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Biomedical subjects

D C Gerhardt

Publications and source records attributed to D C Gerhardt.

12 recordsLinked to original sources
PubMed1990

Gastrointestinal manifestations of mixed connective tissue disease.

We examined the gastrointestinal tract abnormalities in 61 patients with mixed connective tissue disease. The first 34 were part of a prospective longitudinal study that included manometric and radiographic evaluation of the esophagus. Heartburn (48%) and dysphagia (38%) were by far the most common gastrointestinal symptoms. Seventeen percent of patients undergoing manometry had distal esophageal aperistalsis, and 43% low-amplitude peristalsis (less than 30 mmHg). Studies in 10 patients before and after treatment suggested that esophageal dysfunction in mixed connective tissue disease may be responsive to corticosteroids. Upper esophageal sphincter hypotension was also common. One patient had marked upper esophageal sphincter hypotension and recurrent aspiration, which resolved with corticosteroid therapy. Findings on radiographic studies of the stomach and small bowel in 54 patients and barium enemas in 16 patients were reviewed. Our series included one case each of malabsorption, colonic and small bowel perforations due to vasculitis, chronic active hepatitis, and acute pancreatitis. In conclusion, any area of the gastrointestinal tract may be affected by mixed connective tissue disease, although the esophagus is the most common location. The gastrointestinal aspects of mixed connective tissue disease overlap with those of progressive systemic sclerosis, polymyositis, and systemic lupus erythematosus.

Adolescent↗
PubMed1982

Central nervous system lymphoma presenting as dysphagia.

Two patients are presented having lymphomatous involvement of the central nervous system in whom dysphagia was the predominant symptom. All indicated studies failed to reveal evidence of direct esophageal involvement, and the dysphagia improved during treatment of the neural component. Esophageal manometric studies revealed abnormalities of the striated muscle portion of the esophagus. These two case histories suggest that invasion of the central nervous system with lymphoma may produce abnormalities of the neuromuscular control of esophageal function resulting in dysphagia.

Adolescent↗
PubMed1982

Improvement in esophageal motor dysfunction with treatment of reflux esophagitis: a report of two cases.

We report two patients with reflux esophagitis who had decreased lower esophageal sphincter pressures and marked decreased frequency of peristaltic response to swallowing and peristaltic amplitude on pretreatment esophageal motility tracings. Both patients responded to medical therapy of reflux esophagitis with symptomatic clinical improvement, increased lower esophageal sphincter pressures, and increased frequency of peristaltic propagation and amplitude of peristalsis. Measures to treat reflux esophagitis may be effective in some cases, in part, because they permit healing of esophageal inflammation to improve esophageal motor activity, the latter which results in improvement of esophageal acid clearing.

Esophagitis, Peptic↗
PubMed1981

Human esophageal response to rapid swallowing: muscle refractory period or neural inhibition?

The peristaltic response of the normal human esophagus to 10 repeated water swallows separated by varying time intervals (5, 10, 15, 20, and 30 s) between swallows was studied. Pressures measured during the shorter time intervals were of lower amplitude than those at 30-s swallowing intervals throughout the esophagus, with the distal esophagus showing the greatest effect. Frequency of peristalsis was decreased throughout the esophagus with rapid swallowing, especially distally at the 5- and 10-s time intervals. There was no significant change in wave velocity or duration at these time intervals. These data suggest that there is a refractory period in the distal (smooth muscle) esophagus. A series of paired swallows separated by 5 s resulted in a significant decrease in amplitude of the first swallow, and this was more marked in the distal esophagus. These data indicate that there is an inhibition of the progression of peristalsis by a subsequent swallow, probably through a neural mechanism. These studies show that repeated liquid swallows may effect peristalsis by two mechanisms: refractoriness of esophageal smooth muscle and a neural inhibitory discharge.

Adult↗
PubMed1981

Polyposis coli presenting with Streptococcus bovis endocarditis.

Streptococcus bovis bacteremia is an important early clue to the presence of serious and clinically unexpected gastrointestinal disease, particularly carcinoma of the colon. S. bovis bacteremia has also been associated with carcinoma of the esophagus and stomach, gastric lymphoma, pancreatic adenocarcinoma, intestinal diverticulosis and single adenomatous polyps and villous polyps of the colon. We report a patient with S. bovis endocarditis as the initial clinical manifestation of extensive polyposis of the colon and rectum. All patients with S. bovis bacteremia need thorough investigation of their gastrointestinal tract even in the absence of symptoms, signs, or positive laboratory tests suggestive of gastrointestinal pathology.

Adenoma↗
PubMed1980

Cimetidine and hematologic suppression: things are not always as they appear.

A 67-year-old man with a bleeding ulcer developed fever, thrombocytopenia, and neutropenia with eosinophilia coincidental to receiving 3600 mg of cimetidine. Failure to reduplicate the hematologic suppression after cimetidine rechallenge suggests the drug was not responsible for the change in circulating cells. Our patient is similar to the earlier reported cases of cimetidine-associated hematologic suppression. The role of cimetidine in these cases is impossible to determine because of the multifactorial possibilities for bone-marrow suppression. Recently, a fatal case of agranulocytosis associated with cimetidine has been reported. The possible mechanisms of granulocytopenia are reviewed, and it is suggested cimetidine may cause bone-marrow suppression by an idiosyncratic reaction. We believe the possibility of fatal aplastic anemia secondary to cimetidine is very rare and does not preclude a drug rechallenge when the benefit-risk ration warrants.

Aged↗
PubMed1980

Esophageal dysfunction in esophagopharyngeal regurgitation.

Esophageal manometry was performed in 20 patients with esophagopharyngeal regurgitation, in 20 patients with severe chronic heartburn but without regurgitation, and in 20 normal subjects. The purpose of the procedure was to identify possible differences between these groups in upper esophageal sphincter and lower esophageal sphincter resting pressures, and in amplitude of peristaltic contraction in the distal esophagus. The mean peak upper esophageal sphincter pressures in normal subjects and in patients with chronic heartburn were significantly greater than in the patients with esophagopharyngeal regurgitation (101 and 108 vs. 54 mmHg, respectively). In the normal subjects, the mean lower esophageal sphincter resting pressure (19 mmHg) was significantly greater than for the heartburn group (14 mmHg) and for the patients with esophagopharyngeal regurgitation (10 mmHg). The amplitude of peristalsis was significantly lower in the group with regurgitation than in both normal subjects and the group with chronic heartburn. Nine normal subjects responded to intraesophageal infusion of 0.9% NaCl and 0.1 N HCl with a significant increase in upper esophageal sphincter resting pressure, but the group with esophagopharyngeal regurgitation showed no significant change. Patients with esophagopharyngeal regurgitation have lower esophageal sphincter hypotension, diminished peristaltic amplitude, upper esophageal sphincter hypotension, and diminished upper esophageal sphincter response to intraesophageal fluid. We conclude there is in these patients a breakdown of several normal esophageal mechanisms which ordinarily serve as barriers to esophagopharyngeal regurgitation.

Adult↗
PubMed1979

High amplitude, peristaltic esophageal contractions associated with chest pain and/or dysphagia.

Esophageal manometric tracings obtained using low-compliance pneumohydraulic infusion systems were reviewed from patients with symptoms of chest pain and/or dysphagia. Using this sytem, we report on 7 symptomatic patients with markedly increased esophageal peristaltic amplitude. Maximal peristaltic amplitude for these 7 patients (225-430 mmHg) was greater than for normals (75-175 mmHg). Mean peristaltic amplitude for the 7 was 170 mmHg, which was greater than for normals (81 +/- 30 mmHg, mean +/- 2 SD). This finding is believed to reflect the sensitivity of currently available manometric systems. It may be possible with these techniques to define more clearly the bulk of presumed esophageal dysfunction, which is at present poorly characterized. The relationship of clinical symptoms to abnormal esophageal motility is often less than optimal and may result from an inability to define "normal" or from inadequacies of currently available techniques. Our observations of a subset of symptomatic patients having peristaltic contractions with amplitudes exceeding the normal range seem to characterize one form of esophageal motility defect. This abnormality was seen more frequently than diffuse esophageal spasm in our laboratory.

Adult↗