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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This guideline presents recommendations for the diagnosis and management of patients with celiac disease. Celiac disease is an immune-based reaction to dietary gluten (storage protein for wheat, barley, and rye) that primarily affects the small intestine in those with a genetic predisposition and resolves with exclusion of gluten from the diet. There has been a substantial increase in the prevalence of celiac disease over the last 50 years and an increase in the rate of diagnosis in the last 10 years. Celiac disease can present with many symptoms, including typical gastrointestinal symptoms (e.g., diarrhea, steatorrhea, weight loss, bloating, flatulence, abdominal pain) and also non-gastrointestinal abnormalities (e.g., abnormal liver function tests, iron deficiency anemia, bone disease, skin disorders, and many other protean manifestations). Indeed, many individuals with celiac disease may have no symptoms at all. Celiac disease is usually detected by serologic testing of celiac-specific antibodies. The diagnosis is confirmed by duodenal mucosal biopsies. Both serology and biopsy should be performed on a gluten-containing diet. The treatment for celiac disease is primarily a gluten-free diet (GFD), which requires significant patient education, motivation, and follow-up. Non-responsive celiac disease occurs frequently, particularly in those diagnosed in adulthood. Persistent or recurring symptoms should lead to a review of the patient's original diagnosis to exclude alternative diagnoses, a review of the GFD to ensure there is no obvious gluten contamination, and serologic testing to confirm adherence with the GFD. In addition, evaluation for disorders associated with celiac disease that could cause persistent symptoms, such as microscopic colitis, pancreatic exocrine dysfunction, and complications of celiac disease, such as enteropathy-associated lymphoma or refractory celiac disease, should be entertained. Newer therapeutic modalities are being studied in clinical trials, but are not yet approved for use in practice. Given the incomplete response of many patients to a GFD-free diet as well as the difficulty of adherence to the GFD over the long term, development of new effective therapies for symptom control and reversal of inflammation and organ damage are needed. The prevalence of celiac disease is increasing worldwide and many patients with celiac disease remain undiagnosed, highlighting the need for improved strategies in the future for the optimal detection of patients.
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PMID:ACG clinical guidelines: diagnosis and management of celiac disease. 2360 13

We described a 45-year-old previously healthy man presenting with progressively worsening breathlessness for 10 days. Physical examination was suggestive of a left-sided pleural effusion. A chest X-ray was confirmatory. Analysis of aspirated fluid showed a lymphocytic exudate with grossly elevated amylase and lipase levels. CT revealed chronic calcific pancreatitis as the underlying cause of effusion. Retrospective questioning failed to identify classical symptoms of chronic pancreatitis including abdominal pain and steatorrhoea. The patient was managed with intercostal drainage and supportive care. Although unusual, chronic pancreatitis should be kept as a differential diagnosis in patients with unilateral exudative pleural effusion. Elevated fluid levels of amylase and lipase are useful clues to this uncommon diagnosis.
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PMID:Primary presentation of chronic calcific pancreatitis with massive unilateral pleural effusion. 2413 Feb 4

Celiac disease (CD) affects up to 1% of the general population. Classically, it manifests with intestinal symptoms (diarrhea, steatorrhea, abdominal pain or discomfort) associated with weight loss and anemia. Seizure is a rare form of presentation of CD. A 13-year-old female patient with Down syndrome was admitted to the pediatric emergency department with generalized tonicclonic seizure in addition to numbness around the mouth, paresthesias, and muscular cramping for seven days. Investigations revealed severe hypocalcemia and vitamin D deficiency, which were a consequence of malabsorption secondary to histopathologically confirmed CD. Physicians should be aware that unrecognized CD can cause severe hypocalcemia.
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PMID:Hypocalcemic seizure in an adolescent with Down syndrome: a manifestation of unrecognized celiac disease. 2438 37

Whipple's disease is a systemic infectious disease caused by the bacteria Tropheryma whipplei. The most common clinical manifestations of Whipple's disease are weight loss (92%), hypoalbuminemia and steatorrhea (91%, respectively), diarrhea (72%), arthralgia (67%), and abdominal pain (55%). Neurological signs and symptoms from dementia to oculomasticatory myorhythmia or oculofacioskeletal myorhythmia (pathognomonic of Whipple's disease), lymphadenopathy, and fatigue can also be present. Pancytopenia is a rare and less recognized clinical feature in Whipple's disease patients. We are describing a case where a middle-aged Caucasian male diagnosed with Whipple's disease was found to have pancytopenia. Etiology of pancytopenia is postulated to be due to the invasion of bone marrow by T. whipplei. It is important to recognize that bone marrow involvement by the Whipple bacillus is not uncommon. In the presence of lymphadenopathy and pancytopenia, clinicians should think of Whipple's disease as a differential diagnosis apart from lymphoma or other non-specific granulomatous reticuloendothelial disorders.
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PMID:An unusual cause of pancytopenia: Whipple's disease. 2476 56

Cystoisospora belli is an opportunistic protozoan that causes human cystoisosporiasis, an infection characterized by diarrhea, steatorrhea, abdominal pain, fever, and weight loss. The lack of animal models susceptible to C. belli, and the difficulty in obtaining clinical samples with fair amounts of oocysts have limited the research pertaining to the basic biology of this parasite. This study aimed to describe the ultrastructure of endogenous stages of C. belli in Monkey Rhesus Kidney Cells (MK2) and Human Ileocecal Adenocarcinoma cells (HCT-8). Zoites of C. belli exhibited typical morphological features of coccidia, which included a trilaminar pellicle, an apical complex formed by a conoid, polar rings, rhoptries, and micronemes, in addition to dense granules and the endoplasmic reticulum. No crystalloid body was observed but various lipid and amylopectin granules were usually present in the cytoplasm of zoites. We observed a tendency of the endoplasmic reticulum of the host cell to be located near the parasitophorous vacuole membrane. Merozoites were formed by endodyogeny and during replication, the apical complex of the mother cell remained intact. The formation of gametes or oocysts was not observed. The ultrastructural findings of C. belli are further evidence of its proximity to Sarcocystidae family members and corroborate their reclassification as Cystoisospora spp.
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PMID:Ultrastructural aspects of Cystoisospora belli (syn. Isospora belli) in continuous cell lines. 2477 2

Fibrocalculous pancreatic diabetes (FCPD) is an uncommon form of diabetes that occurs as a result of chronic calcific pancreatitis, in the absence of alcohol abuse. The disease is restricted to tropical regions of the world, and southern India has the highest known prevalence of FCPD. The typical patient with FCPD is a lean adolescent or young adult of either sex, presenting with history of recurrent bouts of abdominal pain and steatorrhea. Demonstration of large, discrete pancreatic calculi by plain radiographs or ultrasonography of the abdomen is diagnostic. While the exact etiology of FCPD is unknown, genetic, nutritional and inflammatory factors have been hypothesized to play a role. Diabetes in FCPD is often brittle and difficult to control; most patients require multiple doses of insulin for control of glycemia. However, in spite of high blood glucose levels, patients rarely develop ketosis. Malabsorption responds to pancreatic enzyme supplementation. Surgical removal of stones is indicated for symptomatic relief of intractable pain. While patients with FCPD develop microvascular complications as frequently as those with type 2 diabetes, macrovascular disease is uncommon. Development of pancreatic malignancy is the most dreaded complication and should be suspected in any patient who complains of weight loss, back pain or jaundice.
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PMID:Fibrocalculous pancreatic diabetes (FCPD). 2539 47

Chronic pancreatitis is a common disorder caused by various etiological factors. It usually manifests with abdominal pain and exocrine (steatorrhea, malnutrition) or endocrine insufficiency (diabetes mellitus). Abdominal pain is the dominant symptom in these patients. Medical, endoscopic and surgical modalities are available for therapy. This review focuses on the pharmacological approaches to manage pancreatic pain. Before embarking on medical management of pain it is prudent to exclude complications like pancreatic cancer, pseudocysts, inflammatory mass, biliary or duodenal obstruction which may contribute to abdominal pain. Pharmacological measures for pain relief include central analgesics, enzyme supplements and antioxidants. Other measures include endoscopic and surgical therapy which are not discussed here. Appropriate management of exocrine and endocrine insufficiency and successful control of diabetes are also important in the management of chronic pancreatitis.
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PMID:Medical management of pain in chronic pancreatitis. 2634 64

Fibrocalculous pancreatic diabetes has distinctive features like younger age at onset, presence of large intraductal calculi, aggressive course of the disease, and proneness for pancreatic cancer. Pancreatic calculi are the hallmark for the diagnosis. We report a 32-year-old male patient, a known case of diabetes since 2 years, presented with recurrent pain abdomen, malabsorption, and neuropathic symptoms. The diagnosis was established on the basis of clinical examination, biochemical and radiological investigations. He was prescribed two doses of premix insulin and pancreatic enzyme supplements for relief of abdominal pain and steatorrhea.
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PMID:Fibrocalculous pancreatic diabetes in adult. 2660 23

Chronic pancreatitis is a chronic inflammatory disease of the pancreas characterised by irreversible morphological change and typically causing pain and/or permanent loss of function. This progressive, irreversible disease results in destruction of healthy pancreatic tissue and the development of fibrous scar tissue. Gradual loss of exocrine and endocrine function follows, along with clinical manifestations such as steatorrhoea, abdominal pain and diabetes. Nutrition in chronic pancreatitis has been described as a problem area and, until recently, there was little research on the topic. It is often asserted that >90 % of the pancreas must be damaged before exocrine insufficiency occurs; however, an exploration of the original studies from the 1970s found that the data do not support this assertion. The management of steatorrhoea with pancreatic enzyme replacement therapy is the mainstay of nutritional management, and early identification and treatment is a key. The presence of steatorrhoea, coupled with poor dietary intake (due to intractable abdominal pain, gastrointestinal side effects and often alcoholism) renders the chronic pancreatitis patients at considerable risk for undernutrition, muscle depletion and fat-soluble vitamin deficiency. Premature osteoporosis/osteopenia afflicts two-thirds of patients as a consequence of poor dietary intake of calcium and vitamin D, low physical activity, low sunlight exposure, heavy smoking, as well as chronic low-grade inflammation. Bone metabolism studies show increased bone formation as well as bone resorption in chronic pancreatitis, indicating that bone turnover is abnormally high. Loss of the pancreatic islet cells occurs later in the disease process as the endocrine cells are diffusely distributed throughout the pancreatic parenchyma. Patients may develop type 3c (pancreatogenic) diabetes, which is complicated by concurrent decreased glucagon secretion, and hence an increased risk of hypoglycaemia. Diabetes control is further complicated by poor diet, malabsorption and (for some) alcoholism, and therefore those with type 3c diabetes have clinical characteristics and therapeutic goals that are different from that of type 1 and type 2 diabetes patients. This review describes emerging research and clinical guidelines for nutrition in chronic pancreatitis.
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PMID:Negotiating the complexities of exocrine and endocrine dysfunction in chronic pancreatitis. 2873 75

Pancreatic ductal adenocarcinoma (PDA) is a deadly cancer that resists efforts to identify better chemotherapeutics. PDA is associated with chronic pancreatitis and acinar cell dedifferentiation. This reduces enzyme production by the exocrine pancreas, resulting in digestive insufficiencies. Malabsorption of partially digested food causes bloating, overfilled intestines, abdominal pain, excessive feces, steatorrhea, and malnutrition. These maladies affect quality of life and restrict treatment options for pancreatitis and PDA. Here, we characterize health benefits and risks of dietary pancreatic enzymes in three mouse models of PDA-KC, KCR8-16, and KIC. KC expresses oncogenic KrasG12D in pancreatic tissue whereas KCR8-16 also has deletions of the Rgs8 and Rgs16 genes. Rgs proteins inhibit the release of digestive enzymes evoked by G-protein-coupled-receptor agonists. KC and KCR8-16 mice developed dedifferentiated exocrine pancreata within 2 months of age and became malnourished, underweight, hypoglycemic, and hypothermic. KC mice adapted but KCR8-16 mice rapidly transitioned to starvation after mild metabolic challenges. Dietary pancreatic enzyme supplements reversed these symptoms in KC and KCR8-16 animals, and extended survival. Therefore, we tested the benefits of pancreatic enzymes in an aggressive mouse model of PDA (KIC). Median survival improved with dietary pancreatic enzyme supplements and was extended further when combined with warfarin and gemcitabine chemotherapy. However, dietary pancreatic enzymes stimulated tumor growth in the terminal stages of disease progression in KIC mice.
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PMID:Malnutrition in Pancreatic Ductal Adenocarcinoma (PDA): Dietary Pancreatic Enzymes Improve Short-Term Health but Stimulate Tumor Growth. 2924 57


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