Duodenal carcinoid tumors accounts for 5% of all Gastrointestinal Neuroendocrine Tumors (GI-NETs). Only 4% of all duodenal carcinoid tumors present with a full-blown carcinoid syndrome. We report a case of duodenal carcinoid tumor presenting as carcinoid syndrome in a 58 year old man, who presented with upper abdominal discomfort, diarrhoea, hot flushes and occasional wheezing. Histopathology following endoscopic resection of the tumor and 24 hour urinary 5-Hydroxyindolacetic acid (5-HIAA) confirmed the diagnosis. Duodenal carcinoid tumors are one of the rarest tumors of gastrointestinal tract and their association with a typical carcinoid syndrome is not that common. A high level of suspicion is required for an early diagnosis. With proper resection (endoscopic or surgical) of a localized tumor, recurrence and progression of the disease can be halted. Symptoms of carcinoid syndrome should be controlled by antidiarrheal agents, inhaled βadrenergic agonist bronchodilators and somatostatin analogs (octreotide, lanreotide). Patients should be advised to avoid stress and conditions or substances that precipitate these symptoms. Dietary supplementation with nicotinamide can help in this regard. Patients with hepatic metastases are treated with synthetic analogues of somatostatin (octreotide, lanreotide). Systemic chemotherapy is not recommended in metastatic disease by the current guidelines. Patients should be followed up by monitoring serum chromogranin and urinary 5-HIAA. EUS, CT, MRI & somatostatin receptor scintigraphy can also be used for following up the patients.
Background: Adrenal insufficiency is the clinical manifestation of deficient production or action of glucocorticoids, with or without deficiency of mineralocorticoids and adrenal androgens. It results from primary adrenal failure or secondary adrenal disease due to impairment of the hypothalamic-pituitary axis. Patients often have nonspecific symptoms such as weakness, fatigue, lethargy, anorexia, nausea, vomiting, fever, confusion or coma. Without appropriate therapy, shock progresses to coma and death. The aim of the study was to evaluate the clinical and biochemical parameters at presentation in patients admitted with adrenal insufficiency. Methods: Patients diagnosed with adrenal insufficiency fulfilling the diagnostic criteria were considered as study population. Purposive consecutive type of sampling method was applied. Data was collected in a structured questionnaire. All the data were analysed by SPSS V 22.0. Results: A total of 100 patients of adrenal insufficiency were included in the study. The most were in the age group of 51-60 years (33%), mean age ± SD was 50.82±13.51 years & 38% were male. In our study, 100% patients had generalized weakness, 88% had GI symptoms, 41% had vertigo and 18% had weight loss. Most of them (83%) had vomiting, 70% had nausea and only 17% had anorexia. 38% patients were anaemic and 23% had shock and 33% patients presented with adrenal crisis. In this study, 82% patient were hypotensive, 46% had postural hypotension. In our study, 56% had puffy face, 49% had history of weight gain, 26% had skin thinning. Mean Hb was 10.96 gm/dl, 25% had a serum creatinine of>1.2 mg/dl. Hypoglycaemia was present in 7%, 12% had high blood urea nitrogen, 71% had hyponatraemia, 39% had hyperkalaemia, 12% had hypercalcaemia and 20% had acidosis. Conclusion: Adrenal insufficiency presented with non-specific features like fatigue, weakness, vertigo, GI symptoms, unexplained fever or weight loss and specific pattern of biochemical findings like hyponatraemia, hyperkalaemia, mild acidosis, hypercalcaemia & hypoglycaemia. So, these features should raise the suspicion of adrenal insufficiency.
Background: Several risk factors for development of colorectal adenomas has been studied over the years. But the effect of increased BMI, sedentary lifestyle and metabolic syndrome on the development of colorectal adenoma has been minimally studied. This study describes the influence of increased BMI, sedentary lifestyle & metabolic syndrome on the prevalence of colorectal adenoma. Secondary objective was to determine whether these factors influence the progression of benign adenomas into advanced adenomas or not. Methods: A total of 697 consecutive cases were included. Asymptomatic subjects aged more than 40 years who were undergoing their first colonoscopy were included in the study. Patients with a history of colonic neoplasia, IBD, colonoscopic polypectomy or colectomy were excluded from the study. Details of colonoscopy, polypectomy and histology were recorded. Data were analyzed by SPSS version 22.0. Chi-square (X 2 ) test was done to assess the association of different risk factors with the development of colonic adenomas. Odds ratio (OR) along with its 95% CI was calculated for every individual risk factor under evaluation. A p-value<0.05 was considered as significant. Result: Colonic polyps were detected in 153 (21.95%) subjects. Out of these 153 subjects 81 (11.62%) had histologically proved adenomas. Benign adenomas were detected in 63 (9.03%) cases, whereas advanced adenomas were detected in 18 (2.58%) cases. A BMI of≥30 showed an OR of 2.94 (1.64-4.24) for the development of colorectal adenomas. Presence of metabolic syndrome showed an OR of 1.74 (1.14-2.34) for the development of adenomas. Sedentary lifestyle showed an OR of 1.91 (1.31-2.51) for the development of colorectal adenomas. An age of≥50 years also showed significant effect (OR=1.39) on the development of colonic adenomas. Lastly the presence of increased BMI, sedentary lifestyle and metabolic syndrome was identified as individual risk factors for the progression of adenoma towards advanced adenomas with an OR of 1.67, 2.14 & 2.92 respectively. Conclusion: This study demonstrates that increased BMI, sedentary lifestyle and metabolic syndrome are associated with increased risk of development of colorectal adenomas. Moreover, increasing age (>50 years) also contribute to the increased risk of development of colorectal adenomas. And lastly it has been showed that increased BMI, sedentary lifestyle and metabolic syndrome individually contribute to the increased risk of progression of benign colonic adenomas to a more advanced adenoma.
Background: Bleeding occurs in approximately 1.0−6.1% cases of endoscopic polypectomy. Bleeding can be immediate or delayed. The incidence of delayed post polypectomy bleeding ranges from 0.4% to 1.1%. This study aims at identifying risk factors for delayed post polypectomy bleeding. Methods: A retrospective study was carried out to evaluate the risk factors of delayed Post Polypectomy Bleeding following colonoscopic polypectomy. Patient who had post polypectomy bleeding were assigned to the case group. These patients were age and sex-matched to 57 randomly selected control patients who didn't have post polypectomy bleeding after colonoscopic polypectomy. The baseline characteristics of the case and control groups were similar. No significant differences were identified between the two groups of patients in terms of demographic characteristics, laboratory findings, and comorbidities. Different characteristics of the patients and their polyps (size, location, shape, and histopathological findings) were compared between the case and control group using Chi-square(X 2 ) test. Odds ratio (OR) was calculated for each risk factor to be evaluated. A p-value <0.05 was considered as significant. Statistical analysis was done with SPSS v22. Result: Among the 1073 patients who underwent colonoscopic polypectomy during the study period, 19 (1.77%) experienced delayed PPB. A polyp size of more than 10mm showed significant association with occurrence of delayed PPB with an OR of 6.7. Sessile polyps were more likely to be associated with delayed PPB with an OR of 4.4. Polyps located at the right colon were more prone to delayed PPB with an OR of 4.7. Obese patients with a BMI of more than 25 were more likely to have delayed PPB with an OR of 6.6. Patients aged more than 65 years, patients having cardiovascular disease & patients having CKD were more likely to have delayed PPB in comparison with those who didn't have these comorbidities. Conclusion: The incidence of delayed PPB was 1.77% in our study, and patients with large polyps (>10mm), sessile polyps & polyps located in the right hemi colon showed an increased risk of delayed PPB. In addition, patients with higher BMI (>25) also showed a higher risk of delayed PPB. Patients aged more than 65 years, patients having cardiovascular disease & patients having CKD were more likely to have delayed PPB in comparison with those who didn't have these comorbidities. Polypectomies in patients with these risk factors carry high risk of delayed PPB and should always be delt with extra precaution.
Olmesartan medoxomil is one of eight marketed Angiotensin II Receptor Blocker for the treatment of high blood pressure. Olmesartan Associated Enteropathy has been described in several case reports, subsequently, the United states Food and Drug Administrationincluded severe sprue-like enteropathy as an adverse effect of Olmesartan. Olmesartan Associated Enteropathy mimics celiac disease clinically and pathologically. The pathologic findings are villous atrophy and increased intraepithelial lymphocytes. Clinical presentation of Olmesartan Associated Enteropathy includes nausea, bloating, diarrhea and weight loss. In contrast to celiac disease, tissue transglutaminase is not elevated, and there is no response to a gluten-free diet. Several case reports have described the effects of olmesartan on gut, giving rise to the term of Olmesartan Associated Enteropathy. Clinicians should always be aware that Olmesartan can cause an enteropathy clinically and histologically similar to celiac disease since replacing Olmesartan with an alternative antihypertensive drug can simplify the diagnostic workup and provide both clinical and histologic improvement. We report three cases of Olmesartan Associated Enteropathy in this article. Bangladesh Crit Care J September 2022; 10(2): 154-157
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