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Biomedical subjects

K H Fye

Publications and source records attributed to K H Fye.

At least 19 recordsLinked to original sources
PubMed1992

Renal insufficiency secondary to 2,8-dihydroxyadenine urolithiasis.

A 48-year-old man with a history of recurrent urolithiasis and chronic renal failure underwent a nephrectomy for a renal mass. At surgery the mass proved to be a calculus impacted in a dilated calyx. Gross examination of the kidney revealed chalky white deposits in the deep medulla and papillary tips. Histologic examination revealed chronic interstitial nephritis with brown spicules within some tubular epithelial cells and larger deposits of brown crystals within tubular lumina, the interstitium of the medulla, and papillary tips. Polarization microscopy revealed individual crystals scattered throughout the renal parenchyma. Although the arrangement of the crystals was reminiscent of uric acid, and, in fact, a clinical diagnosis of gouty nephropathy was made, x-ray diffraction analysis demonstrated crystals of 2,8-dihydroxyadenine. Enzymatic studies confirmed the complete absence of adenine phosphoribosyltransferase activity in erythrocyte lysates.

Adenine↗
PubMed1991

Methotrexate and histologic hepatic abnormalities: a meta-analysis.

STUDY OBJECTIVE: To determine the risk of liver toxicity from the long-term administration of methotrexate in patients with rheumatoid arthritis or psoriatic arthritis. DESIGN: A meta-analysis of 15 studies examining the relationship between long-term, low-dose methotrexate administration and biopsy evidence of liver fibrosis. PATIENTS: A total of 636 patients from 15 studies. RESULTS: The incidence of progression of liver disease (defined as worsening of at least one grade on the histologic classification of Roenigk) among 636 patients was 27.9% (95% confidence intervals 24.3 to 31.6). The rate of progression of liver disease in the 15 studies was associated with the cumulative dose of methotrexate (p = 0.01). Patients on average had a 6.7% (95% confidence intervals 2.1 to 11.4) chance of progressing at least one histologic grade on liver biopsy for each gram of methotrexate taken. The overall incidence of advanced pathologic changes on liver biopsy (grades IIIB or IV) among 636 patients was 5.0% (95% confidence intervals 3.5 to 7.0). The development of advanced histologic changes was not associated with the cumulative dose of methotrexate (p = 0.08). Patients who according to their history were heavy drinkers (at least 100 g of alcohol per week) were more likely to have advanced changes on liver biopsy (17.8% versus 4.5%, p = 0.0003) and to show histologic progression (73.3% versus 25.9%, p = 0.0002). Patients with psoriasis were more likely than patients with rheumatoid arthritis to have advanced changes (7.7% versus 2.7%, p = 0.003) and histologic progression (33.1% versus 24.3%, p = 0.02). CONCLUSIONS: The risk of liver toxicity in patients undergoing long-term, low-dose methotrexate therapy is substantial, and that risk increases with the total cumulative dose and with heavy consumption of alcohol. Heavy users of alcohol should not receive long-term methotrexate therapy. For most patients who are not heavy users of alcohol, liver biopsies should be done periodically to monitor for the occurrence of liver toxicity.

Alcohol Drinking↗
PubMed1978

Relationshipp of HLA-Dw3 and HLA-B8 to Sjögren's syndrome.

Nineteen patients with Sjögren's syndrome were evaluated for the presence of HLA-B8 and HLA-Dw3. HLA-B8 was found in 57.8% of patients and 20.1% of 96 controls (P less than 0.001). HLA-Dw3 was detected in 73.7% of the patients and 24.0% of controls (P less than 0.0001). Statistical evaluation of the association of both antigens with Sjögren's syndrome revealed that the primary association was with HLA-Dw3 (P less than 0.005). Patients with HLA-Dw3 had a lower mean parotid salivary flow rate (0.8 +/- 0.3 ml/10 minutes/gland versus 5.6 +/- 1.2 ml/10 minutes/gland, P less than 0.0004) and a more intense lymphocytic infiltration into labial salivary glands (focus score 7.2 +/- 0.9 versus 3.4 +/- 0.9, P less than 0.04) than did patients without HLA-Dw3. The difference in the intensity of the lymphocytic infiltration was even more significant when patients with both HLA-Dw3 and HLA-B8 were compared with patients with neither antigen (focus score 7.5 +/- 1.0 versus 2.8 +/- 0.8, P less than 0.02). In addition, all patients with severe keratoconjunctivitis sicca had both antigens. Our observations suggest that a number of genes may interact to determine susceptibility and severity in Sjögren's syndrome.

Adolescent↗
PubMed1978

HLA-B27 associated arthropathies.

The association between histo-compatibility antigens and disease is reviewed, in particular that between HLA-B27 and spondylitic disorders, i.e., ankylosing spondylitis, Reiter's arthritis, psoriatic arthritis, and ankylosing hyperostosis. We determined whether the presence of HLA-B27 predicted specific radiographic findings and, conversely, whether specific radiographic changes predicted antigenic status. The prevalences of the HLA-B27 antigen in our patients were: ankylosing spondylitis, 100%; Reiter's arthritis, 93%; psoriatic arthritis, 55%; and ankylosing hyperostosis, 12%. The only specific radiographic finding associated with B27 positivity was severe spondylitis in psoriasis.

Arthritis↗
PubMed1977

Immune complexes in hepatitis B antigen-associated periarteritis nodosa. Detection by antibody-dependent cell-mediated cytotoxicity and the Raji cell assay.

A subpopulation of peripheral blood lymphocytes with the ability to lyse target cells coated with specific antibody (antibody-dependent cell-mediated cytotoxicity, ADCC) was serially studied in a patient with hepatitis B antigen-associated periarteritis nodosa. The effector lymphocytes possess FC and complement receptors but do not require complement for functional activity. We found that the patient's ADCC was decreased during periods of disease activity and was almost normal during remission. The patient's serum could block ADCC in normal lymphocytes, and the blocking ability correlated with the concentration of immune complexes as determined by the Raji cell assay (a radioimmunoassay using complement receptors on human cultured lymphoblastoid cells). The concentration of immune complexes and the ADCC blocking ability of ther serum both correlated with disease activity. Serum from five other patients with active vasculitis was found to contain significant amounts of immune complexes and was able to block normal ADCC. It appears that the ADCC assay can be used to detect the presence of circulating immune complexes and to monitor disease activity in periarteritis nodosa.

Adult↗
PubMed1976

In vitro effect of thymosin on T-lymphocyte rosette formation in rheumatic diseases.

The in vitro effect of calf thymosin fraction 5 on T-rosette forming cells (E-RFC) was studied in Sjögren's syndrome (SS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). The baseline percent E-RFC in sixteen normal controls was67-2 +/- 6-9. E-RFC was significantly decreased in SLE (42-6 +/- 17-0, P less than 0-0001) and SS (51-8 +/- 16-9, P less than 0-002) but not in RA (59-7 +/- 14-1). Ten of twenty-five SS patients and two of eleven RA patients had less than 50% E-RFC, and all showed a significant increase after incubation with thymosin (+ 16-5 +/- 6-5%, P less than 0-0001, and + 11 +/- 4-9%, P less than 0-001, respectively). Eleven of sixteen SLE patients had less than 50% E-RFC. Their response to thymosin was less dramatic but still statistically significant (+ 5-3 +/- 6-0%, P = 0-03). There was no response to thymosin in control subjects or in patients with baseline E-RFC greater than 50%. No increase in E-RFC was seen after incubation with calf spleen fraction 5 or known stimulators of cyclic-AMP. Sera from four active SLE patients, as well as the supernatant obtained from overnight culture of the lymphocytes from one SLE patients, were able to block T-rosette formation by normal lymphocytes, even after exposure to thymosin. Two 'blocking' sera were fractionated by sucrose density gradient ultracentrifucation. In one, the blocking capacity was found to reside in the 19S region containing IgM. In the second, the blocking capacity was in the 7S region containing IgG. Four 'blocking' lupus sera were depleted of IgG or IgM by immunoabsorption with goat anti-human IgG or goat anti-human IgM sepharose 4B. The blocking ability in three sera was partially decreased by depletion of either IgG or IgM, and in a fourth, only by removing IgG. The percent of lymphocytes staining with fluorescein labelled goat anti-human immunoglobulin antisera was increased in SLE patients (35-9 +/- 20-2 vs 21-7 +/- 5-9 in controls, P = 0-02). After overnight culture, the percent of staining cells decreased to normal values. These results suggest that thymosin can stimulate the differentiation of T-lymphocytes in patients with SS, SLE, and RA when the baseline E-RFC is decreased. Furthermore, the decreased percent E-RFC in SLE is probably due to cell-bound anti-lymphocyte antibodies that block sheep erythrocyte receptors on the T-cell and, possibly, thymosin receptors on undifferentiated lymphocytes.

Adolescent↗
PubMed1976

Low-dosage heparin in rapidly progressive glomerulonephritis.

Two patients developed acute renal failure; creatinine clearances fell to 13 and 34 ml/min, respectively, and one patient was oliguric. Renal biopsies in both patients gave results that were compatible with rapidly progressive glomerulonephritis (RPGN). Both patients were treated with low-dosage heparin sodium infusion (8,000 units/day) and prednisone for two to four weeks, followed by oral anticoagulant (warfarin) and antithrombotic agents (dipyridamole). In the two patients, creatinine clearance rose to at least 60 ml/min, and no bleeding complications were observed. Repeat renal biopsy specimens that were obtained after three to six months of treatment showed no evidence of active glomerulonephritis in either patient, but there was extensive scarring and fibrosis. Low-dosage heparin infusion may arrest and partially reverse the renal failure associated with RPGN in some cases, while avoiding the bleeding complications that are frequently observed in patients treated with larger dosages of heparin.

Administration, Oral↗
PubMed1975

Vascular manifestations of von Recklinghausen's disease.

A casual relationship between von Recklinghausen's disease, or neurofibromatosis, and arteriolar abnormalities has been reported in the European literature. A patient was seen who had biopsy-proved neurofibromatosis and renovascular hypertension and retroperitoneal bleeding. An arteriographic study showed multiple small aneurysms throughout the coeliac axis, the superior mesenteric artery and in several small intrarenal vessels. Renal vein renin levels were elevated particularly in the right renal vein, supporting the diagnosis of renovascular hypertension. Both the aneurysms seen in angiographic studies and the retroperitoneal hemorrhage are probably vascular manifestations of von Recklinghausen's disease. Support for this conclusion is enhanced by the absence of clinical, laboratory or histologic data supporting the only tenable differential diagnosis, periarteritis nodosa.

Adult↗