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Biomedical subjects

D C Snover

Publications and source records attributed to D C Snover.

At least 37 records · Page 2Linked to original sources
PubMed1992

Septate gallbladder with cholelithiasis: a cause of chronic abdominal pain in a 6-year-old child.

This report describes the case of a 6-year-old girl with septate gallbladder and cholelithiasis without cholecystitis, an uncommon condition associated with chronic abdominal pain. The absence of smooth muscle components within the gallbladder septae supports an embryogenic abnormality that may have occurred early during the maturation of the gallbladder lumen. In concert with other predisposing factors, the septa may have induced gallstones and, thus, the patient's symptoms. Although rare, gallbladder abnormalities may cause abdominal pain in children and should be included in the differential diagnosis. Early ultrasound should be obtained as part of a workup if gallbladder abnormalities are suspected. Elective cholecystectomy is curative.

Abdominal Pain↗
PubMed1992

Adenovirus in the gastrointestinal tracts of immunosuppressed patients.

Adenovirus was cultured from various gastrointestinal sites and one lung specimen from seven immunosuppressed patients, four of whom were bone marrow transplant recipients. Histologic examination and in situ hybridization studies of the lung demonstrated adenovirus in the bronchial epithelium and alveolar lining cells. In contrast, none of the 34 gastrointestinal biopsies performed within 30 days of the positive adenovirus culture showed histologic or molecular evidence of invasive adenovirus in the gastrointestinal mucosa. These results suggest that isolation of adenovirus from gastrointestinal biopsy specimens taken from immunosuppressed patients probably does not indicate an invasive adenoviral infection.

Adenovirus Infections, Human↗
PubMed1992

Bacillary epithelioid angiomatosis involving the liver, spleen, and skin in an AIDS patient with concurrent Kaposi's sarcoma.

The simultaneous findings of bacillary epithelioid angiomatosis and Kaposi's sarcoma of the skin with visceral hepatosplenic bacillary epithelioid angiomatosis is reported in a patient with acquired immune deficiency syndrome. Liver biopsy showed periportal peliotic spindle cell foci that initially were misinterpreted as Kaposi's sarcoma. After antibiotic therapy induced rapid clinical improvement, repeated liver biopsy showed resolution of the previously noted lesions. Although the violaceous skin lesions all appeared similar clinically, some resolved completely and some progressed. One of the latter was biopsied and had the histologic features of Kaposi's sarcoma. The differential diagnosis is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Pathology of the liver in mucopolysaccharidosis: light and electron microscopic assessment before and after bone marrow transplantation.

Serial liver biopsies were obtained in 20 patients undergoing bone marrow transplantation (BMT) for mucopolysaccharidosis (MPS). The 13 patients with MPS I, one with MPS II, four with MPS III, and two with MPS VI underwent liver biopsy prior to and from 1 to 37 months after BMT. The amount of accumulated glycosaminoglycan (GAG) was assessed by semiquantitation of Kupffer cell staining with colloidal iron and by counting the number of hepatocellular GAG-containing lysosomes in electron micrographs. Eleven of 13 patients with MPS I achieved engraftment, and 10 of the 11 cleared the Kupffer cells and hepatocytes of GAG by 3 to 19 months post-BMT. Two patients with autologous recovery demonstrated persistent hepatocyte inclusions. The three patients with MPS II and MPS VI engrafted and showed clearance of hepatocyte and Kupffer cell GAG by 7 months after BMT. All four patients with MPS III engrafted. Although the Kupffer cells in these patients were cleared of GAG by 12 months after BMT, hepatocellular inclusions persisted in all four. For MPS I, II and VI, donor engraftment was associated with resolution of lysosomal storage material in donor-derived Kupffer cells and untransplanted hepatocytes, indicative of transcellular metabolic correction. Failure of hepatocyte clearance in one case of MPS I and all patients with MPS III suggested a diminished capacity of the graft-derived enzyme to enter the hepatocyte lysosomes in these patients.

Bone Marrow Transplantation↗
PubMed1992

Hepatic pathology of chronic granulomatous disease of childhood.

We reviewed the hepatic pathology of seven cases of chronic granulomatous disease of childhood. All patients were male, with an age range of 5 to 41 years. Hepatic biopsy with drainage or wedge resection was performed in five cases to remove abscesses. Autopsy was performed in three cases. Presentation was typical of infection (fever, leukocytosis) with an elevated serum alkaline phosphatase level. Histologically, the most consistent feature was the presence of foamy macrophages that contained a finely granular golden brown pigment, seen in all seven cases. These were present as small collections predominantly in the portal tracts but were also found in the lobules. Palisading granulomas with central necrosis and associated giant cells were seen in four cases, one of which also had occasional lobular epithelioid granulomas. One case showed hyalinized portal and lobular granulomas. Four cases that showed palisading granulomas cultured positive for Staphylococcus aureus. One case cultured Pseudomonas cepacia, and one case cultured Streptococcus intermedius. Although palisading granulomas are typical of chronic granulomatous disease, they are not seen in all cases. These granulomas are similar to granulomas that are seen with Candida and other fungal infections and therefore are not specific for chronic granulomatous disease of childhood. The pigmented macrophages appear to be a consequence of the primary defect of the disease and are not secondary to infection and associated inflammation.

Adolescent↗
PubMed1991

Radiotherapy in mice with yttrium-90-labeled anti-Ly1 monoclonal antibody: therapy of established graft-versus-host disease induced across the major histocompatibility barrier.

A monoclonal antibody recognizing Ly1, the murine homologue of CD5, was labeled with 90Y. In vivo biodistribution studies showed that 90Y-anti-Ly1 selectively localized in lymphoid tissue. Groups of B10,BR mice (H-2k) were lethally irradiated and given major histocompatibility complex-disparate C57BL/6 (H-2b) bone marrow and spleen cells to induce graft-versus-host disease (GVHD). Eight days later, mice with active GVHD were administered a single i.p. injection of 50 microCi90Y-anti-Ly1. Fifty % of these mice were alive 2 months after treatment. Long term (greater than 4-month) survival was significantly higher than in phosphate-buffered saline-treated mice. Survival was slightly improved in groups of mice receiving control irrelevant antibody labeled with 90Y or mice receiving free 90Y. However, survival in these groups was not significantly different from the phosphate-buffered saline-treated control group. The improved survival was supported by data showing improved mean animal weight. An anti-GVHD effect was confirmed by histopathological analysis. Unlabeled anti-Ly1 monoclonal antibody at comparable doses to 90Y-anti-Ly1 was not effective. Animals that died following 50-microCi treatment did not die of radiation toxicity, since all mice receiving 50 microCi 90Y-anti-Ly1 plus syngeneic bone marrow survived. The window of therapy was narrow in our studies, since 100 microCi 90Y-anti-Ly1 did not confer any survival advantage. Animals that did survive long term were studied for evidence of alloengraftment and found to have high levels of circulating donor mononuclear cells. 90Y-Anti-Ly1 localized in the spleen, thymus, liver, kidney and bone marrow but not in the bowel, lung, muscle, or skin. Animals given similar doses of free 90Y, 90Y-anti-Ly1, or labeled irrelevant antibody eliminated free 90Y fastest, followed by 90Y-anti-Ly1 and then labeled irrelevant antibody. Hematological analysis of peripheral blood from 90Y-anti-Ly1-treated mice showed reduction in total WBC counts, absolute lymphocyte numbers, and absolute neutrophil numbers on day 24 after treatment. Myelosuppression recovered by day 38. These findings indicate that Ly1-positive cells are involved in the effector phase of GVHD and that radiolabeled antibodies may be useful as cell-specific probes for studying the GVHD network. 90Y-Anti-Ly1 protected recipients long term from lethal GVHD, and the fact that it had a rather remarkable inhibitory and selective effect on the lymphoid system of mice suggests that these agents may have broader application in the field of transplantation.

Animals↗
PubMed1991

Toxicity and efficacy of anti-T-cell ricin toxin A chain immunotoxins in a murine model of established graft-versus-host disease induced across the major histocompatibility barrier.

Graft-versus-host disease (GVHD) was induced across the murine major histocompatibility complex by injecting C57BL/6 (H-2b) bone marrow and splenocytes into lethally irradiated B10.BR (H-2k) murine recipients. An immunotoxin (IT) composed of a pan T-cell monoclonal antibody called anti-Ly1 (the murine homologue to human anti-CD5) was conjugated to ricin toxin A chain (anti-Ly1-RTA) and used to treat recipient mice. In vitro, IT was as active as free RTA, bound selectively, and inhibited T-cell proliferation even in the absence of potentiators. Mice administered anti-Ly1-RTA in vivo during ongoing GVHD, at a dose of 10 micrograms/d for 5 days, showed lower numbers of splenic Thy1.2+ T cells and significantly improved survival as compared with mice given phosphate-buffered saline (PBS) or irrelevant control RTA IT. Protection was transient because GVHD and weight loss occurred when injections ceased. Survival could not be enhanced by crosslinking RTA30, a low oligosaccharide-containing fraction of purified RTA. Treatment with anti-Ly1-RTA caused a significant elevation in neutrophils, and higher doses were associated with mild hepatotoxicity. In contrast, infusion of identical doses and schedules of another pan T-cell immunotoxin, anti-Thy1.2-RTA, caused a significant decrease in lymphocytes, but not neutrophils; a precipitous increase in weight; a decrease in total plasma protein (TPP); and an increase in pleural and peritoneal effusions reminiscent of vascular leak syndrome (VLS). Although the toxic effects of anti-Thy1.2-RTA were too severe to show a survival advantage in a GVHD model, histopathologic studies showed a definite anti-GVHD effect. The most significant decline in GVHD as compared with the PBS-treated controls was observed in skin, and to a lesser extent, in liver and lung. To investigate the cause of IT toxicity, anti-Thy1.2-RTA was administered intraperitoneally to lethally irradiated B10.BR (H-2k) recipients of syngeneic bone marrow. These recipients showed the same weight gain, hypoproteinuria, and VLS observed in the GVHD model. Death occurred at higher anti-Thy1.2-RTA doses (30 or 50 micrograms/daily injections administered days 8 through 12 posttransplant). Anti-Thy1.2-RTA had a negligible effect on renal function, but histologic studies showed patchy dropout of the renal tubules. Treatment resulted in pulmonary vascular congestion, but there was no pathologic evidence of liver, brain, or colon toxicity. Weight gain was enhanced by irradiation because nonirradiated normal mice did not undergo such a precipitous weight increase.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Intraobserver and interobserver variation in the histopathological assessment of liver allograft rejection. The Liver Transplantation Database (LTD) Investigators.

A study to determine the reproducibility of histopathological findings and diagnoses of rejection was carried out on a series of 42 liver allograft needle biopsy specimens by five pathologists practicing at four liver transplant centers. Pathologists from each of the four centers read each slide independently on two different occasions and were asked to assess 12 histopathological features and render a diagnosis. For all histological variables, the intrarater agreement was higher than the interrater agreement. Moderate to excellent agreement occurred among the pathologists about all histological variables thought to be important in establishing the diagnosis of acute rejection (i.e., portal tract inflammation, subendothelial inflammation and bile duct damage). Other variables such as lobular disarray, bile duct proliferation and particularly arteritis, however, were only fairly or poorly reproducible. Surprisingly, the diagnosis of acute rejection was more reproducible than the individual histopathological findings that were thought to be the basis for the diagnosis. The agreement for the diagnosis of chronic rejection, however, varied according to observer. We noted that relatively inexperienced observers within this group had some difficulties agreeing with more experienced observers in establishing a diagnosis of chronic rejection. These findings demonstrate that the histopathological diagnosis of acute cellular liver allograft rejection is highly reproducible within a group of experienced pathologists and that this diagnosis can be pooled in a common data base with confidence.

Biopsy, Needle↗
PubMed1991

Intestinal ganglioneuromatosis: mucosal and transmural types. A clinicopathologic and immunohistochemical study of six cases.

Six cases of intestinal ganglioneuromatosis (GN) included in this study reveal the occurrence of two morphologic patterns. Transmural GN was characterized by neural hyperplasia in all layers of the bowel wall with predominant involvement of the myenteric plexus. It was found in three patients affected by multiple endocrine neoplasia IIb. Mucosal GN, having predominant involvement of the mucosa without concomitant hyperplasia of the myenteric plexus, was associated with von Recklinghausen's disease, adenocarcinoma of the colon, and multiple adenomas with megacolon in one case each. Clinicopathologic correlations and review of the literature suggest that mucosal GN might represent a distinct entity with a lower morbidity rate than the transmural variant. Immunohistochemical stains reveal considerable heterogeneity. S-100 protein, neuron-specific enolase, and synapto-physin immunostaining followed the distribution of the nervous hyperplasia in the different intestinal layers as identified morphologically and allowed precise determination of the proliferating cells. Increased reactivity for vasoactive intestinal polypeptide, opioid peptides leu-enkephalin and met-enkephalin, and substance P was present in all cases with transmural involvement; mucosal GN showed normal reactivity for opioid peptides and focal increased staining for substance P (one case) and vasoactive intestinal polypeptide (two cases) in the lamina propria. Mild increased immunoreactivity for tyrosine hydroxylase was present in the myenteric plexus of four out of four cases. Histochemical determination of acetylcholinesterase, performed in one case of transmural type, demonstrated hyperplasia of parasympathetic fibers and neurons. Electron microscopic study of another case suggested the presence of several neurotransmitters. These results indicate that the physiopathology of GN is related to a complex hyperplasia of several peptidergic, cholinergic, and probably adrenergic nerve fibers instead of a selective overgrowth of one type of nerve fiber.

Acetylcholinesterase↗
PubMed1991

Chronic rejection after liver transplantation: a study of clinical, histopathological and immunological features.

In an effort to better understand chronic liver transplant rejection, we studied 110 children and adults who survived for at least 2 mo after the transplant procedure. Chronic rejection was defined using a combination of clinical and histopathological criteria and was diagnosed in 10 of the 110 patients for an incidence of 9.1%. All 10 patients were children with the mean age 3.4 yr vs. 21.7 yr for patients without chronic rejection (p less than .001). Males and females were equally represented, and nine received a liver from a gender-matched donor. Four patients were non-Caucasian, resulting in an incidence of 21.7% in non-Caucasian recipients vs. 6.6% in Caucasian recipients (p less than .05). All chronic rejection patients received a liver from an ABO-compatible donor. T-cell crossmatch was negative in all patients in whom it was assessed, and no significant disparity in either the class I or class II human leukocyte antigen loci was noted. Patients who had chronic rejection experienced acute rejection earlier, 11 days vs. 16 days (p less than .05), than patients who did not. In 8 of 10 patients, chronic rejection appeared to evolve directly from early episodes of acute rejection that were unresponsive to immunosuppressive therapy. Two distinct histological presentations were noted. One was progressive loss of bile ducts without hepatocellular injury (four patients), and the other was characterized by worsening ischemic hepatocellular damage and fibrosis (six patients) in addition to severe ductular injury. The first was associated with a more benign clinical course, the second with rapidly deteriorating hepatic function. Three patients recovered spontaneously 9 to 14 mo after transplant, one died awaiting a donor for retransplant, and five had retransplants. We conclude that chronic rejection after the operation is a relatively uncommon complication of liver transplantation with a variable clinical course and unpredictable outcome.

Adolescent↗
PubMed1990

Acute upper gastrointestinal graft-versus-host disease: clinical significance and response to immunosuppressive therapy.

Recognized manifestations of acute graft-versus-host disease (GVHD) of the gastrointestinal (GI) tract include secretory diarrhea, abdominal pain, and, at times, hemorrhage. In a review of 469 patients undergoing allogeneic bone marrow transplantation (BMT) from matched sibling donors at our institution, we have recognized a syndrome of upper GI GVHD. This syndrome, presenting clinically as anorexia, dyspepsia, food intolerance, nausea, and vomiting, was recognized and confirmed histologically in 62 patients (13% by Kaplan-Meier projection) at the initiation of systemic GVHD therapy, a subset of the 197 patients developing grade II through IV GVHD. These 62 patients with upper GI GVHD were significantly older than the overall BMT population and older than the cohort with grade II through IV GVHD, as well. Of the 62 patients, 25 had upper GI GVHD accompanied only by limited (stage 1 and 2) skin GVHD; 13 others with upper GI GVHD plus limited skin involvement at initial presentation later progressed to more extensive multiorgan involvement; 24 others presented with upper GI along with other organ GVHD. This upper GI GVHD syndrome, first recognized at our center in 1983, has been diagnosed with increasing frequency (22% +/- 5%) in the most recent 5-year interval. The upper GI GVHD syndrome is more responsive to immunosuppressive therapy than grade II GVHD defined by Seattle criteria, with complete and continuing responses to treatment observed in 71% +/- 17% (95% confidence interval) of those with the upper GI GVHD syndrome compared with only 37% +/- 10% complete responses in other patients with grade II GVHD (P = .002). Patients failing immunosuppressive therapy for upper GI GVHD often progress to symptomatic lower GI involvement, suggesting that this syndrome may be an earlier and perhaps more treatable manifestation of this unique intestinal immunopathology, which is followed by chronic GVHD in 74% of patients. While upper GI GVHD symptoms are nonspecific and require invasive histologic and microbiologic studies to confirm the diagnosis, we believe this syndrome has been underreported after allogeneic BMT and propose its recognition within the clinical GVHD scoring system.

Acute Disease↗
PubMed1990

The pathology of liver allografts surviving longer than one year.

Although prolonged survival after liver transplantation is now common, the condition of allografts after prolonged survival has not been widely discussed. We reviewed 86 biopsy samples from 38 patients. The samples were obtained between 366 and 1,622 days after transplant. Thirteen patients' biopsy samples were normal or showed minor changes. Six patients' samples showed rejection. Four patients, including two with rejection, demonstrated ischemic change. Three patients showed focal fibrosis, polymorphonuclear infiltration and bile duct proliferation simulating biliary obstruction, although biliary stones were found in only one patient. Three patients had acute hepatitis. Seven patients had a pattern of chronic persistent hepatitis; four had chronic active hepatitis. Follow-up biopsy samples were obtained in seven chronic hepatitis patients. Two of the patients with chronic hepatitis patients. Two of the patients with chronic active hepatitis have shown slight progression of the disease. None has progressed to cirrhosis, but neither has the chronic active hepatitis resolved. It is likely that some of these cases represent non-A, non-B hepatitis. Although histological abnormalities are common after successful transplantation, the clinical significance of many of the changes remains to be determined. Only patients with rejection or vascular thromboses required new transplants.

Acute Disease↗
PubMed1990

Graft-versus-host disease of the gastrointestinal tract.

Gastrointestinal tract disease (GIT) is relatively common following bone marrow transplantation (BMT). Infections, particularly with viral agents, are similar to those affecting any immunosuppressed transplant recipient. However, two unique aspects of BMT are (a) cytotoxic damage caused by the chemotherapy and irradiation used to eradicate the patient's native marrow and (b) gastrointestinal involvement with graft-versus-host disease (GVHD). GVHD may affect any portion of the GIT; therefore, both upper and lower GIT biopsies may provide diagnostic information not evident in biopsy from a single site. The upper GI tract has a higher yield of positive biopsy specimens, but it is more difficult to biopsy. The basic histopathological feature of acute GIT GVHD, which occurs in the first 100 days posttransplant, is necrosis of individual cells in the regenerating compartment of the mucosa. Severe disease may lead to loss of crypts and eventual sloughing of the mucosa. The histology of acute GVHD may be simulated by cytoreductive agents and viral infections, particularly with cytomegalovirus (CMV). Therefore, an absolute biopsy diagnosis of acute GVHD cannot be made in the first 21 days posttransplant or in any mucosa containing CMV inclusions. The GIT is less often involved in chronic than in acute GVHD. The basic pathology of chronic GIT GVHD is fibrosis of the submucosa and subserosa. Therefore, mucosal biopsy is of limited usefulness in the diagnosis of chronic GVHD.

Acute Disease↗
PubMed1989

Nodular regenerative hyperplasia of the liver following bone marrow transplantation.

Liver disease in the early period following bone marrow transplantation may be due to a number of causes, including pretransplant cytoreduction with chemotherapy and irradiation. Although the relationship of venoocclusive disease to these agents has been well established, another process, nodular regenerative hyperplasia, may also occur. In this retrospective study, we evaluated the incidence and clinical signs of these two processes as defined by histological criteria. In 103 patients studied, nine (8.8%) had venoocclusive disease and 23 (22.5%) had nodular regenerative hyperplasia. Venoocclusive disease was significantly associated with transplantation for malignancy other than acute or chronic leukemia and use of busulfan as a cytoreductive agent and occurred in younger patients. Nodular regenerative hyperplasia did not differ from the general transplant population in terms of underlying disease, cytoreductive regimen, graft vs. host disease prophylaxis or age. Both venoocclusive disease and nodular regenerative hyperplasia were associated with ascites. Venoocclusive disease had a poor prognosis, with eight of nine cases dying of or with venoocclusive disease, whereas no case of nodular regenerative hyperplasia died of liver disease and only 5 of 23 died with nodular regenerative hyperplasia. Using retrospective data, five of 11 patients fulfilling clinical criteria for the diagnosis of venoocclusive disease actually had nodular regenerative hyperplasia, as did all of nine patients fulfilling the criteria for "possible" venoocclusive disease. These results indicate that nodular regenerative hyperplasia is a process which occurs commonly following bone marrow transplantation and which may be clinically misdiagnosed as venoocclusive disease.

Bone Marrow Transplantation↗