Diagnosis and Treatment > Investigation > Urinalysis

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E Rapti Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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S Karras Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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M Grammatiki Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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A Mousiolis Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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X Tsekmekidou Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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E Potolidis Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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P Zebekakis Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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M Daniilidis 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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K Kotsa Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

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Summary

Latent autoimmune diabetes in adults (LADA) is a relatively new type of diabetes with a clinical phenotype of type 2 diabetes (T2D) and an immunological milieu characterized by high titers of islet autoantibodies, resembling the immunological profile of type 1 diabetes (T1D). Herein, we report a case of a young male, diagnosed with LADA based on both clinical presentation and positive anti-glutamic acid decarboxylase antibodies (GAD-abs), which were normalized after combined treatment with a dipeptidyl peptidase-4 inhibitor (DPP-4) (sitagliptin) and cholecalciferol.

Learning points

  • Anti-glutamic acid decarboxylase antibodies (GAD-abs) titers in young patients being previously diagnosed as type 2 diabetes (T2D) may help establish the diagnosis of latent autoimmune diabetes in adults (LADA).

  • Sitagliptin administration in patients with LADA might prolong the insulin-free period.

  • Vitamin D administration in patients with LADA might have a protective effect on the progression of the disease.

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Akira Kurozumi First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Yosuke Okada First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Tadashi Arao First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan
Department of Internal Medicine, Japan Labour Health and Welfare Organization, Kyushu Rosai Hospital, Moji Medical Center, Kyushu, Japan

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Yusuke Miyazaki First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Maiko Yoshikawa First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Keiichi Torimoto First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Satoshi Kubo First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Shingo Nakayamada First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Yoshiya Tanaka First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

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Summary

A randomized controlled study of rituximab demonstrated that the drug protects pancreatic function in patients with acute-onset type 1 diabetes mellitus (AOT1DM). However, the mechanism of this protective effect is poorly understood. We examined the effects of rituximab in two patients with AOT1DM in the honeymoon period and the mechanism of these effects. Case 1 was a 40-year-old man and Case 2 was a 45-year-old man, both diagnosed with AOT1DM. Various tests indicated intact capacity for endogenous insulin secretion and that they were in the honeymoon phase of AOT1DM. Treatment with rituximab protected against pancreatic β-cell damage and maintained somewhat the endogenous insulin secretion. In Case 2, HbA1c level was maintained below 6.5% up to 24 months after treatment. However, in Case 1, the patient showed a gradual increase in HbA1c level starting around 9 months but fell at 12 months to >9.0% and required an insulin dose about twice greater than that of Case 2. High spleen tyrosine kinase (Syk) levels were recorded in the two patients before rituximab administration and after the treatment, the levels were further increased in Case 1, but decreased in Case 2. Both patients require continuous careful follow-up for glycemic control, insulin secretion capacity, and adverse reactions in the future. Although the clinical relevance of high Syk levels in AOT1DM patients remains unclear, the difference in the change in Syk level between the two patients may explain the different clinical courses.

Learning points

  • We described the pancreas-protective effect of rituximab in two patients with acute-onset type 1 diabetes mellitus in the honeymoon period and investigated the possible mechanism of action.

  • The present study demonstrated that treatment with rituximab maintained endogenous insulin secretion capacity for 2 years in the two patients.

  • The phosphorylated-spleen tyrosine kinase (p-Syk) data suggest that the differences in HbA1c level and the required insulin dose between the two patients could be due to reactivation or nonreactivation of β-cells.

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A Tabasum Diabetes and Endocrinology, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

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C Shute Diabetes and Endocrinology, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

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D Datta Biochemistry, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

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L George Diabetes and Endocrinology, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

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Summary

Hypokalaemia may present as muscle cramps and Cardiac arrhythmias. This is a condition commonly encountered by endocrinologists and general physicians alike. Herein, we report the case of a 43-year-old gentleman admitted with hypokalaemia, who following subsequent investigations was found to have Gitelman's syndrome (GS). This rare, inherited, autosomal recessive renal tubular disorder is associated with genetic mutations in the thiazide-sensitive sodium chloride co-transporter and magnesium channels in the distal convoluted tubule. Patients with GS typically presents at an older age, and a spectrum of clinical presentations exists, from being asymptomatic to predominant muscular symptoms. Clinical suspicion should be raised in those with hypokalaemic metabolic alkalosis associated with hypomagnesaemia. Treatment of GS consists of long-term potassium and magnesium salt replacement. In general, the long-term prognosis in terms of preserved renal function and life expectancy is excellent. Herein, we discuss the biochemical imbalance in the aetiology of GS, and the case report highlights the need for further investigations in patients with recurrent hypokalaemic episodes.

Learning points

  • Recurrent hypokalaemia with no obvious cause warrants investigation for hereditary renal tubulopathies.

  • GS is the most common inherited renal tubulopathy with a prevalence of 25 per million people.

  • GS typically presents at an older age and clinical suspicion should be raised in those with hypokalaemic metabolic alkalosis associated with hypomagnesaemia.

  • Confirmation of diagnosis is by molecular analysis for mutation in the SLC12A3 gene.

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