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Diagnosis and Treatment > Medication > Alpha-glucosidase inhibitors

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Masato Kotani Center for Diabetes, Endocrinology and Metabolism
Research Support Center, Shizuoka General Hospital, Shizuoka, Shizuoka, Japan
Asahina Shinryoujo, Fujieda, Shizuoka, Japan

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Naohisa Tamura Center for Diabetes, Endocrinology and Metabolism
Research Support Center, Shizuoka General Hospital, Shizuoka, Shizuoka, Japan

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Tatsuhide Inoue Center for Diabetes, Endocrinology and Metabolism

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Issei Tanaka Center for Diabetes, Endocrinology and Metabolism

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Summary

Type B insulin resistance syndrome is characterized by the presence of autoantibodies to the insulin receptor. We present a 57-year-old male admitted to a hospital due to body weight loss of 16 kg and hyperglycemia of 13.6 mmol/L. He was diagnosed with type B insulin resistance syndrome because the anti-insulin receptor antibodies were positive. We informed him that some hyperglycemic cases of this syndrome had been reported to be spontaneously remitted in 5 years, and he did not agree to be treated with high-dose glucocorticoids and/or immunosuppressive agents due to his concern for their adverse effects such as hyperglycemia and immunosuppression. He chose to be treated with insulin and voglibose, but fair glucose control could not be obtained. Six years later, he agreed to be treated with low-dose glucocorticoids practicable in outpatient settings. One milligram per day of betamethasone was tried orally and reduced gradually according to the values of glycated hemoglobin. After 30 months of glucocorticoid treatment, the anti-insulin receptor antibodies became undetectable and his fasting plasma glucose and glycated hemoglobin were normalized. This case suggests that low-dose glucocorticoids could be a choice to treat type B insulin resistance syndrome in outpatient settings.

Learning points:

  • Type B insulin resistance syndrome is an acquired autoimmune disease for insulin receptors.

  • This case suggested the possibility of long-lasting, low-dose glucocorticoid therapy for the syndrome as an alternative for high-dose glucocorticoids or immunosuppressive agents.

  • Since the prevalence of autoimmune nephritis is high in the syndrome, a delay of immunosuppressive therapy initiation might result in an exacerbation of nephropathy.

Taxonomy:
Clinical Overview, Gland/Organ, Kidney, Topic, Diabetes, Hormone, Insulin, Condition/ Syndrome, Autoimmune disorders, Hyperglycaemia, Insulin resistance, Patient Demographics, Age, Adult, Gender, Male, Ethnicity, Asian - Japanese, Country of Treatment, Japan, Diagnosis and Treatment, Signs and Symptoms, Diabetic nephropathy, Glucosuria, Haematuria, Hyperglycaemia, Hyperinsulinaemia, Hypoglycaemia, Insulin resistance, Ketonuria, Proteinuria, Thrombocytopenia, Weight loss, Investigation, Albumin, Alkaline phosphatase, Antinuclear antibody, BMI, C-peptide (24-hour urine), Creatinine (serum), Glucose (blood, fasting), Haemoglobin A1c, Immunoglobulins, Immunoglobulin A, Insulin, Platelet count, Red blood cell count, Urinalysis, Weight, White blood cell count, Medication, Alpha-glucosidase inhibitors, Angiotensin-converting enzyme inhibitors, Betamethasone, Diuretics, Glucocorticoids, Insulin, Voglibose, Related Disciplines, Nephrology, Publication Details, Case Report Type, Novel treatment
DOI:
https://doi.org/10.1530/EDM-19-0115
Volume/Issue:
Volume 2019: Issue 1
Open access
Xin Chen Division of Internal Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

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Dina Kamel Division of Endocrinology, Diabetes, and Metabolism, Keck School of Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

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Braden Barnett Division of Endocrinology, Diabetes, and Metabolism, Keck School of Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

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Evan Yung Division of Pathology, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

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Adrienne Quinn Keck School of Medicine, University of Southern California, Los Angeles, California, USA

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Caroline Nguyen Division of Endocrinology, Diabetes, and Metabolism, Keck School of Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

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Summary

There has been an increasing awareness of post gastric bypass hypoglycemia (PGBH). Histopathologic findings from such patients who underwent partial/total pancreatomy, however, can vary widely from minimal changes to classic nesidioblastosis, making the pathologic diagnosis challenging. PGBH typically presents as postprandial hypoglycemia, as opposed to insulinoma, which presents as fasting hypoglycemia. Herein, we describe an unusual case of a patient with PGBH who initially presented with postprandial hypoglycemia three years after surgery, but later developed fasting hyperinsulinemic hypoglycemia as the disease progressed. Our hypothesis for this phenomenon is that this disease is progressive, and later in its course, the insulin release becomes dissociated from food stimulation and is increased at baseline. Future studies are needed to investigate the prevalence as well as etiology of this progression from postprandial to fasting hypoglycemia.

Learning points:

  • There has been an increasing awareness of post gastric bypass hypoglycemia (PGBH).

  • Histopathologically, PGBH can vary from minimal changes to nesidioblastosis.

  • Although uncommon, patients with PGBH after Roux-en-Y gastric bypass may present with both postprandial and fasting hyperinsulinemic hypoglycemia as disease progresses.

  • Our hypothesis for this phenomenon is that the insulin release becomes dissociated from food stimulation and is increased at baseline with disease progression.

Taxonomy:
Clinical Overview, Gland/Organ, Pancreas, Topic, Obesity, Hormone, Insulin, Condition/ Syndrome, Hyperinsulinaemic hypoglycaemia, Hypoglycaemia, Iatrogenic disorder, Post-prandial hypoglycaemia, Patient Demographics, Age, Adult, Gender, Female, Ethnicity, White, Country of Treatment, United States, Diagnosis and Treatment, Signs and Symptoms, Dizziness, Hyperhidrosis, Hyperinsulinaemia, Hypoglycaemia, Syncope, Tremulousness, Investigation, C-peptide (blood), Glucose (blood), Glucose (blood, fasting), Haematoxylin and eosin staining, Histopathology, Immunohistochemistry, Insulin, Intervention, Bariatric surgery, Diet, Pancreatectomy, Medication, Acarbose, Alpha-glucosidase inhibitors, Diazoxide, Octreotide, Somatostatin analogues, Publication Details, Case Report Type, Unique/unexpected symptoms or presentations of a disease
DOI:
https://doi.org/10.1530/EDM-18-0089
Volume/Issue:
Volume 2018: Issue 1
Open access
Ken Takeshima First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

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Hiroyuki Ariyasu First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

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Tatsuya Ishibashi First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

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Shintaro Kawai First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

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Shinsuke Uraki First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

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Jinsoo Koh Department of Neurology, Wakayama Medical University, Wakayama,, Japan

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Hidefumi Ito Department of Neurology, Wakayama Medical University, Wakayama,, Japan

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Takashi Akamizu First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

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Summary

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystem disease affecting muscles, the eyes and the endocrine organs. Diabetes mellitus and primary hypogonadism are endocrine manifestations typically seen in patients with DM1. Abnormalities of hypothalamic–pituitary–adrenal (HPA) axis have also been reported in some DM1 patients. We present a case of DM1 with a rare combination of multiple endocrinopathies; diabetes mellitus, a combined form of primary and secondary hypogonadism, and dysfunction of the HPA axis. In the present case, diabetes mellitus was characterized by severe insulin resistance with hyperinsulinemia. Glycemic control improved after modification of insulin sensitizers, such as metformin and pioglitazone. Hypogonadism was treated with testosterone replacement therapy. Notably, body composition analysis revealed increase in muscle mass and decrease in fat mass in our patient. This implies that manifestations of hypogonadism could be hidden by symptoms of myotonic dystrophy. Our patient had no symptoms associated with adrenal deficiency, so adrenal dysfunction was carefully followed up without hydrocortisone replacement therapy. In this report, we highlight the necessity for evaluation and treatment of multiple endocrinopathies in patients with DM1.

Learning points:

  • DM1 patients could be affected by a variety of multiple endocrinopathies.

  • Our patients with DM1 presented rare combinations of multiple endocrinopathies; diabetes mellitus, combined form of primary and secondary hypogonadism and dysfunction of HPA axis.

  • Testosterone treatment of hypogonadism in patients with DM1 could improve body composition.

  • The patients with DM1 should be assessed endocrine functions and treated depending on the degree of each endocrine dysfunction.

Taxonomy:
Clinical Overview, Gland/Organ, Adrenal, Topic, Adrenal, Hormone, ACTH, Aldosterone, Cortisol, FSH, IGF1, Insulin, LH, Prolactin, Testosterone, Condition/ Syndrome, Adrenal insufficiency, Autoimmune hypophysitis, Hypergonadotropic hypogonadism, Hyperkalaemia, Hypernatraemia, Hypogonadism, Insulin resistance, Myotonic dystrophy type 1, Patient Demographics, Age, Adult, Gender, Male, Ethnicity, Asian - Japanese, Country of Treatment, Japan, Diagnosis and Treatment, Signs and Symptoms, Diabetes mellitus type 2, Erectile dysfunction, Facies - abnormal, Hyperkalaemia, Hypernatraemia, Hypogonadism, Insulin resistance, Libido reduction/loss, Muscle atrophy, Myasthaenia, Myopathy, Obesity, T-reflex (depressed), Investigation, ACTH, Adrenal function, Aldosterone (24-hour urine), Aldosterone (blood), BMI, Body fat mass, Corticotropin-releasing hormone stimulation test, Cortisol, free (24-hour urine), C-peptide (24-hour urine), C-peptide (blood), CT scan, Electromyography, FSH, Glucose (blood, fasting), Haemoglobin A1c, IGF1, LH, Molecular genetic analysis, Potassium, Prolactin, Respiratory status, Skeletal muscle mass, Sodium, Testosterone, Triglycerides, Waist circumference, White blood cell count, Intervention, Diet, Medication, Alpha-glucosidase inhibitors, DPP4 inhibitors, Insulin, Insulin glargine, Metformin, Pioglitazone, Sitagliptin, Testosterone, Testosterone enanthate esters, Thiazolidinediones, Voglibose, Related Disciplines, Neurology, Publication Details, Case Report Type, Unique/unexpected symptoms or presentations of a disease
DOI:
https://doi.org/10.1530/EDM-17-0143
Volume/Issue:
Volume 2018: Issue 1
Open access