Non-islet cell tumor-induced hypoglycemia associated with macronodular pulmonary metastases from poorly differentiated thyroid carcinoma.

BACKGROUND: Non-islet cell tumor-induced hypoglycemia (NICTH), a major cause of fasting hypoglycemia, is caused by the overproduction of incompletely processed, high molecular-weight insulin-like growth factor-II (IGF-II), termed "big" IGF-II. To the best of our knowledge, only two cases of thyroid carcinoma associated with NICTH have been documented. PATIENT FINDINGS: We report the case of a 72-year-old woman who was brought to the emergency department with impaired consciousness. The patient had a history of pulmonary metastases from poorly differentiated thyroid carcinoma (PDTC), spanning 12 years since initial treatment. Laboratory tests showed decreased plasma glucose levels even though immunoreactive insulin, IGF-I, and growth hormone (GH) were undetectable. Computed tomography (CT) scan revealed macronodular pulmonary metastases the estimated volume of which was 456 mL. Both the biochemical data and imaging results suggested NICTH. The results of Western blot analysis performed on a fractionated serum sample showed an increased expression of big IGF-II, an important indicator in the diagnosis of NICTH. Because the massive pulmonary metastases were considered inoperable, immunohistochemical analysis of stored formalin-fixed, paraffin-embedded tissues was performed. The analysis revealed that the tumor cells were positive for both IGF-II and thyroglobulin. A whole-body CT excluded extrapulmonary metastatic lesions. A retrospective review revealed a gradual decrease in glycohemoglobin levels accompanied by an increase in the estimated volume of pulmonary metastases. These findings suggested that NICTH had been caused by pulmonary metastases from PDTC. CONCLUSIONS: We describe here the third reported case of NICTH associated with thyroid carcinoma. This is also the first case reporting big IGF-II in the serum of a patient with thyroid carcinoma.

Significant correlation between visceral adiposity and high-sensitivity C-reactive protein (hs-CRP) in Japanese subjects.

OBJECTIVE: High-sensitivity C-reactive protein (hs-CRP) is a marker for low-grade inflammation, as well as atherosclerosis, obesity, hyperglycemia and hypertension. Because the factor showing the strongest association with inflammation is currently unknown, we investigated the associations between hs-CRP and clinical and biochemical characteristics in Japanese subjects with mild obesity or impaired glucose tolerance. METHODS: Subjects aged <65 years old, attending the Seirei Medical Examination Center, underwent complete physical and laboratory examinations. A total of 112 subjects (mean age 59.9±5.9 years old, males/females: n=50/62) with a waist circumference of >85 cm in males and >90 cm in females, homeostasis model assessment-insulin resistance (HOMA-IR) ≥1.7, or impaired glucose tolerance were eligible for this study. All subjects had normal albuminuria. RESULTS: Log-transformed hs-CRP concentrations were significantly correlated with BMI (r=0.278, p<0.01), HOMA-IR (r=0.296, p<0.005), 2-h post-challenge IRI during an oral glucose tolerance test (r=0.218, p<0.05), maximum intima-media thickness (r=0.240, p<0.05), visceral fat area evaluated by computed tomography (r=0.423, p<0.0001) and subcutaneous fat area (r=0.231, p<0.05). Multiple linear regression analysis showed that visceral fat was the most significantly correlated factor with hs-CRP. CONCLUSION: Visceral fat mass was a significant and independent predictor for serum hs-CRP levels in Japanese subjects with mild obesity and/or impaired glucose tolerance.