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In cardiovascular homeostasis thyroid hormone plays an important role. We planned to study the changes in thyroid hormone profile in acute coronary syndrome patients admitted in the coronary care unit and compare them between two groups: unstable angina/non-ST elevated Myocardial infarction (UA/NSTEMI) and ST elevated Myocardial infarction (STEMI). This study was a hospital based descriptive cross sectional study which was conducted from 01 March 2018 to 01 February 2019 in Coronary Care Unit of Bangladesh Medical College Hospital and laboratory tests were done in Microbiology Department of Bangladesh Medical College, Dhaka, Bangladesh. Eighty three cases of acute coronary syndromes were taken for the study. Troponin-I was measured as cardiac marker, Electrocardiogram, Complete blood count, blood glucose level, Blood urea, serum creatinine, serum electrolytes, Fasting lipid profile, Thyroid profile, Echocardiography 2D were done. Most of the respondents were distributed in age group 46-60 years where 34(64.15%) male and 19(35.85%) female. Out of 83 Acute Coronary Syndrome (ACS) patients, 27(32.53%) hypertensive, 22(26.50%) diabetic and 16(19.27%) were Chronic kidney disease (CKD). Abnormal lipid profile was present in 30(43.47%) patients. Among total 52 male and 31 female 9(17.30%) male and 6(19.35%) female had abnormal thyroid function. We further elaborated abnormal thyroid function tests in STEMI group and UA/Non STEMI group of ACS patients. We found 10 patients in STEMI group and 5 patients in UA/Non STEMI group with abnormal thyroid function 29.41% and 10.20% respectively which was not statistically significant (p=0.025). This study depicts abnormality in thyroid hormone profile in 18.07% patients of ACS. Abnormal thyroid function increases risk of coronary artery disease. TSH level of ACS patients on hospital admission could be helpful to evaluate further prognosis of the disease.

Ulcerative colitis (UC) affects women of all ages, with a peak incidence in the third and fourth decades, at the prime of their reproductive years [Baiocco PJ, Korelitz BI (1984) The influence of inflammatory bowel disease and its treatment on pregnancy and fetal outcome. J Clin Gastroenterol 6(3):211-216]. We describe a case of fulminating UC at 28 weeks' gestation treated by combined emergency subtotal colectomy and caesarean section with excellent foetal and maternal outcome. A treatment algorithm is suggested, and the literature surrounding inflammatory bowel disease in pregnancy is reviewed.

Background & Aims: Kruppel-like factor 6 (KLF6) is a ubiquitous zinc finger tumor suppressor that is often mutated in prostate cancer. Our aims were to establish the frequency of KLF6 inactivation in sporadic and inflammatory bowel disease (IBD)-associated colorectal cancers (CRC); to correlate these abnormalities with mutation and/or loss of TP53, APC, and K-RAS; and to characterize the behavior of mutant KLF6 in colon-derived cell lines., Methods: We analyzed DNA isolated from 50 microdissected CRC cases, including 35 sporadic and 15 IBD-associated tumors. Microsatellite analysis and direct sequencing were used to establish the incidence of microsatellite instability, KLF6 and TP53 allelic imbalance, and KLF6, K-RAS, TP53, and APC mutation. Loss of growth suppressive function of the CRC-derived KLF6 mutants was characterized by in vitro thymidine incorporation assays and Western blotting., Results: KLF6 was inactivated by loss and/or mutation in most sporadic and IBD-related CRCs. The KLF6 locus was deleted in at least 55% of tumors, and mutations were identified in 44%. Rates of KLF6 loss and mutation were similar to those of TP53 and K-RAS in the same samples. KLF6 mutations were present in tumors with either microsatellite or chromosomal instability and were more common, particularly in the IBD-related cancers, in the presence of wild-type APC. Unlike wild-type KLF6, cancer-derived KLF6 mutants neither suppressed growth nor induced p21 following transfection into cultured cells., Conclusions: Deregulation of KLF6 by a combination of allelic imbalance and mutation may play a role in the development of CRC.

Background: Acute compartment syndrome is both a limb- and life-threatening emergency that requires prompt treatment. To avoid a delay in diagnosis requires vigilance and, if necessary, intracompartmental pressure measurement. This review encompasses both limb and abdominal compartment syndrome, including aetiology, diagnosis, treatment and outcome., Methods: A Pubmed and Cochrane database search was performed. Other articles were cross-referenced., Results and Conclusion: Diagnosis of limb compartment syndrome is based on clinical vigilance and repeated examination. Many techniques exist for tissue pressure measurement but they are indicated only in doubtful cases, the unconscious or obtunded patient, and children. However, monitoring of pressure has no harmful effect and may allow early fasciotomy, although the intracompartmental pressure threshold for such an undertaking is still unclear. Abdominal compartment syndrome requires measurement of intra-abdominal pressure because clinical diagnosis is difficult. Treatment is by abdominal decompression and secondary closure. Both types of compartment syndrome require prompt treatment to avoid significant sequelae.