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RISS 인기검색어
- 검색키워드
- 저자 : ( Maria Azucena Zapata Rivera ) (검색결과 2 건)
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( Rene Rodriguez Gutierrez ),( Karla V Rodriguez Velver ),( Maria Azucena Zapata Rivera ),( Roberto Monreal Robles ),( Fernando J Lavalle Gonzalez ),( Jose G Gonzalez Gonzalezz ),( Jesus Zacarias Vill 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
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 hairiness, 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 initiated. 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”, “prolactioma 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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( Rene Rodriguez Gutierrez ),( Roberto Monreal Robles ),( Maria Azucena Zapata Rivera ),( Karla V Rodriguez Velver ),( Fernando Jj Lavallegonzalez ),( Jose Gerardo Gonzalez Gonzalez ),( Jesus Zacarias 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background and Description: The association of chronic tophaceous gout with severe hypercalcemia is extremely rare and has been usually associated with calcitriol secretion. 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 polyuria, 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-dihydroxyvitamin 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-hydroxylation 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.
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