Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doing a liver test before the use of OCs is advisable for women who face risks, those with previous history of liver disease and familial benign hyperbilirubinemia. For those women who have a negative anamnesis with regard to each of these risk factors, it is not necessary to carry out a liver test before prescribing OCs. The risk of worsening latent chronic hepatitis is very small, and the occurrence of subsequent liver lesions is extremely rare. It is sufficient to carry out the test in women at risk after 3 months and after 1 year of OC use. This applies to patients with intensified cholestatic reactions, which have been asymptomatic, as well as to patients with latent chronic liver disease. The liver test needs to be repeated at regular intervals only when the following clinical symptoms are present: dyspepsia, pruritus, and icterus. Benign and malignant liver tumors cannot be confirmed by liver tests; therefore, there is no justification for this. On the other hand, it is believed that the very low incidence of liver tumors in a small group of women who continue to use OCs for more than 8 years would meet the indication for liver examination. Absolute contraindications for the use of OCs with regard to liver function are considered only for liver disease with prolonged higher liver test values, cholestatic jaundice in pregnancy, and liver tumor.
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PMID:[The effect of hormonal contraception on liver function]. 941 Apr 23

Beyond peptic ulcer disease, Helicobacter pylori infection is associated with intestinal-type gastric cancer and low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is also currently implicated as a possible cause of dyspepsia and extraintestinal disorders such as coronary artery disease, rosacea, chronic urticaria, and delayed growth in children. There are strong epidemiological data from large cohort studies linking H. pylori to gastric adenocarcinoma. Several cofactors, including early childhood acquisition of infection, strain-specific differences, genetic predisposition of the host, and the environment, appear to play a role in the progression of chronic gastritis to gastric cancer. H. pylori infection is seen in over 90% of MALT lymphomas, and about 70% of localized nonbulky tumors will undergo complete histological regression after eradication of the bacterium. Because follow-up data are limited to less than 2 years, those undergoing H. pylori eradication as primary therapy for MALT lymphoma require frequent histological surveillance for tumor recurrence. There are conflicting data from short-term studies regarding the effect of H. pylori eradication on dyspeptic symptoms. The decision to test or not for H. pylori in the dyspeptic patient may become easier when well-controlled studies with longer periods of follow-up become available. Because H. pylori induces a systemic inflammatory response, investigators are beginning to explore possible extraintestinal disease associations with the infection. The global prevalence of both peptic ulcer disease and gastric cancer has led to studies focusing on noninvasive screening for H. pylori in high-risk populations and prevention of primary infection by means of vaccination.
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PMID:Helicobacter pylori: beyond peptic ulcer disease. 953 Nov 10

This a case report of a solid papillary tumor of the pancreas in a young woman of 18 years, who was referred to after having suffered for a period of 8 months with a rather vague symptomatology, characterized by dyspepsia, fatigue and, towards the end of the 8 month period, weight loss (approximately 2 kg). In the last week, as a consequence of a modest abdominal trauma, the patient was submitted to abdominal CT that showed a burden at the head of the pancreas, demonstrating a round neoformation about 6 cm in diameter with solid echogenicity slightly hypodense. Subsequently, she underwent an operation with the diagnosis of pseudocystis of the pancreas. During surgery, a big cystic formation of the head of the pancreas, into which a drain was introduced, was revealed. The histological postoperative examination was compatible with pancreatic tumor with a low grade of malignancy, cystic papillary or solid papillary type. Therefore, the patient came under our observation and underwent an operation of pancreatoduodenectomy. Two years after the operation, the patient had completely recovered. In this case, we discussed the problem of performing certain preoperative diagnoses despite the aid of modern diagnostic imaging, this being a very rare illness that almost exclusively plagues young women (median age 19 years). This diagnosis has an uncertain histological origin and is generally accompanied by a modest and vague symptomatology. The surgical procedure, given the low grade of malignancy of the neoplasm and the excellent long-term prognosis, must be, with respect to the oncological radicality, as conservative as possible.
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PMID:Solid cystic tumor of the head of the pancreas in a young woman. 963 46

Primary gastric lymphoma is the most frequent extra nodal primary site for non-Hodgkin's lymphoma (NHL) and is itself uncommon. Moreover, a massive infiltration of all stomach (from cardias to antrum) simulating a linitis plastica, it's rare. We present a case report of this atypical presentation of primary gastric NHL in a 73 year old females. The patient came to our observation complaining of dyspepsia, epigastric pain and vomiting from 7 months associated with weight loss and asthenia. Physical examination revealed an epigastric palpable mass. Computed tomographic findings has been necessary to confirm that the massive infiltration of gastric wall (from cardias to pylorus) was ascribed to lymphoma. Dawson's criteria was respected to define primary gastric NHL and was performed a total gastrectomy with systematic lymphadenectomy. The histopathological evidences have confirmed clinical diagnosis of primary gastric NHL. Preoperative diagnosis to clarify the nature of lesions (primary or not) and accurate staging of neoplasm before the operation are indispensable for a correct therapeutic approach; in according to the Ann Arbor classification modified by Musshoff our cases was stage IIE and radical gastrectomy with systematic lymphadenectomy was performed. Surgical resection is generally considered to have a definitive role in the treatment of primary gastric lymphoma specially for the stage IE and IIE.
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PMID:[Primary non-Hodgkin's lymphoma of the stomach (a rare case of extensive spread to the entire organ)]. 1057 21

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection plays an important role in pathogenesis of peptic ulcer. Proof for a causal role for HP in peptic ulcer rests in two major points; 1) the majority of ulcer patients are HP infected and the prevalence of this infection for both gastric ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer recurrence. Conclusions regarding the mechanisms by which HP induces peptic ulcer are restricted mainly to studies observing the consequences of its eradication by antibiotics combined with gastric inhibitors or bismuth agents. Several specific virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) as well as other noxious substances including ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF), nitric oxide (NO) and others have been implicated in gastritis and were found to be significantly more frequent in gastric cancer than in gender- and age-matched controls, especially in younger generation. Chronic inflammation, atrophic gastritis, intestinal metaplasia, impaired defense mechanisms combined with hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen metabolites and epithelial cell proliferation have been associated with gastric cancer. This multi-step pathway originally proposed by Correa and his colleagues, long before the HP was discovered in the stomach, leads to cancer but may be reversed by eradication of HP. This is, however, a controversial issue because gastric atrophy and intestinal metaplasia may be also caused by other factors such as bile reflux, dietary irritants, and autoimmunity. The implication of HP in MALT-lymphoma is based on the observations that eradication of HP in early stage of low-grade of this tumor leads to complete remission. The significance of HP in non-ulcer dyspepsia remains questionable and requires further studies.
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PMID:Helicobacter pylori associated gastric pathology. 1069 52

Numerous epidemiological studies demonstrated the association between Helicobacter pylori (H. pylori) infection and gastric cancer but the mechanism of the involvement of H. pylori in gastric cancerogenesis remains virtually unknown. This study was designed to determine the seropositivity of H. pylori and cytotoxin associated gene A (CagA), serum gastrin and gastric lumen gastrin levels under basal conditions and following stimulation with histamine in gastric cancer patients and controls. 100 gastric cancer patients aging from 21 to 60 years and 300 gender- and age-adjusted controls hospitalized with non-ulcer dyspepsia (NUD) entered this study. 13C-Urea Breath Test (UBT), serum immunoglobulin (IgG) antibodies to H. pylori and CagA were used to assess the H. pylori infection and serum levels of IL-1beta, IL-8 and TNFalpha were measured by enzyme-linked immunosorbent assay (ELISA) to evaluate the degree of gastric inflammation by H. pylori . Gastrin-17 mRNA and gastrin receptors (CCK(B)) mRNA expression in gastric mucosal samples taken by biopsy from the macroscopically intact fundic and antral mucosa as well as from the gastric tumor was determined using RT-PCR. The overall H. pylori seropositivity in gastric cancer patients at age 21-60 years was about 92%, compared, respectively, to 68%, in controls. A summary odds ratio (OR) for gastric cancer in H. pylori infected patients was about 5.0 . The H. pylori CagA seropositivity in gastric cancer patients was about 58.5% compared to 32.4% in controls, giving the summary OR for gastric cancer in CagA positive patients about 8.0. The prevalence of H. pylori- and H. pylori CagA-seropositivity was significantly higher in cancers than in controls, irrespective of the histology of gastric tumor (intestinal, diffuse or mixed type). Median IL-1beta and IL-8 reached significantly higher values in gastric cancer patients (9.31 and 30.8 pg/ml) than in controls (0.21 and 3.12, respectively). In contrast, median serum gastrin in cancers (as total group) was several folds higher (62.6 pM) than in controls (19.3 pM). Also median luminal gastrin concentration in gastric cancer patients was many folds higher (310 pM) than in controls (20 pM). This study shows for the first time that cancer patients are capable of releasing large amounts of gastrin into the gastric lumen to increase luminal hormone concentration to the level that was recently reported to stimulate the growth of H. pylori. There was no any correlation between plasma gastrin levels and gastric luminal concentration of gastrin suggesting that: 1) luminal gastrin originates from different source than plasma hormone, most probably from the cancer cells, 2) cancer cells are capable of expressing gastrin and releasing it mainly into the gastric juice and 3) the gastric cancer cells are equipped with gastrin-specific (CCK(B)) receptor so they exhibit the self-growth promoting activity in autocrine fashion. This notion is supported by direct detection of gastrin mRNA and gastrin receptor (CCK(B)-receptors) mRNA using RT-PCR in cancer tissue. To our knowledge this is the first study showing an important role of gastrin as self-stimulant of cancer cells in patients infected with H. pylori. Basal and histamine maximally stimulated acid outputs were significantly lower in gastric cancer patients than in controls despite of enhanced gastrin release, particularly in cancer patients and this might reflect the mucosal inflammatory changes (increased serum levels of proinflammtory interleukins - IL-1beta and IL-8), that are known to increase gastrin release. We conclude that: 1) H. pylori infected patients, particularly those showing CagA-seropositivity, are at greatly increased risk of development of gastric cancer, 2) H. pylori-infected cancer patients produce significantly more IL-1beta and IL-8 that might reflect an H. (ABSTRACT TRUNCATED)
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PMID:Role of gastrin in gastric cancerogenesis in Helicobacter pylori infected humans. 1069 65

The incidence of pancreatic cancer (PC) is increasing in developing countries. Smoking, reduced consumption of fruits and vegetables, chronic pancreatitis appear to be the best established risk factors. PC is often diagnosed at a late stage. We have to look for it when dyspepsia with weight loss, pancreatic pain or impaired glucose tolerance occurs. Tumor markers are briefly exposed and we discuss the place of endoscopic retrograde cholangiopancreatography (ERCP) after non invasive imaging techniques.
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PMID:[Epidemiological aspects, risk factors, and detection of pancreatic cancer]. 1076 72

Sufficient therapy of pain is essential for the treatment of tumor patients. World Health Organisation (WHO)-guidelines recommend a combination of opioids with non-opioid-analgesics (NOA) for patients with medium to strong pain. Cancer pain is often a combination of pain caused by the tumor itself, tumor associated and pain caused by therapy. Various substances act by different mechanisms and therefore combinations may demonstrate superior effects. Opioids ("central analgesics") inhibit neuronal transduction within the spinal cord, enhance inhibiting function of midbrain nuclei on ascending pain transduction and influence pain perception via modulation of the limbic system. NOAs ("peripheral analgesics") inhibit cyclooxygenase hindering activation of the peripheral nociceptor-system. There are 2 different classes of NOAs: 1) non-acidic, antipyretic analgesics like pyrazolones (metamizol) and anilin-derivates (paracetamol) and 2) non-steroidal antirheumatics (NSAR) like salicylates (acetylsalicylic acid), derivates of propionic acid (ibuprofen, naproxen), acetate acid (indomethacin, diclofenac), enolic acid (piroxicam, meloxicam) and anthranil acid (mefenamin). Adjuvant therapy is necessary to control common NSAR-side-effects like dyspepsia, ulcer and gastrointestinal bleeding. Due to its exceptional analgesic, antipyretic and spasmolytic properties, metamizol is an essential substance in tumor therapy. As agranulocytosis-incidence of 1:1,000,000 is low, good gastrointestinal and renal tolerance makes metamizol an excellent alternative to NSAR. There is scientific evidence that adequate combinations of non-opioids, opioids and adjuvant drugs, considering adverse side effects, were effective and safe in the treatment of cancer pain.
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PMID:[Non-opioid analgesics--irreplaceable in cancer pain therapy? 1113 Jan 28

Gastric colonization by Helicobacter pylori is a risk factor for noncardia gastric cancer. The association between H. pylori and cancer may be attributable to increased epithelial cell turnover, possibly related to antigastric antibodies. Two previous studies reported a disproportionate increase in proliferation relative to apoptosis in patients with H. pylori strains expressing the virulence-related cagA gene. This has led to the hypothesis that an abrogation of apoptosis by cagA-positive strains may promote neoplasia. We, therefore, examined the effect of H. pylori on gastric epithelial proliferation, apoptosis, and the presence of serum antiparietal cell antibodies in a large prospective study. Proliferation and apoptosis were evaluated "blindly" using validated immunohistochemical methods in two antral and two gastric corpus biopsies from 60 patients with nonulcer dyspepsia, and results were correlated with the presence of serum antiparietal cell antibodies. H. pylori colonization was assessed by histology, biopsy urease test, and serology. Proliferation was increased 2-fold in both antrum and corpus in H. pylori-positive patients, was not related to H. pylori cagA status, and was positively correlated with histological gastritis. Apoptosis was increased in the antrum and body only in patients with cagA-positive H. pylori strains. Antiparietal cell antibodies were not more prevalent in H. pylori colonization, and their presence was inversely related to epithelial apoptosis scores we therefore conclude that in patients with nonulcer dyspepsia, H. pylori carriage is associated with increased proliferation. Futhermore the cag pathogenicity island is associated with increased apoptosis. Our results do not support the hypothesis that there is a relative deficiency of gastric epithelial cell apoptosis associated with the carriage of cagA-positive strains. Host factors may be more important than bacterial products in determining the long-term outcome of H. pylori colonization.
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PMID:Increased gastric epithelial cell apoptosis associated with colonization with cagA + Helicobacter pylori strains. 1124 42

We report a case of gastric neurofibroma encountered in 41-year-old woman who complained of dyspepsia and physical examination revealed palpable mass in her abdomen. It was not possible to determine the nature and origin of the tumor by radiological and endoscopic investigations. At laparotomy the tumor was found to be pendiculated and growing extramurally from the anterior wall of the stomach. Wedge gastric resection, including the mass, was performed. Histological examination revealed a spindle cell gastric tumor, immunohistochemically differentiated as a neurofibroma.
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PMID:[Gastric neurofibroma--still a diagnostic problem]. 1129 20


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