2013 - Endo · PDF file23-26 October, 2013 Cornelia Diamond Hotel Antalya - Turkey Background: Management of pituitary stalk lesions is a challenging diagnostic problem. Due to advances

2013

Ассоциация эндокринологов

Турецкая ассоциация эндокринологии и обмена веществ

جمعية الغدد الصماء

Bridging the World of EndocrinologyМост, объединяющий мир эндокринологии

توحيد عالم الغدد الصماء

الرابطة التركية الغدد الصماء واأليض

23-26 October, 2013 Cornelia Diamond Hotel Antalya - Turkey23-26 октября 2013 г. Отель “Cornelia Diamond” Анталья - Турция

23- 26 أكتوبر 2013 فندق كورنيليا داميوند أنطاليا - تركيا

w w w . e n d o b r i d g e . o r g

2013

5 23-26 October, 2013 Cornelia Diamond Hotel Antalya - Turkey

Background: Management of pituitary stalk lesions is a challenging diagnostic problem. Due to advances in mag-netic resonance imaging (MRI) technology, pituitary stalk lesions may be identified either incidentally or during eval-uation for symptoms related to hypothalamic - pituitary dysfunction. Pathological processes that involve the hy-pophyseal stalk may extend from the hypothalamus and/or the pituitary gland or may be limited to the stalk itself. The etiological spectrum of these lesions can be divided in 3 cat-egories: neoplastic, inflammatory/infectious, and congeni-tal. Because of the critical location and role of the pituitary stalk, mass lesions in this area are not often biopsied, and the diagnosis may be based on clinical evaluation and imag-ing clues. Here, we report a case of possible neurosarcoid-osis of pituitary hypothalamus without any other systemic involvement.

Case report: A 47-year-old woman presented with polyph-agia and weight gain of about 30 kg in three months. She had been diagnosed as diabetes insipidus 4 years ago and was using vasopressin therapy. Her thyroid hormone levels were consistent with primary hypothyroidism and she was given thyroid hormone replacement [TSH: 19.7 μIU/m sT4: 0,41 ng/dl (0.74-1.79)]. Serum levels of anti-thyroid peroxi-dase were negative. On progressive worsening of symptoms of general weakness and menstrual irregularities, her pitu-itary function tests revealed panhypopituitarism one month ago. Her sella MRI showed a mass 1x1.4 cm in size, infil-

trating the hypothalamus without extension to the stalk or hypophysis. Since the differential diagnosis of infiltrative lesion in hypothalamus included sarcoidosis, serum angio-tensin converting enzyme (ACE) levels were tested and re-ported within normal limits. Her chest computed tomograhy was normal. A pituitary biopsy was advised but could not be performed because of lack of patient consent. A lumbar puncture was performed and her ACE levels in CSF was con-sistent with neurosarcoidosis (ACE in CSF: 1.6 mumol/l/min and ACE in peripheral blood: 57.5 mumol/l/min). High dose steroid and cyclophoshamide treatment was started and she is under follow up now.

Conclusion: Sarcoidosis is a chronic inflammatory disease of unknown etiology that is characterized by noncaseating granulomatous inflammation and involvement of almost en-tire system of the body. Only about 1.3% of sarcoidosis cases involve the nervous system. Intracranial neurosarcoidosis often affects the leptomeninges and commonly presents as nodular and/or diffuse infiltrative growing lesions. Most patients with neurosarcoidosis presented with a uniformly thickened pituitary stalk on MRI. Hypothalamic infiltration have been described rarely. Sarcoidal granulomas produce ACE which is elevated in about 60% of patients with sarcoid-osis. However, the value of serum ACE levels in the diagnosis of sarcoidosis remains controversial due to its inadequate sensitivity and specificity.

(Pituitary)

A RARE CASE OF NEUROSARCOIDOSIS INVOLVING THE HYPOTHALAMUS

Nese Cinar, Nafiye Helvaci, Miyase BayraktarHacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Sihhiye, Ankara

2013


Background: Proximal muscle weakness and diabetic ketoac-idosis are only rarely first clinical presentations of acromegaly.

Clinical Case: A 30 years old male patient presented with mus-cle weakness, weight loss of 12 kg in the last 5 months, plydipsia and polyuria. He had acral and facial enlargement prominent in last year. In the last week he was diagnosed with diabetes due to elevated blood sugar levels. His personal and family histo-ry did not reveal any relevant disease. He was referred to our center for his diabetes. His general condition was fair. He had prognatism and coarse facial features, swollen hands and feet. His height was 180 cm, weight was 76.5 kg, blood pressure was 140/80 mmHg. He had proximal muscle weakness (3/5 bilater-ally) and he could barely walk. His blood glucose level was 501 mg/dl, venous ph was 7.21 and acetone was (+) in urine analy-sis. Additional laboratory results are presented in Table 1 and Table 2. He was hospitalized with diabetic ketoacidosis. Intra-venous isotonic saline infusion with a total of 20 mEq KCl was initated. After s.c bolus of 10 U rapid acting insulin, 0.1 U/kg/hr i.v insulin infusion was initiated. Serum glucose was mea-sured every hour, while serum electrolytes and venous pH were measured every four hours. When the serum glucose reached 250 mg/dL, additionally i.v dextrose solution was initiated. His GH level 80 ng/ml (N:0-4 ng/ml), while the concomitant blood glucose level was 500 mg/dl. IGF-1 level was IGF1: 821 ng/mL (N:115-358), so he was diagnosed with acromegaly. Sella MRI revealed a 54x24 mm macroadenoma infiltrating cavernous si-nus on both sides. Despite Vitamin D replacement his muscle weakness did not improve. EMG revealed prolonged latency of sensory and motor responses of median nerve bilaterally, prolonged F responses of proximal extremity and prominently prolonged motor response amptitutes in lower extremity. For acromegaly long acting octreotide analogue (20 mg, s.c) was administered and he was transferred to neurosurgery with ongoing insulin infusion. Pathology of the hypophysectomy material showed an adenoma with scarce PRL positivity and 95% positivity for GH. LH and TSH were 5% and 20% positive, respectively. P53 was <%1 and Ki67 was %1. After operation

blood glucose levels decresed to 70-80 mg/dl so insulin was discontinued and metformin was added. In early postoperative period steroid and thyroid hormone replacements were initiat-ed due to hypopituitarism and octreotide analogue was contin-ued. At postoperative 8 months his muscle weakness resolved completely, his GH level was 0.25 ng/ml, IGF-1 was 126.7 ng/ml (N:115- 358), fasting blood glucose level was 93 mg/dl and HbA1c was 6.7 (figure 1). Conclusion: Although rare proximal muscle weakness and diabetic ketoacidosis can be the first presentation in cases with acromegaly. With efficient treatment of acromegaly these complications can also regress.

Table 1

Table 2

(Pituitary)

A CASE WITH ACROMEGALY PRESENTING WITH PROXIMAL MUSCLE WEAKNESS AND DIABETIC

KETOACIDOSISEsra Hatipoglu, Pinar Kadioglu, Sadi Gundogdu

Dıvısıon Of Endocrınology And Metabolısm, Department Of Internal Medıcıne, Cerrahpasa Medıcal School, Unıversıty Of Istanbul, Istanbul, Turkey

2013


Figure 1

2013


Hereditary hemochromatosis is an autosomal recessive ge-netically transmitted disorder due to the mutation of HFE gen(C282Y). HFE protein is responsible for control of iron in duodenal cript cells. Besides from accumulation of iron in various tissues such as skin, liver, kidneys, many endo-crin organs may be affected. A 35 year old woman without any known illness admitted with menstrual irregularity and darkening of the skin. She had one live birth. On physical examination she had only sligth alopecia and hyperpigmen-tation. Laboratory results are shown on the Table. She was diagnosed hemochromatosis because of high transferin saturation and high ferritin levels and she was searched for organ involvement. Abdominal USG was normal. Abdominal MRI showed diffuse signal attenuation consistent with he-

mosiderosis or hemochromatosis without any other patho-logical finding. Hormon profile revealed hypogonadothropic hypogonadism with low FSH and LH levels with other hyph-ophysis hormones in normal range. In our case hypophysis MRI supported iron accumulation. Although she had insu-lin resistance; as she had normal body weight and repeated blood glucose levels and HbA1C level were normal, we only recommended her to follow up blood sugar. We performed genetic analysis for HFE gen mutation. HD3D mutation was found positive heterozigotically. Gynecological examination and visual field were normal. We performed liver biopsy. Iron accumulation was seen in all hepatocytes with Prussian blue in granular pattern. After consultation with hematolo-gist filebotomy was planned according to Htc values.

(Pituitary)

A WOMAN WITH HIPOPITUITARY HEMOCHROMATOSIS

Füsun Erdenen, Rengin Altınok, Ebru Pekgüç, Ayşe Üzüm, Mustafa Boz, Cüneyt Müderrisoğlu, Yeşim Karagöz, Esma Altunoğlu

Istanbul Training and Research Hospital

2013


Introduction: Thyroid hormone resistance(THR) is an end organ hyporesponsiveness in tissues. Main cause of THR is dominant negatif inhibitory effect of thyroid hormone recep-tor mutations.The clinical symptoms can be so variable. The patients can be euthyroid, hyperthyroid or hypothyroid. And there are some ways to follow up metabolic and tissue ef-fects of thyroid hormone. One of them is systolic time inter-val index (Preejection period (PEP) / Left ventricular ejection time (LVET)), which is useful in the follow-up of the tissue effects of the thyroid hormone. The normal reliable healthy population values of PEP / LVET ratios are 0.29-0.34 in males and 0.30-0.35 in females. Here we present a patient with thy-roid hormone resistance. We use systolic time interval index to follow up patient’s metabolic response with treatment.

Case Presentation: A 72 year old male patient had been re-ferred to Akdeniz University Endocrinology Division because of high thyroid hormone levels on routine screening. His TSH level was found 9.95 μIU/mL (normal range 0,35-5,5); his free T3(fT3) level was found 5,27 pg/mL (normal range 2.3-4.2); and free T4(fT4) level was found 2.22 ng/dL (normal range 0,89-1,76). He had tachycardia but any other symptoms. He did not have a family history of thyroid disease. He had no neck tenderness and his thyroid gland was not palpable. He had no hand fine tremor. Hypophyseal MRI was scheduled to

rule out a TSH-secreting adenoma. But his hypophyseal MRI had normal appearance.His systolic time interval index was 0,185 (normal range: 0.29-0.34 in males) before treatment. The patient was considered as clinically hyperthroid accord-ing to the thyroid hormone’s tissue effect. He had increased TSH, free T4 and free T3 levels, although he had peripheral thyrotoxicosis. We considered he has thyroid hormone resis-tance. We started methimazole two times(2x5) a day. After one month treatment we measured his systolic time interval index with echocardiography again to follow up the periph-eral thyrotoxicosis. His systolic time interval index increased up to 0,238. His TSH, free T4, free T3 levels were 26.59 μIU/mL, 0.89 ng/dL and 3.05 pg/mL respectively. And he had no longer tachycardia. Methimazole was stopped and planned to follow up his thyroid hormones two weeks later.

Conclusion: Misdiagnosis of TRH in clinics are common and it causes treatment failures in patients. Nearly one-third of patients was misdiagnosed as primary hyperthyroidism and treated inappropriately. And systolic time interval index measurement is also a reliable way to follow-up treatment of hyperthyroxinemia. Furthermore, we should always con-sider TRH, in our differential diagnosis in case of high thy-roid hormone levels.

(Thyroid)

CASE REPORT: THYROID HORMONE RESISTANCE FOLLOWED UP WITH SYSTOLIC TIME INTERVAL

INDEX MEASUREMENTAlparslan Merdin1, Mustafa Kemal Balci2, Fatma Avci1, Hasan Altunbas2

1 Department of Internal Medicine, University of Akdeniz 2 University of Akdeniz, Department of Internal Medicine and Endocrinology, Antalya

2013


Background: Fine-needle aspiration (FNA) plays an essen-tial role for the evaluation of most thyroid nodules larger than 1 cm. Of all thyroid FNAs, 3-6% are reported as atypia of undetermined significance (AUS). The usual follow-up of AUS is repeating the FNA; however if the clinician has clin-ically or sonographically suspicion for malignancy, patient can be referred to surgery.

Case Report: A 58 year-old female was found to have a 2-cm, incidentally discovered thyroid nodule on the right lobe while undergoing chest computed tomography scanning when she was admitted to emergency department for dyspnea. The patient was known to have systemic lupus erithema-tosus and asthma but no prior thyroid illness. Assessment of serum TSH concentration revealed a value of 3.16 mIU/mL (normal 0.27– 4.2 mIU/mL). The patient underwent ul-trasound evaluation of thyroid, a 25x 18x12 cm nodule on the inferior part of the right thyroid lobe, with peripheral

hypoechoic halo and microcalsifications and both peripher-al and internal vascularisations was seen. The patient was recommended for ultrasound-guided fine-needle aspiration of the nodule. The cytology result was reported as atypia of undetermined significance. The patient was referred to surgery and total thyroidectomy was performed. The biop-sy material was reported as chronic lymphocytic thyroiditis. The immunohistochemical evaluation of the nodule with CK19, HBME-1,Galaktin 3 were all reported as negative and the Ki-67 proliferation index was ≤1.

Conclusion: Due to the fact that some thyroid FNAs are not classified as benign, malignant or suspicious, in the Bethes-da System for reporting thyroid cytopathology, such FNAs are reported as atypia of undetermined significance, which is 3-6% of all FNAs. Depending on the clinically or sono-graphically suspicion, patient is referred to repeat the FNA, follow-up or surgery.

(Thyroid)

MANAGEMENT OF A PATIENT WITH ATYPIA OF UNDETERMINED SIGNIFICANCE IN THYROID NODULE

FINE NEEDLE ASPIRATION CYTOLOGYAyşe Bahar Keleşoğlu1, Safak Akin², Alper Gurlek²

1 Hacettepe University School of Medicine, Department of Internal Medicine, Sihhiye, Ankara 2 Hacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Sihhiye, Ankara

2013


Background: Papillary thyroid microcarcinomas are defined as papillary carcinomas ≤1 cm in diameter. Recent studies have indicated that total thyroidectomy decreases overall recurrence rate and is the treatment of choice. Although microcarcinomas have excellent prognosis, recurrence is possible, especially when multifocality and lymph node me-tastasis exists. The use of RAI ablation in thyroid microcarci-noma cases is generally not recommended. However, there is a caveat that patients with papillary thyroid carcinoma and concerning risk factors such as multifocality or lymphade-nopathy may be considered for RAI ablation.

Case: A 44-year-old female patient was found to have a mul-tinodular goiter in routine controls. She was referred to our hospital. Her thyroid function tests were normal. A heteroge-neous hypoechoic nodule of 9.5 x 7.5 mm in size with irreg-

ular borders and lymphadenopathies with the largest node of 21.5 x 8.5 mm on the neck were detected by ultrasound. A thyroid fine needle aspiration biopsy was performed. Cy-tology specimen was compatible with papillary carcinoma. A total thyroidectomy and central neck lymph node dissection was performed. Histopathologic examination revealed three thyroid papillary microcarcinoma foci of 0,8 cm, 0.2 cm, and 0,1 cm; reactive lymph nodes; and two parathyroid glands. There were no residual thyroid gland on postoperative thy-roid scintigraphy. 100 mCi I-131 ablation was performed.

Conclusion: Multifocal disease have been shown to have a higher recurrence rate. Thus, radioactive iodine ablation af-ter total thyroidectomy would be safer in the management of papilary microcarcinomas when multifocality exists.

(Thyroid)

RADIOACTIVE IODINE ABLATION THERAPY IN THYROID MULTIFOCAL PAPILLARY CARCINOMA:

A CASE REPORTBerfu Korucu¹, Nafiye Helvaci², Alper Gurlek²

1 Hacettepe University School of Medicine, Department of Internal Medicine, Sihhiye, Ankara 2 Hacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Sihhiye, Ankara

2013


Background: Interferon/Ribavirin combination has been reported to induce thyroid dysfunction and autoimmunity ranging from hypothyroidism to thyrotoxicoses. Thyrotoxico-ses are induced either by destructive thyroidities or Graves disease.

Clinical Case : We report the case of a 63 year-old , HCV positive, female with a history of HTN on coversyl 4mg, who was referred to our Clinic in May 2011. She received a first cycle of interferon/ribavirin combination in 2008 with no complication. Thyroid function and AntiTpo at base line and after interferon was negative. In 2009 she developed high grade ventricular arrhythmia, for which she was started on amiodarone therapy. After 6 months, she developed prima-ry hypothyroidism, antiTpo was negative. Amiodarone was stopped and the patient was started on beta core 80 mg . Because hypothyroidism persisted, she was started on L thyroxine 75 mg. She remained euthyroid on this dose for 4 years . At presentation, she was biochemically and clinical-

ly euthyroid on thyroxine 75 mg . In October 2012, she was restarted on interferon /ribavirin combination therapy by a hepatologist. After 5 months of treatment, she became thy-rotoxic. Thyroxine doses were gradually lowered / tapered, then treatment was discontinued. Anti TPO was negative . As the Anti TSH receptor antibody and RAI scan was not avail-able in Libya the patient went to Tunisia to do them . Anti TSH receptor was positive, and TC99m scan revealed high up-take. Interferon was stopped by the hepatologis as the PCR was negative and the patient underwent RAI 131 therapy in Tunisia . After 6 weeks of RAI therapy she return to follow up our clinic with thyroid function TSH was 100 mUI/l, T4 & T 3 very low . L thyroxine 100 µg treatment restarted gradually.

Conclusion : To our knowledge, this is the first report of a case of long term hypothyroidism induced by amiodarone therapy evolving into thyrotoxic Graves disease induced by interferon/ ribavirin combination therapy in libya .

(Thyroid)

INTERFERON-INDUCED TOXIC GRAVES DISEASE IN A PATIENT WITH AMIODARONE-INDUCED

HYPOTHYROIDISM ON THYROXINE REPLACEMENTAdela Ebsat

Endocrine And Diabetes Unit /Hawri Teaching Hospital/ Benghazi Unversity

2013


History and Admission Findings: We report about a male patient with Graves’ disease and immune thrombocytopenia (ITP). He was started antithyroid treatment for Graves’ dis-ease and steroid therapy for ITP. He developed diabetes un-der steroid treatment which resolved after discontinuation a three month long steroid therapy.

Diagnosis, Treatment and Course: TSH receptor antibod-ies (TRAb) were elevated. Cytologic examinations of the pe-ripheral blood count showed a distinctive thrombocytopenia and giant platelets. The results were interpreted as ITP and concomitant Graves’. The patient received steroid thepapy for three months for ITP. There was a significant improve-

ment after this therapy but the patient developed diabetes. As treatment for diabetes the patient received insulin during this period. Finally, normalisation of glucose levels occured after cessation of ITP. Also a normalisation of the platelet count was observed after discontinuation of ITP treatment.

Conclusion: It is known that the association of idiopath-ic thrombocytopenic purpura and Graves’ disease is rare. Hence, little is known about the outcomes of these two diseases when associated. In our case, successful man-agement of Graves‘ disease including efficient antithyroid therapy may also have contributed to normalisation of the platelet count.

(Thyroid)

IMMUNE THROMBOCYTOPENIA AND GRAVES’ DISEASE: A RARE COMBINATION OF TWO IMMUNE

MEDIATED DISEASEKevser Onbasi1, Türkan Paşali Kilit1, Sadrettin Özge Erez2

1 Dumlupinar University Kütahya Turkey 2 Kütahya Evliya Çelebi Training And Education Hospital

2013


Introduction: Acute suppurative thyroiditis (ST) is rare, but potentially life threatening condition usually caused by bac-terial infection of the thyroid gland. The organisms most often isolated from ST patients are aerobic bacteria but anaerobic bacteria, viruses, and parasites are encountered infrequently, too. Neck ultrasonography (USG) often shows abscess formation and facilitates guided drainage when necessary. Herein we present a case of ST with thyroid ab-scess accompanied by thyrotoxicosis on postpartum period caused by Peptostreptococcus, which is also rarely encoun-tered.

Case Report: A 24-year-old female presented to our clinic on the fifth postpartum day with severe neck pain on swal-lowing, chills and fever. She had been diagnosed with acute tonsillitis 6 days before delivery and had used oral amoxicil-lin for 5 days. Physical examination revealed fever (38 °C), tachycardia, and an erythematous non-fluctuant mass over the left thyroid lobe. Laboratory findings were as follows: elevated WBC count: 14,490 (neutrophils 85%); erythrocyte sedimentation rate: 30 mm/h; C-reactive protein (CRP): 127 mg/L. Thyroid function test results were as follows: free T4 (thyroxine): 3.12 ng/dL (normal range: 0.93-1.7); free T3 (triiodothyronine): 6.72 pg/mL (normal range: 2.0-4.4); TSH (thyroid-stimulating hormone): 0.01 μIU/mL (normal range: 0.27-4.2). Technetium 99m (99mTc) sodium pertechnetate neck scan showed no uptake in the thyroid beds. The results

were compatible with thyrotoxicosis due to thyroid tissue destruction. Thyroid USG showed a 10.1 ´ 14.5 ´ 25.6 mm heterogeneous hypoechoic lesion in the left lobe. Approxi-mately 5 cc of purulent yellow-brown foul-smelling fluid was obtained at the first USG-guided aspiration, a portion of which has been cultivated. The patient has been adminis-tered sulbactam/ampicillin for initial therapy. Thyroid aspi-rate cultures showed Peptostreptococcus growth which was sensitive to sulbactam/ampicillin. Two weeks later thyroid USG showed that the abscess shrank to 2.2 x 3.1 ´ 4.2 mm. On the 20th day of antimicrobial therapy, all clinically and laboratuary signs and symptoms of infection were resolved.

Discussion: ST may occur as a result of haematogenous and lymphatic spread as well as by direct invasion from sur-rounding infected tissues. In untreated cases abscess for-mation may also develop. In our patient, ST and abscess had probably developed after an upper respiratory tract infection via direct invasion of Peptostreptococcus which may have been facilitated by pregnancy-induced immunosuppression. In the presented case a rarely seen anaerobe “Peptostrepto-coccus” was isolated from the patient’s thyroid abscess and she was treated successfully with parenteral sulbactam/ampicillin therapy and multiple thyroid abscess aspirations. Thyrotoxicosis has resolved with no medications. During the follow-up period the patient’s prognosis had been excellent with no complications.

(Thyroid)

POSTPARTUM THYROTOXICOSIS WITH ACUTE SUPPURATIVE THYROIDITIS CAUSED BY

PEPTOSTREPTOCOCCUSNarin Nasiroglu Imga1, Yasemin Tütüncü1, Mazhar Müslüm Tuna1, Dilek Berker1, Serdar Güler2

1 Ankara Numune Education And Research Hospital, Department Of Endocrinology; Sihhiye, Ankara, Turkey 2 Hitit University Faculty Of Medicine, Department Of Endocrinology, Çorum, Turkey 2

2013


Introduction: Primary squamous cell carcinoma (SCC) of thyroid gland is an enormously rare disease. Infrequently primary SCC of the thyroid gland is accompanied by other thyroid diseases such as Hashimoto’s thyroiditis (HT). We present a 48 year-old woman with HT who had primary SCC. Also, we further reviewed the clinical characteristics, dis-ease stage for primary SCC cases with or without lympho-cytic thyroiditis (LT), and compared with each other. Meth-ods: Review of English language literature associated with primary SCC of thyroid gland.

Results: We could access only 46 full papers. The 16 and 77 cases with primary SCC of thyroid gland described with and without LT, respectively. The lymph node metastasis, local invasion did not differ in between two groups. The distant metastasis in patients with LT were not absent whereas the cases among in patients without LT had 13 (16.9%) distant metastasis. Advanced stage disease (stage IV A-B-C) in pa-tients without LT is significantly higher than the patients with LT (p < 0.05).

Conclusions: Coexisting LT in patients with primary SCC of thyroid gland was identified as an early stage disease. Also, routine central lymph node dissection may be helpful in these patients with or without gross lymph node metastasis.

(Thyroid)

PRIMARY SQUAMOUS CELL CARCINOMA OF THYROID GLAND WITH CONCOMITANT LYMPHOCYTIC

THYROIDITIS PRESENT WITH LESS AGGRESSIVE DISEASE STAGE

Mehmet Asik1, Emine Binnetoglu1, Hacer Sen1, Fahri Gunes1, Asli Muratli1, Duygu Kankaya2, Fatma Uysal1, Mustafa Sahin2, Kubilay Ukinc1

1 Çanakkale Onsekiz Mart University 2 Ankara University3

Figure 1:Ultrasound image of the right nodule 14 years ago. b. Ultrasound images of a left lobe heterogeneous appear-ance. c. Ultrasound images of a right malignant nodule. Transverse view of right posteriorly located a combination of hypoechogenicity, irregular borders, and central macrocal-cifications in the same solitary thyroid nodule has a strong correlation with thyroid cancer. d. Ultrasound image of a lev-el 4 lymph node containing metastatic cancer. (white arrow).

2013


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2013


Introduction: The prevalence of autoimmune thyroid disease (AITD) has progressively increased. Circulating autoantibod-ies associated with AITD may affect the result of laboratory analyses and cause incorrect conclusions in the assessment of thyroid hormone status. In this report, we presented a pa-tient with Hashimoto’s thyroiditis with high thyrotrophin and free thyroxine (fT4) and triiodothyronine (fT3) levels due to the presence of auto-antibodies to iodothyronines.

Case: A 59-year old female patient presented to our outpa-tient clinic with symptoms of fatigue and exhaustion. Previ-ous laboratory analysis showed high serum levels of TSH, FT4 and FT3 for at least 6 years. Her physical examination was in normal limit except 2/6 systolic ejection murmur and a trace pretibial non-pitting edema. She has type 2 diabetes mellitus and hypertension for 12 years. TSH level was 29.6 μIU/ml (normal range 0.35-5.5 μIU/ml), FT4 3.56 ng/dl (NR 0.74-1.79 ng/dl, FT3 >40 pg/ml (NR 2.3-4.2 pg/ml). Magnetic resonance imaging was not compatible with TSH-secreting pituitary adenoma and the possibilities were resistance to thyroid hormone or to TSH was considered. Blood sample were collected from the patient and first degree relatives. Sequencing of the THRB and TSH receptor genes showed no abnormalities. TPO and TG antibodies were detected (Fu-jirebro, Japan) in the serum of the proband indicating the presence of AITD. She also had low total T4 and reverse T3 (rT3) measured using the Elecsys (Roche, Indianapolis, IN) platform and low free T4 index (FT4I) estimated by measur-ing the serum T4-binding capacity. The later measurements suggested hypothyroidism a diagnosis confirmed by a high serum TSH concentration. Antibodies to T4, T3 and rT3 were also identified by precipitation with polyethylene glycol of

radioiodinated tracers of these iodothyronines added to the subject’s serum. This was not the case in her unaffected brother. Four first degree relatives, two sibling and two of her children had also AITD , all had normal tests of thyroid function, except for a mild increase in the FT4I in her broth-er (Fig. 1). Treatment with L-thyroxine was initiated and the dose was adjusted according to her serum TSH levels. Serum free hormone levels were not taken into consider-ation for dose adjustement. Nine months later, on 75 mcg of L-thyroxine, TSH level was 2.74 mU/L,

Conclusions: Antibodies develop against the specific iodo-thyronine epitopes in the TG molecule. It has been report-ed that the incidence of T4 or T3 autoantibodies is 1.8% and these autoantibodies can coexist with TPO autoantibodies. Depending on the immunometric method these antibod-ies can result in free and total iodothyronine levels that are falsely high or low. In patients with discrepancies in the clin-ical status and thyroid function tests, iodothyronine auto-an-tibodies should be measured. If present, TSH levels should be used to adjuste the hormone replacement dose.

Figure 1

(Thyroid)

FALSE ELEVATION OF FREE THYROXINE AND TRIIODOTHYRONINE DUE TO THE PRESENCE OF

ANTIBODIES TO IODOTHYRONINES: CASE REPORTOrkide Kutlu¹, Caecilie Crawley Larsen2, Solomon Maximo Greenberg², Alfonso Massimiliano Ferrara²,

Ferda Sevimli Burnik3, Samil Ecirli¹, Samuel Refetoff², Cevdet Duran31 Konya Training And Research Hospital, Department Of Internal Medicine, Konya, Turkey

2 The University Of Chicago, Department Of Medicine, Chicago, Il, USA 3 Konya Training And Research Hospital, Department Of Internal Medicine And Endocrinology, Konya, Turkey

2013


Introduction: Adrenal venous sampling (AVS) is a widely used method to lateralize the source of aldosterone hyper-secretion in primary aldosteronism. It is also used in the management of patients with bilateral adrenal masses and corticotropin (ACTH)-independent Cushing syndrome (CS). However, there is hardly enough experience about AVS in adrenal CS with normal imaging studies. This case report shows that AVS can be a good choice to detect the focus of hypercortizolemia in these patients.

Clinical Case: A 30-year-old woman was presented with 2 years of fatigue, hirsutizm, amenorrhea, purple striae and weight gain. She had elevated 24-h urinary free cortisol excretion rate and midnight serum cortizole levels. Both 1 mg and 2 mg dexamethazon supression tests were not su-pressed, and the serum ACTH level was suppressed. In light of the undetectable baseline morning ACTH levels and un-supressed results of the 1 mg and 2 mg DST, the diagnosis of corticotropin-independent CS was made. As the imaging

studies revealed normal adrenal glands AVS was performed in order to make a diagnosis and formulate a management plan. According to the result of the AVS cortizole level was significantly higher in left adrenal gland which was surgi-cally removed thereafter. Pathological examination revealed primary pigmented nodular adrenal hyperplasia (PPNAH). The clinical symptoms significantly improved after the sur-gical removal of the left adrenal gland.

Conclusion: In this case we performed AVS in the adrenal CS which is not found any focus of hypercortizolemia. AVS may be an important step in the differential diagnosis of CS and local¬ization of the source of cortisol excess. It may re-veale the lateralization of the cortizole excess and may avoid unnecessary bilateral adrenalectomy. It can also ensure that the correct operation is completed, if required, and thus avoid the increased morbidity and mortality associated with repeated surgical interventions.

(Adrenal)

ADRENAL VENOUS SAMPLING IN THE DIAGNOSIS OF CUSHING SYNDROME

Aydogan Aydogdu¹, Cem Haymana¹, Turhal Ibrahimov¹, M. Sahin Ugurel², Mukerrem Safali3, Mahmut Yazici¹, Abdullah Taslipinar¹, Alper Sonmez¹, Omer Azal¹

1 Gulhane Faculty Of Medicine, Department Of Endocrinology And Metabolism 2 Gulhane Faculty Of Medicine, Department Of Radiology 3 Gulhane Faculty Of Medicine, Department Of Pathology

2013


Background: The main cause of primary adrenocortical defi-ciency is autoimmune adrenalitis. We present a case refracto-ry to treatment with high dose methylprednisolone (MP).

Clinical Case: A 58 year old male patient was referred to en-docrinology unit due to weakness, poor appetite, vertigo, and weight loss for 20 days. He denied any chronic illness and medication usage. Hyperpigmentation was evident in the palm creases and gingiva and over the knuckles and face (Figure).

Diagnostic Evaluation: Abnormal admission values were: sodium 122 mmol/l, potassium (K+) 5.6 mmol/l, cortisol 2.9 mcg/dl, and ACTH 1250 pg/ml. Addison’s disease was di-agnosed. Anti endomysium, antigliadin, anti TPO, and anti GAD antibodies were negative. Anti 21 hydroxylase antibody was unavailable. Treatment: During first 24 hours intrave-nous (IV) 20 mg q 6 hrs MP was given. Parenteral HC is not available in Turkey. The second day MP dose was halved and continued for four days. Then the dose halved again and he was on 20 mg/d IV MP therapy for 3 days before discharge. Electrolytes were normal at discharge. He was prescribed oral prednisolone in split doses until oral HC was available.

Follow-up: Eleven days after discharge he was again admit-ted to hospital with complaints of weakness and muscular cramps. He denied discontinuation of oral steroid until vom-iting ensued. He had MP shot according to recommendations

before discharge. Hyponatremia and hyperkalemia did not improve despite IV 80 mg MP. On the contrary electrolytes deteriorated with any dose reduction. During therapy liver enzymes began to rise. Viral hepatitis markers for HCV and HBV as well as autoimmune hepatitis markers were nega-tive. The deterioration in liver enzymes was attributed to high dose steroid. Meanwhile glucose levels began to rise up to 350 mg/dl. FC was available at last and started immediately at a dose of 0.1 mg q 12 hrs. MP was halved every day. He was discharged on HC 10 mg q 8 hrs along with FC 0.1 mg q 8 hrs. Twelve days after discharge electrolytes improved. The next week he came to the office again complaining ankle oedema. Bilateral edema in pretibial region and ankle was detected. Blood pressure was normal. Urinary protein excretion was normal despite low albumin (2.8 g/dl). Two weeks later albu-min normalized and oedema disappeared. Conclusion: High dose MP doesn’t obviate the need for FC therapy in case of Addison’s disease. Discussion: Corticosteroids are classified according to anti-inflammatory and mineralocorticoid activity. MP has half of the mineralocorticoid activity of HC. HC shows mineralocorticoid activity at doses over 50 mg/day. In practice daily FC need in patients on HC therapy is 50-250 mcg/day. The dose doubles in patients on prednisolone therapy. In our case even 80 mg/d MP was insufficient to maintain electrolyte balance. There may be individual differences in mineralocor-ticoid activity of synthetic steroids.

(Adrenal)

TWO EDGES OF THE SWORD: MINERALOCORTICOID ACTIVITY VS. COMPLICATIONS OF

METHYLPREDNISOLONEBengur Taskiran¹, Eylem Bahadir², Ruya Mutluay3

1 Eskisehir Yunus Emre State Hospital 2 Eskisehir Yunus Emre State Hospital, Department Of Radiology

3 Eskisehir Yunus Emre State Hospital, Department Of Nephrology

Initial and repeat electrolytes and glucose levels in accordance with methyl prednisolone dose

2013


Miscellaneous laboratory data

2013


Introduction: Disseminated cryptococcus neoformans in-fection commonly occurs in immunocompromised patients. We report a patient with cryptococcal adrenal insufficien-cy and meningitis who had otherwise normal immunologic status. Although the adrenal glands are able to be involved in disseminated cryptococcosis, adrenal insufficiency is uncommon. In previous reports, most cases of adrenal in-sufficiency caused by cryptococcosis were accompanied by meningoencephalitis. Several authors have reported that adrenal cryptococcosis presenting with adrenal insufficien-cy is refractory to antifungal chemotherapy. In such cases, bilateral adrenalectomy was effective for controlling crypto-coccal meningoencephalitis.

Clinical Case: A 37-year-old man with adrenal insufficiency is presented. A year before his admission, he had intractable headaches and was diagnosed to have a temporal lobe mass lesion on magnetic resonance imaging (MRI). After refusing to have a diagnostic brain biopsy procedure, he had been in good health until his admission to a local hospital with an-orexia, weight loss, nausea, and increased skin pigmenta-tion. Having obtained low serum sodium (122 mEq/L),with low baseline morning cortisol 2,63 mcg/dl and elevated plasma adrenocorticotropic hormone (ACTH) levels [856,6

pg/ml (normal <60pg/ml)]. Abdominal MRI demonstrated bilateral enlargement of the adrenal glands. Ultrasonically guided adrenal biopsy was performed but the cytology report was not diagnostic. Being under cortisole replacement for about a year, he was than admitted to our Institute for fur-ther evaluation and management of his suspected adrenal insufficiency. On control MRI series, bilateral mass lesions were enlarged and the brain lesion was in the same location with the same size. Laparoscopic unilateral adrenalectomy was performed. Histologic studies of the resected adre-nal glands revealed massive caseating necrosis containing yeast-like particules that was diagnostic for Cryptococcus neoformans. An increased leucocyte count was found in the lomber punction. Systemic antifungal therapy was started along with the corticosteroid replacement. Patient is in good health in the 6th month of the follow up.

Conclusion: Although adrenal insufficiency due to dissem-inated cryptococcosis is rare in healthy hosts, it should be recalled in differential diagnosis of unilateral or bilateral ad-renal masses. When the effect of antifungal therapy was in-sufficient, surgical removal of the focus is an effective mea-sure for the treatment of the meningitis as well.

(Adrenal)

BILATERAL ADRENAL MASSES PRESENTING WITH PRIMARY ADRENAL INSUFFICIENCY AND MENINGOENCEPHALITIS: A CASE REPORT OF

DISSEMINATED CRYPTOCOCCOSISAydogan Aydogdu¹, Coskun Meric¹, Kamil Baskoy¹, Tural Ibrahimov¹, Cem Haymana¹, Zafer Kilbas²,

Ahmet Karakas3, Mehmet Gamsizkan4, Abdullah Taslipinar1, Y. Alper Sonmez¹, Omer Azal¹1 Gulhane School Of Medicine, Department Of Endocrinology

2 Gulhane School Of Medicine, Department Of Surgery 3 Gulhane School Of Medicine, Department Of Infectious Diseases

4 Gulhane School Of Medicine, Department Of Pathology

2013


Background: Most of the pheochromocytomas (pheos) are not diagnosed during life. Incidentally detected adrenal masses provides opportunity to diagnose pheos. Pheos bear potentially lethal complications. Plasma or urinary cate-cholamine levels are used for diagnosis. Alpha blockage was done before surgery to avoid hypertensive crisis during operation.

Clinical Case: A 60 year old female patient was evaluated in endocrinology ward due to incidentally discovered right adrenal mass. She had thyroidectomy five years ago. She had hypertension and type 2 diabetes of 9 years’ duration. She was on candesartan, hydrochlorothiazide, pioglitazone, metformin, and levothyroxine therapy. Blood pressure was under control. Diagnostic evaluation: The mass was 32*27 mm in size and had internal cystic areas. The density of the solid component was 20 HU on non-contrast phase CT and 50 HU on porto-venous contrast CT. The image was not com-patible with benign adenoma. Therefore possible metastasis was considered. Mammography, cervical smear, upper gas-trointestinal endoscopy, and CT scan of head, neck, thorax, and abdomen were nonsignificant otherwise. Resting ECG was normal. Urinary catecholamine values were in normal range. Low dose dexamethasone test was suppressed.

Treatment: Because of suspicipous features on CT, surgery was planned. Pulmonary oedema and hypoxemia developed after laparoscopic surgery. Pulmonary oedema resolved with diuretic therapy. Follow-up: Biochemically silent pheo was diagnosed. PASS was 3 in pathologic evaluation. Chro-mogranin and synaptophysin was positive. S100 was positive in sustentacular cells. Ki-67 was 1-2 %. She attended cardi-ology unit due to chest pain 2 weeks after discharge. Con-secutive %80 and %90 stenotic lesions in proximal LAD were detected on angiography. Urinary catecholamines 3 months after surgery was normal.

Conclusion: Normal urinary catecholamine values cannot assure the safety of surgical removal of biochemically silent adrenal masses.

Discussion: Our patient had normal uriary catecholamine values before operation. Blood pressure was under control. Resting ECG was normal. Typical angina pectoris was ab-sent. Therefore alpha blockade was not done prior to sur-gery. Immediately after surgery pulmonary oedema ensued. There is a number of case reports about biochemically silent pheos. Pheos may intermittantly secrete catecholamines. In patients with normal catecholamine values alpha blockade may be considered before surgery in case of suspicious ra-diologic findings compatible with pheos.

cxr PULMONARY OEDEMA

(Adrenal)

PULMONARY OEDEMA COMPLICATING SURGICAL REMOVAL OF SILENT PHEOCHROMOCYTOMA

Bengur Taskiran, Serdar Akyuz, Betul Peker Cengiz, Eylem Bahadir, Ozgur KirdokEskisehir Yunus Emre State Hospital

2013


CONTRAST CT IMAGE

TABLE GIF

2013


Introduction: Polycystic ovary syndrome (PCOS) is one of the most serious and frequent endocrine diseases among reproductive age women associated with metabolic syn-drome, obesity, type 2 diabetes and cardiovascular disease.

Case Report: A 33 years old Caucasian female was consult-ed by endocrinologist due to obesity, hirsutism, sliding hair, fatigue and irregular menses. In childhood she had over-weight, at age of 18 her weight was 62 kg, at 21 weighed 75 kg. She gave birth 12 years ago and after had been gaining weight steadily - at 30 she weighed 90 kg, at 33 up to 100 kg. At 25 face and abdominal hairiness became obvious. She could not conceive for the last 6 years. Last two years had a menstrual cycle every 6 months. She had pelvic ultrasound confirming the presence of bilateral polycystic ovaries. Her family history was positive for obesity (mother, sister and brother were obese and father was overweight and bald). On examination she had central obesity: weight – 98.5 kg, height – 167.5 cm, BMI – 35.1 kg/m2, waist circumference – 109.5 cm, hip circumference – 104.8 cm; waist to hip ra-tio – 1.05; signs of insulin resistance – acanthosis nigricans at neck, elbows, hands regions; hirsutism by modified Fer-riman-Gallwey score of 10; hypertension (blood pressure – 148/106 mmHg). Laboratory tests revealed hyperandroge-naemia (testosterone – 2.68 nmol/l, SHBG – 16,17 nmol/l; FAI – 16.57), impaired glucose tolerance (fasting glucose

– 6.4 mmol/l, 2-h glucose – 9.3 mmol/l), insulin resistance (HOMA-IR – 4.26), dyslipidaemia (total cholesterol – 5.44 mmol/l, HDL – 0.86 mmol/l), LDL – 3.54 mmol/l, TG – 2.32 mmol/l), increased cardiovascular risk by CRP (CRP – 3.8 mg/l), fatty liver signs – GGT – 24.7 U/l, AST – 34.31 U/l, ALT – 57.86 U/l. Prolactin, 17OHP, FSH, LH were within normal limits. The patient started 1500 calories diet and metformin for 12 months. During the follow up period weight decreased by 18 kg, waist circumference decreased by 9 cm, menses became regular, ovulation was detected by progesterone level and analyses improved resulting in increasing of SHBG, normalizing of glucose tolerance, lipids level, decreasing in liver enzymes.

Conclusions: Obese PCOS women having classic phenotype have tendency to android fat distribution, metabolic syn-drome and cardiovascular risk. Weight loss might be an op-tion for the risk reduction.

Declaration of Interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

(Female Reproductive Endocrinology)

METABOLIC AND FERTILITY BENEFITS OF WEIGHT LOSS IN PATIENT WITH POLYCYSTIC OVARY

SYNDROMELina Zabuliene¹, Jurgita Urboniene2

1 Clinics Of Rheumatology, Traumatology-Orthopedics And Reconstructive Surgery, Faculty Of Medicine, Vilnius, Lithuania; Antakalnio Out-Patient Clinic, Vilnius, Lithuania

2 Infectious Diseases And Tuberculosis Hospital, Vilnius University Hospital Santariskiu Klinikos, Vilnius, Lithuania

2013


Introduction: The virilizing ovarian tumors are a rare cause of hyperandrogenism. They account for 1-2 % of all ovari-an tumors which the Leydig cell tumor is the most common one. The signs of hyperandrogenism in reproductive aged women could be hirsutism, alopecia and oligo-amenorrhea due to endometrial atrophy.

Clinical Case: Forty-five year old woman being amenorrheic since 10 years, admitted to Endocrinology and Metabolism Clinic with the complaint of hirsutism and alopecia. Her past medical history, she was diagnosed as menopause without laboratory evaluation, even though she had no complaint of menopausal symptoms. The complaints of hirsutism and al-opecia were increased day by day. On physical examination she had dorsal, facial and peri-umbilical hirsutism (score 11) and alopecia. There was no cliteromegaly, stria or voice thickening. Laboratory tests showed normal ACTH, cortisol, DHEA-S but elevated testosteron levels. She had normal FSL, LH and estrogen levels. The total and free testosteron levels were 262.7ng/dl (normal range: 6-88) and 5.62 pg/mL

(normal range: 0-2.1). We performed 1 mg dexamethazon supression test and cortisol was supressed. The 17-0H pro-gesteron level was 1.3 ng/ml. With these results, Cushing disease and late onset congenital adrenal hyperplasia were excluded. Abdomino-pelvic CT revealed that there was no adrenal mass but there was a 3-cm solid lesion on the right ovary. She was referred to Gynecology Clinic with ovarian mass which was suspected as androgen secreting tumor. Total Abdominal Hysterectomy and Bilateral Salpingo-Oo-pherectomy (TAH-BSO) was performed. Histopathological studies revealed a 3 cm ovarian Sertoli-Leydig cell tumor. Postoperatively, testosterone levels declined to normal range. The significant improvement on alopecia and hirsut-ism were observed throughout following 6 months.

Conclusion: The misdiagnosed premature menopause due to high testosterone level that would lead to endometrial at-rophy and the complaints of hirsutism and alopecia in late stage of reproductive women should be remind to have an androgen secreting tumors.

(Female Reproductive Endocrinology)

HIRSUTISM IN THE LATE STAGE OF REPRODUCTIONFiliz Ekşi Haydardedeoğlu

Adana Numune Research and Training Hospital Endocrinology and Metabolism Clinic

2013


Background: Exenatide, a glucagon-like peptide receptor-1 agonist have been recently used in clinical management of type 2 diabetes mellitus. With introduction of GLP-1 agonists in clinical practice,the question how to combine this medica-tion with insulin has gained significant attention . Exenatide therapy often results in weight loss, which further assists in decreasing insulin resistance and this makes the drug a good therapeutic option for obese patients. Here, we report the use of exenatide in an obese, 64-year-old woman with poorly controlled type 2 diabetes mellitus.

Case Report: A 64-year-old woman with a body-mass index of 38 kg/m2 was referred to our clinic with a complaint of difficulty in controlling blood sugar levels. Her medical his-tory included coronary artery disease, hypertension, and hy-perlipidemia. She had type 2 diabetes mellitus for 20 years with macrovascular and microvascular complications. She had been using insulin since 2002 and on admission, her to-

tal dose of basal insulin was 90U/day and bolus insulin was 130U/day. She also used 1 gr metformin twice a day. Despite the high doses of intensive insulin treatment, her capillary glucose measurements usually ranged between 300-450 mg/dl. HbA1C was found to be 9.2%. After searching for the secondary causes of insulin resistance, insulin therapy was adjusted with NPH and regular insulin. Despite the dose ad-justments, target levels can not be reached and exenatide therapy was started in combination with insulin therapy. No gastrointestinal side effects were seen and final dose was 5 mcg twice a day. After 5 weeks in follow-up, 7 kg of weight loss was achieved and her fasting and postprandial plasma glucose levels ranged between 170-200 mg/dl and 200-250 mg/dl, respectively.

Conclusion: Exenatide may be an effective adjunct thera-py for obese patients with poorly controlled type 2 diabetes mellitus.

(Diabetes)

EARLY EFFECTS OF GLP-1 ANALOGUE AND INSULIN COMBINATION THERAPY IN AN OBESE PATIENT

WITH TYPE 2 DIABETES MELLITUSBasak Bolayir¹, Nafiye Helvaci², Bulent Okan Yildiz²

1Hacettepe University School of Medicine, Department of Internal Medicine, Sihhiye, Ankara 2 Hacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Sihhiye, Ankara

2013


Introduction: Studies have shown that, when implemented early in the course of type 2 diabetes mellitus, intensive in-sulin therapy can induce a glycaemic remission, quick res-toration of euglycemia and preserve beta cell function on a long term basis. Addition of metformin results in superior glycemic control. There are very few case reports of hypogly-cemia in diabetic patients on Metformin monotherapy.

Case Summary: Mr. A S, A 61 years old male patient referred to Benghazi medical centre; diabetic outpatient clinic for the continuity of care on 24/1/2012 as newly diagnosed type 2 diabetes and hypertension, first presentation was polyurea, polydepsia and BS of 1000mg/dL, he was discharged from the hospital on intensive insulin regimen 0.6 U/Kg Insulin aspart at meals, glargine bed time and metformin 1.5g/d plus life style modification and Enalopril tablets 10mg/day. On the first visit, he was asymptomatic, he had never been smoker and never drinks alcohol, his BP was 168/72 mmHg, weight was 89Kg, height was 188 cm, BMI was 25.2kg/m2 , other systemic, feet and retinal examinations were normal (N). HBA1C 12.7%, estimated GFR N, liver and renal func-tion tests were N, LDL N, HDL 39 mg/dL, TG N, HBN,Urine for microalubuminurea N. After two months SMBG revealed; premeal blood glucose (BG) values < 118 mg/dL and 2 hours post meal values of < 117 mg/dL and HBA1C was 6.5%. Three months later, premeal BG values were 55-147 mg/dL and Post meals 49-177 mg/dL and HBA1C 5.7% insulin dose was

reduced through these months to 0.36 U/Kg; Hypoglycemia all occur pre lunch and post lunch. After one year insulin was stopped, and he continued on Metformin 850mg/day, his HBA1C 5.1%, Premeal BG values between 60-128mg/dL and 2 hours post meals 65-164 mg/dL. Two months later, he was on Metformin 850mg/day and he developed pre-lunch hypo-glycemia of 56-69 mg/dL, thyroid function test was normal, insulin level and C peptide level were normal for the hypo-glycemia, synacthen test was negative. When the patient re-duces Metformin to 250-500mg/day or stops Metformin, he had no hypoglycemia and hypoglycemic attacks occur when he is on a dose of 850-1.5 g/day. During Ramadan fasting month he was on Metformin 500mg/day, he fasted the whole month of Ramadan without hypoglycemia with pre-iftar BG values between 75-103mg/dL.

Conclusion: Early initiation of insulin therapy in type 2 dia-betes is associated with effective glycemic control with ear-ly restoration of physiologic insulin secretion and glycemic control could be, followed by therapies to prolong mainte-nance of euglycemia. Patients presenting with significant hyperglycemia may benefit from early initiation of insulin therapy that can rapidly correct their metabolic derange-ment and reverse glucotoxicity and lipotoxicity. Although rare, Metformin induced hypoglycemia can occur and in this case it was a dose dependent and mainly with delayed meal, ACE inhibitors might add to hypoglycemia risk.

(Diabetes)

EARLY INTENSIVE INSULIN THERAPY IN COMBINATION WITH METFORMIN IN A TYPE TWO DIABETIC PATIENT MAINTAINS NORMOGLYCEMIA

WITH METFORMIN MONOTHERAPY AFTER STOPPING INSULIN AND DEVELOPMENT OF HYPOGLYCEMIA

WITH METFORMINNajat Buzaid¹, Adela Ebsat²

1 Benghazi Medical Centre 2 Alhawari General Hospital

2013


Introduction: Onset time of insulin glargine is 2-4 hours, duration of action is 20-24 hours. Insulin glargine’s duration of action may have some individual differences like other in-sulin analoques. We are going to share a case that injected 300 iu insulin glargin subcutaneous mistakenly and applied to our emergency service.

Case Report: A 59 years-old male patient had the diagnosis of diabetes (dm) and hypertension for two years, however he had not used any medication before. The patient was pre-scribed 1x100 mg tablets losartan, 2x1000 mg tablets met-formin, insulin glargine (lantus) 1x12 iu and he was given education of insulin / diabetes. The patient was admitted to our emergency department with a complaint of high-dose insulin glargine (lantus) application by mistake. When he injected insulin glargine 12 iu at 21:30 he thought that he didn’t take right dose. So that he made multiple different doses of insulin repeatedly. When he realized that he fin-ished insulin pen which includes 3 ml insulin (100 iu/ml) he applied to emergency service. In his first examination he was conscious, orianted, cooperated, slightly anxious.T.A:150/80 mmhg pulse:98/m fever:36,2 c respiratory rate(rr):18/m. His physical examination was clearly normal. His blood glucose was measured as 98 mg/dl by glucometer and immediately he was given 10% dextrose infusion. At the beginning in his blood: glucose was 87 mg/dl, k:3,45 mmol/l, ca:9,9 mg/dl, p:3,3mg/dl and mg was 1,4 mg/dl. He was continued to treat

with 10% and 20% dextrose infusion under strict control of glycemia. At 24th hour of his hospitalisation, dextrose infu-sion was reduced to 25 cc/h. When it was seen that patient was tend to hypoglicemia, we continued 100cc/h dextrose in-fusion, 40 meq k was added to every 1000 cc dextrose solu-tion and started oral mg replacement. Patient needed dex-trose infusion until 38th hour of hospitalisation. After 3-day follow-up patient was discharged under glycemic regulation.

Conclusion: Over dose use of insulin glargine cases are rare, nearly all of them are suicidal reasons.Mistakenly high dose insulin usage hasn’t been reported yet. Insulin half-life be-comes longer than expected in high dose insulin used cases. In literature, doses are between 400 and 2000, and average duration of action is between 40 and 100 hours in overdose insulin taken cases. In massive insulin intake continuous dextrose infusion, free oral nutrition, glucagon / octreotide when needed and strict follow up / replacement of serum electrolyte levels are the main treatment approach our case backs up prolongation of half-life like previously reported overdose insulin intake cases. But when we compare with previous cases, hypoglycemic episodes continued less than expected (38 hours). In such cases, glycemic control can be achieved with only dextrose infusion if the patient is hospi-talized early. In addition, strict glycemic monitoring should be done without considering the known half-life of insulin

(Diabetes)

INSULIN GLARGINE (LANTUS) OVERDOSE: A CASE REPORT

Veysel Özalper¹, Ramazan Arikan¹, Ferhat Deniz², Arif Yönem²1 GATA Haydarpaşa Hospital Internal Medicine Clinic

2 GATA HEH Endocrinology Clinic

2013


Introduction: Hypertriglyceridemia is a well known phe-nomenon of pregnancy. It occurs due to physiologic changes in sex hormone levels. One of the most important compli-cations of hypertriglyceridemia in pregnancy is acute pan-creatitis which causes significant morbidity and mortality for both mother and the fetus. Here, we report a case of repeat-ed hypertriglyceridemia in pregnancy.

Clinical Case: A 38- year- old woman was admitted to our hospital at the 13th gestational week of her third pregnan-cy. She didn’t have a previous personal and family history of abnormal lipid metabolism. She had a past history of two miscarriages. At her second pregnancy, when she was 27 years old, she was admitted to the hospital because of ab-dominal pain. Her serum triglyceride level was found to be 1825 mg/dl. Serum lipase and amylase levels were elevated. She was diagnosed with acute pancreatitis secondary to hy-pertriglyceridemia and required plasma exchange. Despite repeated plasmapheresis, intrauterine death of the fetus happened by 22th gestational week. Then, she was start-

ed to use fenofibrate. After she was discharged, she didn’t come to hospital visits regularly. 4 years later, she was di-agnosed with type 2 diabetes mellitus and started to use an oral antidiabetic agent. In 2010, her antidiabetic medication was switched to intensive insulin therapy because of preg-nancy plans. In 2011, when she applied to our hospital at the 13th gestational week of her third pregnancy, her serum triglyceride level was 1599 mg/dl. Since she had a history of acute pancreatitis due to hypertriglyceridemia, she was im-mediately started on plasmapheresis to avert pancreatitis. After repeated plasmapheresis, her third pregnancy result-ed in delivery of a healthy newborn with caesarean section on 34th gestational week.

Conclusion: Early diagnosis and treatment is necessary to prevent the development of pancreatitis and to preserve the lives of the mother and the fetus in gestational hypertri-glyceridemia. Therapeutic plasma exchange appears to be useful and effective in this situation.

(Lipids/Obesity/Hypertension)

SEVERE HYPERTRIGLYCERIDEMIA IN PREGNANCYGurkan Guner¹, Safak Akin², Miyase Bayraktar²

¹ Hacettepe University School of Medicine, Department of Internal Medicine, Sihhiye, Ankara ²Hacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Sihhiye, Ankara

2013


Introduction: Barakat syndrome syndrome. Patients has Hypoparathyroidism ,sensory neural deafness ,Renal dis-ease includes nephrotic syndrome, hypoplasia or a plasia.

Clinical Case : We report a case of 25 year- old female Lib-yan patient with one daughter , with history of recurrent abortion , who was referred from Elkofra hospital at18-July 2013 as a case of hypocalcemia and convulsion for evalua-tion .On review of here history the patient was diagnosed as eclamptic toxemia at 19 –may 2013 with fetal death delivery, complicated with rhabdomylses and acute renal and liver failure with sever hypocalcemia. Her condition was improved but calcium level and phosphorous continued to be low and high respectively for which diagnoses of hypoparathyroidim was made .The patient was discharged at 12 – June 2013 on high calcium and vitamin D replacement. After 10 days the patient had seeking advice in Tunisia . Here investigation in contrast showed hypercalcemia and hyperphosphatemia with low PTH and VITD . Renal impairment, moderately high lipase and amylase level table 1. MRI abdomen showed nor-mal pancreas , Hypo plastic right kidney . figure 1 . Echo showed piller anterolateral calcification . figure 2 Vitamin D and calcium was stopped, Rehydration had started .Bi-sphosponate was prescribed at discharge . After arrival to Libya the patient had developed Hypocalcaemic convulsion treated in Elkofra hospital and then transferred to Benghazi

. At arrival to our hospital she was conscious , BP 160/100 , Mildly deaf patient ,small hard nodules in forearms. She developed attack of convulsion just after admission. Bio-chemical screen showed hypocalcemia, hyperphosphatemia , hypomagnesaemia , high Alp, LDH ,CPK , amylase and li-pase, Slightly high creatinine. Low PTH ,Total vitamin D , D25 and albumin . 24 hour urine protein more than 2 gm/dl, Cre-atinine clearance was 31 ml/min . table2. Calcium infusion started .USS pancreas were normal. Diagnoses of hypopara-thyoidism with vitamin D deficiency was made .The presence of right renal hypoplasia had raised the suspicion of Barakat syndrome. CT for CNS calcification was ordered and came positive . figure 3 . pure tone audiometry had reveal mod-erate sensor neural deafness. figure 4 . X-ray of both fore-arms showed query calcifications which was confirmed by CT .figure 5 Tenormin was started for high blood pressure. Genetic study for GATA3 mutation not available. The patient discharged on calcium and vitamin D supplement .

Discussion: Our diagnoses of barakat syndrome was based on presence of hypoparathyroidism, renal hypoplasia ,mod-erate sensory neural deafness . To our knowledge presence of cardiac calcification was not observed before in hypopara-thyrodism . Conclusion : To our knowledge this is the first reported case of barakat syndrome in Libya . No grants sup-porting the writing of the abstract .

(Bone/Calcium)

BARAKAT (HYPOPARATHYROIDISM, DEAFNESS RENAL HYPOPLASIA; HDR) SYNDROME IN AN ADULT

LIBYAN WOMENAdela Ebsat¹, Ibrahim Elamami², Abdul Hakim Ali²

1 Endocrine And Diabetes Unit /Hawari Teaching Hospital/ Benghazi Unversity 2 Radiology Department //Hawari Teaching Hospital/ Benghazi Unversity2

2013


Table 124June 25 June 28 June 29 June 3 July

Calcium 16.5mg/dl 17.6mg/dl 11mg/dl 9.5mg/dlPhosphorous 7.5mg/dl 4.4mg/dlMagnesium 1.6mg/dl

Parathyriod hormone 3.9pg/ml 5.6pg/mlvitaminD25 10ng/l

Haemoglobin 9.7g%WBC 7.6^3

Platlet 332?^3Prothrombin time 12.5 sec

INR 1Urea 40

Creatinine 2.6mg/dl 2.2mg/dlBlood glucose 95mg/dl

Sodium 138mmol/lPotassium 4.7mmol/lChloride 100mmol/l

FT4 23.8pmol/l 21.3pmol/lTSH 1.4miu/lESR 80 73

D dimer 584ng/ml24 hour calcium excretion 476mg/24hr normal range (150-300mg)

showed the investigation of our patient during admission to Tunisia hospital

Table 218 July 21 July 22 July 23July 24July At discharge

Calcium 3mg/dl 5 4.5 5.7 6 7.8Albumin 2.9g/dl 3.2 2.7 2.7Protien 5.9g/dl

Corrected calcium 3.88mg/dl 5.64 5.3 6.7 7.04 8.48Phosphorous 8.7mg/dl 8.6 4.8Magnesium 1.4mg/dl 3.1

ALP 700u/l 593 413LDH 778u/l 433u/l

CK(total) 464u/lPotassium 4.1mmol/l 4.3

Sodium 138mmol/l 145Urea 15.9mg/dl 34.7 41

Creatinine 1.3mg/dl 1 1.4Chloride 98.1mmol/l 99.8

ALT 5.7u/lAST 17.3u/l

Blood suger 78mgu/lAmylase 148u/l 137 180 164Lipase 299u/l 346

Cholesterol 160mg/dlTriglyceride 151.2mg/dl

PT\INR 16/1.3Haemoglobin 8.4g/dl 9.2 9.3

WBC 7^3Platelet 325^3

PTH 4.9pg/ml 5.9Vitamin D 25 8.8 4.9

PH( ABG ) 7.4HCO3 24.4

T3 1.4nmol/lT4 105nmol/l

TSH 1.43ulu/mlUrine albumin ++ ++

24hr urine protein 2.o93mg/dayCreatinine clearance 31.2ml/min

showed the investigations of our patient during admission to our hospital

2013


Introduction: Surgical cure of parathyroid adenomas is around 95%. The main reason for surgical failure is the pres-ence of persistent disease, usually due to an ectopic adeno-ma or hyperplasia of the glands. A second problem may be the presence of a ‘sleeping tumor’, where there is hyper-function of an adenoma after the removal of a dominant ad-enoma. We present here a case where there is an ectopically located sleeping tumor.

Clinical Case: A 60 year old woman who has had thyroid-ectomy at the age of 30 came first with a calcium level of 12.5mg/dL. The other laboratory findings confirmed prima-ry hyperparathyroidism. The adenoma was then localized, and adenectomy was performed. During the follow-up the calcium levels were within normal ranges at the postopera-tive period until when she showed up with a new calcium of

12.0mg/dl after a time period of 6 months. Again the ade-noma was localized with ultrasonography and scintigraphy and surgery was performed. At the postoperative period her calcium levels did not decline. Conservative measures were not adequate to keep her calcium within normal ranges. A last operation was performed were tha gamma probe was used to localize the adenoma intraoperatively, where it was found to be located within the residual thyroid tissue. The postoperative calcium levels were within normal ranges and stayed so at the follow-up.

Conclusion: A ‘sleeping adenoma’ should be kept in mind in recurrent primary hyperthyroidism. Intraoperative gam-ma-probe may be useful in localizing diffucult-to-find ecto-pic parathyroid adenomas.

(Bone/Calcium)

AN ECTOPIC SLEEPING PARATHYROID ADENOMADilek Yazici, Sule Temizkan, Oguzhan Deyneli, Dilek Yavuz

2013


Introduction: Tertiary hyperparathyroidism (THPT) is an important complication in patients with advanced renal in-sufficiency. Total parathyroidectomy with immediate partial parathyroid autotransplantation is an alternative method for treatment of THPT. The state of high impact parathormone levels (iPTH) continuing after surgery is called parathyroma-tosis. The frequency of parathyromatosis in forearm auto-transplantations are reported between 0.11% and 58%. Here we presented a patient with total parathyroidectomy and ½ parathyroid tissue autotransplantation to right brachioradial muscles in the forearm operation (contralateral to the arte-rious-venous fistulae) has been performed due to tertiary hyperparathyroidism.

Case: A fifty-six year old male, having chronic kidney fail-ure and hemodialysis treatment for 15 years. 10 years ago, total parathyroidectomy and ½ parathyroid gland autotrans-plantation to the brachioradial muscle in the right forearm operation had been performed due to tertiary hyperparathy-roidism. Renal transplantation had been performed 4 years ago. Before the transplantation, iPTH levels were between 90 and 477 pg/ml (N: 11-67 pg/ml), after renal transplanta-tion iPTH levels were between 190 and 1853 pg/ml. Parathy-roidomatosis had been suspected and scintigraphic imaging

had been done and no focus found in another center. When he admitted to our out-patient clinic, his laboratory analy-sis showed; iPTH value was 2382 pg/ml, calcium 9,2 mg/dl (N: 8,4-10,2 mg/dl), phosphorus 4,2 mg/dl (N: 2,5-4,5 mg/dl), albumin 3,9 gr/dl (N: 3,5-5 gr/dl), creatinine 1.51 mg/dl (N: 0,7-1,3 mg/dl). In order to understand whether the raised level of iPTH values are due to the area; samples were tak-en both from the right arm (proximal and distal region of implant) and from the left (contralateral) arm. iPTH values were detected as 1863 pg/ml from the right forearm proxi-mal; 75,6 pg/ml from the distal and 30 pg/ml from the left arm. It became apparent that the differences between the iPTH values are due to the place of the blood samples taken.

Discussion: In patients with renal failure, it is avoided to take blood samples from arm with arterious-venous fistulae that causes factitious extremely high iPTH values if blood sam-ples are taken from the proximal region of arm having auto-transplantation. In order to avoid misdiagnosis and leading to unnecessary and incorrect procedures, the blood sample should be taken from the contralateral or distal site of the autotransplantation. In the evaluation of parathyroid func-tions, biochemical parameters should be assessed together with PTH level at the same time.

(Bone/Calcium)

FALSE HIGH PARATHORMONE LEVELS DUE TO PREANALYTICAL DIFFERENCES IN PATIENT WITH PARATHYROID GLAND AUTOTRANSPLANTATION

Cevdet Duran¹, Orkide Kutlu², Mustafa Cayci², Ferda Sevimli Burnik¹, Omer Karahan3, Uysaler Aslan², Samil Ecirli²

1 Konya Training And Research Hospital, Department Of Internal Medicine And Endocrinology, Konya, Turkey 2 Konya Training And Research Hospital, Department Of Internal Medicine, Konya, Turkey 3 Konya Training And Research Hospital, Department Of General Surgery, Konya, Turkey

2013


Introduction: Insulin producing islet cell tumor is very rare.The chaotic release of insulin results hypoglycemia after ex-ercise or prolonged fasting. We report two clinical cases of insulinoma who have different phenotypes.

Clinical Case 1: A 85-year-old woman presented with hy-poglycemia and psychotic attack. Biochemical testing re-vealed insulinoma (Table 1). Abdominal contrast computed tomography demonstrated a hypervascular tumor of 16 mm in diameter in the pancreatic tail.Further, an adrenal nodule of 6 mm in diameter in the left was detected. Also, she had a subcutaneous fibrolipoma 25 mm in diameter in the cra-nium. Her family preferred medical therapy with diazoxide because of a high risk for surgery.

Clinical Case 2: A 30-year-old woman presented with hy-poglycemia. She had hypopituitarism 10 years after a pitu-itary surgery and conventional radiotherapy for macropro-lactinoma.She was taking replacement therapy for gonadal axis ,only. We started replacement therapy for adrenal and thyroid axes.But hypoglycemia did nor resolve.Biochemical testing revealed insulinoma (Table 2). Abdominal contrast computed tomography demonstrated a hypervascular tumor of 22 mm in diameter in the pancreatic body. Additionally, a parathyroid adenoma in the inferior of the left lobe of thy-roid was detected. She was diagnosed as Multiple Endocrine Neoplasia type 1 (MEN 1). She was prepared for surgery with diazoxide.

Conclusion: We presented two clinical cases of insulinoma in different age groups. Clinical case 1 did not have the diag-nostic criteria for MEN 1. Clinical case 2 had the diagnostic criteria for MEN 1 presenting prolactinoma as the first sign. We could not study the MEN 1 gene. MEN 1 can present with combinations of different endocrine and nonendocrine tu-mors and also the tumors of MEN 1 have a wide range of penetrance incresing with age.

Table 1: Glucose 45 mg/dl

Insulin 37.62 microU/ml

C peptide 6.09 ng/ml

FSH 37.06 mIU/ml

LH 23.89 mIU/ml

Prolactin 16.67 ng/ml

FT4 1.25 ng/dl

TSH 1.48 microIU/ml

Cortisol 19.36 microg/dl

Plasma Renin Activity 11 ng/ml/hour

Plasma Aldosteron 14.33 ng/dl

Urine Metanephrine 91.7 microg/day

Urine Normetanephrine 118.5 microg/day

Urine VMA 3.8 mg/day

1 mg Dexametasone suppression 5.96 microg/dl

Biochemical test results

Table 2FT3 2.43 pg/ml

FT4 0.766 ng/dl

TSH 1.11 microIU/ml

Cortisol 3.42 microg/dl

Ca 10.4 mg/dl

PTH 170.8 pg/ml

FSH 3.89 mIU/ml

LH 3.35 mIU/ml

Prolactin 0.871 ng/ml

GH 0.39 mIU/ml

Somatostatin-C 118 ng/ml

Glucose 50 mg/dl

Insulin 24.13 microU/ml

C peptide 5.53 ng/ml

Gastrin 35.39 pg/ml

CA-19-9 5.21 U/ml

Biochemical test results

(Neuroendocrine Tumors)

THE PRESENTATION OF INSULINOMA; TWO CLINICAL CASE REPORTS

S. Nur Boysan1, Mesut Ozkaya², H. Sancar Bozkurt¹, M. Sait Menzilcioglu¹, Tuna Sahin¹, Serdal Citil¹, Serkan Çaglar¹, B. Kemal Sonmez¹, I. Gurkan Cikim¹

1 Kahramanmaras Necip Fazil City Hospital 2 Gaziantep Univercity Medical Faculty

2013


Introduction: Metastatic pheochromocytomas are rare and challenging tumors. Current therapies include surgery, sys-temic chemotherapy, and radiopharmacoutical agents. Nov-el therapeutic strategies such as tyrosine kinase inhibitors, show encouraging results but need to be evaluated in pro-spective clinical trials. Iodine-131 metaiodobenzylguanidine (I-131 MIBG) is a useful technique in the diagnostic work-up of pheochromocytomas and has been introduced as a mo-lecular nuclear therapy in the management of neuroendo-crine tumors. Here, we report a case of malign pheochromo-cytoma with multiple metastases treated with I-131 MIBG.

Clinical Case: A 53-year-old woman was admitted to the hospital for the evaluation of a mass on her chest. Bone scin-tigraphy showed increased osteoblastic activity and expan-sion at the fifth rib on the left. Computed tomography of the thorax and abdomen revealed a heterogenous mass mea-suring 10.5x10 cm in the region of left adrenal gland along with multiple metastatic solid lesions in liver and spleen, a destructive lesion mesuring 5x3.3 cm at the fifth left-sided rib, and a lymph node measuring 22x18 mm at the left para-sternal region which was also thought to be metastatic. Al-though the patient wasn’t presented with the symptoms and signs of pheochromocytoma, the diagnosis was confirmed

by markedly elevated 24-hour urinary levels of cathechol-amines and metanephrines as well as positive I-131 MIBG scintigraphy showing tracer uptake at the regions of prima-ry mass in the left upper quadrant of the abdomen and its metastases. Since I-131 MIBG scintigraphy showed marked uptake at the primary mass and its metastases, the patient was thought to benefit from high dose I-131 MIBG radiother-apy. A debulking surgery was planned in order to reduce the tumor burden and increase the success of I-131 MIBG treat-ment but the patient refused the surgery. She underwent in-travenous injection of 100 millicuries of I-131 MIBG. There were no serious adverse events associated with the treat-ment and she was discharged from the hospital two days af-ter the first cycle. Five days after MIBG therapy, whole body single-photon emission computed tomography/computed tomography was performed showing increased I-131 uptake at the left parasternal region, lesion which destructs the fifth rib on the left hemithorax, multiple foci in liver, primary mass in the region of left adrenal gland, and the sacrum.

Conclusion: Given the limited role for other systemic thera-pies such as chemotherapy, I-131 MIBG treatment can be a valuable option for the patients with metastatic or unresect-able pheochromocytomas with limited side effects.

(Neuroendocrine Tumors)

IODINE-131 METAIODOBENZYLGUANIDINE (I-131 MIBG) THERAPY IN METASTATIC

PHEOCHROMOCYTOMASNafiye Helvaci, Nese Cinar, Bulent Okan Yildiz

Hacettepe University School of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism, Sihhiye, Ankara

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