruction is extensive [ 4 ]. Type B (less common) is caused by IGF-2 overproduction as it is partially processed by tumoral cells.…”

Section: Discussionmentioning

confidence: 99%

“…Most patients are treated with intravenous glucose infusions; despite this, response rates are bad, and second-line therapy is usually required [ 4 ].…”

Section: Discussionmentioning

confidence: 99%