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Biomedical subjects

V Boonpucknavig

Publications and source records attributed to V Boonpucknavig.

At least 37 records · Page 2Linked to original sources
PubMed1985

IgA nephropathy associated with enteric fever.

3 cases of enteric fever (2 paratyphoid and 1 typhoid) associated with IgA nephropathy were reported. Salmonella Vi antigen was demonstrated in the glomeruli. The clinical syndrome disappeared after enteric fever was treated. Possible pathogenesis was discussed relating this intestinal infection to IgA nephropathy.

Adolescent↗
PubMed1984

Renal histopathology in the hemolytic-uremic syndrome following shigellosis.

The hemolytic-uremic syndrome (HUS) following dysentery caused by S. dysenteriae Type 1, characterized by microangiopathic hemolytic anemia and acute renal insufficiency, is clinically similar but not identical to the idiopathic HUS. We studied renal necropsy specimens of nine children who died of HUS following shigellosis by light and immunofluorescent microscopy and compared them to 12 controls: six cases with severe shigellosis without HUS, and six with pneumonia or sepsis. Eight of nine HUS cases showed cortical necrosis, extensive glomerular thrombosis or arterial thrombosis. Cases without HUS showed only scattered glomerular fibrin thrombin and widening of the mesangium. Among seven HUS cases studied by immunofluorescent microscopy, three demonstrated deposition of glomerular IgM and complement (C3) and one of the three had IgG and IgA as well; four cases had neither immunoglobulin or complement deposits. Among nine controls, two demonstrated IgM and three IgG, but none had C3. Both HUS and non-HUS cases had fibrin deposition. In the three HUS cases studied by electron microscopy intracapillary material (fibrin and platelets) was seen in all three, and sparse electron-dense deposits in mesangial matrix in one. The data indicate that the renal histopathology in the HUS following shigellosis consistently presents as a severe thrombotic microangiopathy, but lacks the characteristic endothelial and mesangial lesions of idiopathic HUS. The infrequent demonstration of glomerular immunoglobulin deposition fails to support an immunoglobulin-mediated pathogenesis.

Anemia, Hemolytic↗
PubMed1983

Immunopathology of acute rheumatic fever and rheumatic heart disease. The demonstration of Coxsackie group B viral antigen in the myocardium.

Immunopathologic studies were performed on heart tissue of patients with acute rheumatic fever with carditis and chronic rheumatic heart disease. Coxsackie group B viral antigen was demonstrated in 3 heart specimens of patients clinically compatible with active rheumatic fever. In two of these the pathologic findings were compatible with acute rheumatic carditis. Immunoglobulin was detected in 2 and complement in one of these heart specimens. All of the chronic rheumatic heart specimens and the controls were negative. These findings suggested that Coxsackie group B virus may be etiologically related to the pathogenesis of acute rheumatic fever.

Acute Disease↗
PubMed1981

Infection of young adult mice with dengue virus type 2.

Young adult female mice, five to six weeks old, were injected intraperitoneally with 2.5 x 10(6.3) LD50 of dengue-2 virus, New Guinea C strain. The mice were killed on day 1, 2, 3, 4, 5, 6, 7, 10, 14, 21, 28, and 35 respectively. By means of the immunofluorescent antibody technique, viral antigen appeared as irregular granules in the reticuloendothelial cells of liver, lymph nodes and spleen of infected mice on the first day after inoculation and then diminished. From the fifth to sixth day of infection dengue antigen appeared again as homogeneous staining in the cytoplasm of single or groups of mononuclear cells in the lymphatic sinuses only. Later, by the third week of infection, dengue antigen could be seen in the mononuclear cells located in the marginal zone of lymphoid follicle of the spleen, the pattern of staining changing to bright spherical granules. At the same time, the deposition of immune complexes (composed of dengue antigen, mouse gamma and beta 1C globulin) could be seen in the renal glomeruli of infected mice. Serum antibody to dengue virus was found at low levels, being maximal on the 14th day after infection. Dengue virus was not isolated from the sera or from the infected organs. Granulomatous inflammation developed in lymph nodes and liver of mice infected with dengue virus and in mice inoculated with normal mouse brain suspension. Proliferative glomerular lesion was observed on day 14 after inoculation without definite abnormal urine findings.

Animals↗
PubMed1980

Renal involvement in human trichinosis.

A renal clinicopathologic study was made in five patients with trichinosis. The patients had mild proteinuria and abnormal urinary sediment that disappeared after the disease was under control. Creatinine clearance was normal in all cases. p-Aminohippurate clearance was decreased in two patients who had hypoalbuminemia. A renal biopsy specimen showed mesangial proliferative glomerulonephritis with deposition of immunoglobulins and C3 in the mesangial areas and along the capillary loops. Glomerular fibrin deposition was noted in one case. Deposition of hyaline material and C3 was observed in the arteriolar wall. Tubular interstitial changes were not present.

Adult↗
PubMed1979

Immunofluorescence study of skin rash in patients with dengue hemorrhagic fever.

Fifty-three skin biopsy specimens obtained from the cutaneous rashes of patients who had dengue hemorrhagic fever (DHF) were studied by immunofluorescence technique. Six specimens showed deposits of IgM, beta 1 C-globulin, dengue antigen, and fibrinogen during the first week of fever. Some but not all of these components (IgM, beta 1 C, dengue antigen) were demonstrated in 29 specimens. Twenty-three of them yielded negative results. Granular deposits of IgM and beta 1 C appeared in the blood vessel walls of dermal papillae. Dengue antigen was seen in mononuclear cells that were closely infiltrated around the blood vessel wall in dermal papillae. Fibrinogen was located within or about the blood vessels. The findings suggest that the cutaneous rashes occurring in DHF are caused by an immunopathologic process.

Antigens, Viral↗
PubMed1979

Immunopathological studies of Plasmodium berghei infected mice: (effect of carbon particles).

An attempt was made to block the role of the macrophages in the immune response by saturating them with carbon particles. The experiment was performed on Swiss albino female mice injected intraperitoneally with 10(5) P. berghei berghei. These mice were injected with carbon particles of 20 mgs on the day before the inoculation and again 10 mgs on day 4 and day 9 after the inoculation. The degree of parasitaemia was slightly higher throughout the experiment in the infected mice treated with carbon than in those untreated. By direct immunofluorescent method the free floating form of malaria antigen was detected in the infected organs (liver, kidney and spleen) on day 3 of infection onwards. The antigen was more intense in the carbon treated mice than in the untreated ones. The granular form of the antigen in the walls of glomerular capillaries of the kidney, in the Kupffer cells of the liver and in the reticulo-endothelial cells of the spleen, the malarial antibody and the immune complex (malaria antigen, antibody and mouse beta 1 C globulin) in the kidney were detected later on (day 11).

Animals↗
PubMed1979

Plasmodium berghei--infected mice. Focal glomerulonephritis in hyperimmune state.

Twenty-one male Swiss albino mice were injected intraperitoneally with 2 x 10(5) Plasmodium berghei berghei-infected cells. Twenty-four mice were used as a noninfected control group. On the tenth day after infection, three mice were killed and the remainder were treated with chloroquine phosphate (0.025% solution) given orally. The dosage was subsequently adjusted to keep the parasitemia below 5%. Eighteen of the controls received the same chloroquine dosage. Diffuse proliferative glomerulonephritis was seen from day 10 of infection up to two months after treatment. Granular deposits of immune complex were seen in all glomeruli. At the end of third month and thereafter, all experimental mice were in a hyperimmune state, and the kidneys showed the characteristic of focal glomerulonephritis resembling some types of human focal glomerulonephritis.

Animals↗