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.
Objectives. This study aimed to compare the severity of COVID-19, inflammatory parameters and clinical outcomes among patients with normal and subnormal levels of Vitamin D.Methodology. This is a retrospective cohort study of 135 patients admitted in a tertiary hospital for COVID-19. Patients were grouped according to their Vitamin D level. Primary outcome measure was the composite of all-cause mortality and morbidity. Other outcome measures determined were the comparison among the groups on the severity of COVID-19 infection, changes in inflammatory parameters, length of hospital stay and duration of respiratory support.Results. There was a significant trend of higher ICU admission (p-value=0.024), mortality (p-value=0.006) and poor clinical outcome (p-value=0.009) among the Vitamin D deficient group. No significant difference was found for most of the inflammatory parameters, duration of hospital stay and respiratory support. Overall, patients with deficient, but not insufficient Vitamin D level had 6 times higher odds of composite poor outcome than those with normal Vitamin D (crude OR=5.18, adjusted OR =6.3,. Conclusion. The inverse relationship between Vitamin D level and poor composite outcome observed in our studysuggests that low Vitamin D may be a risk factor for poor prognosis among patients admitted for COVID-19.
BACKGROUND Chronic hypoparathyroidism in adults is usually secondary to previous thyroid surgery and is characterized by low calcuim and inappropriately low circulating PTH levels. The clinical presentation of hypoparathyroidism can vary with the serum calcium levels and chronicity of hypocalcemia. Hypoparathyroidism can cause intracranial calcifications but extensive intracranial calcifications are rare. Brain calcinosis syndrome is defined as bilateral calcium accumulation in the brain parenchyma, most often within the basal ganglia. Such intracranial calcifications occur in 0.3-1.5% of patients with hypoparathyroidism, often detected incidentally. The mechanism of intracranial calcification is not completely understood. Its occurrence with hypocalcemia suggests that increased calcium-phosphorus complex formation plays a role. THE CASE A 63-year old female was admitted due to dizziness. She had a fall prior confinement due to loss of consciousness lasting for less than 5 minutes, however, recovered afterwards. No head injury was detected at the referring hospital. She is hypertensive with good BP control on Amlodipine 2.5 mg and Losartan 50 mg taken once daily. She had total thyroidectomy for colloid adenoma 20 years ago, prescribed with Levothyroxine 100 mcg once daily but taken with poor compliance. She had episodes of cold intolerance, hoarseness, and weight gain. On examination, she was conscious and coherent. Blood pressure was 95/60 mm Hg, heart rate of 67 beats per minute. A midline neck scar from previous surgery was visible, no palpable neck mass or lymph nodes. Notable on the neurological examination were positive Rhomberg test and dysmetria evaluated by finger-to-nose test. Chvostek’s and Trosseau’s signs were negative. Motor, sensory and cranial nerve functions were intact. Plain cranial CT scan showed extensive cranial calcifications on both basal ganglia, corona radiata, brainstem and cerebellum. Blood tests revealed low levels of ionized calcium (0.91 mmol/L; N 1.12-1.32 mmol/L)), intact PTH (0.51 pg/ml; N 15-65 pg/ml), and FT4 (5.54 pmol/L; N 12-22 pmol/L). TSH was elevated (32.85 uIU/ml; N 0.27- 4.2 uIU/ml). Calcium with active vitamin D and levothyroxine were given. Physical rehabilitation initiated. Patient was eventually discharged improved, with decreased dizziness. CONCLUSION Basal ganglia calcifications present with diverse manifestations and include seizures, mental deterioration and disorders of the cerebellar or extrapyramidal function. Treatment usually involves calcium and vitamin D supplementation. Marked clinical improvement usually results from treatment of hypoparathyroidism. Measurement and monitoring of serum calcium, phosphorus and intact PTH is warranted. REFERENCE: Ramen C. Basak. A Case Report of Basal Ganglia Calcification - A Rare Finding of Hypoparathyroidism. Oman Med J. 2009 Jul; 24(3): 220-222.
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 scintigraphywas 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 inour 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: No date and time listed
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