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Acute Renal Failure Due to Vitamin D Intoxication

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WCIM 2014 SEOUL KOREA 97

Poster Session

The Korean Journal of Internal Medicine Vol. 29, No. 5 (Suppl. 1)

PS 0195 Endocrinology

Acute Renal Failure Due to Vitamin D Intoxication

Yusuf HANCERLI1, Veysel OZALPER1, Ibrahim CETINTAGLI1, Barbaros BASBUG1, Seyid Ahmet AY2, Ramazan ARIKAN1, Yalcin ONEM1

GATA Haydarpasa Training Hospital, Turkey1, GATA Haydarpasa Training Hospital, Turkey2

Objective: Vitamin D defi ciency is associated with multpl diseases.Vitamin D becomes more popular every day with the increasing studies. Vitamin D replacement therapy cases increase as well as Vitamin D intoxication cases. We present a 80-old-female patient who developed acute renal failure due to vitamin D intoxication.

Case: Patient came to the emergency room with the complaints of 4-day continuing nausea, vomiting and loss of appetite. Mucosa of the patient was dry and she was dehydrate.Tests results were urea:186mg/dL, creatinine:3.64mg/dl, albumin:3.26 g/dL, calcium:12.7mg/dL and venous blood gas results were pH:7,41,pCO2:41.9 HCO3:26.6.

Calcium,urea and creatinine levels were normal in a test that was performed 2 months ago. She was diagnosed with acute pre-renal failure connected to dehydration. A detailed medical history showed that 2.5 months ago, the patient was tested vitamin d3-25-0H (kalsifediyol):6.2 ng/ml and vitamin d3 300 000 IU bulb total of 3 was prescribed to her to be taken orally once a week, however, it was realized that the relatives of the patient gave her total of 10, once a week. After this fi nding, performed test results were detected as vitamin d3-25-0H (kalsifediyol):365 ng/ml, parathyroid hormone:16.8pg/ml. The patient was hospitalized with a diagnosis of vitamin D intox- ication and intravenous hydration with saline and IV furosemide infusion therapy was applied. At the end of second day her complaints have decreased and at the end of third day calcium level were 9.3mg/dl. At the tenth day test results were urea:30 mg/

dL,creatinine:1.12 mg/dL, and the patient was discharged.

Conclusion: Due to growing interest in vitamin D, it is very important that clinicans should be aware and alerted of that overdose vitamin D replacement therapy can cause vitamin D intoxication.

PS 0196 Endocrinology

A Case of Recurrent Multifocal Diabetic Myonecrosis

Hwa-Sun PARK1, Sang Min LEE1, Wookyung CHUNG1, Ie Byung PARK1 Gachon University Gil Hospital, Korea1

Diabetic myonecrosis is a rare complication associated with poorly controlled diabetes.

Although diabetes may be a common disease, diabeteic myonecrosis is a rare compli- cation. The usual presentation is sudden onset of pain at the involved muscles associ- ated with swelling and tenderness without previous trauma or fever. Diagnosis is clini- cal but MRI is the best investigation for diagnosis. Muscle biopsy is necessary in cases of doubt or to confi rm the imaging diagnosis. Management consists of conservative measures including analgesia and rest. We report one case of diabetic myonecrosis admitted in a tertiary care hospital. We present the case of a 37-year-old male, with 10 years history of well controlled diabetes mellitus type 2, on insulin therapy. Diabetic neuropathy, nephropathy requiring regular hemodialysis, retinopathy, hypertension and dyslipidemia were clinically evident. There was no history of injury of the right thigh.

Right thigh was hot, swollen, tender and fi rm with non-pitting edema. MRI revealed T2 high signal intensity and swelling of the vastus lateralis, distal vastus intermedius and medialis, rectus femoris, and short head of biceps femoris muscles. We performed ultrasound-guided muscle biopsy. It showed that multifocal necrosis and fi brosis with atrophy of muscle fi ber and some lymphocytic infi ltration. He was treated conserva- tively with analgesics and antibiotics. The pain improved in a period of 3-4 weeks. But he complained the pain of the left thigh 4 month later. Early differential diagnosis of diabetic myonecrosis is important. The diagnosis of diabetic myonecrosis is a clinical one that can be supported by MRI. Muscle biopsy is important, to exclude other caus- es such as pyomyositis, necrotising fasciitis, and neoplasm. Conservatively manage- ment including tight glycemic control should be achieved. Nonsurgical therapy appears to provide the most favorable outcome.

PS 0197 Endocrinology

Severe Hypercalcemia: Chronic Tophaceous Gout the Responsible Cause?

RENE RODRIGUEZ-GUTIERREZ1, ROBERTO MONREAL-ROBLES1, MARIA AZUCENA ZAPATA-RIVERA1, KARLA V RODRIGUEZ-VELVER1, FERNANDO JJ LAVALLE- GONZALEZ1, JOSE Gerardo GONZALEZ-GONZALEZ1, JESUS ZACARIAS VILLARREAL- PEREZ1

Endocrinology Division, Internal Medicine Department, University Hospital, Mexico1

Background and Description: The association of chronic tophaceous gout with severe hypercalcemia is extremely rare and has been usually associated with calcitriol se- cretion. PTHrP has never been described as the responsible cause. A 42-year old man with a long stand history of chronic gout initiated a week before admission with poly- uria, polypsia and progressive altered mental status. Neurological examination revealed only lethargy. Characteristic, multiple, non-tender tophi were obvious at inspection (Figures 1-3). Initial laboratory work up revealed a uric acid of 14.0 mg/dl, calcium of 14.5 mg/dl, phosphorous of 6.3 mg/dl, creatinine of 5.4 mg/dl, blood nitrogen urea of 56, a MDRD GFR of 16 ml/min.

Diagnostic and Therapeutic Approach: PTH was suppressed (< 3.0 pg/ml), 25-di- hydroxyvitamin D was normal, PTHrP was elevated 45.0 pg/ml, and calcitriol normal (19.6 pg/ml). Radiographs revealed bone erosions (Figure 1-3). Bone scan and a PET-CT were negative for metastasis and malignancy. Treatment was initiated with calcitonin, hydration and prednisone. PTH, 25-dihydroxyvitamin D, PTHrP, and calcitriol returned to normal values. At 6 months follow-up he referred no pain, tophi had improved and calcium levels were within normal range.

Discussion and Conclusion: A systemic research on PubMed, Medline, Embase and MedConsult with the search criteria; “Tophaceous gout”, hypercalcemia”, “calcitriol”,

“PTHrP”, was made. The proposed mechanism has being an enhanced 1a-hydrox- ylation of vitamin D in a proliferative chronic synovitis. In this case calcitriol levels were normal. PTHrP had never been, until now, described as the responsible cause of hypercalcemia in gout. In our case baseline PTHrP and calcium values were elevated and after medical treatment both returned to normal values. Immobilization is another well-known cause of mild calcium elevations. It is likely that in this case this was an exacerbating rather than the primary factor.

PS 0198 Endocrinology

Giant Cystic Prolactinoma in a Woman: Do Not Forget the Hook Effect

RENE RODRIGUEZ-GUTIERREZ1, KARLA V RODRIGUEZ-VELVER1, MARIA AZUCENA ZAPATA-RIVERA1, ROBERTO MONREAL-ROBLES1, FERNANDO J LAVALLE-GONZALEZ1, JOSE G GONZALEZ-GONZALEZZ1, JESUS ZACARIAS VILLARREAL-PEREZ1

Endocrinology Division, University Hospital, Mexico1

Background and Case Presentation: Cystic prolactinomas correspond to = 1% of all prolactinomas and its association with a giant pituitary macroadenoma in a woman has been seldom reported. A 43-year old woman was evaluated for a suprasellar tumor. She had absence of menses since 2 years. Three months before she started to have progressive headache. She also referred asthenia, adynamia, fatigue, dry hairi- ness, decreased libido, vaginal atrophy, and chronic constipation. Hair in armpits and pubic area was insignificant and osteotendinous reflex relaxation phase was slow.

Galactorrhea was absent and presented bitemporal hemianopsia.

Diagnostic and Therapeutic Approach: MRI scan revealed a 5 x 3.5 cm suprasellar mass and a 8.1 x 3.6 cm cystic component (Figures 1-3). Cortisol level 2.2 mg/dl, FSH and LH were low, estradiol < 0.05 pg/mL, IGF-1 normal and a serum prolactin of 125 ng/mL. Serial dilutions 1:10 and 1:100 were made. Diluted prolactine was 12,500 ng/

mL (hook effect). Treatment with cabergoline, prednisone and levothyroxine were ini- tiated. At two months follow-up prolactin serum levels decreased to 32.1 ng/mL.

Discussion and Conclusion: A systemic research on PubMed, Medline, Embase and MedConsult with the search criteria: “Giant Cystic Prolactinoma”, “prolactin”, “prol- actioma and “hook effect” was made. Due to the clinical signs of hypogonadism, the image in the MRI and the low/moderate high serum prolactin levels serial dilutions of prolactin were made. Serum prolactin assays can greatly underestimate extremely high levels of hormone, the so called “hook effect”. In present case, a high level of suspicion along with low/moderate prolactin levels and the MRI image consistent with a pituitary adenoma made us ask for diluted prolactin samples. If missed, this would have delayed the diagnosis and consequently would have changed the treatment plan and prognosis of the patient.

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