Objective. This study aims to determine the relationship between the different factors associated with the severity of Fibroscan with CAP findings among patients with Type 2 diabetes and fatty liver.Methodology. This is a cross-sectional study. Seven hundred four Fibroscan with Controlled Attenuation Parameter (CAP) results were electronically retrieved from a diagnostic center. 285 charts of diabetic patients with fatty liver on ultrasound were reviewed. 164 patients with fatty liver on ultrasound and Fibroscan with CAP were included in the study. Several factors were analysed in relation to the severity of Fibroscan with CAP findings in the study group.Results. Fifty five point five percent (55.5%) (91/164) had significant fibrosis and cirrhosis. Hepatic steatosis prevalence was 96% (158/164). Diabetes >5 years (OR 1.75), HbA1c >7% (OR 2.25) and high SGPT levels (OR 2.39) were associated with liver fibrosis and cirrhosis. BMI >25 kg/m 2 (OR 1.45), triglyceride levels >150 mg/dl (OR 1.31) and HbA1c >7% (OR 1.74) were associated with hepatic steatosis. Conclusion.Factors associated with the severity of hepatic fibrosis, cirrhosis and steatosis included above normal BMI, disease duration of >5 years, poor glycemic control and elevated levels of ALT, and serum triglycerides.
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 Pituitary apoplexy is characterized by acute neuroophthalmologic features due to bleeding in pituitary adenoma. Clinical manifestations occur due to local mass effect, spread of blood in subarachnoid space and deficiency of pituitary hormones. Clinical features include headache, visual impairment, external ophthalmoparesis, altered sensorium and hormone deficiencies. Causes of pituitary apoplexy are infarction, bleeding within the pituitary adenoma or metastasis. Surgery is indicated for decompression and relief of neuroophthalmic features. THE CASE A 65-year old male was admitted due to right eye ptosis, diplopia and blurring of vision. Two days prior, he was rushed to hospital due to headache and BP elevations. Plain cranial CT scan revealed age-related brain atrophy and gliosis. He was then discharged, with Losartan 100mg once daily, taken with good compliance. Examination showed stable vital signs. He was awake, coherent and oriented. Cranial nerves examination revealed right eye ptosis with medial, upward and downward gaze palsy. Pupillary sizes were 3 mm O.D. with nonreactive light reflex, 2 mm O.S. with brisk light reflex; no bitemporal hemianopsia. He was unable to read from 1.5 feet with both eyes. CT angiogram revealed suprasellar mass (1.4 x 2.3 x 1.2 cm), no evidence of vascular malformation. Cranial MRI with contrast defined the mass to be 2.6 cm lobulated sellar-suprasellar mass, compressing the optic chiasm, consistent of hemorrhagic pituitary macroadenoma. Hormonal studies showed low levels of serum cortisol (11.3 nmol/L; N 171- 536 nmol/L), FT4 (5.07 pmol/L N; 12-22 pmol/L), FT3 (2.5 pmol/L; N 3.1-6.8 pmol/L), LH (0.19 mIU/ml; N 0.57- 12.07 mIU/ml), testosterone (0.03 ng/mL; N 2.8-8ng/ml) and prolactin (2.26 ng/ml; N 3.46-19 ng/ml). TSH (0.30 uIU/ml; N 0.27-4.2 uIU/ml) and FSH (1.35 mIU/ml; N 0.95-11.95 mIU/ml) were normal. Hydrocortisone IV and levothyroxine were administered prior surgery. Patient underwent transphenoidal excision of pituitary tumor with no intraoperative complications. Biopsy of tumor revealed pituitary adenoma. Patient manifested postoperatively with improvement of ptosis and extraocular muscle movement on right eye. There was full lateral and downward gaze. Gradual recovery of upward and medial gaze on right eye was also seen. Patient was discharged with steroid and hormone replacement. CONCLUSION Pituitary apoplexy is a rare but life-threatening condition. Commonly implicated cause is pituitary macroadenoma. Immediate recognition allows prompt steroid administration and surgical decompression. Long-term hormone replacement is required. Recovery of visual symptoms is commonly realized. REFERENCE Rajesh Verma et al. Pituitary apoplexy syndrome as the manifestation of intracranial tuberculoma. BMJ Case Rep. 2014
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