Background: Toxicity by pesticide has become a global health issue and leaves a harmful impact on human health via various ways. The people exposed to pesticides in the rural population get affected by the harmful effects of it as they enter the human body system through skin, inhalation, oral administration, food chain and many more ways. The present work is designed to study the toxic effect of endosulfan in male (n=30) and female (n=30) Swiss albino mice. Endosulfan was administered by oral gavage (oral administration) method, at the dose of 3.5 mg/Kg body weight daily for period of 3 weeks, 5 weeks and 7 weeks. After the completion of the treatment, the mice were sacrificed and their ovary and testis tissues were dissected out to check the degeneration. The blood was collected for karyotyping, biochemical and hormonal analysis of pesticide induced genotoxicity. After 7 weeks of administration with Endosulfan, various abnormalities were observed in male and female mice. Results: Treatment with endosulfan at the dose of 3.5 mg/Kg body weight caused a higher degree of degeneration in the reproductive organ of Swiss albino mice . Treatment by this pesticide generated degeneration in long duration of dosage for 3,5 and 7 weeks. Ovaries of endosulfan administered groups showed degenerated germinal epithelium, Graffian follicles and corpus luteum. In testis of endosulfan treated mice, microscopic examination showed that there is significant damage and reduction in the tissue of seminiferous tubules and primordial germ cells. High degree of degeneration caused the disarrangement and deformation of spermatogonia with the decrease in the number of Sertoli cells. Biochemical and hormonal properties was also affected by endosulfan treatment. There was significant 5 folds decrease in the testosterone value of endosulfan in 7 weeks treated mice in comparison to control (p < 0.0001) and similarly there was significant elevation in the estrogen levels found in 7th week endosulfan treated mice. It also influenced the level of free radicals as there was significant decrease (p < 0.0001) in the value in catalase levels in 7 weeks endosulfan treated male and female mice, while significant (p < 0.0001) increase in the values of lipid peroxidation levels as 8 folds and 10 folds in 7 weeks endosulfan treated male and female Swiss albino mice respectively. This study hence speculates that the endosulfan exposed population are at the risk of reproductive health hazards. Conclusions The present study thus concludes that, endosulfan after 7 weeks of exposure caused significant reproductive damage to both male and female Swiss albino mice groups. Moreover, the karyotyping study also correlated the genotoxic damage in the mice.

Purpose: The purpose of this study was to determine the pattern of human leukocyte antigen (HLA)-DQ genotype in children diagnosed with celiac disease (CD) (biopsy proven), and to compare this with a control group; and secondarily, to correlate HLA genotypes with clinical profiles of CD. Methods: This cross-sectional comparative observational study included 26 controls and 52 patients diagnosed with CD who presented at Sir Padampat Mother and Child Health Institute, Jaipur, from May, 2017 to October, 2018. HLA DQ genotype was assessed for each patients and correlated with clinical profiles. Results: HLA DQ2/DQ8 genotypes were significantly more common in CD (present in 100.0% cases) than in controls (23.1%) in Northern India (Rajasthan). When HLA DQ2.5 and DQ8 were present together, individuals had significantly more atypical presentations and severe findings on duodenal biopsy. Similarly, patients with the HLA DQ 2.5 genotype were also predisposed to more severe endoscopic findings, while HLA DQ2.2 predisposed them to less severe biopsy findings. HLA DQ8 was significantly associated with later age at diagnosis (>5 years) and shorter stature. The highest HLA DQ relative risk (RR) for CD development was associated with HLA DQ2.5 and DQ2.2 in combination, followed by HLA DQ2.5 and DQ8 in combination, while HLA DQx.5 and HLA DQ2.2 together had the lowest risk. Conclusion HLA DQ2/DQ8 genotypes are strongly associated with pediatric CD patients in northern India. These genotypes and their combinations may be associated with different clinical presentations of CD, and may help predict severity of CD.

Acute traumatic aortic injuries, which have substantial lethal outcomes at the time of admission, are fatal in 80% to 90% of cases. These injuries are relatively rare and have nonspecific clinical presentations. Radiologists and emergency physicians need to identify the radiological signs of acute traumatic aortic injury and differentiate them from common imaging errors to ensure accurate diagnosis and determine appropriate management protocols. In combination with image-guided interventions, advances in cross-sectional imaging have enabled nonsurgical management of acute traumatic aortic injuries. Timely and precise diagnoses of these injuries following prompt treatment are essential as up to 90% of patients presenting at the hospital can undergo early repair.

Fibrous dysplasia (FD) is sometimes accompanied by extraskeletal manifestations that can include any combination of café-au-lait macules, hyperfunctioning endocrinopathies, such as gonadotropin-independent precocious puberty, hyperthyroidism, growth hormone excess, FGF23-mediated renal phosphate wasting, and/or Cushing’s syndrome, as well as other less common features. The combination of any of these findings, with or without FD, is known as McCune-Albright syndrome (MAS). The broad spectrum of involved tissues and the unpredictable combination of findings is because of a molecular defect due to dominant activating mutations in the widely expressed signalling protein Gsα. These mutations arise sporadically, often early in development, prior to gastrulation and can distribute across many or few tissues.1,2 We present a case of a 3½ year-old-girl who presented simultaneously with precocious puberty and hypophosphatemic rickets, along with fibrous dysplasia and café au lait macules.
Fibrous Dysplasia, Polyostotic ; Puberty, Precocious ; Rickets, Hypophosphatemic

Background: Celiac disease is frequently associated with type 1 diabetes mellitus, but is usually ill-defined and not usually suspected until the disease becomes advanced. Objective: To study the prevalence and clinical profile of celiac disease among patients with type 1 diabetes mellitus in a tertiary care referral centre in north India. Methodology: Two hundred and fifty six patients were screened (149 males and 107 females) during the study period of two years, patients were evaluated for the clinical signs, biochemical investigations and family history of celiac disease in tertiary care health center in western Uttar Pradesh. Results: Twenty four (9.37%) patients were diagnosed to have celiac disease; the mean age at diagnosis of diabetes was 9.34 ± 7.3 years. Only 1/24 patients with celiac disease had been diagnosed before detection of diabetes mellitus. The common manifestations were normocytic normochromic anemia (66.6%) followed by diarrhoea (62.5%), abdominal pain/bloating sensation (58.3%) and short stature (58.3%). Some uncommon manifestations were also observed in small number of patients: rickets (20.8%), recurrent hypoglycemia (16.6%), carpopedal spasm (8.3%), and night blindness (8.3%). Conclusion Celiac disease was found in about 10% of patients with type 1 diabetes, almost 10-20 times higher than that observed in general pediatric population. Atypical manifestations (rickets, recurrent hypoglycemia, carpopedal spasm and night blindness) were found to be common in patients with type 1 diabetes as compared to the general population. Unexplained anemia, diarrhoea, short stature and rickets should raise suspicion for the possibility of undiagnosed celiac disease in type 1 diabetes mellitus.
Diabetes Mellitus, Type 1 ; Anemia

Blepharophimosis ptosis epicanthus inversus (BPES) is a relatively rare congenital disorder, which usually presents with classical eye manifestations. In some cases, it is associated with premature ovarian failure (POF). BPES is of two types, type I and type II. Type I is associated with POF along with eyelid malformations, while Type 2 has only eyelid malformations. Here, we report a family of BPES, in whom two sisters presented with secondary amenorrhea. On eye examination, they have blepharophimosis, ptosis, epicanthus inversus and telecanthus. Investigations revealed hypergonadotropic hypogonadism. Their father also has similar eye manifestations. Diagnosis of BPES type I was made and both were started on hormone replacement therapy. To make timely diagnosis of BPES, every patient with POF should specifically be checked for eye manifestations.
Blepharophimosis, Ptosis, and Epicanthus Inversus ; Blepharophimosis

Inflammatory bowel disease (IBD), once considered a disease of the Western hemisphere, has emerged as a global disease. As the disease prevalence is on a steady rise, management of IBD has come under the spotlight. 5-Aminosalicylates, corticosteroids, immunosuppressive agents and biologics are the backbone of treatment of IBD. With the advent of biologics and small molecules, the need for surgery and hospitalization has decreased. However, economic viability and acceptability is an important determinant of local prescription patterns. Nearly one-third of the patients in West receive biologics as the first/initial therapy. The scenario is different in developing countries where biologics are used only in a small proportion of patients with IBD. Increased risk of reactivation of tuberculosis and high cost of the therapy are limitations to their use. Thiopurines hence become critical for optimal management of patients with IBD in these regions. However, approximately one-third of patients are intolerant or develop adverse effects with their use. This has led to suboptimal use of thiopurines in clinical practice. This review article discusses the clinical aspects of thiopurine use in patients with IBD with the aim of optimizing their use to full therapeutic potential.

Background: Celiac disease is frequently associated with uncontrolled blood sugar and impaired linear growth in a child with type 1 diabetes mellitus. Objective: To study the impact of a gluten-free diet on several growth parameters in children with type 1 diabetes mellitus and celiac disease. Methodology: Two hundred and fifty six patients with Type 1 diabetes mellitus were screened (149 males and 107 females) during the study period of two years. Patients were evaluated for the clinical signs, biochemical investigations and family history of celiac disease in a tertiary care health centre in Western Uttar Pradesh, India. Results: Twenty four (9.3%) patients were diagnosed to have celiac disease; the mean age at diagnosis of diabetes was 9.37±7 years. Only one out of twenty four patients with celiac disease had been diagnosed before the detection of diabetes mellitus. Weight standard deviation score (SDS) increased from -0.12±1.3 at the start of gluten free diet to 0.8±0.9 after 12 months (p<0.004). Height SDS decreased from -2.46±1.1 at the start of gluten free diet to -2.14±0.9 after 12 months later (p=0.087). Bone age SDS increased from 9.2±6.3 at the start of gluten free diet to 10.3±6.7 after 12 months later. Height velocity increased from 4.7±0.7 cm/year in the year before treatment to 5.1+1.2 cm/year during treatment (p=0.05). The increase in Haemoglobin, serum calcium, and serum iron was statistically significant (p<0.05). Conclusion Patients with celiac disease associated with type 1 diabetes mellitus frequently have poor glycemic control and impairment in several growth parameters. When these patients are put on a gluten restricted diet, they show signs of improvement in terms of weight gain, height, serum Ca, serum iron, haemoglobin, and in height velocity.
Diabetes Mellitus, Type 1

Objective: Short stature can be caused by a great variety of congenital and acquired conditions, some of which present with additional symptoms and signs. Overall, the number of patients seeking medical attention for short stature may be considered as the tip of the iceberg. The objective of this study was to determine the pattern and etiological factors of short stature in children. Methodology: A cross-sectional study was carried out in the Department of Endocrinology at a tertiary care health center in north India from August 2012 to June 2015. Four hundred and fifty one children (280 boys and 171 girls), ranging from 4 to 18 years presenting with short stature were studied. Anthropometric measurements were plotted on Indian standard growth charts. Results: In this study, the male to female ratio was found to be 1.6:1, with mean chronological age of 11.6+3.2 years, and mean bone age of 7.8+2.8 years. The common etiologic factors in the order of frequency were constitutional delay in growth and puberty (41.2%), familial short stature (15.9%), type 1 diabetes mellitus (9.9%), and hypothyroidism (8.6%) while growth hormone deficiency (2.4%) was a relatively uncommon cause. The most common pathological cause for proportionate short stature was type 1 diabetes and for disproportionate short stature was hypothyroidism. Hypothyroidism caused the maximum retardation of bone age while the least bone age retardation was noticed in familial short stature. Conclusion Physiological/normal variants outnumbered the pathological causes of short stature. Endocrinological causes were found in almost one fourth of children with short stature; however, growth hormone deficiency was found in only 2.4% of the children.
Diabetes Mellitus, Type 1 ; Growth Hormone