The International Journal of Romanian Society of Endocrinology / Registered in 1938

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  • Book Review

    Miron R

    The Washington Manual of Medical Therapeutics

    Acta Endo (Buc) 2007 3(4): 531-531 doi: 10.4183/aeb.2007.531

  • Letter to the Editor

    Onbasi K, Hatipoglu H, Ucgun S, Güngör Hatipoglu M

    May Dental Extraction Trigger Subacute Thyroiditis? Report of Two Cases

    Acta Endo (Buc) 2015 11(4): 532-535 doi: 10.4183/aeb.2015.532

    Introduction. Subacute thyroiditis (SAT) is a self-limiting thyroid disease associated with a triphasic clinical direction of hyperthyroidism, hypothyroidism and back to normal thyroid function. Precise etiology of this clinical condition is unknown. Generally diagnosis is based on clinical-laboratory parameters. Considerable cases of SAT develop after several types of viral infections. We herein describe two cases that developed SAT after dental extraction. Cases. Two-female patients in the forties ages experienced fever and neck pain after dental extraction. The patients presented elevated sedimentation rates and SAT symptoms. After clinical diagnosis and therapy administration, symptoms resolved after one week. Conclusion. We have presented two cases experiencing SAT after dental extraction. The management and possible association with current literature were discussed.
  • Case Report

    Genc S, Evren B, Bozbay A, Aydin ES, Genc O, Sahin I

    Could Covid-19 Trigger Type 1 Diabetes? Presentation of Covid-19 Case Presented with Diabetic Ketoacidosis

    Acta Endo (Buc) 2021 17(4): 532-536 doi: 10.4183/aeb.2021.532

    COVID-19 is a viral disease that is recognized now as a pandemic by the World Health Organization. It is known that some viral infections may trigger autoimmune diseases. It has been revealed that COVID-19 may also lead to the pathogenesis of some autoimmune diseases, including Type 1 DM (T1DM) and autoimmune thyroid diseases. Here, we aimed to present a young female patient with COVID-19, who we followed up in our clinic, who presented with diabetic ketoacidosis (DKA), and developed Hashimoto’s disease during the treatment process. In order to emphasize that COVID-19 may trigger the emergence of T1DM, that it may mask nonspecific DKA symptoms like nausea and vomiting, that it may cause delay in diagnosis of DKA, and also to emphasize the importance of evaluating other autoimmune diseases accompanying COVID-19, we found it appropriate to present this case.
  • General Endocrinology

    Attakpa ES, Sezan A, B Seri

    PPAR-{alpha} Role in Obesity-Diabetes in Mice

    Acta Endo (Buc) 2013 9(4): 533-542 doi: 10.4183/aeb.2013.533

    Background. Peroxisome proliferator– activated receptors (PPAR) α and γ are ligand-activated transcription factors and members of the nuclear hormone receptor superfamily that regulate the metabolism of glucose and lipids. Aim. This study investigated the effects of PPARα deficiency on body weight in wild type and PPAR-αnull mice. Materials and methods. The study was performed on male wild type (WT) mice and homozygous PPAR-αnull (PPARα-knockout) mice of C57BL/6J genetic background. The mRNA expression was quantitatively analyzed by the real time of polymerase chain reaction (RTPCR). Liver TG content was measured by using a commercially available kit. Serum triglyceride (TG) content was measured using enzymatic methods. Serum insulin was determined using an ELISA kit. Serum glucose was determined by the glucose oxidase method using a glucose analyser. Results. Compared with WT, PPAR-αnull mice had high relative adipose tissue weight. These mice exhibited high adiposity state. PPAR-αnull mice also expressed high adiponectin and leptin mRNA levels compared to wild type animals. The PPAR-αnull mice had significantly higher body weight than WT. Hepatic TG and FFA were higher in PPAR- αnull mice as compared to WT animals. PPAR-αnull mice had a high accumulation of TG and FFA in the plasma. Serum insulin concentrations and its pancreatic mRNA transcripts were downregulated in PPAR-αnull mice, suggesting that PPARα gene deletion contributes to low insulin gene transcription. We have reported that PPARα deficiency leads to hypoglycaemia in mice. Conclusion. It is suggested a role of PPARα in obesity-diabetes in mice by studying PPARα-knockout mice.
  • Case Report

    Aydin Y, Direktor N, Berker D, Onder E, Gungor A, Celbek G

    Gliclazid induced thrombocytopenia

    Acta Endo (Buc) 2009 5(4): 533-536 doi: 10.4183/aeb.2009.533

    Background. Drug induced thrombocytopenia is mostly related with nonsteroidal\r\nanti-inflammatory drugs (NSAID), anticonvulsants, sulfonamides, diuretics, cinchona\r\nalkaloid derivatives, penicillamine and gold salts. Oral sulfonylureas such as glibenclamide,\r\nchlorpropamide and glimepiride are known to induce thrombocytopenia.\r\nCase report. We report a 42 year old female admitted to emergency department with\r\na complaint of hematochesia. She has been using oral gliclazide for three years. Laboratory\r\nresults revealed bicytopenia: haemoglobin=8.9 g/dL (N=12.3-15.3), white blood count\r\n(WBC)=12100/μL (N=4400-11300), platelet count=4000/μL (N=150000-450000). All\r\nexaminations to etiology of thrombocytopenia were negative including autoimmune,\r\ninfectious (viral-bacterial) and haematological diseases. Colonoscopic examination showed\r\n50% construction of the lumen in the first 15 cm segment of the colon by an ulcerovegetant\r\nmass. Pathological examination was reported as adenocarcinoma. Thrombocyte levels\r\nincreased on the 4th day after stopping gliclazid treatment.\r\nConclusions. It is the first case of gliclazid induced thrombocytopenia in literature. So\r\nwe recommended that platelet count should be regularly checked in all patients receiving\r\nsulfonylurea drugs including gliclazid.
  • Case Report

    Laway BA, Shah T, Bahir M, Dada A, Zargar AH

    Acute onset psychosis following steroid replacement in Sheehan's syndrome

    Acta Endo (Buc) 2010 6(4): 533-538 doi: 10.4183/aeb.2010.533

    Psychosis following steroid replacement in Sheehan's syndrome is rarely encountered. We present the clinical course of two patients who developed severe psychosis after starting them on low dose prednisolone. Psychosis subsided after either stopping or decreasing the dose together with use of antipsychotic medications. Glucocorticoids restarted a week later in low doses were well tolerated. Both the patients were reviewed after three months and were psychosis free.
  • Case Report

    Iliescu L, Mercan-Stanciu A, Toma L, Ioanitescu ES

    A Severe Case of Hyperglycemia in a Kidney Transplant Recipient Undergoing Interferon-Free Therapy for Chronic Hepatitis C

    Acta Endo (Buc) 2018 14(4): 533-538 doi: 10.4183/aeb.2018.533

    Context. Hepatitis C and diabetes represent important health problems globally. The new-onset diabetes after transplantation is a particular entity that appears due to the use of immunosuppression among transplanted patients. Objective. We aim to describe the clinical and biological aspects of severe hyperglycemia in a kidney transplant recipient undergoing Interferon-free therapy for chronic hepatitis C, discussing the interference of different factors with the glucose metabolism. Design. The occurrence of diabetes in a patient with history of renal transplantation and Interferon-free treated hepatitis C was studied from both clinical and paraclinical points of view. Subjects and methods. When presenting to the hospital, extensive blood tests were performed on the patient, revealing significant hyperglycemia and an elevated level of blood tacrolimus. Creatinine clearance was calculated. ECG presented T-wave alterations. Intensive insulin protocol was applied, the case being managed in a multidisciplinary approach. Results. Blood glucose and tacrolimus were slowly normalized, under therapy. The antiviral treatment was continued, with the achievement of sustained virologic response. Conclusions. Diabetes mellitus can have many causes, hepatitis C and transplantation both having an impact on glucose metabolism. The association of the three entities should be carefully managed, due to its enhancing effect on morbidity and mortality.
  • Book Review

    Badiu C


    Acta Endo (Buc) 2020 16(4): 535-535 doi: 10.4183/aeb.2020.535

  • Case Report

    Dema A, Taban S, Borda A, Lazureanu C, Muresan A, Cornianu M, Lazar E, Herman D, Onet D, Popovici D

    Neuroendocrine Dedifferentiation of a Prostate Adenocarcinoma after Hormonal Treatment - A Case Study

    Acta Endo (Buc) 2011 7(4): 535-544 doi: 10.4183/aeb.2011.535

    Background. The concept of NE differentiation in prostate carcinoma has two major aspects: prostate tumors with\r\nprimary NE differentiation and NE differentiation occurred during hormonal therapy for prostate adenocarcinoma, with\r\nthe extreme case of tumor dedifferentiation into a NE hormone resistant carcinoma.\r\nMaterial and method. The patient, 62 years old, with a history of poorly differentiated prostate adenocarcinoma,\r\nhormonally treated with the decrease and then constant maintenance of serum PSA level to 0.01 ng/mL was admitted in the hospital, 8 years after prostate tumor diagnosis, and 3 years after ceasing of hormone therapy, with multiple bone and liver metastases of unknown primary source.\r\nResults. The serum levels of CgA, NSE, CEA, CA19.9, serotonin were elevated. The histopathological examination\r\nof the needle biopsy fragment from a liver metastatic lesion revealed small cell neuroendocrine carcinoma. Despite the\r\nprompt chemotherapy, the disease has progressed, with the occurrence of brain metastases and the patient?s death\r\n6 months after detection of the metastatic disease.\r\nConclusions. The present case confirms the diagnostic difficulties in llymetastatic undifferentiated small cells\r\ntumors, and on the other hand, draws attention to the possibility of NE dedifferentiation as a result of hormone\r\ndeprivation in patients with prostate cancer.
  • Actualities in medicine

    Dobrescu R, Badiu C

    An Expanding Class in the Treatment of Thyroid Cancer: Tyrosine Kinase Inhibitors

    Acta Endo (Buc) 2015 11(4): 536-539 doi: 10.4183/aeb.2015.536

    Thyroid cancer, the most frequent endocrine malignancy, is in most patients a treatable disease, with excellent outcome and cure rate. However, a few patients present with rapidly progressive metastatic differentiated thyroid cancer which loses the radioiodine uptake capacity. These rare cases are prone to a rapid evolution and poor prognosis. Medullary thyroid cancer is a neuroendocrine tumor occurring sporadically or as part of endocrine tumor syndromes, genetic tests being part of standard clinical evaluation. Current knowledge of tumor biology in thyroid cancer allowed development of a new class of drugs, thyrosine kinase inhibitors (TKI). Their use in clinical trials allowed the development of more specific drugs, increasingly effective and with less adverse reactions, interfering with multiple thyrosine kinase enzymes. Improvement of the progression free survival, decrease of tumor volume and tumor markers, as well as patients with stable disease on TKI are strong arguments for including patients in clinical trials. Currently, only four TKI are approved by FDA: sorafenib and lenvatinib for DTC; vandetanib and cabozantinib for MTC. In this paper we present this new class of drugs used in the treatment of aggressive thyroid cancer.