Tuberculosis is ancient disease known to mankind. Diagnosis and management of spinal tuberculosis has immensely improved in last few decades. Imaging, particularly MRI, plays important role in diagnosis of spinal tuberculosis and its complications. Four common imaging patterns of spinal tuberculosis include paradiscal type, central type, Anterior subligamentous type, and posterior type. Imaging also plays important role in differentiation of spinal tuberculosis from its mimics, particularly pyogenic spondylitis, and metastasis. Radiological interventions, such as CT guided vertebral biopsy, and percutaneous drainage of cold abscess, are commonly used in management of spinal tuberculosis. Monitoring of therapeutic response is often based on clinical evaluation and imaging. MRI is most common imaging modality used. Signs of healing include bony ankylosis, resolution of marrow edema, decrease in contrast enhancement, and fatty change with in bone marrow. PET CT is recently evaluated for response assessment with promising results. This review summarizes pathophysiology, clinical presentation, imaging features, radiological interventions, and response assessment in spinal tuberculosis.
Objectives: The objective of this study was to evaluate the diagnostic accuracy of multiparametric magnetic resonance imaging (mpMRI) and 68 Ga prostate-specific membrane antigen positron emission tomography–computed tomography (PSMA PET-CT) and respective quantitative parameters (K trans – influx rate contrast, K ep – efflux rate constant, ADC – apparent diffusion coefficient, and SUVmax ratio – prostate SUVmax to background SUVmax ratio) in detection and localization of clinically significant prostate cancer (CSPCa) in D’Amico intermediate- and high-risk group patients (prostate-specific antigen [PSA] >10 ng/ml). Methodology: The study included thirty-three consecutive adult men with serum prostate specific antigen >10ng/ml, and systematic 12 core prostate biopsy proven prostate cancer. All the 33 patients, were evaluated with mpMRI, and 68 Ga PSMA PET-CT. The biopsy specimens and imaging were evaluated for 12 sectors per prostate by a predetermined scheme. Results: MpMRI Prostate Imaging Reporting and Data System version 2 (PI-RADS v2) score ≥3 showed higher sensitivity than 68 Ga PSMA PET-CT (96.3% vs. 82.4%), with similar specificity (54.5% vs. 54.5%) ( n = 33 patients, 396 sectors). Combined use of MRI and 68 Ga PSMA PET-CT in parallel increased sensitivity (99.5%) and NPV (98.7%) for detection of CSPCa and combined use of MRI and 68 Ga PSMA PET-CT in series increased specificity (71.8%) and PPV (71.5%) ( n = 33 patients, 396 sectors). ADC showed a strong negative correlation with Gleason score (r = −0.77), and the highest discriminative ability for detection and localization of CSPCa (area under curve [AUC]: 0.91), followed by K trans ( r = 0.74; AUC: 0.89), PI-RADS (0.73; 0.86), SUVmax ratio (0.49; 0.74), and K ep (0.24; 0.66). Conclusion: MpMRI PI-RADS v2 score and 68 Ga PSMA PET-CT (individually as well as in combination) are reliable tool for detection and localization of CSPCa. Quantitative MRI and 68 Ga PSMA PET-CT parameters have potential to predict Gleason score and detect CSPCa.
Introduction Primary hyperparathyroidism (PHPT) is a disease that is usually diagnosed in an asymptomatic state during routine biochemical screening. It generally manifests as a sporadic disease in post-menopausal women. However, in India and developing countries, we continue to see severe skeletal and renal manifestations of the disease. Case report Herein, we describe the case of a 16-year-old adolescent girl who presented with severe manifestations of primary hyperparathyroidism. Biochemically, she had severe parathyroid hormone (PTH)-dependent hypercalcaemia with hypophosphataemia and vitamin D deficiency (serum total Ca – 18.5 mg/dl [8.5–10.5 mg/dl], serum PO4 – 1.9 mg/dl [2.5–4.5 mg/dl], serum ALP – 2015 IU/l [80–240 IU/l], serum 25[OH]D – 19.1 ng/ml [30–100 ng/ml] and serum iPTH > 5000 pg/ml [15–65 pg/ml]). Pre-operatively, she required management with saline diuresis, bisphosphonate, and calcitonin. After surgery, the patient had severe hungry bone syndrome (serum Ca – 4.1 mg/dl, serum PO4 – 2.1 mg/dl, serum ALP > 10,000 IU/l) that required treatment with calcium infusions for almost 3 months. Although the clinical and biochemical picture was suggestive of parathyroid carcinoma, histopathology revealed atypical parathyroid adenoma with low proliferative index. Atypical parathyroid adenoma is a term applied to a neoplasm with ‘worrisome’ features but not fulfilling the ‘absolute histopathological criteria of malignancy’. Conclusions Atypical parathyroid adenoma, a rare cause of PHPT, may be associated with severe manifestations. Although malignancy was not discerned in the immediate post-operative period, we plan to continue long-term follow-up of the patient to look for any signs of recurrence or development of parathyroid carcinoma.
Cushing’s syndrome is a rare disease in the paediatric age group. Adrenocortical carcinomas (ACC) constitute the most common cause of Cushing’s syndrome between 1 and 5 years of age. Often, adrenocortical carcinomas co-secrete other hormones such as androgens (testosterone), deoxy-corticosterone (DOCA), or 17-hydroxy-progesterone [17(OH)P] in addition to cortisol. This may manifest with symptoms and signs of precocious puberty along with Cushing’s syndrome. It is rare for a benign adrenocortical adenoma to co-secrete androgens and other hormones in addition to cortisol. Differentiation between adenoma and carcinoma is difficult in all aspects: clinical, radiological, and histopathological. Here, we describe the case of a 2.5-year-old male child who presented with Cushing’s syndrome and virilization. Although we suspected ACC clinically, the radiological and histopathological findings were suggestive of benign adrenocortical adenoma. Our case represents the diagnostic challenge that exists in paediatric adrenocortical tumours.
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