Browse

You are looking at 1 - 5 of 5 items

Takatoshi Anno Department of General Internal Medicine 1, Kawasaki Medical School, Okayama, Japan

Search for other papers by Takatoshi Anno in
Google Scholar
PubMed
Close
,
Hideaki Kaneto Department of Diabetes, Metabolism and Endocrinology, Kawasaki Medical School, Kurashiki, Japan

Search for other papers by Hideaki Kaneto in
Google Scholar
PubMed
Close
,
Ryo Shigemoto Department of General Internal Medicine 1, Kawasaki Medical School, Okayama, Japan

Search for other papers by Ryo Shigemoto in
Google Scholar
PubMed
Close
,
Fumiko Kawasaki Department of General Internal Medicine 1, Kawasaki Medical School, Okayama, Japan

Search for other papers by Fumiko Kawasaki in
Google Scholar
PubMed
Close
,
Yasuhiro Kawai Department of General Internal Medicine 1, Kawasaki Medical School, Okayama, Japan

Search for other papers by Yasuhiro Kawai in
Google Scholar
PubMed
Close
,
Noriyo Urata Department of General Internal Medicine 2, Kawasaki Medical School, Okayama, Japan

Search for other papers by Noriyo Urata in
Google Scholar
PubMed
Close
,
Hirofumi Kawamoto Department of General Internal Medicine 2, Kawasaki Medical School, Okayama, Japan

Search for other papers by Hirofumi Kawamoto in
Google Scholar
PubMed
Close
,
Kohei Kaku Department of General Internal Medicine 1, Kawasaki Medical School, Okayama, Japan

Search for other papers by Kohei Kaku in
Google Scholar
PubMed
Close
, and
Niro Okimoto Department of General Internal Medicine 1, Kawasaki Medical School, Okayama, Japan

Search for other papers by Niro Okimoto in
Google Scholar
PubMed
Close

Summary

Hypoglycemia is induced by many causes, especially over-dose of insulin or oral hypoglycemic agents in diabetic subjects. In such a case, hyperinsulinemic hypoglycemia is usually observed. On the other hand, it is important to classify secondary hypoglycemia and hypoinsulinemic hypoglycemia. Liver injury-induced hypoglycemia is one of the causes of hypoinsulinemic hypoglycemia but rarely observed in clinical practice. Herein, we experienced similar 2 cases of non-diabetic hypoinsulinemic hypoglycemia. Both of them were elderly subjects with low body weight. Furthermore, it is likely that hypoinsulinemic hypoglycemia in both subjects was triggered by severe liver injury, at least in part, due to possible limited liver glycogen store. In elderly subjects with low body weight and/or malnutrition, metabolism in the liver is reduced and glycogen accumulation is decreased. Such alteration brings out acute and marked liver injury, which finally leads to the onset of severe hypoglycemia. It is known that not only liver injury but also multiple organ failure could be induced due to extreme emaciation in subjects. It is likely that in elderly subjects with low body weight and/or malnutrition, multiple organ failure including liver failure could be induced due to the similar reason. Therefore, we should be very careful of such subjects in order to avoid the development of multiple organ failure which leads to life-threatening situations. In conclusion, we should keep in mind the possibility of hypoinsulinemic hypoglycemia when we examine severe liver injury, especially in elderly or starving subjects with low body weight and limited liver glycogen stores.

Learning points:

  • It is important to classify secondary hypoglycemia and hypoinsulinemic hypoglycemia.

  • Liver injury-induced hypoglycemia is one of the causes of hypoinsulinemic hypoglycemia but rarely observed in everyday clinical practice.

  • Herein, we reported similar 2 cases of hypoinsulinemic hypoglycemia without diabetes presumably triggered by severe liver injury.

  • In both cases, hypoglycemia was improved by glucose infusion, although their liver injury was not improved.

  • We should keep in mind the possibility of hypoinsulinemic hypoglycemia when we examine severe liver injury, especially in elderly subjects with low body weight.

Open access
Mads Ryø Jochumsen Department of Nuclear Medicine & PET Centre, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Mads Ryø Jochumsen in
Google Scholar
PubMed
Close
,
Peter Iversen Department of Nuclear Medicine & PET Centre, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Peter Iversen in
Google Scholar
PubMed
Close
, and
Anne Kirstine Arveschoug Department of Nuclear Medicine & PET Centre, Aarhus University Hospital, Aarhus, Denmark

Search for other papers by Anne Kirstine Arveschoug in
Google Scholar
PubMed
Close

Summary

A case of follicular thyroid cancer with intense focal Methionine uptake on 11C-Methionine PET/CT is reported here. The use of 11C-Methionine PET in differentiated thyroid cancer is currently being investigated as a surrogate tracer compared to the more widely used 18F-FDG PET. This case illustrates the potential incremental value of this modality, not only in the localizing of parathyroid adenoma, but also indicating that 11C-Methionine PET might have a potential of increasing the pretest likelihood of thyroid malignancy in a cold nodule with highly increased Sestamibi uptake.

Learning points:

  • 11C-Methionine PET/CT and 18F-Fluorocholine PET/CT often visualizes the parathyroid adenoma in case of negative Tc-99m-MIBI SPECT/CT.

  • A cold nodule in Tc-99m Pertechnetat thyroid scintigraphy with a negative Sestamibi scintigraphy has a very low probability of being malignant.

  • However, the pretest likelihood of thyroid cancer in a cold nodule with increased Sestamibi uptake is low.

  • 11C-Methionine PET might have a potential incremental value in increasing the pretest likelihood of thyroid malignancy in a cold nodule with highly increased Sestamibi uptake.

Open access
Maria Cabrer Endocrine Unit, Hospital Comarcal d’Inca, Inca, Spain

Search for other papers by Maria Cabrer in
Google Scholar
PubMed
Close
,
Guillermo Serra Endocrine Unit, Hospital Universitari Son Espases, Palma, Spain

Search for other papers by Guillermo Serra in
Google Scholar
PubMed
Close
,
María Soledad Gogorza Endocrine Unit, Hospital Universitari Son Espases, Palma, Spain

Search for other papers by María Soledad Gogorza in
Google Scholar
PubMed
Close
, and
Vicente Pereg Endocrine Unit, Hospital Universitari Son Espases, Palma, Spain

Search for other papers by Vicente Pereg in
Google Scholar
PubMed
Close

Summary

Chromosome 22q11.2 deletion syndrome (22q11.2DS) is a genetic syndrome that may present with hypocalcemia due to primary hypoparathyroidism (PH) at any age. We report a new diagnosis of 22q11.2DS in a 57-year-old man who presented with symptomatic hypocalcemia. It is important to consider genetic causes of hypocalcemia due to PH regardless of age.

Learning points:

  • It is important to discard genetic cause of primary hypoparathyroidism in a patient without autoimmune disease or prior neck surgery.

  • A new diagnosis of a hereditary disease has familial implications and needs genetic counselling.

  • It is also important to discard other syndrome’s comorbidities.

Open access
S A A van den Berg Departments of Clinical Chemistry and Hematology

Search for other papers by S A A van den Berg in
Google Scholar
PubMed
Close
and
C G Krol Departments of Clinical Chemistry and Hematology

Search for other papers by C G Krol in
Google Scholar
PubMed
Close

Summary

We present a patient (87 years, female) who was admitted to the emergency department because of loss of consciousness. Previous medical history included advanced-stage hepatocellular carcinoma and associated weight loss. She was found on the ground in an unresponsive state by her daughter and was determined to be hypoglycaemic. Upon bolus administration of 100 mL intravenous glucose (10%), glucose levels increased to 2.9 mmol/L and the patient regained full consciousness. She was admitted to the hospital for further examination, and treatment and continuous intravenous glucose infusion was initiated. As the patient was known to suffer from advanced-stage hepatocellular carcinoma, tumour-associated hypoglycaemia was suspected. Insulin, c-peptide and IGF1 concentrations were indeed low, cortisol concentration was high and IGF2 and Pro-IGF2 were borderline low and borderline high normal respectively. IGF2:IGF1 ratio was 23, confirming the diagnosis of non-islet cell tumour hypoglycaemia. During the initial phase of treatment, euglycaemia was maintained by continuous variable glucose infusion (5%, varying between 1 and 2 L/24 h), and the patient was advised to eat small snacks throughout the day. After euglycaemia was established and the diagnosis was confirmed, prednisolone was started (30 mg, 1 dd) and glucose infusions were halted. Under prednisolone treatment, glucose levels were slightly increased and no further hypoglycaemic episodes occurred. At her request, no surgery was performed. After 19 days, the patient was discharged to a hospice and died 3 weeks later.

Learning points:

  • Hepatocellular carcinoma may be associated with non-islet cell tumour hypoglycaemia (NICTH).

  • NICTH-induced hypoglycaemia is associated with low insulin and IGF1.

  • Measurement of IGF2 only (without measurement of Pro-IGF2 and IGF1) may be insufficient to prove NICTH.

Open access
Katia Regina Marchetti Department of General Medicine

Search for other papers by Katia Regina Marchetti in
Google Scholar
PubMed
Close
,
Maria Adelaide Albergaria Pereira Department of Endocrinology, Clinics Hospital, University of Sao Paulo School of Medicine, Sao Paulo, SP, Brazil

Search for other papers by Maria Adelaide Albergaria Pereira in
Google Scholar
PubMed
Close
,
Arnaldo Lichtenstein Department of General Medicine

Search for other papers by Arnaldo Lichtenstein in
Google Scholar
PubMed
Close
, and
Edison Ferreira Paiva Department of General Medicine

Search for other papers by Edison Ferreira Paiva in
Google Scholar
PubMed
Close

Summary

Adrenacarcinomas are rare, and hypoglycemic syndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by these tumors have been described infrequently. This study describes the case of a young woman with severe persistent hypoglycemia and a large adrenal tumor and discusses the physiopathological mechanisms involved in hypoglycemia. The case is described as a 21-year-old woman who presented with 8 months of general symptoms and, in the preceding 3 months, with episodes of mental confusion and visual blurring secondary to hypoglycemia. A functional assessment of the adrenal cortex revealed ACTH-independent hypercortisolism and hyperandrogenism. Hypoglycemia, hypoinsulinemia, low C-peptide and no ketones were also detected. An evaluation of the GH–IGF axis revealed GH blockade (0.03; reference: up to 4.4 ng/mL), greatly reduced IGF-I levels (9.0 ng/mL; reference: 180–780 ng/mL), slightly reduced IGF-II levels (197 ng/mL; reference: 267–616 ng/mL) and an elevated IGF-II/IGF-I ratio (21.9; reference: ~3). CT scan revealed a large expansive mass in the right adrenal gland and pulmonary and liver metastases. During hospitalization, the patient experienced frequent difficult-to-control hypoglycemia and hypokalemia episodes. Octreotide was ineffective in controlling hypoglycemia. Due to unresectability, chemotherapy was tried, but after 3 months, the patient’s condition worsened and progressed to death. In conclusion, our patient presented with a functional adrenal cortical carcinoma, with hyperandrogenism associated with hypoinsulinemic hypoglycemia and blockage of the GH–IGF-I axis. Patient’s data suggested a diagnosis of hypoglycemia induced by an IGF-II or a large IGF-II-producing tumor (low levels of GH, greatly decreased IGF-I, slightly decreased IGF-II and an elevated IGF-II/IGF-I ratio).

Learning points:

  • Hypoglycemyndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by adrenal tumors is a rare condition.

  • Hypoinsulinemic hypoglycemia associated with hyperandrogenism and blockage of the GH–IGF-I axis suggests hypoglycemia induced by an IGF-II or a large IGF-II-producing tumor.

  • Hypoglycemia in cases of NICTH should be treated with glucocorticoids, glucagon, somatostatin analogs and hGH.

Open access