Biomedical subjects

M N Ehrinpreis

Publications and source records attributed to M N Ehrinpreis.

11 recordsLinked to original sources

PubMed1992

Taurine deficiency after intensive chemotherapy and/or radiation.

Taurine, a nonessential amino acid (AA), is the most abundant free AA in the intracellular space. We measured plasma AA concentrations in 36 patients 7-28 d after intensive chemotherapy and/or radiation. Plasma taurine concentrations were uniformly low in all patients (20.0 +/- 6.4 mumol/L, mean +/- SD). Plasma taurine in 11 healthy volunteer control subjects was 45.0 +/- 20.3 mumol/L (P less than 0.001). Other AA concentrations, specifically those of precursor AAs methionine and cystine, were normal. We prospectively measured plasma AA concentrations in 12 patients before starting and 6-10 d after completing intensive cytotoxic treatment. Values before treatment were 37.2 +/- 11.6, 109.6 +/- 30.7, and 18.5 +/- 4.8 for taurine, cystine, and methionine, respectively, and were 24.3 +/- 6.0, 111.2 +/- 23.8, and 24.0 +/- 14.5 after treatment. Pretreatment plasma taurine correlated directly with the magnitude of decrease in plasma taurine during cytotoxic treatment (n = 12, r = 0.85, P less than 0.01). Intensive cytotoxic chemotherapy and/or radiation leads to a reduction in plasma taurine concentrations without any change in its precursor AAs, methionine and cystine. The clinical relevance of plasma taurine depletion will need further study.

Adolescent↗

PubMed1990

Candida-associated diarrhea in hospitalized patients.

Ten hospitalized patients with severe diarrhea associated with intestinal Candida overgrowth are reported. Candida-associated diarrhea is predominantly of the secretory type, characterized by frequent watery stools, usually without blood, mucus, tenesmus, or abdominal pain. The patients were elderly, malnourished, and critically ill, or suffered from chronic debilitating illness. Their hospital stays were prolonged, and the majority were being treated with multiple antibiotics or chemotherapeutic agents. Diarrhea often led to dehydration, prerenal azotemia, hyperchloremic metabolic acidosis, and electrolyte imbalance. Stool culture most frequently isolated Cand. albicans in association with decreased normal flora. Colonoscopy showed no evidence of colitis. Diagnosis was made based on the absence of diarrhea-producing medications, the continuation of diarrhea despite fasting, the exclusion of other infections, inflammatory conditions and other causes of secretory diarrhea, and a dramatic response to a short course of nystatin.

Aged↗

PubMed1990

Increased colonic mucosal angiotensin I and II concentrations in Crohn's colitis.

To define a potential role for the angiotensin system in Crohn's colitis, the colonic mucosal levels of angiotensin I and II were measured in endoscopic biopsy samples from patients with active Crohn's colitis (n = 20), ulcerative colitis (n = 13), other forms of colitis (n = 3), and normal controls (n = 17). Colonic mucosal levels of angiotensin I and II were greater in patients with Crohn's colitis than in normal subjects (p less than 0.001 and p less than 0.001, respectively). Mucosal levels of angiotensin I and II were also higher in Crohn's colitis than in ulcerative colitis (p less than 0.001 and p less than 0.001, respectively), and levels of angiotensin II were higher in Crohn's than in other forms of colitis (p = 0.014). Mucosal levels of angiotensin I and II correlated well with the degree of macroscopic inflammation in Crohn's colitis (r = 0.86, p less than 0.001 and r = 0.68, p less than 0.001, respectively). Mucosal levels of angiotensin I correlated fairly well with the Crohn's Disease Activity Index (r = 0.46, p less than 0.05) while angiotensin II levels correlated poorly. These studies suggest that angiotensin I and II may have a role in the inflammation associated with Crohn's colitis.

Angiotensin I↗

PubMed1989

Cimetidine-induced galactorrhea.

Various breast abnormalities have been described in patients treated chronically with cimetidine, but galactorrhea has been reported only twice in the medical literature. In both cases, there appeared to be an associated hyperprolactinemia. These problems could well represent a consequence of histamine2-receptor blockade. We report here a female patient with hepatic cirrhosis and portal hypertension who developed hyperprolactinemia and galactorrhea while on long-term cimetidine therapy. Both the hyperprolactinemia and the galactorrhea disappeared when the patient was switched to ranitidine, an alternative H2-receptor blocker. A review of the previous case reports and relevant literature is included.

Cimetidine↗

PubMed1988

Ornithine decarboxylase as a marker for colorectal polyps and cancer.

There is as yet no specific chromosomal abnormality or gene marker identified for colorectal polyps and cancer. Thus available markers include only phenotypic markers. Tumor markers that have been studied include tetraploidy and increased colonic mucosal proliferation; and these markers have identified those patients that are at high risk for colon cancer. The current "gold standard" of colorectal cancer markers is the carcinoembryonic antigen (CEA). CEA is best used as a monitor of disease and recurrence, and not as a screening or diagnostic test. Newer carbohydrate markers include CA 19-9, incompatible A and B antigens, and T and Lewis antigens. These markers have not shown increased specificity or sensitivity compared to CEA. An interesting recently described marker is ornithine decarboxylase (ODC), which serves as a simple overall index of colonic mucosal proliferation. Ornithine decarboxylase levels have shown correlation with the progression from normal mucosa to adenoma and carcinoma, especially in hereditary polyposis syndromes. This enzyme may also serve as a potential therapeutic target. Many markers have been found useless in further clinical trials. Ornithine decarboxylase needs to be studied in greater detail to determine its sensitivity and specificity, in patients with hereditary colonic neoplasia and in patients without genetic syndromes.

Biomarkers, Tumor↗

PubMed1988

Clinical features, evaluation, and detection of colorectal cancer.

The most common presentation of colorectal carcinoma is in the symptomatic patient, most often with complaints of rectal bleeding, abdominal pain, or change in bowel habits. Symptomatic patients often have advanced disease and, because surgical resection is the only effective therapy at present, their chance for cure is poor. Until effective treatment is available, therefore, we must identify patients at high risk for lifelong screening. In addition, more effective means of surveillance of the general population need to be developed in order to diagnose patients at risk for sporadic colorectal cancer, given that this represents the majority of patients with disease. Tumor markers also would be useful to find residual disease while it is still resectable in patients who have undergone surgery for curative resection.

Colorectal Neoplasms↗

PubMed1988

Management of the malignant polyp.

Colonoscopy and endoscopic polypectomy are being utilized more frequently these days with the increased emphasis on the prevention, early detection, and treatment of colon cancer. Consequently, the problem of managing the malignant polyp is likely to be more frequently encountered. Many attempts have been made to clarify the management principles involved. Although the studies conducted have been imperfect in their design, the variety of information obtained from these studies is making the picture clearer. A more conservative approach is evolving. Many malignant polyps may be managed by endoscopic polypectomy alone. The criteria for which patients are to be managed in this fashion seem to be relatively simple ones, though technical problems with polypectomy performance and histologic evaluation are still frequently encountered. More carefully designed long-term studies are needed to create firm guidelines for the management of malignant polyps. Should screening and surveillance result in the discovery of earlier and more readily treatable forms of invasive colon cancer, endoscopic polypectomy will most certainly be a cornerstone of their treatment.

Adenocarcinoma↗

PubMed1988

Colonoscopic polypectomy.

Since the advent of fiberoptic endoscopy and the introduction of colonoscopic polypectomy, a simple and cost-effective procedure has been available to deal with an exceedingly common problem, the colonic polyp. Although polyps in the gastrointestinal tract have a varied natural history, there is strong evidence that adenomatous colonic polyps have a potential for malignant degeneration and that virtually all colorectal cancers arise from adenomatous polyps. This article will review some basic features of the endoscopic approaches and problems associated with polypectomy.

Colonic Polyps↗

PubMed1987

Gold induced ulcerative proctitis: report and review of the literature.

A case of ulcerative proctitis complicating chrysotherapy for rheumatoid arthritis and a literature review of gold induced enterocolitis is presented. Only 26 patients have been reported with this complication. No specific therapy is available, except supportive measures and cessation of gold therapy.

Arthritis, Rheumatoid↗

PubMed1984

Genetics of carbon tetrachloride-induced liver injury in mice. II. Multigenic regulation.

Mice from many different congenic inbred strains were given an intramuscular injection of carbon tetrachloride (CCl4) in olive oil to determine the genetic influences on induction of, and recovery from, liver damage. Liver and blood samples were taken at days 1, 4 and 7. The degree of necrosis and lymphoid infiltration appeared to be controlled, qualitatively and quantitatively, by both H-2-linked and Ah-linked genes. Strain differences were noted in the patterns of hepatocellular necrosis and the proportions of lymphoid, monocytic and other inflammatory cells which characterized the infiltrating population. Kinetic studies of F1 hybrids from matings between the susceptible BALB/cJ male parent and the resistant SJL/J female parent suggested that two dominant genetic influences play a major role in CCl4-induced liver damage. The gene contributed from the BALB/cJ parent affects the extent of liver necrosis and a second gene from SJL/J augments recovery. These results suggest, therefore, that the CCl4-induced liver damage and subsequent recovery are under multigenic control by H-2, Ah and possibly other genes.

Animals↗

PubMed1981

Effect of SQ 14225, an inhibitor of angiotensin I-converting enzyme, on the granulomatous response to Schistosoma mansoni eggs in mice.

Murine schistosomiasis is a granulomatous disease associated with high serum and granuloma angiotensin I-converting enzyme (ACE) activity. SQ 14225, a specific competitive inhibitor of ACE, was administered to normal mice and mice infected with Schistosoma mansoni to determine whether this compound could inhibit granuloma ACE activity and modify the size of the granulomatous response to schistosome eggs. Peroral administration of SQ 14225 for 5 wk to infected mice with peak granulomatous responses decreased ACE activity in isolated liver granulomas. Treated mice demonstrated a decrease in granuloma size in the liver, colon, and ileum, and hydroxyproline concentration of isolated liver granulomas was increased. Mean diameters of synchronous pulmonary granulomas, induced by the pulmonary embolization of schistosome eggs into normal and sensitized mice, were decreased by a similar dose of SQ 14225. Withdrawal of SQ 14225 from unsensitized mice with 2-wk-old synchronous pulmonary granulomas induced an increase in inflammation. Infected, but not normal mice receiving SQ 14225 demonstrated reduced portal pressure, liver weight, and body weight. Both normal and infected mice experienced dipsogenesis, expanded intravascular volume, and increased serum ACE. These observations suggest that SQ 14225 can partially inhibit the granulomatous response to schistosome eggs and the pathological manifestations of schistosomiasis. It is possible that ACE has an inflammatory role in granulomatous inflammation.

Angiotensin-Converting Enzyme Inhibitors↗