H2 receptor antagonist therapy has been shown to produce rebound acid hypersecretion. The clinical significance of this phenomenon is not known. We performed this study to determine whether withdrawal of H2 receptor antagonist therapy results in dyspepsia in previously asymptomatic volunteers.Thirty-five Helicobacter pylori-positive asymptomatic volunteers were randomized in double-blind fashion to receive 2 months' treatment with either ranitidine 300 mg nocte or placebo. Dyspeptic symptoms were measured before starting treatment and over the course of 10 days after stopping treatment by means of a validated questionnaire.Thirty-one subjects completed the study; 17 were randomized to ranitidine. The pretreatment median aggregate dyspepsia score of the placebo group was 0 (0-4), as was that of the ranitidine group (0-8) (N.S.). During the 10 days after completion of ranitidine, the median aggregate dyspepsia score was 1.4 (0-30), compared with 0 (0-6.3) after placebo (p < 0.01). Of those given ranitidine, 59% experienced dyspepsia after treatment, compared with only 14% who took placebo. In the subgroup that developed dyspepsia after active therapy, the median duration of symptoms was 2 days, symptom severity being maximal on the second day after completion of the tablets. On the days when dyspepsia was experienced, the median daily dyspepsia score was 5 (range, 2-10), which was similar to that of a control group with active duodenal ulcer disease (5; range, 0-11).Withdrawal of a 2-month course of ranitidine 300 mg nocte results in the development of dyspeptic symptoms in a proportion of previously asymptomatic subjects. Patients receiving ranitidine should be warned about this rebound dyspepsia and advised not to immediately resume treatment, as rebound symptoms are likely to improve within a few days.
The discovery of H. pylori infection and the recognition of its effects on gastric physiology has significantly advanced our understanding of the pathophysiology of ulcer disease, In DU patients H. pylori gastritis is mainly confined to the antral mucosa. It stimulates increased release of gastrin by the antral mucosa and this is accompanied by high acid output by the oxyntic mucosa. This high acid response to gastrin stimulation by the oxyntic mucosa in DU patients is due to the combination of a high parietal cell mass and the fact that the function of these parietal cells is not impaired by any body gastritis. The increased acid secretion results in an increased duodenal acid load with the development of gastric metaplasia within the duodenal bulb and then actual ulceration. The reason why only some subjects develop this antral predominant pattern of H. pylori gastritis and associated acid hypersecretion is unclear but may be explained by a premorbid high acid output protecting the oxyntic mucosa form H. pylori gastritis.
Article abstract-Nerve growth factor (NGF) plays a biologic role in the development and maintenance of sympathetic and small sensory neurons. Because it facilitates nerve fiber regeneration, lowers heat-pain threshold (hyperalgesia), and prevents or improves nerve dysfunction in experimental neuropathy, it is being considered as a putative treatment for certain human polyneuropathies. In 16 healthy subjects, we tested whether intradermal injection of minute doses of recombinant human NGF (1 or 3 micro g) compared with saline induces hyperalgesia or alters cutaneous sensation (at the site of injection) as measured by symptom scores, clinical examination, or quantitative sensory testing with Computer Assisted Sensory Examination (CASE IV). Most subjects had, as their only symptom, localized tenderness of the NGF-injected site and only when the site was bumped or compressed. Slight discomfort developed in volar wrist structures (with flexion of fingers) or tenderness of deep structures to palpation over the bicipital groove or supraclavicular region. The Neuropathy Symptoms and Change questionnaire indicated that pressure allodynia was significantly localized to the NGF-injected side from 3 hours to 21 days after injections. Light stroking of the skin did not induce tactile allodynia. Compression of injected sites induced pressure allodynia that occurred more frequently and significantly on the NGF-injected side after 3 hours and was maintained for several weeks. No abnormality of vibratory or cooling detection threshold developed from NGF injection. By contrast, heat-pain threshold (HP 0.5, p = 0.003) and an intermediate level of heat-pain (HP 5.0, p < 0.001) were significantly lowered 1, 3, and 7 days (and in some cases at 3 hours and 14 and 21 days) after NGF injection. The time course of pressure allodynia and heat-pain hyperalgesia is too rapid to be explained by uptake of NGF by nociception terminals, retrograde transport, and upregulation of pain modulators. Local tissue mechanisms appear to be implicated. It remains to be tested whether recombinant human NGF prevents, stabilizes, or ameliorates small fiber human neuropathies. NEUROLOGY 1997;48: 501-505
We performed infrared telethermography in 55 patients with the clinical diagnosis of lumbosacral radiculopathy and in 37 normal controls. Five readers interpreted the thermograms in a blinded fashion. A moderate degree of agreement was noted in tests of intraobserver and interobserver variability. The sensitivity of thermography ranged from 78% to 94% compared with 81% to 92% for imaging studies and 77% for EMG. The specificity of thermography ranged from 20% to 44%. Thermography predicted the level of the radiculopathy correctly in less than 50% of cases. Thermography has little or no utility in the diagnosis of lumbosacral radiculopathy.
Helicobacter pylori infection is now recognized to be an important acquired factor in the pathogenesis of duodenal ulcer disease. There is also an association between H pylori and the subsequent development of gastric cancer. The mechanism of the association between the infection and those disorders is incompletely understood but there is increasing evidence that H pylori-induced disturbances of gastric function play a pivotal role. In this article we review the role of H pylori infection in the pathophysiology of these important upper gastrointestinal diseases.
Background: Acid secretion is intimately associated with most upper gastrointestinal diseases. Helicobacter pylori infection is a major environmental factor modifying acid secretion. Aim: To study the association between the pattern of H pylori gastritis and gastric secretory function in a large number of subjects without specific upper gastrointestinal disease. Methods and materials: Maximal acid output (MAO) was measured in 255 patients with dyspepsia showing normal endoscopy. Activity and severity of gastritis, atrophy and H pylori infection were assessed in body and antral biopsies. The correlations of histological parameters as well as age, sex, height, weight, smoking, serum gastrin, pepsinogen I and II, and their ratio with MAO were determined. Multiple linear regression was used to show the best possible predictors of MAO. Results: Negative relationships: Body atrophy and body-combined (active and chronic) inflammatory scores showed a potent inverse correlation with MAO (correlation coefficients (CC) 0.59 and 0.50, respectively). Body:antral chronic gastritis ratio and body:antral combined inflammation ratio (both with CC = 0.49) and age (CC = 0.44) were also inversely correlated with MAO. Intestinal metaplasia at both antral and body sites had negative relationships with acid output with CC = 0.23 and 0.20, respectively. Positive relationships: Serum pepsinogen I, body H pylori density:combined inflammation ratio and pepsinogen I:II ratio with CC of 0.38, 0.38 and 0.30, respectively, correlated with MAO. The H pylori density: combined inflammation of both antrum and body positively correlated with MAO (CC = 0.29 and 0.38, respectively). Male sex and patient height also positively correlated with acid output. Modelling showed that body combined inflammatory score, body atrophy, age and serum pepsinogen I are independent predictors of acid output (R 2 = 0.62). Conclusion: Combination of body gastritis, body atrophy, age and serum pepsinogen I can be used as predictors of acid-secretory state in populations infected with H pylori .
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