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Biomedical subjects

M R Gottfried

Publications and source records attributed to M R Gottfried.

36 records · Page 2Linked to original sources
PubMed1993

Cooccurrence of collagenous colitis with seronegative spondyloarthropathy: report of a case and literature review.

Collagenous colitis is an uncommon cause of chronic watery diarrhea, characterized by colonic deposition of collagen. Nonerosive, oligoarticular, peripheral arthritis has previously been noted in about 7% of patients with collagenous colitis. We describe a patient with collagenous colitis who concurrently developed erosive, seronegative spondyloarthropathy affecting peripheral and axial joints. Synovial histology was characterized by a conspicuous inflammatory infiltrate comprised of histiocytes, lymphocytes and plasma cells. Collagenous colitis is suggested to be a systemic autoimmune disorder, with extraintestinal features such as thyroiditis and arthritis.

Colitis↗
PubMed1991

Gastrointestinal cryptococcosis.

Cryptococcal infection of the gastrointestinal (GI) tract is rarely reported, either in disseminated disease or as an isolated finding. We report a case of gastric cryptococcal infection diagnosed by endoscopic biopsy as the initial presentation of the acquired immunodeficiency syndrome (AIDS), and an additional seven cases found by reviewing 23 other autopsy cases of disseminated or pulmonary cryptococcal infection. The patient with gastric cryptococcosis was a 38-year-old man who presented with symptoms of gastroesophageal reflux including odynophagia. Upper GI endoscopy showed Candida esophagitis and gastric nodules. Biopsy of the nodules revealed cryptococcal infection and granulomatous inflammation of the fundic mucosa and submucosa. The patient died 3 weeks later despite anti-fungal therapy. Autopsy revealed widespread cryptococcal infection involving the cecum but not the stomach, suggesting that the gastric lesions resolved with therapy. The sites of infection in the seven other cases were esophagus (three), stomach (one), terminal ileum (one), colon (three), gallbladder (one), and in a focus of Kaposi's sarcoma in the wall of the small bowel (one). Esophageal candidiasis was also present in two of the cases of esophageal cryptococcal infection. Predisposing factors were AIDS (3), hematologic malignancy (3), and corticosteroid therapy (1). In summary, we report a case of gastric cryptococcosis and conclude that cryptococcal infection involves the GI tract more commonly than has been previously reported, with 8/24 (33%) cases positive in our autopsy series. Of clinical significance is the observation that GI cryptococcal infection may be the initial presentation of disseminated disease in the immunocompromised patient, and cryptococcal infection of the esophagus may be found in the setting of esophageal candidiasis.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Helicobacter pylori-like microorganisms and chronic active gastritis in ferrets.

To determine the prevalence and histology of Helicobacter pylori (HP) associated gastritis in young ferrets, we examined 36 normal 2- to 4-month old ferrets. Identification of HP-like microorganisms included Warthin Starry stains of tissue sections, rapid urease test on fresh tissue, and culture. HP-like microorganisms were found in the stomachs of 35/36 ferrets. The highest density of microorganisms was seen in the antrum, where HP-like microorganisms were present in the pits and in deep glands. HP-like microorganisms were also seen in the cardia and on the foveolar epithelium of the fundus, but not in fundic glands. Chronic active gastritis was seen in all animals with HP-like microorganisms, but involved only the antrum. The distal antrum was most severely involved. One animal had no evidence of HP-like microorganisms on tissue sections or by rapid urease test. Gastric tissue sections from this animal showed only minimal infiltration of the lamina propria by polymorphonuclear leukocytes and lymphocytes. Gastritis associated with HP-like microorganisms is common in ferrets and is acquired at a young age. It is associated with chronic active antral gastritis similar to that seen in humans, suggesting that ferrets should provide a useful experimental model for HP-associated gastritis and peptic ulcer.

Animals↗
PubMed1989

Incomplete intestinal metaplasia in the diagnosis of columnar lined esophagus (Barrett's esophagus).

To investigate the distribution and specificity of intestinal metaplasia (IM) in columnar lined esophagus (CLE), the authors reviewed biopsies of the hiatal hernia pouch (HHP) and esophagus from 17 patients with CLE (84 biopsies) and 10 controls (25 biopsies). The proximal margin of the gastric folds was used as an endoscopic landmark, corresponding to the gastroesophageal muscular junction (GEMJ). No biopsies obtained above the GEMJ in control patients showed columnar mucosa. No goblet cell metaplasia was seen in 21 biopsies of the HHP from patients with CLE or in 13 corresponding biopsies from controls. In contrast, alcian blue (AB) stains showed diffuse acid mucins in 3 of 21 biopsies of the HHP from patients with CLE and in 10 of 13 corresponding biopsies from controls, demonstrating that goblet cell metaplasia clearly distinguishes biopsies of CLE from the HHP (P less than 0.01), whereas small amounts of diffuse acid mucin on AB stains do not. IM evidenced by goblet cell metaplasia was frequently seen in biopsies only 2-3 cm above the GEMJ, and CLE was limited to that area in three patients, suggesting that the distal esophagus cannot be dismissed as a site for metaplastic and possibly premalignant mucosa. Adenocarcinoma was diagnosed during the course of the study in one patient with only 5 cm of columnar mucosa above the GEMJ.

Adult↗
PubMed1987

Early diagnosis of columnar-lined esophagus: a new endoscopic diagnostic criterion.

The relationship between the proximal margins of the gastric mucosal folds and the squamocolumnar mucosal junction (SCMJ) in normal subjects and in patients with columnar-lined esophagus (CLE) was studied. Results indicate that in the normal esophagus, the SCMJ is located within 2 cm of the proximal margin of the gastric folds. The proximal margin of the gastric folds in a hiatal hernia pouch provide a fixed, reproducible, anatomic landmark at endoscopy, which designates the junction of the muscular wall of the esophagus and stomach and permits one to predict the expected normal location of the SCMJ. The diagnosis of CLE should be considered at endoscopy when either the SCMJ is located or columnar epithelium is obtained by biopsy at a site greater than 2 cm above the proximal margin of the gastric folds located within a hiatal hernia pouch. This study provides an endoscopic criterion to permit a more accurate diagnosis of CLE in its earliest stages and may permit a better assessment of its prevalence.

Barrett Esophagus↗
PubMed1987

Benign papilloma of the male breast following chronic phenothiazine therapy.

Benign intraductal papilloma is a rare lesion in the male breast. The authors report the occurrence of an intraductal papilloma in a male with more than a ten-year history of phenothiazine therapy (Mellaril and Prolixin). Phenothiazines have been demonstrated to cause elevated serum prolactin levels. The literature regarding the relationship between prolactin and mammary tumors in rodents and in humans remains controversial. The occurrence of this rare male breast tumor in the setting of chronic phenothiazine therapy raises further questions as to the role of prolactin in the development of mammary tumors.

Aged↗
PubMed1986

Extensive squamous metaplasia in gynecomastia.

Extensive squamous metaplasia is described in a case of gynecomastia. Numerous ducts in all sections of breast tissue revealed multiple foci of squamous metaplasia, many of which included large, papillary excrescences of keratinizing squamous cells into duct lumens, with foci of dyskeratosis. Review of four years of gynecomastia cases from our surgical pathology files revealed a total incidence of squamous metaplasia equaling six of 40 cases of gynecomastia, including the case reported here. The other five cases included only one or two small foci of squamous metaplasia. These findings demonstrate that squamous metaplasia in gynecomastia is not rare, but is usually very limited. However, an unusual case, such as that reported here, may show extensive, florid squamous metaplasia, without associated inflammation or neoplasm.

Adult↗
PubMed1985

Congenital giant axonal neuropathy.

Giant axonal neuropathy (GAN) is a distal sensorimotor neuropathy, characterized by neurofilamentous axonal swellings, with usual onset at 2 to 3 years of age. We report a case of congenital GAN with hypotonia at birth. At 7 months of age, nerve conduction studies showed almost complete lack of sensory and motor responses in the lower extremities. A sural nerve biopsy specimen disclosed absence of myelinated axons. Autopsy, following death at 15 months of age, revealed axonal swellings in peripheral nerves and distal degeneration of long spinal cord tracts. The neurofilamentous content of the axonal swellings was confirmed by Glees-Marsland staining and immunoperoxidase reaction with antibodies to neurofilaments. Axonal swellings did not stain with periodic acid-Schiff and were not seen in the cerebral cortex or brain stem, distinguishing this process from infantile neuroaxonal dystrophy. This patient illustrates congenital GAN with subsequent rapid progression.

Axons↗
PubMed1985

The morphology of carbon disulfide neurotoxicity.

The morphology of carbon disulfide induced peripheral neuropathy was studied in rats exposed to three concentrations of carbon disulfide by inhalation for 90 days. Rats exposed to 800 ppm developed neurofilamentous axonal swellings in the distal portions of long fibers, including the dorsal ascending sensory and corticospinal tracts of the spinal cord. In peripheral nerve the predominant effect was seen at the level of the posterior tibial nerve. Teased fiber preparations of the muscular branch of the posterior tibial nerve showed numerous paranodal and internodal swellings as well as Wallerian degeneration. Ultrastructurally the swellings were characterized by neurofilament accumulations, decreased numbers of microtubules and thin myelin. Other features included segregation of axoplasmic organelles and cytoskeletal components, intrusion of Schwann cell processes into the axoplasm, Schwann cells with increased cytoplasmic contents, and Schwann cell proliferation around many swollen and demyelinated axons. These features draw important parallels between the morphology of carbon disulfide neuropathy and the neurofilamentous neuropathies induced by hexacarbons and beta,beta' iminodipropionitrile (IDPN).

Animals↗
PubMed1985

Covalent crosslinking of neurofilaments in the pathogenesis of n-hexane neuropathy.

These studies test the hypothesis that in n-hexane neuropathy the gamma-diketone metabolite 2,5-hexanedione (2,5-HD) results in covalent crosslinking of neurofilaments via nucleophilic attack on oxidized pyrrole rings formed from the reaction of 2,5-HD with epsilon-amino groups of lysyl residues. The 2,5-HD analogue and gamma-diketone,3,4-dimethyl-2,5-hexanedione (DMHD), was found to result in more rapid pyrrole formation, pyrrole autoxidation, and protein crosslinking when compared with 2,5-HD. DMHD was 20-30 times more potent than 2,5-HD in producing hindlimb paralysis. Following 2,5-HD intoxication the neurofilament filled axonal swellings were found in the distal, subterminal axon. After treatment with DMHD, swellings were present in the proximal axon, similar to those seen after intoxication with beta,beta'-iminodipropionitrile (IDPN). DMHD was proposed as a connecting link between the proximal neurofilamentous axonopathy caused by IDPN and the distal neurofilamentous axonopathies from n-hexane, acrylamide, and carbon disulfide intoxication. [14C]DMHD was found to alkylate nerve protein and to result in polymers of radiolabeled protein too large to pass through nitrocellulose filters with pore sizes as large as 12 nm. An even greater proportion of radiolabeled protein was retained by nitrocellulose filters when DMHD was reacted with nerve in which SCa (slow component a of axonal transport) had been pulse-labeled with [35S] methionine. Radiolabeled nerve proteins acylated with [125I]Bolton-Hunter reagent were minimally retained by nitrocellulose filters, suggesting that filter retention reflects polymerization rather than non-specific adsorption.

Acrylamide↗
PubMed1982

Veno-occlusive disease of the liver after high-dose mitomycin C therapy and autologous bone marrow transplantation.

Twenty-nine patients with refractory malignancies underwent intensive therapy with mitomycin C (60, 75, or 90 mg/m2 IV) and autologous marrow transplantation. Six patients developed the clinical syndrome of hepatic veno-occlusive disease (VOD) characterized by progressive abnormalities in liver function, abdominal pain, and ascites 15-70 days after mitomycin C therapy. Postmortem material was available in 16 patients, including four patients who had the clinical syndrome. VOD of the central and sublobular hepatic veins was noted in these four patients. VOD was discovered incidentally at autopsy in one of 12 patients without antemortem clinical evidence of disease. Two patients with abnormalities of liver function but without ascites or right upper quadrant pain had no evidence of VOD at autopsy. Although not statistically significant, there was a greater incidence of VOD with increasing doses of mitomycin C. When bone marrow toxicity of mitomycin C was overcome by autologous bone marrow transplantation, the development of VOD appeared to be the limiting factor in dose escalation.

Adult↗
PubMed1982

Hepatic veno-occlusive disease after high-dose mitomycin C and autologous bone marrow transplantation therapy.

Three cases of veno-occlusive disease of the liver were diagnosed in four autopsied patients who had received high-dose mitomycin C therapy followed by autologous bone marrow transplantation, and the pathologic finding are reported. Review of 27 liver, examined post mortem, of patients receiving other high-dose chemotherapeutic regimens, 15 of them with subsequent autologous bone marrow transplantation, revealed no evidence of veno-occlusive disease. Veno-occlusive disease may now become a dose-limiting factor in the use of the combined high-dose mitomycin C-bone marrow transplantation therapy. Attention is also drawn to the increasing number of veno-occlusive disease cases being reported in associated with alkylating agents.

Adult↗
PubMedDate not supplied

Ultrastructure of experimental cocaine hepatotoxicity.

Cocaine is a potent hepatotoxin in mice. It is converted in the liver by a minor oxidative pathway to the active metabolite, norcocaine nitroxide. Previous studies have shown evidence of a lipid peroxidative mechanism of toxicity, including increased conjugated diene absorption by hepatic microsomal lipids following a single 60 mg per kg i.p. dose of cocaine in DBA/2Ha mice. To explore this mechanism further, morphologic changes in the livers of DBA/2Ha mice were examined following the same dose of cocaine. The first ultrastructural change seen was dilatation of rough endoplasmic reticulum in centrilobular hepatocytes 1 hr following cocaine injection, coincident with the previously observed onset of increased conjugated diene absorption in microsomal lipids. During the previously observed period of peak conjugated diene absorption (2 to 4 hr), ultrastructural changes in centrilobular hepatocytes progressed. These included focal mitochondrial membrane disruption followed by more extensive mitochondrial swelling and disruption with increased swelling of rough endoplasmic reticulum. Changes in size, shape and concentration of histochemically labeled, morphometrically studied peroxisomes were also seen during this interval. Injury of centrilobular hepatocytes advanced to cell death in 6 to 8 hr. The time course and nature of these morphologic findings correlate with previously observed evidence of lipid peroxidation, supporting the hypothesis that this is the mechanism of cocaine hepatoxicity.

Animals↗
PubMedDate not supplied

Staging of pancreatic cancer before and after neoadjuvant chemoradiation.

Neoadjuvant chemoradiation therapy is used at many institutions for treatment of localized adenocarcinoma of the pancreas. Accurate staging before neoadjuvant therapy identifies patients with distant metastatic disease, and restaging after neoadjuvant therapy selects patients for laparotomy and attempted resection. The aims of this study were to (1) determine the utility of staging laparoscopy in candidates for neoadjuvant therapy and (2) evaluate the accuracy of restaging CT following chemoradiation. Staging laparoscopy was performed in 98 patients with radiographically potentially resectable (no evidence of arterial abutment or venous occlusion) or locally advanced (arterial abutment or venous occlusion) adenocarcinoma of the pancreas. Unsuspected distant metastasis was identified in 8 (18%) of 45 patients with potentially resectable tumors and 13 (24%) of 55 patients with locally advanced tumors by CT. Neoadjuvant chemoradiation therapy and restaging CT were completed in a total of 103 patients. Thirty-three patients with potentially resectable tumors by restaging CT underwent surgical exploration and resections were performed in 27 (82%). Eleven (22%) of 49 patients with locally advanced tumors by restaging CT were resected, with negative margins in 55%; the tumors in these 11 patients had been considered locally advanced because of arterial involvement on restaging CT. Staging laparoscopy is useful for the exclusion of patients with unsuspected metastatic disease from aggressive neoadjuvant chemoradiation protocols. Following neoadjuvant chemoradiation, restaging CT guides the selection of patients for laparotomy but may overestimate unresectability to a greater extent than does prechemoradiation CT.

Adenocarcinoma↗
PubMedDate not supplied

Pathology of the liver in severe combined immunodeficiency and DiGeorge syndrome.

Review of liver biopsy or autopsy material from 33 patients with severe combined immunodeficiency or combined immunodeficiency and four patients with DiGeorge syndrome revealed a wide range of hepatic pathology. The most common abnormality was graft-versus-host disease (16 patients), followed by viral infection (4 patients had adenovirus hepatitis, 3 had cytomegalovirus hepatitis). Centrilobular fibrosis with or without veno-occlusive disease was seen in five patients. Three patients had nonspecific hepatitis, four had changes attributed to total parenteral nutrition, and two had lymphoproliferative disorders involving the liver. Both patients with lymphoproliferative disorders had received transplants. Two patients had resolving necrosis probably secondary to non-A, non-B hepatitis. One had atypical mycobacterial infection. Hemosiderosis was a common nonspecific abnormality, seen in nine patients. All patients with hepatic graft-versus-host disease had received transplants or nonirradiated blood products. Hepatic graft-versus-host disease varied in severity from hepatic necrosis with destruction of both large and small bile ducts in a transfusion-associated case to subtle damage to interlobular bile ducts. Even minimal bile duct changes correlated with the clinical impression of graft-versus-host disease in these patients. Late chronic graft-versus-host disease was not seen in any patient, although acute graft-versus-host disease sometimes occurred late after transplant.

Bone Marrow Transplantation↗
PubMedDate not supplied

Cross-species extrapolation in hydrocarbon neuropathy.

Not all species demonstrate the same vulnerability to hydrocarbon neuropathy. These differences are related to axonal length and diameter as well as to variations in toxicokinetics. While cross-species extrapolation is made difficult by these factors, understanding the basis for the differences provides insight into pathogenesis.

Animals↗