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Biomedical subjects

K Hohloch

Publications and source records attributed to K Hohloch.

8 recordsLinked to original sources
PubMed2004

Combination chemotherapy with gemcitabine plus oxaliplatin in patients with intensively pretreated or refractory germ cell cancer: a study of the German Testicular Cancer Study Group.

PURPOSE: Long-term survival is rarely achieved in patients with cisplatin-refractory germ cell cancer (GCT). Both single-agent gemcitabine and oxaliplatin have shown activity in patients who experience relapse or are refractory to cisplatin treatment. This study investigates the activity of a gemcitabine plus oxaliplatin regimen in these patients. PATIENTS AND METHODS: Gemcitabine was administered at a dose of 1,000 mg/m(2) on days 1 and 8; oxaliplatin was administered at a dose of 130 mg/m(2) on day 1. Response was evaluated every 4 weeks. RESULTS: Thirty-five patients with a median age of 37 years (range, 21 to 54 years) were enrolled onto the study. Primary tumor localization was gonadal, retroperitoneal, or mediastinal in 30, one, and four patients, respectively. Patients had been pretreated with a median of six platinum-containing cycles (range, four to 13 cycles) and 89% of patients previously had experienced treatment failure after high-dose chemotherapy with peripheral-blood stem-cell transplantation. Sixty-three percent of patients were considered absolutely cisplatin-refractory or cisplatin-refractory. A median of two cycles (range, 1 to 6 cycles) per patient were applied. Toxicity consisted mainly of myelosuppression, with Common Toxicity Criteria grade 3 occurring in 54% of patients. Only 9% of patients developed neutropenic fever. Three patients attained a complete remission (CR), two patients attained a marker-negative partial remission, and 11 patients attained a marker-positive partial remission, resulting in an overall response rate of 46% (95% CI, 30% to 64%). All three patients with CR and one patient with a marker-negative partial remission remained disease free at 16+, 12+, 4+, and 2+ months of follow-up. Seven (44%) of these 16 responses, including one CR, occurred in cisplatin-refractory patients. CONCLUSION: Gemcitabine plus oxaliplatin demonstrates antitumor activity with acceptable toxicity in heavily pretreated patients with relapsed or cisplatin-refractory GCT, and may offer a chance of long-term survival for selected patients.

Adult↗
PubMed2002

Lichen planus with oesophageal involvement. A case report and review of the literature.

BACKGROUND: Lichen planus is a common mucocutaneous disease of unknown aetiology. Oral disease affecting the mouth and the pharynx occurs in 30-70% of the cases. Oesophageal disease is considered to be extremely rare. The diagnosis of oesophageal involvement is often not made until complications occur. CASE REPORT: A 56-year-old woman with oral and genital erosive lichen planus for more than 4 years complained of odynophagia and dysphagia. Episodes of oesophageal bolus obstruction started 2 months earlier. Upper endoscopy revealed a high-grade concentric stenosis at 21-24 cm from the incisors. Biopsy specimens taken after bougienage showed a squamous epithelium with dense leukocyte infiltration and Civatte bodies. The bougienage led to complete relief, but due to recurrent symptomatic stenosis, endoscopic dilatation had to be performed another four times within 5 years of follow-up. Immunosuppressive therapy with systemic and local steroid application did not prevent recurrent stenosis. CONCLUSIONS: Patients with lichen planus should be evaluated for gastrointestinal symptoms because oesophageal involvement is a rare but severe complication leading to inflammatory stenosis. The benefit of immunosuppressive therapy in the prevention of recurrent stenosis is not established. A review of all reported cases is done with particular regard to therapy.

Dilatation↗
PubMed1999

Rapid mucosal CD4(+) T-cell depletion and enteropathy in simian immunodeficiency virus-infected rhesus macaques.

BACKGROUND & AIMS: Human immunodeficiency virus (HIV) infection leads to severe immunologic and functional disturbances in the intestinal tract in late stages of the disease. Information on mucosal pathology directly after infection is limited. We characterized this early phase in rhesus macaques infected with simian immunodeficiency virus (SIV). METHODS: Eight rhesus macaques were infected with SIV. Upper endoscopy was performed at defined times before and after infection. Viral load, percentage of CD4(+) T cells, villus height, crypt depth, and Ki-67-positive crypt cells were analyzed in duodenal biopsy specimens. Serum beta-carotene and vitamin D levels were assessed. RESULTS: A rapid increase of duodenal SIV core protein (p27) concentration and an almost complete loss of intestinal CD4(+) T cells was found within 2 weeks after infection. A decrease of villus height was observed, and the percentage of Ki-67-positive (proliferating) crypt cells increased. Serum concentrations of vitamin D decreased in 6 of 8 animals, and beta-carotene concentrations decreased in 3 of 8 animals after infection. CONCLUSIONS: Mucosal SIV replication and intestinal CD4(+) T cell depletion are early events in SIV-infected rhesus macaques. The structural changes of the mucosa strongly support the concept of HIV/SIV-induced enteropathy. In contrast to late-stage human HIV infection, early small intestinal villous atrophy in SIV infection is associated with crypt hyperplasia.

Animals↗
PubMed1998

HIV/SIV enteropathy.

Evidence is increasing that HIV/SIV-induced changes in the highly differentiated gut-associated immune system play a central role in the pathogenesis of gastrointestinal manifestations in HIV/SIV infection. It has been shown in both humans infected with HIV and in nonhuman primates infected with SIV that a rapid, very early, and more pronounced loss of CD4+ T-cells occurs in the mucosa in comparison to the peripheral blood. The loss of this important regulatory T-cell subset might explain mucosal immunodeficiency with the consequence of opportunistic mucosal infections. In addition, there is evidence that small intestinal damage occurs independently of secondary infections (HIV/SIV enteropathy). In late-stage human disease, HIV enteropathy is characterized by villous atrophy with hyporegeneration and dysmaturation of intestinal epithelial cells. In SIV infection of macaques, villous atrophy is a very early event; however, it is accompanied by crypt cell hyperproliferation. Early- and late-stage enteropathy in immunodeficiency virus infection may represent two types of immunologically mediated mucosal transformation in which the number and state of activation of regulatory T cells determine whether hypo- or hyperproliferative villous atrophy occurs.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Iron release from transferrin by pyoverdin and elastase from Pseudomonas aeruginosa.

Pseudomonas aeruginosa produces the siderophores pyoverdin and pyochelin as well as receptors for siderophores in response to iron deprivation. Previously, it has been shown in vitro that at neutral pH purified pyoverdin acquires iron from transferrin only in the presence of P. aeruginosa elastase (LasB), which proteolytically degrades transferrin. We constructed a LasB-negative mutant, PAO1E, by insertional mutagenesis to investigate whether this mutant differs in growth from the parental strain PAO1 in an iron-depleted medium supplemented with transferrin or human serum. PAO1 and PAO1E did not differ in growth with 1.25 microM Fe2-transferrin as the only iron source. Urea gel electrophoresis indicated iron release from intact transferrin during the logarithmic growth phase of PAO1 and PAO1E. A total of 333 microM LasB was synthesized from PAO1 after onset of stationary-phase growth. Quantification of pyoverdin by spectroscopy revealed that up to 900 microM pyroverdin was produced during growth of the strains in medium supplemented with Fe2-transferrin or 10% human serum. Incubation of Fe2-transferrin and purified pyoverdin in concentrations similar to those found in the culture supernatant resulted in release iron from transferrin after 10 h at 37 degrees C. However, LasB significantly enhanced the rate constant for iron acquisition of pyoverdin from transferrin. We conclude that P. aeruginosa can use transferrin as an iron source without further need of LasB or pH changes. This is further supported by experiments with P. aeruginosa K437, which has a defective iron uptake system, and its LasB-negative mutant, K437E. Though K437 and K437E did not differ in growth with Fe2-transferrin as the only iron source, their growth was significantly reduced relative to that of PAO1 and PAO1E.

Bacterial Proteins↗