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Your search keyword '"Deepthi, Bobbity"' showing total 78 results
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78 results on '"Deepthi, Bobbity"'

56. Chondrodysplasia punctata with severe airway stenosis

Author

Deepthi, Bobbity, Chhapola, Viswas, Kanwal, Sandeep, Sharma, Ankita, and Kumar, Virendra

Subjects
Pediatric research, Chondrodysplasia punctata -- Diagnosis -- Case studies, Health
Abstract

Byline: Bobbity. Deepthi, Viswas. Chhapola, Sandeep. Kanwal, Ankita. Sharma, Virendra. Kumar Chondrodysplasia punctata (CDP) is a group of skeletal dysplasias characterized primarily by punctate calcifications in cartilage. It is a [...]

Published
2018

68. Infantile nephrotic syndrome secondary to cytomegalovirus infection in a 7-month-old girl: resolution with ganciclovir.

Author

Kaur, Jasleen, Deepthi, Bobbity, Dhull, Rachita Singh, Faruq, M. D., and Saha, Abhijeet

Subjects
*NEPHROTIC syndrome, *CYTOMEGALOVIRUS diseases, *GANCICLOVIR, *POLYMERASE chain reaction, *INFANTS, *FOCAL segmental glomerulosclerosis
Abstract

Infantile nephrotic syndrome is a rare disorder which is frequently caused by genetic defects. A 7-month-old girl presented with fever, loose stools and anasarca and was diagnosed with nephrotic syndrome. Work-up for a genetic cause was negative. Cytomegalovirus polymerase chain reaction (CMV PCR) was positive and the infant was treated with ganciclovir for 6 weeks, followed by valganciclovir for 10 weeks. All symptoms resolved within 2 weeks of commencing treatment and she attained complete remission within 4 weeks. CMV PCR was negative within 4 weeks of antiviral therapy. At 18 months follow-up she remained well. Appropriate treatment of infantile nephrotic syndrome secondary to CMV should result in recovery. [ABSTRACT FROM AUTHOR]

Published
2021
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74. Plasma Free Homocysteine Levels in Children with Idiopathic Nephrotic Syndrome.

Author

Arumugam, Venkatesh, Saha, Abhijeet, Kaur, Manpreet, Deepthi, Bobbity, Basak, Trayambak, Sengupta, Shantanu, Bhatt, Ajay, Batra, Vineeta V., and Upadhyay, Ashish D.

Subjects
NEPHROTIC syndrome diagnosis, AGE factors in disease, CHOLESTEROL, DRUG resistance, ENDOTHELIUM, EPITHELIAL cells, HIGH performance liquid chromatography, LONGITUDINAL method, NEPHROTIC syndrome, PEDIATRICS, RISK assessment, SERUM albumin, SEX distribution, STEROIDS, HOMOCYSTEINE, DISEASE remission
Abstract

Altered metabolism of homocysteine in children with idiopathic nephrotic syndrome leads to raised plasma-free homocysteine levels. Elevated free homocysteine causes endothelial cell dysfunction and promotes early atherosclerosis and glomerulosclerosis. In this analytical study with a longitudinal follow-up, 29 children with first episode of nephrotic syndrome (FENS) aged 1-16 years along with 30 age andgender-matched healthy controls were enrolled. Plasma-free homocysteine was measured using high-performance liquid chromatography (HPLC). Other variables were measured using standard biochemical methods. The primary outcome measure was plasma-free homocysteine level in children with FENS and in controls. The secondary outcome measure was to observe the levels of plasma-free homocysteine in children with FENS at 12 weeks in remission and in steroid resistant states. Plasma-free homocysteine levels were significantly elevated in children with FENS at disease onset [Median (IQR) 2.170 (1.54-2.71); N = 29; P < 0.001], at 12 weeks of steroid-induced remission [Median (IQR) 1.946 (1.53-2.71); N = 22; P < 0.001], and in steroid-resistant states [Median (IQR) 2.262 (1.53-2.74); N = 7; P < 0.001] compared to controls. The levels did not decrease significantly at 12 weeks of steroid-induced remission compared to onset of nephrotic syndrome. Plasma-free homocysteine levels correlated positively with serum total cholesterol (P = 0.005; r = 0.362) and negatively with serum albumin (P = 0.032; r = 0.281). Plasma-free homocysteine levels are raised in children with FENS posing a risk of endothelial dysfunction which persists at least in short term. Long-term effects of raised plasma-free homocysteine needs to be studied. [ABSTRACT FROM AUTHOR]

Published
2019
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78. Vitamin D-dependent rickets (VDDR) type 1: case series of two siblings with a CYP27B1 mutation and review of the literature.

Author

Dhull RS, Jain R, Deepthi B, Cheong HI, Saha A, Mehndiratta M, and Basu S

Subjects
Humans, Mutation, Siblings, Vitamin D, 25-Hydroxyvitamin D3 1-alpha-Hydroxylase genetics, Familial Hypophosphatemic Rickets diagnosis, Familial Hypophosphatemic Rickets genetics
Abstract

Two siblings presented with clinical and biochemical features of rickets, initially suspected as hypophosphatemic rickets. There was no improvement initially, hence the siblings were reinvestigated and later diagnosed as having vitamin D-dependent rickets (VDDR) type 1 due to a rare mutation in the CYP27B1 gene encoding the 1α-hydroxylase enzyme. Both siblings improved with calcitriol supplementation. The initial presentation of VDDR is often confusing and algorithmic evaluation helps in diagnosis. We also present a brief review of the literature, including genetics.

Published
2020
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