Objectives: Coronavirus disease 2019 (COVID-19)–associated mucormycosis (CAM) has emerged as a formidable infection in patients with COVID-19. The aggressive management ofCAM affects quality of life (QOL); thus, this study was designed to assess the QOL in patients with CAM at a tertiary healthcare institution. Methods: This cross-sectional study of 57 patients with CAM was conducted over 6 monthsusing a semi-structured standard questionnaire (the abbreviated World Health Organization Quality of Life questionnaire [WHO-BREF]) and a self-rated improvement (SRI) scale ranging from 0 to 9. Cut-off values of ≤52 and < 7 were considered to indicate poor QOL and poor improvement, respectively. The correlations of QOL and SRI scores were evaluated using Spearman rho values. Results: In total, 27 patients (47.4%; 95% confidence interval [CI], 34.9%–60.1%) and 26 patients (45.6%; 95% CI, 33.4%–58.4%) had poor QOL and poor SRI scores, respectively. The overall median (interquartile range) QOL score was 52 (41–63). Headache (adjusted B, −12.3), localized facial puffiness (adjusted B , −16.4), facial discoloration (adjusted B, −23.4), loosening of teeth (adjusted B, −18.7), and facial palsy (adjusted B, −38.5) wer e significantly associated with the QOL score in patients with CAM. Conclusion Approximately 1 in 2 patients with CAM had poor QOL and poor improvement.Various CAM symptoms were associated with QOL in these patients. Early recognition is the key to optimal treatment, improved outcomes, and improved QOL in patients with CAM.

Respiratory failure and chronic ventilator dependence in tetraplegics following cervical injuries located high on the spine (C1–C3) constitute significant challenges in the rehabilitation of patients given the occurrence of repeated hospitalizations and an ever-increasing financial burden. A 30-year-old man presented with posttraumatic tetraplegia following an unstable injury at the C1–C2 level with cord compression; he was managed by posterior stabilization and decompression followed by ventilator dependence and no rehabilitation until 6 months postinjury. We implanted phrenic nerve stimulator electrodes bilaterally for indirect diaphragm pacing by an implantable pulse generator that allowed for weaning from mechanical ventilation and spontaneous ventilator-free breathing at 20 weeks post-implantation and which facilitated post-tetraplegia rehabilitation. At 36 months after implantation, the patient is ventilator- free without any procedure-related complications or respiratory infections. Diaphragm pacing with phrenic nerve stimulation may be a way forward for ventilator-dependent tetraplegics in developing countries to pursue effective rehabilitation and improved quality of life.

Various patterns of calcifications may be seen in thyroid cancers on ultrasonography (USG) of thyroid.1 Coarse calcifications seen in medullary thyroid carcinoma (MTC) are generally associated with posterior shadowing on thyroid ultrasound.2 We briefly report this case of MTC with an emphasis on its radiological features.
Thyroid cancer, medullary

Rickets, one of the leading causes of bony deformities and short stature, can be calciopenic (inciting event is defective intestinal calcium absorption) or phosphopenic (inciting event is phosphaturia). Early diagnosis and timely treatment of rickets are crucial for correction of the limb deformities. Guidelines exist for nutritional rickets, but the diagnosis and management of the relatively uncommon forms of rickets are complex. This consensus aims to formulate a simplified diagnostic approach for rickets, especially in resource-limited settings. The consensus statement has been formulated by a 29-member committee from the Endocrine Society of Bengal. The process included forming a working group, conducting a literature review, identifying controversies, drafting, and discussion at a consensus meeting. Participants rated their agreement with the clinical practice points, and a 70% consensus was required. Input integration and further review led to the final consensus statements. Children with suspected rickets should initially be examined for distinctive skeletal deformities. The diagnosis of rickets should be confirmed with characteristic radiographic abnormalities. It is advisable to order tests for serum calcium, inorganic phosphorus (Pi), liver function, 25-hydroxyvitamin D (25OHD), parathyroid hormone, creatinine, and potassium in all patients with rickets. In cases of refractory rickets, it is also recommended that assessments be conducted for spot urine calcium, Pi, creatinine, and, blood gas analysis. In children with rickets and metabolic acidosis, tests for glycosuria, uricosuria, aminoaciduria, low molecular weight proteinuria, and albuminuria should be conducted. In children with resistant calciopenic rickets and sufficient serum 25OHD levels, serum 1,25(OH)2D concentration should be tested. 1,25(OH)2 D and fibroblast growth factor 23 estimation is useful for certain forms of phosphopenic rickets.

Rickets, one of the leading causes of bony deformities and short stature, can be calciopenic (inciting event is defective intestinal calcium absorption) or phosphopenic (inciting event is phosphaturia). Early diagnosis and timely treatment of rickets are crucial for correction of the limb deformities. Guidelines exist for nutritional rickets, but the diagnosis and management of the relatively uncommon forms of rickets are complex. This consensus aims to formulate a simplified diagnostic approach for rickets, especially in resource-limited settings. The consensus statement has been formulated by a 29-member committee from the Endocrine Society of Bengal. The process included forming a working group, conducting a literature review, identifying controversies, drafting, and discussion at a consensus meeting. Participants rated their agreement with the clinical practice points, and a 70% consensus was required. Input integration and further review led to the final consensus statements. Children with suspected rickets should initially be examined for distinctive skeletal deformities. The diagnosis of rickets should be confirmed with characteristic radiographic abnormalities. It is advisable to order tests for serum calcium, inorganic phosphorus (Pi), liver function, 25-hydroxyvitamin D (25OHD), parathyroid hormone, creatinine, and potassium in all patients with rickets. In cases of refractory rickets, it is also recommended that assessments be conducted for spot urine calcium, Pi, creatinine, and, blood gas analysis. In children with rickets and metabolic acidosis, tests for glycosuria, uricosuria, aminoaciduria, low molecular weight proteinuria, and albuminuria should be conducted. In children with resistant calciopenic rickets and sufficient serum 25OHD levels, serum 1,25(OH)2D concentration should be tested. 1,25(OH)2 D and fibroblast growth factor 23 estimation is useful for certain forms of phosphopenic rickets.

Rickets, one of the leading causes of bony deformities and short stature, can be calciopenic (inciting event is defective intestinal calcium absorption) or phosphopenic (inciting event is phosphaturia). Early diagnosis and timely treatment of rickets are crucial for correction of the limb deformities. Guidelines exist for nutritional rickets, but the diagnosis and management of the relatively uncommon forms of rickets are complex. This consensus aims to formulate a simplified diagnostic approach for rickets, especially in resource-limited settings. The consensus statement has been formulated by a 29-member committee from the Endocrine Society of Bengal. The process included forming a working group, conducting a literature review, identifying controversies, drafting, and discussion at a consensus meeting. Participants rated their agreement with the clinical practice points, and a 70% consensus was required. Input integration and further review led to the final consensus statements. Children with suspected rickets should initially be examined for distinctive skeletal deformities. The diagnosis of rickets should be confirmed with characteristic radiographic abnormalities. It is advisable to order tests for serum calcium, inorganic phosphorus (Pi), liver function, 25-hydroxyvitamin D (25OHD), parathyroid hormone, creatinine, and potassium in all patients with rickets. In cases of refractory rickets, it is also recommended that assessments be conducted for spot urine calcium, Pi, creatinine, and, blood gas analysis. In children with rickets and metabolic acidosis, tests for glycosuria, uricosuria, aminoaciduria, low molecular weight proteinuria, and albuminuria should be conducted. In children with resistant calciopenic rickets and sufficient serum 25OHD levels, serum 1,25(OH)2D concentration should be tested. 1,25(OH)2 D and fibroblast growth factor 23 estimation is useful for certain forms of phosphopenic rickets.

We report three cases of Bardet-Biedl syndrome (BBS) among which a young female and two siblings from a separate family, presented with common features of obesity, postaxial (ulnar) polydactyly, speech delay, developmental delay with learning difficulties and progressive deterioration of vision. Fundus examination revealed maculopathy and other remarkable findings in these patients. In this image of endocrinology, we describe the BBS phenotypes of these cases highlighting the fundus photography features with a plan for close follow up on obesity and endocrine complications.
Polydactyly ; Obesity ; Macular Degeneration ; Bardet-Biedl Syndrome

Rickets, one of the leading causes of bony deformities and short stature, can be calciopenic (inciting event is defective intestinal calcium absorption) or phosphopenic (inciting event is phosphaturia). Early diagnosis and timely treatment of rickets are crucial for correction of the limb deformities. Guidelines exist for nutritional rickets, but the diagnosis and management of the relatively uncommon forms of rickets are complex. This consensus aims to formulate a simplified diagnostic approach for rickets, especially in resource-limited settings. The consensus statement has been formulated by a 29-member committee from the Endocrine Society of Bengal. The process included forming a working group, conducting a literature review, identifying controversies, drafting, and discussion at a consensus meeting. Participants rated their agreement with the clinical practice points, and a 70% consensus was required. Input integration and further review led to the final consensus statements. Children with suspected rickets should initially be examined for distinctive skeletal deformities. The diagnosis of rickets should be confirmed with characteristic radiographic abnormalities. It is advisable to order tests for serum calcium, inorganic phosphorus (Pi), liver function, 25-hydroxyvitamin D (25OHD), parathyroid hormone, creatinine, and potassium in all patients with rickets. In cases of refractory rickets, it is also recommended that assessments be conducted for spot urine calcium, Pi, creatinine, and, blood gas analysis. In children with rickets and metabolic acidosis, tests for glycosuria, uricosuria, aminoaciduria, low molecular weight proteinuria, and albuminuria should be conducted. In children with resistant calciopenic rickets and sufficient serum 25OHD levels, serum 1,25(OH)2D concentration should be tested. 1,25(OH)2 D and fibroblast growth factor 23 estimation is useful for certain forms of phosphopenic rickets.