Clinical Overview > Condition/ Syndrome > Diabetes mellitus type 2

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Jiman Kim
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Eulsun Moon Seoul 365 Medical Clinic, Seoul, Korea

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Seungwon Kwon Department of Cardiovascular and Neurologic Diseases, College of Korean Medicine, KyungHee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-702, Korea

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Summary

Diabetic nephropathy, a microvascular complication of diabetes, is a progressive kidney disease caused by angiopathy of the capillaries in the kidney glomeruli. Herein, we report a case of a 62-year-old patient with a 30 year history of diabetes, who showed a substantial improvement in diabetic nephropathy on administration of 30 g of Astragalus membranaceus extract per day. After 1 month, estimated glomerular filtration rate increased from 47 to 72 ml/min per 1.73 m2 and was subsequently maintained at the 1-month follow-up. Urinary protein levels also decreased following treatment. Herein, we present and discuss the evidence and mechanism of A. membranaceus on diabetic nephropathy in this patient.

Learning points

  • Diabetic nephropathy is a progressive kidney disease.

  • Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are currently used to prevent and delay the progression of diabetic nephropathy. However, their effects are not sufficient to prevent a decline in kidney function.

  • Furthermore, combination therapy with an ACE inhibitor and an ARB can produce adverse effects without additional benefits.

  • In the early phase of diabetic nephropathy, administration of Astragalus membranaceus can be a therapeutic option.

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M S Draman Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital, Blanchardstown, Dublin 15

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H Thabit Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital, Blanchardstown, Dublin 15

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T J Kiernan Department of Cardiology, University of Limerick, Limerick, Ireland

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J O'Neill Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital, Blanchardstown, Dublin 15

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S Sreenan Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital, Blanchardstown, Dublin 15

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J H McDermott Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital, Blanchardstown, Dublin 15

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Summary

Silent myocardial ischaemia (SMI), defined as objective evidence of myocardial ischaemia in the absence of symptoms, has important clinical implications for the patient with coronary artery disease. We present a dramatic case of SMI in a diabetes patient who attended annual review clinic with ST elevation myocardial infarction. His troponin was normal on admission but raised to 10.7 ng/ml (normal <0.5) when repeated the next day. His angiogram showed diffused coronary artery disease. We here discuss the implications of silent ischaemia for the patient and for the physician caring for patients with diabetes.

Learning points

  • Silent myocardial ischaemia (SMI) is an important clinical entity.

  • SMI is common and occurs with increased frequency in patients with diabetes.

  • SMI is an independent predictor of mortality.

  • Recognition may lead to early intervention.

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Vivienne Yoon Department of Internal Medicine/Division of Endocrinology and Metabolism, VA North Texas Health Care System and the University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8857, USA

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Aliya Heyliger Department of Internal Medicine/Division of Endocrinology and Metabolism, VA North Texas Health Care System and the University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8857, USA

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Takashi Maekawa Department of Pathology, Tohoku University School of Medicine and Hospital at Sendai, Sendai, Japan

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Hironobu Sasano Department of Pathology, Tohoku University School of Medicine and Hospital at Sendai, Sendai, Japan

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Kelley Carrick Departments of Pathology

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Stacey Woodruff Surgery, University of Texas Southwestern Medical Center, Dallas, Texas, USA

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Jennifer Rabaglia Surgery, University of Texas Southwestern Medical Center, Dallas, Texas, USA

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Richard J Auchus Department of Internal Medicine/Division of Metabolism, Endocrinology and Diabetes, University of Michigan Health System, Ann Arbor, Michigan, USA

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Hans K Ghayee Department of Internal Medicine/Division of Endocrinology and Metabolism, VA North Texas Health Care System and the University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8857, USA

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Summary

Objective: To recognize that benign adrenal adenomas can co-secrete excess aldosterone and cortisol, which can change clinical management.

Methods: We reviewed the clinical and histological features of an adrenal tumor co-secreting aldosterone and cortisol in a patient. Biochemical testing as well as postoperative immunohistochemistry was carried out on tissue samples for assessing enzymes involved in steroidogenesis.

Results: A patient presented with hypertension, hypokalemia, and symptoms related to hypercortisolism. The case demonstrated suppressed renin concentrations with an elevated aldosterone:renin ratio, abnormal dexamethasone suppression test results, and elevated midnight salivary cortisol concentrations. The patient had a right adrenal nodule with autonomous cortisol production and interval growth. Right adrenalectomy was carried out. Postoperatively, the patient tolerated the surgery, but he was placed on a short course of steroid replacement given a subnormal postoperative serum cortisol concentration. Long-term follow-up of the patient showed that his blood pressure and glucose levels had improved. Histopathology slides showed positive staining for 3β-hydroxysteroid dehydrogenase, 11β-hydroxylase, and 21 hydroxylase.

Conclusion: In addition to the clinical manifestations and laboratory values, the presence of these enzymes in this type of tumor provides support that the tumor in this patient was able to produce mineralocorticoids and glucocorticoids. The recognition of patients with a tumor that is co-secreting aldosterone and cortisol can affect decisions to treat with glucocorticoids perioperatively to avoid adrenal crisis.

Learning points

  • Recognition of the presence of adrenal adenomas co-secreting mineralocorticoids and glucocorticoids.

  • Consideration for perioperative and postoperative glucocorticoid use in the treatment of co-secreting adrenal adenomas.

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Rajesh Rajendran Department of Diabetes and Endocrinology, The Ipswich Hospital NHS Trust, Ipswich IP4 5PD, UK

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Sarita Naik Department of Diabetes and Endocrinology, Royal United Hospital Bath NHS Trust, Bath BA1 3NG, UK

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Derek D Sandeman Department of Diabetes and Endocrinology, University Hospital of Southampton NHS Foundation Trust, Southampton SO16 6YD, UK

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Azraai B Nasruddin Department of Diabetes and Endocrinology, University Hospital of Southampton NHS Foundation Trust, Southampton SO16 6YD, UK

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Summary

We report the use of pasireotide in a rare and unusual case of pituitary macroadenoma co-secreting GH, prolactin and ACTH. A 62-year-old Caucasian man presented with impotence. Clinically, he appeared acromegalic and subsequent investigations confirmed GH excess and hyperprolactinaemia. Magnetic resonance imaging (MRI) of pituitary revealed a large pituitary macroadenoma. He underwent trans-sphenoidal surgery and histology confirmed an adenoma with immunohistochemistry positive for ACTH, GH and prolactin. Acromegaly was not cured following surgery and inadequately controlled despite subsequent octreotide therapy. He underwent further debulking pituitary surgery, following which IGF1 levels improved but still high. This time adenoma cells showed immunohistochemistry positivity for ACTH only, following which subsequent investigations confirmed intermittent hypercortisolaemia compatible with pituitary Cushing's disease. We recommended radiotherapy, but in view of the pluripotential nature of the tumour, we proceeded with a trial of s.c. pasireotide therapy on the basis that it may control both his acromegaly and Cushing's disease. After 3 months of pasireotide therapy, his mean GH and IGF1 levels improved significantly, with improvement in his symptoms but intermittent hypercortisolaemia persists. His glycaemic control deteriorated requiring addition of new anti-diabetic medication. MRI imaging showed loss of contrast uptake within the tumour following pasireotide therapy but no change in size. We conclude that our patient has had a partial response to pasireotide therapy. Long-term follow-up studies are needed to establish its safety and efficacy in patients with acromegaly and/or Cushing's disease.

Learning points

  • Plurihormonal pituitary adenomas are rare and unusual.

  • Patients with pituitary adenomas co-secreting ACTH and GH are more likely to present with acromegaly because GH excess can mask hypercortisolaemia.

  • Pasireotide holds potential where conventional somatostatin analogues are not effective in acromegaly due to higher affinity for somatostatin receptor subtypes 1, 2, 3 and 5.

  • Significant deterioration in glycaemic control remains a concern in the use of pasireotide.

  • Currently, long-term safety and efficacy of pasireotide in patients with acromegaly and/or Cushing's disease are not fully clear.

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