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Biomedical subjects

H D Appelman

Publications and source records attributed to H D Appelman.

At least 55 records · Page 3Linked to original sources
PubMed1992

Recurrence of hepatitis B and delta hepatitis after orthotopic liver transplantation.

The clinical course of 10 liver transplant recipients who had hepatitis B virus (HBV) and five recipients with HBV and D (delta) infection before transplantation is described. Six patients who underwent eight transplants died. The estimated one and two year survival rates in patients with HBV only before transplantation were 74% and 67% respectively. The estimated one and two year survival in patients with HBV and HDV infection beforehand was 100%. Graft infection by HBV occurred in 8 of 10 patients infected with HBV only; and in 4 of 5 patients with previous HBV and HDV infection. There was a widely variable time from transplantation to the appearance of HBV markers in liver or serum, ranging from 6-331 days. Hepatitis D antigen (HDAg) appeared in three grafts very rapidly after transplantation at 4, 8, and 37 days respectively. Graft infection by HBV was accompanied by significant liver injury in six allografts in five recipients. In particular, there was a striking morphological appearance in five infected livers in which the hepatocytes became progressively enlarged and distorted as they accumulated huge amounts of hepatitis B surface and core antigens (HBsAg, HBcAg). These features were accompanied by pericellular fibrosis and cholestasis but little associated inflammation. This syndrome carried a poor prognosis. A gradual progression to cirrhosis occurred in one additional liver. Finally, recurrent HBV infection was a principal or a contributing factor in all deaths. The presence of HBcAg and inflammation in he native liver increased the risk of HBV induced tissue damaged in the graft whereas HDV infection in the host liver seemed to reduce the risk of significant HBV induced tissue damage in the allograft. These data suggest that post transplant HBV infection is accompanied by a variety of changes in the liver allograft, some of which are unique to the transplanted liver and may result in impaired allograft function.

Adolescent↗
PubMed1992

Appendiceal involvement in ulcerative colitis.

Little information has been published regarding appendiceal changes in ulcerative colitis of any extent. An early study has shown the appendix to be involved in over 50% of all cases of ulcerative colitis for which a proctocolectomy was performed, but the extent of the colitis was not always defined. While some investigators have found appendiceal involvement only in continuity with adjacent involved cecum, others believed it may occur as a skip lesion. In this study, the colons and nonobliterated appendices of 87 patients who underwent total proctocolectomy for ulcerative pancolitis were examined to determine the frequency of appendiceal involvement and to determine the frequency with which such involvement truly occurs as a skip lesion. All 87 cases had ulcerative pancolitis, and 66 (62%) had colitic changes in the appendix. In the remaining 21 cases, there was no appendiceal inflammation. In all cases in which the appendix was involved, the cecum was also involved. Cecal activity or lack of activity correlated with appendiceal activity in 52 of the 87 cases (60%). Of the 35 cases in which there was some discrepancy in disease activity between the appendix and cecum, nine had more active disease in the appendix, and 26 had greater activity in the cecum, but in none of the cases where the cecum was normal or near normal was the appendix more severely involved. These data suggest that appendiceal involvement in resected ulcerative pancolitis always occurs in continuity with adjacent involved cecum, although there may be differences in disease activity between the two sites.

Adolescent↗
PubMed1991

Thymosin treatment of chronic hepatitis B: a placebo-controlled pilot trial.

Chronic hepatitis B is a severe and frequently progressive disease. We assessed the safety and efficacy of thymosin fraction 5 and thymosin-alpha 1 in a prospective, placebo-controlled trial in 12 patients with chronic hepatitis B. All patients had histological and biochemical evidence of active liver disease for at least 6 mo before treatment and were positive for serum hepatitis B virus DNA and HBsAg. Seven patients received thymosin fraction 5 or thymosin-alpha 1 and five patients received placebo twice weekly for 6 mo. By the conclusion of the study (1 yr), serum aminotransferase levels had improved significantly in thymosin-treated patients, but not in the placebo group. Six (86%) of the thymosin treated patients and one (20%) patient given placebo cleared hepatitis B virus DNA from serum (p less than 0.04, Fisher's exact test). After treatment, replicative forms of hepatitis B virus DNA were present in the liver specimens of four of five placebo-treated patients but in only one of seven thymosin-treated patients (p less than 0.04, Fisher's exact test). Response to thymosin therapy was associated with significant improvements in peripheral blood lymphocyte and CD3 and CD4 counts and in in vitro production of interferon-gamma over initial values. No significant side effects were observed in patients given thymosin or in placebo-treated patients. Clinical, biochemical and serological improvement in patients responding to thymosin were sustained during 26 +/- 3 mo of follow-up. The results of this pilot trial suggest that thymosin therapy promotes disease remission and cessation of hepatitis B virus replication in patients with chronic viral infection.

Adolescent↗
PubMed1990

Phenotypic variation in colorectal adenoma/cancer expression in two families. Hereditary flat adenoma syndrome.

Clinical, pathologic, and genetic studies on two colorectal cancer-prone families have disclosed right-sided colonic flat adenomas and colorectal cancer. Adenomatous polyp counts exceeded those found in hereditary nonpolyposis colorectal cancer (HNPCC) but were fewer than in familial adenomatous polyposis (FAP). Colon cancer occurred at a later age than in HNPCC or FAP and showed right-sided predominance. The older age of patients with colonic cancer, the right-sided predominance of colon cancer, and the paucity of rectal adenomas make FAP unlikely. Vertical transmission of polyps and colon cancer fit the pattern of autosomal dominant inheritance. A characteristic feature of this phenotype is the predominance of flat adenomas. Molecular genetic studies, with careful description of phenotype, should help clarify classification.

Adenocarcinoma↗
PubMed1990

Colorectal adenomas in the Lynch syndromes. Results of a colonoscopy screening program.

Forty-four asymptomatic putative Lynch syndrome patients participated in a colonoscopy screening program. There were 18 men and 26 women; mean age was 44 yr. Thirty percent of Lynch syndrome patients had at least one adenoma; 20% had multiple adenomas. In 18% of the patients, adenomas were discovered proximal to the splenic flexure. In a reference group of 88 age- and sex-matched patients, 11% had adenomas, 4% had multiple adenomas, and 1% had right-sided adenomas. Twenty-one Lynch syndrome patients had follow-up colonoscopies. Of 7 patients with adenomas on initial examinations, 6 had adenomas at follow-up. Of 14 patients with negative initial examination results, 3 had adenomas at follow-up. The prevalence of adenomas in the Lynch syndromes is greater than in an unselected reference group. The adenomas are more proximally located, corresponding to the site of cancer distribution in the Lynch syndromes. A high rate of synchronous and metachronous lesions is found. Our findings support the hypothesis that adenomatous changes are the premalignant lesion in the Lynch syndromes. We also found evidence of heterogeneity among Lynch syndrome families in adenoma incidence.

Adenoma↗
PubMed1990

Crohn's-like lymphoid reaction and colorectal carcinoma: a potential histologic prognosticator.

A distinctive Crohn's disease-like reaction (CLR) consisting of discrete lymphoid aggregates, some with germinal centers, and surrounding stellate fibrosis is commonly found around colorectal adenocarcinomas in the absence of clinical or pathologic evidence of prior Crohn's disease. Most lymphoid aggregates are located one or more millimeters beyond the advancing tumor fronts, mainly in muscularis propria and pericolic adipose tissue. The intensity of this reaction was graded as absent, mild, or intense for 100 consecutive colorectal carcinomas. These tumors also were evaluated for invasion beyond muscularis propria, lymphoid infiltrates at the tumor margin, and nodal metastases. The degree of CLR was correlated with survival. Results indicated that CLR is more likely to occur in transmurally invasive carcinomas than in those confined to the colonic wall, especially in the right side. An intense CLR is associated with an intense lymphoid infiltrate at the tumor edge, a lower incidence of nodal metastases, and a statistically significant increase in 10-yr survival. These results suggest that the Crohn's-like reaction around colorectal carcinomas may be a favorable host response, similar to lymphocytic infiltrates at the advancing tumor edge. Analysis of more cases should clarify whether this CLR is independent of other variables.

Adenocarcinoma↗
PubMed1989

The integrated value of serum procollagen III peptide over time predicts hepatic hydroxyproline content and stainable collagen in a model of dietary cirrhosis in the rat.

To determine whether a serum parameter of collagen metabolism, serum procollagen type III peptide, correlated with hepatic collagen in a model of diet-induced fibrosis, rats were fed a control or cirrhogenic diet for 6 months and treated with either subcutaneous vehicle or the hepatoprotective prostaglandin 16,16-dimethyl prostaglandin E2 (100 micrograms per kg) twice daily. Pair-fed rats from each group were killed after 2, 4 or 6 months. The value of serum procollagen type III peptide to body weight integrated over time (Kt) correlated linearly with hepatic hydroxyproline content (r = 0.97) at killing time t. Good correlations were also seen between Kt and histopathological assessment of aniline blue-stainable collagen (r = 0.93) and between the histopathology and hydroxyproline content (r = 0.97). Rats receiving 16,16-dimethyl prostaglandin E2 had lower values of all three parameters compared to rats receiving vehicle, confirming the previously demonstrated hepatoprotective effect of 16,16-dimethyl prostaglandin E2. The excellent correlation between Kt and the two other traditional parameters of hepatic collagen suggest that sequential measurements of serum procollagen type III peptide can be used to predict alterations in liver collagen deposition in rats.

16,16-Dimethylprostaglandin E2↗
PubMed1989

Campylobacter pylori is not associated with gastroparesis.

There is a high incidence of Campylobacter pylori in the gastric mucosa of patients with duodenal ulcer, gastric ulcer, and nonulcer dyspepsia. Factors that lead to development of this infection are unknown. We hypothesized that delayed solid-phase gastric emptying, a condition characterized by antral stasis, might predispose to Campylobacter pylori infection. We prospectively studied 51 patients with symptoms of gastroparesis using a solid-phase gastric emptying study and upper endoscopy. Patients were excluded if they had predominant symptoms of epigastric pain or an abnormal endoscopy. Three biopsies were obtained from the antrum and stained with H&E. When any inflammation was present, a Warthin-Starry stain was also performed. These were blindly examined for chronic inflammation, activity, and presence of Campylobacter pylori. Campylobacter pylori was not more common in patients with gastroparesis, documented by delayed gastric emptying, than in patients with a normal emptying study. On the contrary, there was a significantly lower incidence of Campylobacter pylori in those with delayed emptying compared to those with normal emptying (5% vs 31%, P less than 0.05). Gastritis activity correlated closely with Campylobacter presence. Inactive chronic gastritis with Campylobacter was equally common in those with delayed or normal gastric emptying. Diabetics were no more likely to harbor Campylobacter pylori than nondiabetics (16% vs 25%). The 5% incidence of Campylobacter in the gastroparesis group is less than, but approaches, that previously reported in asymptomatic controls. The 31% incidence of Campylobacter in the group with symptoms of gastroparesis but normal gastric emptying approaches that reported for nonulcer dyspepsia. Our data suggest that gastroparesis does not predispose to Campylobacter pylori infection or histologic chronic gastritis.

Adult↗
PubMed1989

Treatment of Campylobacter pylori does not alter gastric acid secretion.

The effect of treatment of Campylobacter pylori-associated gastritis on acid secretion was studied to examine further the strong association between C. pylori and peptic diseases. Twelve symptomatic patients with non-ulcer dyspepsia and C. pylori-associated histologic gastritis had basal and pentagastrin-stimulated gastric acid analysis before and after a 14-day course of amoxicillin 250 mg qid and bismuth subsalicylate 524 mg qid. Endoscopy, antral biopsies, and symptom questionnaires were obtained at entry and at the conclusion of the study. C. pylori was identified by Warthin-Starry stain. Biopsy specimens were also graded for the severity of chronic inflammation and the presence of neutrophils in the epithelium. The treatment regimen cleared C. pylori in 10 of 12 patients. Dyspeptic symptoms improved in 10 of 12 patients, two of whom did not clear the organism, and were unchanged in the remaining two patients, both of whom cleared the bacteria. Neutrophil infiltration in the antral biopsies resolved in 10 patients, including nine with C. pylori clearance and one with persistence of the organism. The severity of the underlying chronic inflammation improved in only one of the 10 organism-free patients and one of the two persistently infected individuals. Pretreatment gastric acid analysis demonstrated hypochlorhydria in three of 12 patients, mild hyperchlorhydria in three of 12 patients, mild hyperchlorhydria in two of 12, and normal acid secretion in the remaining seven patients. Posttreatment acid studies revealed that four of 12 patients were hypochlorhydric, one of 12 had hyperchlorhydria, and seven of 12 were normochlorhydric. After treatment, there was no significant change in basal or maximal acid secretion in the 10 patients who cleared the organism. The two patients who failed to clear C. pylori had insignificant increases in acid secretion after treatment. Our data show no consistent pretreatment pattern of acid secretion in patients with C. pylori-associated gastritis. In addition, gastric acid output did not show a consistent change after treatment for C. pylori. This suggests that the association between C. pylori infection and peptic diseases does not occur via altered acid secretion.

Amoxicillin↗
PubMed1988

Flat adenomas in a colon cancer-prone kindred.

We describe new pathologic findings in a hereditary nonpolyposis colorectal cancer family. Affected family members developed multiple small adenomas with right-sided predominance; many adenomas had an unusual appearance featuring slightly elevated lesions with adenomatous changes confined to the upper regions of the colonic crypts. We have adopted the previously established term "flat adenoma" for these lesions. This phenotype may be a morphologic marker for at least one subset of hereditary nonpolyposis colorectal cancer.

Adenoma↗
PubMed1988

Cell markers in gastrointestinal stromal tumors.

Stromal tumors of the gastrointestinal (GI) tract have generated considerable controversy about their direction and level of differentiation, particularly about whether the tumor cells are smooth muscle or Schwann cells. In an attempt to characterize these tumors, the immunohistochemical staining patterns of desmin, vimentin, actin, and S-100 protein were studied in 41 GI stromal tumors, using the avidin-biotin method, and compared with normal host smooth muscle and nerve and with esophageal and uterine leiomyomas. Twenty gastric and one rectal tumor stained diffusely with vimentin and actin, but not with desmin, and had scattered strongly S-100-positive cells that might either be trapped Schwann cells or tumor cells. Twenty small bowel tumors stained similarly to the gastric tumors with regard to vimentin, actin, and desmin, but most (17/20) had a unique, strongly positive geographic staining pattern with S-100. No differences in staining were noted between benign and malignant tumors in either gastric or small bowel sites, and most histologic patterns in tumors from similar locations stained similarly. These results suggest that GI stromal tumors are not truly "leiomyomas and leiomyosarcomas," but relatively undifferentiated tumors, with the expression of various antigens depending on their location in the gut.

Actins↗
PubMed1988

Candida hepatitis. Histopathologic diagnosis.

Candida hepatitis, usually a manifestation of disseminated candidiasis in immunocompromised patients, is difficult to diagnose antemortem. We studied six patients with proven hepatic candidiasis to assess features helpful in deriving a correct diagnosis. Five patients were immunosuppressed as a result for treatment for leukemia; one was immunosuppressed due to renal transplantation. All had sustained fevers greater than 101 degrees F, elevated alkaline phosphatase levels, and multiple hepatic and splenic defects--presumably abscesses--on abdominal CT scan. Twelve liver biopsies (nine needle, three wedge) were examined. Biopsies from four patients contained identifiable Candida organisms within suppurative granulomas; a biopsy from a fifth patient grew Candida albicans in cultures. In the sixth patient, the first biopsy was culture positive for Candida albicans, and the second biopsy, a fine-needle aspirate, contained Candida organisms and purulent material. In all of the nondiagnostic biopsies, as well as in regions of the diagnostic biopsies around the suppurative granulomas, mass-associated obstructive changes were noted. These included pericentral sinusoidal dilatation and cholestatic inflammation characterized by periportal ductular proliferation with surrounding neutrophils and edema. We conclude that in the appropriate clinical setting, these mass-associated histologic findings are suggestive of adjacent Candida abscesses. Definite diagnosis requires either the identification of Candida organisms within inflammatory hepatic lesions or positive culture of Candida from the liver biopsy.

Adolescent↗
PubMed1987

Histopathology differentiates acute self-limited colitis from ulcerative colitis.

Acute self-limited colitis (ASLC) must be distinguished from chronic ulcerative colitis (CUC) for the proper early management of patients with the acute onset of bloody diarrhea. This study was undertaken to determine if any clinical, endoscopic, microbiologic, or histologic parameters can be used to make this distinction reliably and quickly. Forty-eight patients with ASLC, 36 patients with chronic ulcerative colitis during their first attack [CUC(F)], and 84 patients with recurrent flares of chronic ulcerative colitis [CUC(R)] were studied prospectively. The presence of fever (temperature greater than 100 degrees F), abdominal pain, or the time from onset of bloody diarrhea to presentation were not discriminatory. Overall clinical and endoscopic severity were identical among the three groups. Microbiologic studies identified an infectious agent in only 42% of patients with ASLC. Histopathologic features always distinguished patients with CUC from those with ASLC. No case of ASLC was misdiagnosed histologically as CUC or vice versa. Plasmacytosis in the lamina propria extending to the mucosal base and mucosal distortion were present in all cases of CUC(F) and CUC(R), but were absent in all cases of ASLC. The finding of focal cryptitis during the resolving phase of ASLC could be confused with similar lesions in biopsy specimens from patients with Crohn's disease and mandates clinical follow-up. Histopathology is thus the only reliable diagnostic tool for the rapid differentiation of ASLC from CUC. However, biopsy specimens are only diagnostic when obtained during the acute phase of illness; that is, usually within the first 4 days from the onset of symptoms.

Acute Disease↗