Mucosal biopsies from rabbit ileum were organ cultured for 24 h. The influence of triamcinolone and somatostatin on villus height and diameter as well as crypt depth and the number of mitoses was measured at various times during 24 h of culture as indices of cell proliferation and tissue maintenance. It could be shown that triamcinolone reduced cell proliferation slightly but preserved mucosal structure in organ culture. Somatostatin inhibited crypt cell proliferation, without any effect on other morphological parameters.

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Waterhouse-Friderichsen syndrome (WFS) is a rare, highly fatal disease that is the result of adrenal gland hemorrhage and infarction, typically due to Neisseria meningitidis infection. [1] We report a case of a patient who developed WFS secondary to Haemophilus influenzae type b (Hib) bacteremia. CASE PRESENTATION:A 19-year-old male with no medical history presented with vomiting and diarrhea for 2 days. Patient was febrile to 103.1 degrees Fahrenheit, hypotensive to 60/23, and tachycardic to 170/min. Labs showed WBC 7.9, platelets 98, creatinine 5.3, lactic acid 9.9, procalcitonin 256, and troponin peak 44.509. Respiratory viral panel and blood cultures were positive for rhinovirus and Hib, respectively. CT chest revealed scattered bilateral groundglass opacities. Patient had cardiac arrest x2. He was intubated and started on vasopressors/inotropes, antimicrobials, and renal replacement therapy. Echocardiogram showed ejection fraction (EF) 10-15%, necessitating intra-aortic balloon pump placement and veno-arterial extracorporeal membrane oxygenation (VA ECMO). Hospital course was complicated by the development of purpura fulminans, disseminated intravascular coagulation (DIC), rhabdomyolysis, heart block requiring transvenous pacemaker, and candida albicans fungemia. Patient was ultimately diagnosed with WFS and treated with hydrocortisone, resulting in hemodynamic improvement and weaning of circulatory support. Despite this, he eventually succumbed to his illness and the complications mentioned above. DISCUSSION: While Neisseria meningitidis accounts for the majority of cases of WFS, other bacteria, such as Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas aeruginosa, have been implicated.[2] Suspicion should be raised in any patient presenting with fever, purpura, coagulopathy, and signs of adrenal insufficiency. [1] Diagnosis is confirmed by CT scan showing adrenal hemorrhage.[2] Mortality rates are as high as 50%, particularly when there are delays in diagnosis and subsequent treatment with corticosteroids.[1,2]Our patient presented with Hib bacteremia of unclear etiology. One possible explanation is pneumonia, as evidenced by groundglass opacities on CT chest, but these may be better explained by concurrent rhinovirus infection. He developed the bacteremia despite being up to date on immunizations and having vaccine titers, including Hib, within the protective range. Other immune deficiency workup was unrevealing. WFS was suspected but could not be confirmed with imaging due to hemodynamic instability and significant vasopressor support.CONCLUSIONS: WFS is an uncommon cause of adrenal insufficiency that requires prompt diagnosis and treatment. It should be considered in any patient presenting with septic shock, regardless of the causative organism.

INTRODUCTION: Homeostasis of the GI mucosal environment depends on gut motility and normal gastric acid secretion. The autonomic nervous system plays an important role in these processes. Diabetes has been shown to injure the enteric nervous system, resulting in slowed motility. Gastroparesis and small intestinal bacterial overgrowth are two consequences of the enteric injury associated with diabetes. CASE DESCRIPTION/METHODS: A 23-year-old male with type 1 diabetes presented with 6 months of diffuse abdominal pain and diarrhea, which had recently worsened. He noted 4-6 loose bowel movements daily and vomiting after food. He had previously been seen by gastroenterology and had an unremarkable colonoscopy, EGD, and celiac testing. He had been trialed on rifaximin and neomycin, which improved his symptoms for a short period. He tried eluxadoline with little effect. On presentation, he was hemodynamically stable with labs significant only for mildly elevated AST (58 units/L). WBC, ESR, CRP, feces ova and parasites, and C. difficile Ag were all unremarkable. A gastric emptying study revealed moderate (24%) gastroparesis. A right upper quadrant ultrasound was unremarkable. Small intestinal bacterial overgrowth related to gastroparesis was suspected. A trial of rifaximin and metoclopramide improved his symptoms leading to empiric diagnosis of SIBO. DISCUSSION: Small intestinal bacterial overgrowth occurs when the normal homeostatic mechanisms that control bacterial populations are in some way disrupted. Frequently, this occurs with decreased gastric acid secretion or dysmotility of the small intestine. The most common symptoms of SIBO include bloating, abdominal discomfort and distention, chronic diarrhea, weight loss, and malabsorption. One proposed theory for SIBO in gastroparesis is the idea that phase 3 migratory motor complexes may be diminished in frequency or altogether absent. While the gold standard for diagnosis requires jejunal aspirate, lactulose and glucose breath testing have been used as indirect measures of SIBO. Multiple studies have been done to analyze the relationship between gastroparesis and SIBO with results showing up to 60-70% of study participants with gastroparesis test positive for SIBO via lactulose breath testing. Once the diagnosis of SIBO has been established, the goal of therapy is to correct the underlying cause, provide nutritional support, and treat overgrowth with a course of antibiotics.