Abnormal serum lipid levels in subjects with gastric xanthoma.
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Biomedical subjects
Publications and source records attributed to F Y Chang.
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The serodiagnosis of tuberculosis (TB) by using an enzyme-linked immunosorbent assay (ELISA) to detect IgG against mycobacterial antigen 60 (A60) was evaluated. Forty-three controls (10 healthy adults, 19 patients with non-tuberculous pulmonary diseases and 14 patients with non-pulmonary infectious diseases) and 63 patients with TB in different disease activity (50 patients with active TB and 13 patients with old pulmonary TB) were studied. When a cut-off value of 200 units was selected, the results obtained with controls were: 100% negative in IgG titers in healthy adults and patients with non-pulmonary infectious diseases, 89% negative in IgG titers in patients with non-tuberculous pulmonary diseases. The overall "false positive" rate was 5% in the control groups. The percentage of serologically positive cases of active TB was: 82% in smear-positive, 67% in smear-negative/culture-positive and 38% in culture-negative. Of the 13 patients with calcified pulmonary TB, four had a positive serological response (31%). Four out of eight patients with active TB showed an elevation in IgG titer 1 to 3 months after diagnosis and anti-TB chemotherapy. The positive and negative predictive values of the test may provide valuable information according to the prevalence of TB in different populations. When the TB prevalence is high, a positive IgG ELISA test may support the diagnosis of active TB.
To evaluate the clinical aspects of gram-negative bacillary meningitis (GNBM), we reviewed 41 adult patients with bacteriologically proven gram-negative bacillary meningitis, seen from 1985 to 1990. Thirty-two patients had post-neurosurgical GNBM and nine patients had spontaneous GNBM. Spontaneous GNBM appeared to have a sudden onset, a relatively fulminant course, and was caused most often by Escherichia coli. Post-neurosurgical GNBM, however, had a more insidious onset, a more protracted course, and was more often caused by nosocomial organisms which were resistant to multiple antibiotics. The overall mortality was 39%. Patients treated with combined aminoglycoside therapy had a lower mortality rate than those treated with intravenous aminoglycoside (17% vs 48%). The use of third-generation cephalosporins has made a significant therapeutic advance in the treatment of GNBM, with a lower mortality of 21%. We recommend treatment of GNBM with third-generation cephalosporins and aminoglycosides. If aminoglycosides are to be employed, it is suggested that they be administered both intravenously and directly into the central nervous system.
We report on a 25-year-old man who had scrub typhus with the unusual complication of acute renal failure. The clinical features of fever, headache, high Weil-Felix OX-K agglutination and Rickettsia tsutsugamushi immunofluorescence titers confirmed the diagnosis of scrub typhus. Acute renal failure was proven by oliguria, urinary diagnostic indices and renal biopsy. The patient had a complete recovery after adequate medical treatment.
Vibrio parahemolyticus is a halophilic marine vibrio commonly associated with outbreaks of acute gastroenteritis which also sometimes causes serious wound infection. It is an uncommon cause of septicemia. A few reports suggest that patients with chronic liver disease and leukemia are more susceptible. A case of liver cirrhosis with septicemia caused by this organism is discussed. The patient's condition rapidly deteriorated, and he died 12 hours after admission.
Serum pepsinogen I (PGI) levels were measured in 231 duodenal ulcer (DU) patients and 100 sex- and age-comparable healthy controls. Significantly higher mean serum PGI levels were found in DU patients than in controls (124.7 +/- 3.4 ng/ml v. 92.9 +/- 2.3 ng/ml; P < 0.001) (mean +/- SE). These levels were higher in male DU patients than in female DU patients (128.5 +/- 3.9 ng/ml v. 107.4 +/- 6.4 ng/ml; P < 0.05). Smoking was associated with elevated serum PGI levels in DU patients (145.3 +/- 5.1 ng/ml v. 109.0 +/- 4.2 ng/ml; P < 0.001). Healed DUs were associated with lower mean serum PGI levels than active ulcers (110.9 +/- 7.6 ng/ml v. 129.4 +/- 3.8 ng/ml, P < 0.05). Whether patients were positive or negative for Helicobacter pylori, infection did not affect mean serum PGI levels. All the risk factors for DU may not affect serum PGI levels and DU may therefore be considered a multifactorial disease.
Endoscopic experience in patients with acquired immunodeficiency syndrome (AIDS) has rarely been reported in Taiwan. We present our experience in 9 AIDS patients (8 male and 1 female, age from 26 to 63 years) with 12 examinations. The risk factor of these patients were bisexual in 3, homosexual in 2, hemophilia in 1, drug abuse in 1, and paid-sex in 2. Odynophagia or dysphagia was the major complaints. Oral ulcers or/and thrush were noted in 8 patients. Endoscopic findings included negative (6/12), candidiasis (3/12), erosions (1/12), ulcers (1/12) and ulcer scar (1/12) in esophagus; negative (8/12), gastritis (1/12), erosions (1/12), ulcers (1/12) and Kaposi's sarcoma (1/12) in stomach; and negative (11/12) and duodenitis (1/12) in duodenum. Patients with esophageal candidiasis always had oral thrush. Dysphagia was highly correlated with positive endoscopic findings in esophagus. It is important for an endoscopist to identify clinical symptoms and to examine patient's oral cavity before an endoscopic examination. The endoscopist must keep himself from being infected by exposure to contaminated blood and secretion and avoid dissemination of this horrible disease by undisinfected instruments.
To examine the relation between gastric ulcer (GU) location and serum pepsinogen I (PGI) level, we measured this marker in 284 endoscopically proved GU patients. Their ulcer locations were further divided according to Johnson's criteria modified to the corpus (type 1a), gastric angle (type 1b), combined with duodenal ulcer (type 2) and prepyloric area (type 3). The number of each subset were 96, 81, 58 and 49, respectively. Mean serum PGI level (99.6 +/- 44.8 ng/ml) of all GU patients showed no difference from that of their sex and age matched controls. Mean serum PGI levels in both type 1a and 1b patients, did not differ from each other but were significantly lower than in controls, in contrast to those in type 2 and 3 patients which were significantly higher than in controls and comparable to the PGI levels of patients with duodenal ulcer. Smoking did not affect mean serum PGI levels in all subsets except the smoking type 2 patients who manifested a significantly higher mean PGI level. Helicobacter pylori infection did not show different serum PGI levels in any subset. In conclusion, different location of ulcer in the stomach results in a characteristic serum PGI level.
Serum pepsinogen I (PGI) levels were measured in 192 gastric carcinoma (GC) patients and 70 controls. Among GC patients serum PGI levels were not influenced by the following variables: age, sex, smoking, Borrmann's or Lauren's classification, tumor size, cellular differentiation, and layer of invasion. The mean serum PGI levels of tumors restricted to the body, antrum, or involving both areas were 64.8 +/- 37.6 ng/ml, 76.0 +/- 47.0 ng/ml, and 51.1 +/- 25.5 ng/ml, respectively (P < 0.005). Odds ratios of GC patients from the quartile of 262 serum PGI levels in the limits > or = 100 ng/ml, 70-99.9 ng/ml, 45-69.9 ng/ml, and < 45 ng/ml were 1.00, 0.76, 3.44, and 37.1, respectively (P < 0.001). The lower serum PGI levels of Chinese GC patients seem to be related to disease location rather than other characters of the tumor.
Neurokinins (NK) are a group of peptides that share a common C-terminal and play an important role in control of the motor functions of the mammalian gut. Neurokinin receptors such as NK1, NK2 are certainly present in any segment of gut, whereas the NK3 receptors are probably present in the ileum of the Guinea pig and duodenum of the rat. We measured gastrointestinal responses with natural NK and their very specific agonists to determine the probable receptors in the stomach and small intestine of Sprague-Dawley rats. After overnight fasting, the rats were intubated with a catheter to feed saline liquid meal that contained 10% charcoal. Simultaneously, various doses of NK ranged selected from 10(-10) and 10(-7) mol kg-1 included substance P (SP), neurokinin A (NKA), neurokinin B (NKB), septide, [Nle10]-NKA4-10, senktide, and vehicle were intraperitoneally injected. At 15 min after being fed test meal, the rats were sacrificed. Then we removed entire gut including the stomach to measure the total length of small intestine and transit length of the charcoal, from which the transit ratio was calculated. In comparison with ratios of rats treated with vehicle, the inhibited transit ratios for charcoal were seen among SP at 10(-10) mol kg-1, NKA at 10(-10) and 10(-7) mol kg-1, [Nle10]-NKA4-10 at 10(-7) mol kg-1, and senktide at all doses except 10(-8) mol kg-1. Enhanced transit ratios were seen for septide at the doses 10(-8) and 10(-7) mol kg-1. Likewise the mean total intestinal lengths of rats if they received various treatments of peptides except that rats treated with NKB had somewhat diminished length than those of vehicle-treated rats. Some natural NK and their very specific receptor agonists mainly inhibited rat gastrointestinal charcoal transits. We suggest the probable presence of NK1, NK2 and NK3 receptors in the small intestine and stomach including pylorus of the rat.
Human neutrophils, alone, did not kill Trichomonas vaginalis. More than 90% of T. vaginalis (10(5)/ml) survived in the presence of 10% normal human serum (NHS) while 90% of these organisms were killed in the presence of a combination of neutrophils (10(6)/ml) and 10% NHS. Mechanisms responsible for this serum-mediated neutrophil killing of T. vaginalis were demonstrated through a process of lucigenin-amplified neutrophil chemiluminescence. As evidenced by indirect immunofluorescence, NHS showed specific immunoglobulin G (IgG) titre of 1:8 for T. vaginalis. Purified IgG, at 1.6 mg/ml, showed no direct opsonizing or lytic effect on this organism. Formalin-fixed trichomonads opsonized by C2 deficient human serum promote 4 times more neutrophil chemiluminescence than those opsonized by Factor B deficient human serum. With the addition of purified IgG (5 mg/ml) neutrophil chemiluminescence was increased by 4 times and further improved trichomonal killing by neutrophils (from 5 +/- 4% to 78 +/- 16%) via activation of the classical complement pathway, but did not alter that due to activation of the alternative complement pathway. These studies indicate that both an IgG-enhanced classical complement pathway activation and an antibody-independent alternative complement pathway activation provide opsonin (C3) for T. vaginalis to facilitate the neutrophil killing mechanism.
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Previous study demonstrated that platelet activating factor (PAF) was a potent inducer of polymorphonuclear leukocyte (PMN) activation. This study used a luminometer to measure the chemiluminescence (CL) of peripheral blood (PB) PMNs in 15 patients with rheumatoid arthritis (RA). Superoxide production from PB and synovial fluid (SF) PMNs was also determined by inhibiting reduction of ferricytochrome C with superoxide dismutase. Neutrophils obtained from 12 age- and sex-matched healthy subjects (HS) were used as controls. The results showed that PAF at both 1 microM and 10 microM significantly increased neutrophil CL in both RA (1.40 +/- 0.90 mv, 1.87 +/- 1.18 vs control 0.66 +/- 0.18) and HS (1.70 +/- 0.72, 2.22 +/- 1.25 vs control 0.67 +/- 0.13), with no significant difference between the two groups. Both PMA and zymosan also significantly enhanced PMN CL in both RA (41.51 +/- 17.42, 40.0 +/- 26.51) and HS (43.42 +/- 17.28, 39.91 +/- 27.24), and those values were much higher than those of controls or via PAF stimulation, but, again, there was no difference between RA and HS groups. Lipopolysaccharide (LPS)-stimulated mononuclear cell supernatant can induce neutrophil activity, too. Like CL, PAF had a weak effect on the generation of superoxide from PMNs. Neutrophils from seven RA SF stimulated with PMA or PAF showed a significant increase in superoxide production (76.05 +/- 2.14, 2.83 +/- 0.18) and these were higher than in PB of either RA patients (54.35 +/- 12.46, 1.03 +/- 0.74) and HS (55.70 +/- 17.9; 1.08 +/- 1.12) (p less than 0.05). These findings demonstrated the PMNs were more activated in SF than those in PB of RA patients and HS, suggesting some unidentified factors in SF provoked PMNs activation.
Parallel measurements of circulating thyroglobulin (Tg), microsomal [TPO(mic)] and TSH-receptor antibodies [TSH-R(rr)] were performed in 30 cases of Graves' hyperthyroid patients who received antithyroid drug (ATD) therapy for 2.8 +/- 1.7 years (range: 0.5-5.0 years). Before ATD therapy, positive Tg, TPO(mic) and TSH-R(rr) antibodies were found in 33.3%, 83.3% and 86.7% of our patients with Graves' disease, respectively. The titers of Tg and TPO(mic) antibodies remained unchanged in most patients after ATD treatment. However, the TSH-R(rr) antibody titers decreased in 46.7%, elevated in 26.7% and unchanged in 26.7% after ATD therapy. Six cases got long-term remission. Measurements of Tg and TPO antibodies have no value in forecasting the outcome of the disease. The change of circulating TSH-R(rr) antibody from positive to negative is more predictive of remission after ATD therapy than the decrease of thyrotropin-binding inhibiting immunoglobulin index only. However, the former change indicating a persistent remission is not certain.
An elderly man was admitted to hospital with dull abdominal pain and marked weight loss. Ileocolic intussusception was shown on colonoscopy and later confirmed at laparotomy. The main feature was a caecal lipoma. A review of the subject and comparison with two other cases is included in the report. If the colonoscopy reveals a coil-spring polypoid mass, intussusception must be considered as a diagnosis in patients with abdominal pain.
The participation of antibody and complement in cell-mediated adherence and cytotoxicity to infected larvae (L3) of Angiostrongylus cantonensis was investigated in vitro. Of the different cell types involved in the reaction, neutrophils were seen to have a predominant role in immune serum--dependent adherence and cytotoxicity to L3. In the presence of immune serum, cytotoxicity to L3 by neutrophils from infected rats was twice that of neutrophils from normal rats. Although mononuclear cells and eosinophils from infected rats significantly increased the adherence to L3, they had little lethal effect on L3. A further study using gel filtration (Sephacryl S-200) and affinity chromatography (protein A) revealed that immunoglobulin G (IgG) alone was responsible for the complement activation in neutrophil-mediated killing of L3. Neither adherence nor cytotoxicity to L3 by neutrophils were affected when immune serum was heated to 50 degrees C or treated with zymosan, but they were markedly decreased when immune serum was treated with Mg2(+)-ethylene glycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. The results of this study indicate that the neutrophil-mediated adherence and cytotoxicity to L3 of A. cantonensis are mediated through IgG-dependent classical complement pathway activation.
The effect of cefodizime on the function in vitro of neutrophils from poorly-controlled, non-insulin-dependent diabetics was demonstrated by the chemotactic index and by chemiluminescence. Without cefodizime treatment, the chemotactic index for diabetic neutrophils was significantly lower than that for healthy controls (1.0 +/- 0.1 vs 3.6 +/- 0.7; mean +/- S.E.M., P less than 0.01). When neutrophils were pretreated with cefodizime at 1 or 10 mg/l, cefodizime restored the chemotactic activity of diabetic neutrophils (1.0 +/- 0.1 vs 2.7 +/- 0.3, P less than 0.01), but did not affect the activity in healthy controls. Conversely, cefodizime at 100 mg/l had no enhancing effect on diabetic neutrophil chemotaxis, but decreased the chemotactic activity of healthy neutrophils (1.1 +/- 0.2 vs 3.6 +/- 0.7, P less than 0.01). A difference in neutrophil chemiluminescence was also found between diabetics and healthy subjects but no influence of cefodizime on chemiluminescence was noted in neutrophils from either diabetics or healthy subjects.
The effect of actinomycin D (ACT-D) on human neutrophil chemotaxis, chemiluminescence (CL), superoxide (O2-) production, phagocytic uptake, and intracellular bacterial killing has been examined. The viability of the ACT-D-treated neutrophils was 98% even at a concentration of 10 micrograms/ml for 4 hr. Using fMLP as the chemotactic factor, depressed chemotaxis was demonstrated following ACT-D (1-10 micrograms/ml) pretreatment of neutrophils as compared with the non-treated controls. Similar ACT-D pretreatment produced the depressed responses in phorbol myristate acetate-induced CL and superoxide production by neutrophils. Moreover, using heat-inactivated human serum as an opsonin for Salmonella enteritidis (NCTC 6676), there was a significant difference in intracellular killing (P less than 0.01) but no difference in phagocytic uptake between ACT-D-treated and non-treated neutrophils. These studies indicate that ACT-D profoundly impairs both intracellular bacterial killing by human neutrophil through an effect on respiratory burst activity and directed cell migration of human neutrophils.