Background Derangements of calcium metabolism are common in patients with cancer.1 Unlike hypercalcemia which is well-recognized, little is known about hypocalcemia of malignancy.2 In fact, there were only 2 studies published to date that investigated its incidence among cancer patients. 2,3 Clinical Case: A 40-year-old male consulted an ENT specialist for a 2×2 cm left parotid mass of 3 years duration. There was no fever, cough, night sweats or significant weight loss. Histological analysis of the mass revealed parotid gland adenocarcinoma. Tumor metastases to lung and spine were seen on PET CT scan. Consequently, he received 18 cycles of chemotherapy and 10 sessions of radiotherapy without surgery because of the advanced stage. He initially exhibited good response with the treatment. A year after, he developed shortness of breath, numbness of hands with seizure episode. Chest x-ray showed pleural effusion and osteoblastic changes while cranial CT scan revealed brain metastasis. Bone scintigraphy was evident for multiple osseous metastases. He underwent stereotactic brain surgery, and thoracentesis with pleural fluid analysis consistent with malignancy. Biochemical tests were remarkable for hypocalcemia (0.99, n>1.12 mmol/L, normomagnesemia (0.89, n>0.74 mmol/L), low vitamin D (11.6, n>30 ng/mL), elevated phosphate (1.73; n: <1.49 mg/dL), and elevated intact PTH which eventually dropped (157.7 to 9, n>15 pg/mL). Ultrasound of the neck revealed diffuse thyroid calcifications. Despite oral calcium supplementation (14.4 grams elemental calcium), calcium infusion (1.35 mg/kg/hour elemental calcium) and vitamin D supplementation (6000 IU cholecalciferol and 0.5 mg calcitriol daily), he remained hypocalcemic. His condition eventually worsened, and he succumbed to death in due course despite aggressive measures provided. Conclusion To our knowledge, this is the first case illustrating the therapeutic challenge in addressing an intractable hypocalcemia in the setting of an advanced parotid carcinoma in our country.Reference: (1)Carl Blomqvist. A Hospital Survey of Hypocalcemia in Patients with Malignant Disease. Acta Med Scand. 1986;220. (2) Schattner et al. Hypocalcaemia of Malignancy. The Netherlands Journal of Medicine. July 2016, Vol. 74, No. 6. (3) Goncalves. Hypocalcemia in cancer patients: An exploratory Study. Porto Biomed. J. (2019) 4: 4 Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
Background Turner syndrome and Congenital adrenal hyperplasia are distinct examples of disorders of sexual development. Because they share common clinical features, their coexistence is difficult to diagnose.1 Currently, only ten cases have been reported in the literature.2 Clinical Case: A 54-year-old, born and raised as a female, consulted a gynecologist because of ambiguous genitalia. Her late presentation was due to reluctance of medical care. During her teenage years, she had cyclic hypogastric cramps but never had menstrual bleeding. In her late 20s, she noted virilizing features such as receding hairline, hirsutism and deepening of voice. None of her parents and siblings presented the same features. She had a short stature (height: 147.32 cm), wide spaced nipples with absent breast bud and shortened 4th metatarsals. Genital examination showed a pair of labia without palpable mass and testes, and a prominent phallic structure measuring 3-4 cm (Prader Stage V). Hormonal assays revealed low normal FSH (4.58, >3. 03 mIU/mL, low LH (0.48, >1.8 mIU/mL), elevated testosterone (4.7, n<0.75 ng/mL) and progesterone (14.47, <1.4 ng/mL), and normal estradiol (66, n: 23-139 pg/mL). Tumor markers such as ß-hCG, ɑ-fetoprotein, LDH and CA-125, electrolyte analysis and thyroid function test showed no abnormalities. Both pelvic ultrasonography and abdominal MRI demonstrated a large abdominopelvic mass (14.7×17.1×8.4 cm) with no identifiable normal looking uterus, ovaries, or testes. She underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy. Histopathologic analysis of the specimen revealed submucous and intramural leiomyoma uteri, atrophic endometrium without abnormality on both ovaries and fallopian tubes. Karyotype analysis indicated 45×[2] / 46, XX [48], Mosaic 45,×/ 46 XX consistent with Turner's syndrome. Because virilization is not a typical feature, further evaluation using 17-hydroxyprogesterone was performed. The result yielded elevated basal (235, n<6 nmol/L) and postsynacthen result (60 minutes) (241, n<30 nmol/L), hence, the diagnosis of non-classic congenital adrenal hyperplasia was established. Conclusion The individual incidence of Turner syndrome and non-classic congenital adrenal hyperplasia is not uncommon, but their coexistence is rare. In the absence of Y chromosome in Turner syndrome, presence of virilization should warrant investigation for congenital adrenal hyperplasia. Presentation: No date and time listed
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