Sejal Shah, MD

  • Sejal H Shah



Trabajo y Educación

Formación Profesional

Northwestern University Medical School, Chicago, IL, 2005


Rainbow Babies And Childrens, Cleveland, OH, 2006


Rainbow Babies And Childrens, Cleveland, OH, 2008


Stanford University Pediatric Residency, Palo Alto, CA, 2012

Certificaciones Médicas

Pediatric Endocrinology, American Board of Pediatrics

Pediatrics, American Board of Pediatrics



Condiciones Tratadas

Adrenal Disorders

Diabetes (Type 1 and Type 2)

Early and Delayed Puberty

Glucose Related Problems

Growth Disorders



Pituitary Gland Disorders


Thyroid Disorders

Turner Syndrome

Todo Publicaciones

Large Doses of Vitamin D Fail to Increase 25-Hydroxyvitamin D Levels ortoAlter Cardiovascular Risk Factors in Obese Adolescents: A Pilot Study. journal of adolescent health Shah, S., Wilson, D. M., Bachrach, L. K. 2015; 57 (1): 19-23


Vitamin D deficiency and cardiometabolic risk factors are common in obese adolescents. Observational studies demonstrate an inverse relationship among serum 25-hydroxyvitamin D (25OHD) and obesity, insulin resistance, and inflammatory cytokines. This pilot study explores if vitamin D supplementation could reduce serum concentrations of inflammatory cytokines (interleukin [IL] 6, IL-10, tumor necrosis factor ), adiponectin, lipids, hemoglobin A1C, and high-sensitivity C-reactive protein (hs-CRP). A secondary aim was to determine the associations between baseline serum 25OHD concentrations and body mass index (BMI), hs-CRP, inflammatory cytokines, and lipids.Overweight and obese adolescents enrolled in this 24-week, randomized, double-blind study were given 150,000 IU ergocalciferol or placebo at baseline and 12weeks. Outcome measurements included serum 25OHD, inflammatory cytokines, adiponectin, hs-CRP, lipids, hemoglobin A1C, and BMI at baseline, 12, and 24weeks.Of 40 participants, 31 (78%) completed the study. Mean standard error 25OHD levels were similar in vitamin D and placebo groups at baseline (19.6 5.3 vs. 25.8 10.8ng/mL) and 24weeks (20.1 3.4 vs. 24.6 8.4ng/mL). Inflammatory and cardiovascular markers were not significantly different between groups at 24weeks. Serum 25OHD at baseline was associated with BMI (r=-.44 [95% confidence interval,-.66 to-.15]) but not with other outcome measures.Supplementation with vitamin D at 150,000 IU every 3months failed to increase serum 25OHD or alter inflammatory markers and lipids in overweight and obese youth. Further studies are needed to establish the dose of vitamin D required to increase 25OHD and determine potential effects on metabolic risk factors in obese teens.

View details for DOI 10.1016/j.jadohealth.2015.02.006

View details for PubMedID 25873553

A randomized trial of transdermal and oral estrogen therapy in adolescent girls with hypogonadism. International journal of pediatric endocrinology Shah, S., Forghani, N., Durham, E., Neely, E. K. 2014; 2014 (1): 12-?


Adolescent females with ovarian failure require estrogen therapy for induction of puberty and other important physiologic effects. Currently, health care providers have varying practices without evidence-based standards, thus investigating potential differences between oral and transdermal preparations is essential. The purpose of this study was to compare the differential effects of treatment with oral conjugated equine estrogen (OCEE), oral 17 estradiol (OBE), or transdermal 17 estradiol (TBE) on biochemical profiles and feminization in girls with ovarian failure.20 prepubertal adolescent females with ovarian failure, ages 12-18 years, were randomized to OCEE (n=8), OBE (n=7), or TBE (n=5) for 24months. Estrogen replacement was initiated at a low dose (0.15mg OCEE, 0.25mg OBE, or 0.0125mg TBE) and doubled every 6months to a maximum dose of 0.625mg/d OCEE, 1mg/d OBE, or 0.05mg/d TBE. At 18months, micronized progesterone was added to induce menstrual cycles. Biochemical markers including sex hormones, inflammatory markers, liver enzymes, coagulation factors, and lipids were obtained at baseline and 6month intervals. Differences in levels of treatment parameters between the groups were evaluated with one-way analysis of variance (ANOVA). The effect of progesterone on biochemical markers was evaluated with the paired t-test.Mean (SE) estradiol levels at maximum estrogen dose (18months) were higher in the TBE group (5319pg/mL) compared to OCEE (145pg/mL) and OBE (125pg/mL) (p0.01). The TBE and OBE groups had more effective feminization (100% Tanner 3 breast stage at 18months). There were no statistical differences in other biochemical markers between treatment groups at 18months or after the introduction of progesterone.Treatment with transdermal 17 estradiol resulted in higher estradiol levels and more effective feminization compared to oral conjugated equine estrogen but did not result in an otherwise different biochemical profile in this limited number of heterogeneous patients. OBE and TBE provide safe and effective alternatives to OCEE to induce puberty in girls, but larger prospective randomized trials are required.NCT01023178.

View details for DOI 10.1186/1687-9856-2014-12

View details for PubMedID 24982681

View details for PubMedCentralID PMC4074834

Adrenal Suppression from Topical and Subconjunctival Steroids after Pediatric Cataract Surgery. Ophthalmology Lambert, S. R., Shah, S. 2018; 125 (10): 164445

View details for DOI 10.1016/j.ophtha.2018.06.012

View details for PubMedID 30243335

Newborn with prenatally diagnosed choroidal fissure cyst and panhypopituitarism and review of the literature. AJP reports Chitkara, R., Rajani, A., Bernstein, J., Shah, S., Hahn, J. S., Barnes, P., Hintz, S. R. 2011; 1 (2): 111-114


Little has been reported on fetal diagnosis of choroidal fissure cysts and prediction of the clinical complications that can result. We describe the case of a near-term male infant with prenatally diagnosed choroidal fissure cyst and bilateral clubfeet. His prolonged course in the neonatal intensive care nursery was marked by severe panhypopituitarism, late-onset diabetes insipidus, placement of a cystoperitoneal shunt, and episodes of sepsis. Postnatal genetic evaluation also revealed an interstitial deletion involving most of band 10q26.12 and the proximal half of band 10q26.13. The patient had multiple readmissions for medical and surgical indications and died at 6 months of age. This case represents the severe end of the spectrum of medical complications for children with choroidal fissure cysts. It highlights not only the importance of comprehensive evaluation and multidisciplinary management and counseling in such cases, but also the need for heightened vigilance in these patients.

View details for DOI 10.1055/s-0031-1293512

View details for PubMedID 23705098

View details for PubMedCentralID PMC3653523

Interaction of PIMT with transcriptional coactivators CBP, p300, and PBP differential role in transcriptional regulation JOURNAL OF BIOLOGICAL CHEMISTRY Misra, P., Qi, C., Yu, S. T., Shah, S. H., Cao, W. Q., Rao, M. S., Thimmapaya, B., Zhu, Y. J., Reddy, J. K. 2002; 277 (22): 20011-20019


PIMT (PRIP-interacting protein with methyltransferase domain), an RNA-binding protein with a methyltransferase domain capable of binding S-adenosylmethionine, has been shown previously to interact with nuclear receptor coactivator PRIP (peroxisome proliferator-activated receptor (PPAR)-interacting protein) and enhance its coactivator function. We now report that PIMT strongly interacts with transcriptional coactivators, CBP, p300, and PBP but not with SRC-1 and PGC-1alpha under in vitro and in vivo conditions. The PIMT binding sites on CBP and p300 are located in the cysteine-histidine-rich C/H1 and C/H3 domains, and the PIMT binding site on PBP is in the region encompassing amino acids 1101-1560. The N-terminal of PIMT (residues 1-369) containing the RNA binding domain interacts with both C/H1 and C/H3 domains of CBP and p300 and with the C-terminal portion of PBP that encompasses amino acids 1371-1560. The C-terminal of PIMT (residues 611-852), which binds S-adenosyl-l-methionine, interacts respectively with the C/H3 domain of CBP/p300 and with a region encompassing amino acids 1101-1370 of PBP. Immunoprecipitation data showed that PIMT forms a complex in vivo with CBP, p300, PBP, and PRIP. PIMT appeared to be co-localized in the nucleus with CBP, p300, and PBP. PIMT enhanced PBP-mediated transcriptional activity of the PPARgamma, as it did for PRIP, indicating synergism between PIMT and PBP. In contrast, PIMT functioned as a repressor of CBP/p300-mediated transactivation of PPARgamma. Based on these observations, we suggest that PIMT bridges the CBP/p300-anchored coactivator complex with the PBP-anchored coactivator complex but differentially modulates coactivator function such that inhibition of the CBP/p300 effect may be designed to enhance the activity of PBP and PRIP.

View details for DOI 10.1074/jbc.M201739200

View details for Web of Science ID 000175894800101

View details for PubMedID 11912212