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Open access

Katia Regina Marchetti, Maria Adelaide Albergaria Pereira, Arnaldo Lichtenstein and Edison Ferreira Paiva

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

M Nwokolo and J Fletcher

Summary

A 46-year-old woman presented multiple times in a 4-month period with hypotension, sepsis, hypoglycaemia and psychosis. A low random cortisol in combination with her presenting complaint made adrenal insufficiency the likely diagnosis. Fluid resuscitation and i.v. steroid therapy led to clinical improvement; however, a short synacthen test (SST) demonstrated an apparently satisfactory cortisol response. The test was repeated on a later admission and revealed a peak cortisol level of 25 nmol/l (>550 nmol/l). Concurrent treatment with i.v. hydrocortisone had led to a false-negative SST. ACTH was <5 ng/l (>10 ng/l), indicating secondary adrenal failure. We discuss the challenges surrounding the diagnosis of adrenal insufficiency and hypopituitarism, the rare complication of psychosis and a presumptive diagnosis of autoimmune lymphocytic hypophysitis (ALH).

Learning points

  • Adrenocortical insufficiency must be considered in the shocked, hypovolaemic and hypoglycaemic patient with electrolyte imbalance. Rapid treatment with fluid resuscitation and i.v. corticosteroids is vital.

  • Polymorphic presentations to multiple specialities are common. Generalised myalgia, abdominal pain and delirium are well recognised, psychosis is rare.

  • A random cortisol can be taken with baseline bloods. Once the patient is stable, meticulous dynamic testing must follow to confirm the clinical diagnosis.

  • The chronic disease progression of ALH is hypothesised to be expansion then atrophy of the pituitary gland resulting in empty sella turcica and hypopituitarism.

  • If hypopituitarism is suspected, an ACTH deficiency should be treated prior to commencing thyroxine (T4) therapy as unopposed T4 may worsen features of cortisol deficiency.