Acute Exacerbation of Pulmonary Fibrosis in Syndrome of Combined Pulmonary Fibrosis and Emphysema Following Lung Surgery : A Report of Two Cases

We herein report two cases of an acute exacerbation of pulmonary fibrosis in the syndrome of combined pulmonary fibrosis and emphysema (CPFE) following lung surgery, and also review the relevant literature. One is a 76-year-old man, who had been diagnosed with CPFE and lung cancer and undergone lobectomy. He was admitted to our hospital because of aggravation of dyspnea 50 days after lung surgery. The other is a 69-yearold man who had been diagnosed with pulmonary bulla, pulmonary emphysema and idiopathic interstitial pneumonia at 53 years old and was complicated by lung cancer. He underwent right lower lobectomy and presented with slight fever and desaturation 18 days after lung surgery. In both cases, chest computed tomography showed diffuse bilateral ground-glass opacities superimposed on preceding reticular opacities in the lower lung field. They were diagnosed as acute exacerbation of pulmonary fibrosis in CPFE.A strict followup is required, because the prevalence of lung cancer may be higher, and acute exacerbation may occur following lung surgery in CPFE patients. HRCT plays an important role in evaluating the occurrence of lung cancer at an early stage and for determining whether there is an acute exacerbation of pulmonary fibrosis in CPFE patients.Article信州医学雑誌 60(3): 149-156(2012)journal articl

In situ evaluation of podocin in normal and glomerular diseases

In situ evaluation of podocin in normal and glomerular diseases.BackgroundMutations of the NPHS2 gene are responsible for autosomal-recessive steroid-resistant nephrotic syndrome. Its product, podocin, faces the slit diaphragm area with its two ends in the cytoplasm of foot processes.MethodsWe generated rabbit polyclonal antibodies against conjugated peptides from human podocin N- and C-termini, and studied podocin and synaptopodin using kidney tissues of normal humans and those with glomerular diseases.ResultsAntipodocin antibodies detected the original 42 kD fragment and an extra smaller fragment by Western blot analysis using human isolated mature glomeruli. RNA analysis showed two bands, the original and the other of a decreased length. Immunohistochemically, podocin was detected in a linear pattern along the glomerular capillary loop. Antipodocin antibody (C-terminal) stained the smooth muscles of renal arterioles and aorta. Among 42 patients, podocin was normally expressed in glomeruli in purpura nephritis, IgA nephropathy (IgAN), and minimal-change disease (MCD), while it was either decreased or absent in most subjects with focal segmental glomerulosclerosis (FSGS). The expression of synaptopodin was similar to that of podocin, although some discrepancy existed.ConclusionAlthough indirect, our data suggest the existence of a vascular isoform of podocin with a different molecular mass. We propose that examination of podocin expression may help differentiate MCD from FSGS

Impact of a learning health system on acute care and medical complications after intracerebral hemorrhage

Introduction: Patients with stroke often experience pneumonia during the acute stage after stroke onset. Oral care may be effective in reducing the risk of stroke‐associated pneumonia (SAP). We aimed to determine the changes in oral care, as well as the incidence of SAP, in patients with intracerebral hemorrhage, following implementation of a learning health system in our hospital. Methods: We retrospectively analyzed the data of 1716 patients with intracerebral hemorrhage who were hospitalized at a single stroke center in Japan between January 2012 and December 2018. Data were stratified on the basis of three periods of evolving oral care: period A, during which conventional, empirically driven oral care was provided (n = 725); period B, during which standardized oral care was introduced, with SAP prophylaxis based on known risk factors (n = 469); and period C, during which oral care was risk‐appropriate based on learning health system data (n = 522). Logistic regression analysis was performed to evaluate associations between each of the three treatment approaches and the risk of SAP. Results: Among the included patients, the mean age was 71.3 ± 13.6 years; 52.6% of patients were men. During the course of each period, the frequency of oral care within 24 hours of admission increased (P < .001), as did the adherence rate to oral care ≥3 times per day (P < .001). After adjustment for confounding factors, a change in the risk of SAP was not observed in period B; however, the risk significantly decreased in period C (odds ratio 0.61; 95% confidence interval 0.43‐0.87) compared with period A. These associations were maintained for SAP diagnosed using strict clinical criteria or after exclusion of 174 patients who underwent neurosurgical treatment. Conclusions: Risk‐appropriate care informed by the use of learning health system data could improve care and potentially reduce the risk of SAP in patients with intracerebral hemorrhage in the acute stage

A variant Philadelphia chromosome (Ph1) positive chronic myelocytic leukemia.

A rare case of variant Philadelphia (Ph1) chromosome positive [46, XX, t (9; 22) (q34; q11), inv (9) (9q22; 22q13)] chronic myelocytic leukemia (CML) was described. The patient, 73 years old female, was hospitalized to our hospital because of leukocytosis. Hematological findings corresponded to those of CMLs. However, this case lacked hepatosplenomegaly. Southern blot analysis using a 3 breakpoint cluster region (bcr) probe revealed a bcr rearrangement. The patient has been in the chronic phase for sixteen months without treatment. Clinical and chromosomal changes are under observation in order to get accumulate data for a pathophysiological analysis of variant Ph1 positive CMLs.</p

A human T cell leukemia virus type-I carrier with recurrent thrombocytopenia and various autoantibodies.

A 34-year-old woman infected with human T cell leukemia virus type-I(HTLV-I) with recurrent thrombocytopenia and various autoantibodies is described. The platelet counts fluctuated between 1.3 x 10(4)/microliters and 14.8 x 10(4)/microliters without any medical treatment, and thrombocytopenia improved with a decrease of platelet-associated IgG (PA-IgG). Autoantibodies such as rheumatoid factor, antinuclear factor, anti-Sm, anti-RNP and anti-SSA antibodies were also recognized. Marker analysis of peripheral mononuclear cells showed an increase in the proportion of CD 25+ cells, CD 3+ HLA-DR+ cells, CD4+ HLA-DR+ cells and CD8+ HLA-DR+ cells. The recurrent thrombocytopenia and development of various autoantibodies in this HTLV-I carrier are speculated to be due to the alteration of B cell functions by T cells infected with HTLV-I.</p

Etiological factors in primary hepatic B-cell lymphoma

Sixty-four cases of malignant lymphoma involving the liver were examined. Of these, 20 cases were histologically confirmed to be primary hepatic B-cell lymphoma. Twelve of these 20 cases were diffuse large B-cell lymphoma (DLBCL) and eight cases were mucosa-associated lymphoid tissue (MALT) lymphoma. Of the 12 cases of DLBCL, six were immunohistologically positive for CD10 and/or Bcl6 (indicating a germinal center phenotype), six were positive for Bcl2, and five were positive for CD25. Eight of the 12 DLBCL cases (66.7%) and two of the eight MALT lymphoma cases (25%) had serum anti-hepatitis C virus (HCV) antibodies and HCV RNA. The incidence of HCV infection was significantly higher in the hepatic DLBCL cases than in systemic intravascular large B-cell cases with liver involvement (one of 11 cases, 9.1%) and T/NK-cell lymphoma cases (one of 19 cases, 5.3%) (p < 0.01 for both). Two hepatic DLBCL cases (16.7%) had rheumatoid arthritis treated with methotrexate, and four MALT lymphoma cases (50%) had Sjögren’s syndrome, primary biliary cirrhosis, or autoimmune hepatitis; one case in each of these two groups was complicated by chronic HCV-seropositive hepatitis. Although primary hepatic lymphoma is rare, persistent inflammatory processes associated with HCV infection or autoimmune disease may play independent roles in the lymphomagenesis of hepatic B cells