Midgut malrotation and incomplete rotation are common causes of neonatal intestinal obstruction. At end of 10 week of intrauterine life, cecum will be placed in subhepatic region temporarily and descends to right lower quadrant by eleventh week. Arrest of cecum in subhepatic region or undescended cecum is a rare congenital anomaly of mid gut. Usually, it remains asymptomatic and is diagnosed incidentally. If any pathology occurs in anomalous part, like appendicitis then the diagnosis and treatment will be challenging in all age groups. Variation in blood supply have also been reported with anomalies leading to iatrogenic injuries during colonoscopy and surgeries. Lack of knowledge of these rare variations may lead to delayed diagnosis of appendicitis leading to perforation and surgical emergencies. In the present case, we describe an undescended cecum and its associated variation in branching pattern of superior mesenteric artery.
Appendicitis ; Arteries* ; Cecum* ; Colic* ; Colonoscopy ; Delayed Diagnosis ; Diagnosis ; Emergencies ; Humans ; Intestinal Obstruction ; Mesenteric Artery, Superior ; Pathology

BACKGROUND: Aberrant myeloid antigen (MA) co-expression and high expression of CD34 antigen on the blasts of acute lymphoblastic leukemia (ALL) patients are independently reported to have a role in pathogenesis and prognosis. This study was conducted to determine whether these two parameters are related. METHODS: A total of 204 cases of ALL were included in an analysis of blast immunophenotypic data. CD34 expression was categorized as low when less than 50% of blasts were CD34-positive (CD34low) and as high when 50% or more were CD34-positive (CD34high). RESULTS: Of 204 cases of ALL, 163 and 41 were of B-cell origin (B-ALL) and T-cell origin (T-ALL), respectively. Of all cases, 132 (64.7%) showed co-expression of MA and among these, 101 (76.51%) were CD34high, while the remaining 31 (23.48%) were CD34low. Of 72 cases without MA co-expression, 25 (34.72%) were CD34high and 47 (67.25%) were CD34low. Furthermore, of 163 cases of B-ALL, 111 showed co-expression of MA and 84 of these were CD34high. Of 52 cases of B-ALL without MA expression, 22 were CD34high. Among 41 cases of T-ALL, 21 co-expressed MA, 17 of which were CD34high. Moreover, all 20 cases of T-ALL without co-expression of MA were CD34low. These differences were statistically significant. CONCLUSION: We observed a strong correlation between aberrant MA expression and CD34high expression on the blasts of ALL. We hypothesize that these different patient subsets may represent unique prognostic characteristics.
Antigens, CD34 ; B-Lymphocytes ; Flow Cytometry ; Humans ; Immunophenotyping ; Precursor Cell Lymphoblastic Leukemia-Lymphoma* ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; Prognosis ; T-Lymphocytes ; Tertiary Care Centers*

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