PubMed Health⌕ Search

Biomedical subjects

E Atillasoy

Publications and source records attributed to E Atillasoy.

15 recordsLinked to original sources
PubMed2001

Short-duration oral terbinafine for the treatment of tinea pedis in HIV-positive patients.

Management of tinea pedis in patients who have the human immunodeficiency virus (HIV) is problematic; in those patients, dermatophytoses may be more difficult to treat than in the general population. This prospective, open-label, multicenter, randomized study evaluated the efficacy and safety of a short course of oral terbinafine for tinea pedis in patients who are HIV positive. Twenty-seven patients were randomized to receive oral terbinafine 250 mg once daily for 2 or 4 weeks; 17 patients with positive initial cultures and follow-up cultures were evaluable for efficacy at week 8. Mycological cure (defined as negative potassium hydroxide [KOH] microscopy and culture results) occurred in 47% (8) of patients; and modified mycological cure (defined as negative follow-up cultures) occurred in 65% (11) of patients. All 27 patients were evaluated for safety. Clinical cure (defined as minimal residual signs and symptoms) occurred in 82% (14) of patients. Oral terbinafine was well tolerated, indicating that regimens of 2 or 4 weeks are safe and effective for the treatment of tinea pedis in patients who are HIV positive.

Administration, Oral↗
PubMed1999

Etiology and outcome for 295 patients with acute liver failure in the United States.

Little information is available on acute liver failure (ALF) in the United States. We gathered demographic data retrospectively for a 2-year period from July 1994 to June 1996 on all cases of ALF from 13 hospitals (12 liver transplant centers). Data on the patients included age, hepatic coma grade on admission, presumed cause, transplantation, and outcome. Among 295 patients, 74 (25%) survived spontaneously, 121 (41%) underwent transplantation, and 99 (34%) died without undergoing transplantation. Ninety-two of 121 patients (76%) survived 1 year after transplantation. Acetaminophen overdose was the most frequent cause (60 patients; 20%), followed by cryptogenic/non A non B non C (NANBNC; 15%), idiosyncratic drug reactions (12%), hepatitis B (10%), and hepatitis A (7%). Spontaneous survival rates were highest for patients with acetaminophen overdose (57%) and hepatitis A (40%) and lowest for those with Wilson's disease (no survivors of 18 patients). The transplantation rate was highest for Wilson's disease (17 of 18 patients; 94%) and lowest for autoimmune hepatitis (29%) and acetaminophen overdose (12%). Age did not differ between survivors and nonsurvivors, perhaps reflecting a selection bias for patients transferred to liver transplant centers. Coma grade on admission was not a significant determinant of outcome, but showed a trend toward affecting both survival and transplantation rate. These findings on retrospectively studied patients from the United States differ from those previously gathered in the United Kingdom and France, highlighting the need for further study of trends in each country.

Acetaminophen↗
PubMed1998

Ultraviolet B-induced squamous epithelial and melanocytic cell changes in a xenograft model of cancer development in human skin.

We previously demonstrated that precancers (actinic keratoses and dysplasias) and squamous cell carcinomas (SCCs) develop in one quarter of human neonatal foreskins grafted onto recombinase-activating gene-1-knockout mice treated once with 7,12-dimethylbenz[a]anthracene (DMBA) followed by chronic intermediate-range ultraviolet (UV) B light irradiation. The goals of this study were to determine if a longer UVB exposure followed by further observation would increase the number of precancers and invasive cancers and to evaluate whether this model results in changes in p53 expression and cell proliferation similar to those seen in sun-damaged normal skin, actinic keratoses, and SCCs. The treatment consisted of a single dose of DMBA followed by 500 J/m2 UVB radiation administered three times weekly for at least 5 mo. Histologic changes (cysts, hyperplasias, precancers, and/or invasive cancers) were seen in 24 of 25 treated xenografts but not in controls. Ten of 25 grafts (40%) had two or more histological changes, and two human SCCs developed. After seven or more months of UV exposure and a total time from DMBA treatment to killing of 12-18 mo, 83% (15 of 18) of specimens developed squamous precancer or SCC of human origin, and 44% (eight of 18) developed melanocytic hyperplasia or melanoma. The change from moderate dysplasias to SCC required longer UV exposure (median, 11 mo), and 5 mo more observation than did the development of mild dysplasias (median UV exposure, 7 mo; median DMBA to death time, 12 mo). There was a direct correlation between both p53 expression and cell proliferation and the degree of histologic alteration both in squamous epithelial and melanocytic cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Fatal fungemia resulting from an infected transjugular intrahepatic portosystemic shunt stent.

Placement of a transjugular intrahepatic portosystemic shunt is a well accepted treatment in the management of gastroesophageal variceal bleeding. Although morbidity and mortality associated with the use of transjugular intrahepatic portosystemic shunts have dramatically decreased, complications still occur. We report a case of fatal fungemia resulting from an infected transjugular intrahepatic portosystemic shunt stent.

Aged↗
PubMed1996

Effects of acarbose on fecal nutrients, colonic pH, and short-chain fatty acids and rectal proliferative indices.

Acarbose, an alpha-glycosidase inhibitor, treats diabetes mellitus by delaying the digestion and intestinal absorption of dietary carbohydrates. In effective doses, acarbose induces some passage of carbohydrates into the colon. The effect of such chronic carbohydrate transfer on colonic structure and function is unknown. We studied the effects of 1 year of acarbose administration in diabetes mellitus on fecal energy, protein, and fat, including short-chain fatty acids (SCFA) output, fecal pH, and several metabolizing bacterial species. Changes in colonic histology and epithelial cell proliferation were investigated in rectal biopsies. Fecal macronutrient output was unaffected by acarbose, but pH decreased and total SCFA, butyrate, and acetate output were markedly greater. Breath hydrogen output increased after acarbose, but digoxin-metabolizing bacteria and diacylglycerol (DAG) production were unaltered. Compared with the control, acarbose did not induce hyperplasia or change rectal proliferation. However, total fecal SCFA and butyrate output correlated inversely with proliferation in the rectal upper crypt-a biomarker of risk for colonic neoplasia. In conclusion, long-term acarbose administration does not adversely affect colonic function or fecal nutrient output. If increased fecal SCFA and butyrate reduces upper-crypt proliferation, then acarbose may reduce the risk of colonic neoplasia.

Acarbose↗
PubMed1996

Recurrent toxin-mediated perineal erythema.

BACKGROUND: Important new diseases due to bacterial toxins functioning as superantigens have been described with increasing frequency within recent years. Toxic shock syndrome, recalcitrant erythematous desquamating disorder, streptococcal toxic shock-like syndrome, and, most recently, mucocutaneous lymph node syndrome (Kawasaki disease) have been etiologically linked with certain staphylococcal and streptococcal toxins. We describe two patients with a novel clinical presentation of toxin-mediated disease, which shares certain clinical features with mucocutaneous lymph node syndrome. OBSERVATIONS: Two otherwise healthy young male adults developed recurrent erysipelaslike perineal erythema, which regularly erupted within 1 to 2 days of the onset of acute pharyngitis. Accompanying signs included mucosal changes and acral erythema with desquamation. Throat cultures obtained during the acute episodes yielded toxin-producing Staphylococcus aureus from one patient and toxin-producing Streptococcus pyogenes from the other. CONCLUSION: The recurrent nature, age predilection, and clinical presentation suggest that our patients display a unique clinical syndrome due to toxin-producing bacteria.

Adolescent↗
PubMed1996

Identification of bipotential progenitor cells in human liver regeneration.

Recent studies, including our own, suggest that intermediate filament proteins, particularly bile duct-specific cytokeratin 19 (CK19) and the hepatocyte-specific HepPar1 antigen define the developmental stages of hepatic progenitor cells during liver morphogenesis. We hypothesized that the HepPar1+ CK19+ progenitor cells are activated during human liver regeneration after massive hepatic necrosis and proliferate with the formation of so-called ductular hepatocytes or neocholangioles. We demonstrated previously that the ductular hepatocytes proliferate and share phenotypic characteristics with hepatocytes and biliary epithelial cells. In this investigation, we compared the expression pattern of intermediate filament proteins and HepPar1 antigen in ductular hepatocytes with that of bipotential hepatic progenitor cells. CK14, CK19, vimentin, and HepPar1 antigen were localized by immunoperoxidase staining in 13 human livers with regeneration after massive hepatic necrosis. Double immunostaining of three cases for CK14/CK19 and HepPar1/CK19 was also performed. CK19 reaction exhibited diffuse staining of the cytoplasm of many ductular hepatocytes and bile ducts in all cases. CK14 was expressed in the cytoplasm of ductular hepatocytes and few bile ducts in 5 of 12 specimens. HepPar1 staining was positive in many ductular hepatocytes in 11 of 13 cases. Vimentin was detected in the perinuclear cytoplasm of ductular hepatocytes and some bile duct epithelial cells in all regenerating livers. Double immunostaining for HepPar1/CK19 demonstrated that the ductular hepatocytes contained either HepPar1 or CK19 and that some ductular hepatocytes coexpressed both antigens. CK14, CK19, vimentin, and HepPar1 expression in ductular hepatocytes in human liver regeneration resembles the pattern seen in the developing human liver from 4 to 16 weeks' gestation. This suggests that the ductular hepatocytes recapitulate the developmental stages of bipotential liver progenitor cells and differentiate in steps marked by the acquisition or loss of specific phenotypic characteristics.

Adolescent↗
PubMed1995

Fulminant hepatic failure: pathophysiology, treatment, and survival.

Fulminant hepatic failure is characterized by severe metabolic derangements, neurologic complications and, ultimately, multiorgan failure. In the past three decades, improved intensive care has increased mean survival from 15% to 50% in certain patient groups by providing metabolic support and management of specific, frequent, and potentially fatal complications. However, outcome remains highly dependent on etiology. While intensive care is sufficient therapy in some patients (Group I), those with irreparable hepatic damage (Group III) can only survive if transplanted. In intermediate cases (Group II), the liver retains the potential to regenerate if the patient receives hepatic functional support. Major areas of current research in this field include development of hepatic support devices, strategies to accelerate and maximize hepatic regeneration, and criteria for accurate prognostic classification of patients.

Cause of Death↗
PubMed1993

Gastrointestinal proliferation and aging.

The gastrointestinal tract represents an organ system that is characterized by rapid proliferation and by cells that demonstrate differentiation from immature stem cells to terminal differentiated mature cells. Aging gastrointestinal tissues illustrate markedly different phenomena from aged post-mitotic cells. Contrary to generally held prejudices, a state of hyperproliferation, not hypoproliferation, occurs in the epithelial cells of the stomach, the small intestine, and the large intestine of stable-fed, aged rodents when compared to young mature rodents. Furthermore, abnormalities of proliferative and differentiation responses become evident when gastrointestinal tissues are stimulated by injury, or by starvation and refeeding. We speculate that such changes in proliferation and differentiation expose aging gastrointestinal epithelial cells to genotoxic effects that may increase the susceptibility to gastrointestinal cancers.

Aging↗
PubMed1988

Hydroxydesipramine in the elderly.

Elevation of the hydroxy metabolites of the tricyclic antidepressants in the elderly has been demonstrated for nortriptyline and suggested for desipramine by a study reporting elevated hydroxydesipramine (OH-DMI) plasma levels in four older patients. In the current study, patients treated with desipramine (DMI) were studied to determine whether OH-DMI was elevated in two larger samples of depressed elderly patients and to determine the magnitude of the increase, if present. In Sample I, which consisted of 68 patients of whom 23 were over 60 years of age, a fixed target dose of DMI was employed. Sample II, in which 20 of the 56 patients were over 60, received a dose adjusted to attain a fixed target DMI blood level. OH-DMI levels were higher in patients over 60 than in younger patients but the differences were not significant in either sample individually. In the two samples combined, average OH-DMI levels were 11 ng/ml higher in patients over 60 and the difference was significant (t = 2.30, p = 0.02). If variations in dose are accounted for, OH-DMI concentrations are positively correlated with age in both samples. OH-DMI/DMI ratios were not higher in the patients over 60 in these samples, but OH-DMI/DMI ratios may be higher in patients on lower doses with low DMI levels, as is common in the treatment of elderly patients. If comparable dosage is administered, nonlinear increases in DMI levels result in lower OH-DMI/DMI ratios similar to those in younger patients. Although our findings of elevated hydroxy levels in the elderly are consistent with prior reports, the clinical importance of an 11 ng/ml difference, particularly in relation to total drug levels averaging 220 ng/ml, is questioned.

Administration, Oral↗
PubMedDate not supplied

Abnormal cell proliferation and p52/p35-CSK expression in the colons of aging rats.

In rodents and in humans, aging is associated with increased gastrointestinal epithelial cell proliferation and an expanded crypt proliferative compartment similar to that seen in the preneoplastic bowel. We have compared the distribution of a series of cytoskeletal antigens that are modified when colonic cancer cells differentiate in vitro in the colon of young (4-7 month) and aging (22-26 month) Fischer 344 rats. Two such proteins, p52 and p35, (that are increased in cultured senescent cells) differ in their position in the crypt axis and subcellular localization between young and aging rats. In young rats, immunoreactive p52 protein is present solely near the colonic crypt surface epithelium but in aging rats p52 expressing cells are found deeper in crypts. The intracellular localization of p35 also differs markedly in young and aging animals. The distribution of these proteins appears to be a reproducible biomarker of aging. Antigenic changes similar to those observed in aging colons also are seen in crypt cells of patients with ulcerative colitis and in the flat colonic mucosa of patients with adenomatous polyps and colon cancer. The combination of proliferative and differentiation changes suggest that the flat mucosa of the colon of aging rats has preneoplastic features.

Aging↗
PubMedDate not supplied

Selective decontamination of the digestive tract helps prevent bacterial infections in the early postoperative period after liver transplant.

UNLABELLED: In liver transplant (LTx) recipients, gut-associated bacterial and fungal organisms produce significant postoperative morbidity and mortality. We sought to assess the role of selective digestive decontamination (SDD) in preventing postoperative infections in a large single-center cohort of liver recipients transplanted under two non-simultaneous protocols. In 212 consecutive patients transplanted between 1/1/91 and 7/31/92, SDD (gentamicin 80 mg, polymyxin B 100 mg, nystatin suspension 10 mL) was employed, starting after induction of anesthesia and continued until POD 21 (SDD Group). In 157 consecutive patients transplanted between 1/1/93 and 12/31/93, SDD was not used (non-SDD Group). Both groups received IV vancomycin and cefotaxime prophylaxis. All culture-positive infections within the first 30 days post-LTx were recorded and classified as bacterial or fungal. Infection-related mortality (patients who died of infectious complications without any technical complication) was recorded. Groups did not differ in patient demographics, United Network for Organ Sharing (UNOS) status, use of veno-venous bypass, total/warm ischemia, or length of ICU stay. Infections developed in fewer SDD patients (56/212; 26%) than non-SDD patients (69/157; 44%) (p<0.001). The incidence of gram-negative infection was less in the SDD group (11% vs. 26%, p<0. 001) as was gram-positive infection (16% vs. 26%, p<0.001). Among patients who developed infection, there was no difference between groups in infections per patient. Primary graft non-function (PNF) developed in 20 SDD patients (7/20 had infections) and 8 non-SDD patients (6/8 had infections) (p=0.06). There were no differences in incidence of fungal infections or of infection-related mortality between groups. In the SDD group, there were fewer abdominal (p<0. 001), lung (p<0.001), wound (p<0.01), and urinary tract infections (p<0.05). CONCLUSION: Use of SDD in liver recipients early after transplant was associated with significantly fewer infections in the early postoperative period.

Adolescent↗
PubMedDate not supplied

Fecal diacylglycerol concentrations and calcium supplementation.

Growth factors are known to stimulate colonic proliferation via activation of protein kinase C by production of diacylglycerol (DAG) from membrane phosphatidyl inositol. Previous studies from our laboratories have shown that fecal bacteria can produce and metabolize DAG and that DAG can be absorbed by colonocytes, and thus might contribute to neoplasia. Calcium is a putative chemopreventive agent, and we have shown that calcium administration reduces fecal DAG concentrations, as well as rectal proliferation in patients after jejuno-ileal bypass surgery. The present study in normal volunteers eating self-selected diets demonstrates that fecal DAG concentrations are very constant with a coefficient of variation from 6.7 to 10.2%. Calcium administration showed a trend to reduce fecal DAG by 11% (P < 0.08). We conclude that fecal DAG levels can be determined in individuals on a self-selected diet from a single stool determination. If the trend to reduce fecal DAG by calcium is verified in more extensive studies, then the effects of calcium used in chemopreventive might, in part, reflect changes in the luminal lipid content.

Calcium, Dietary↗