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Biomedical subjects

Y Taguchi

Publications and source records attributed to Y Taguchi.

At least 91 records · Page 5Linked to original sources

[Secondary osteoporosis in gynecology].

Several diseases and medications are known to induce secondary osteoporosis. Among them, same situations are related to gynecological field. They include Turner's syndrome, anorexia nervosa, ovarian dysfunction, oophorectomy, GnRH agonist therapy, and osteoporosis associated with pregnancy. We briefly describe these secondary osteoporosis in this article as follows. Several studies have found osteoporosis to be a common complication of Turner's syndrome and hormone replacement therapy has been used as a possible management; in anorexic patient, low body weight, prolonged amenorrhea, early onset of anorexia nervosa, and hypercortisolism have been reported to be risks for bone demineralization; since oophorectomy which is a common intervention in gynecology leads osteoporosis, it is important to prevent osteoporosis caused by surgery as well as postmenopausal osteoporosis; GnRH agonist, which induces estrogen deficient state and affect bone mass, is commonly used as a management for endometriosis and leiomyoma of uterus; associated with pregnancy, post-pregnancy spinal osteoporosis and transient osteoporosis of the hip are clinically considered to be important and heparin therapy and magnesium sulfate therapy are commonly employed during pregnancy, affecting calcium homeostasis.

Anorexia Nervosa↗

[Significance of serum surfactant protein-D (SP-D) level in patients with pulmonary tuberculosis].

Elevated levels of serum surfactant protein-D (SP-D) have been previously reported in patients with idiopathic pulmonary fibrosis (IPF) and pulmonary alveolar proteinosis. To determine whether the same change is seen in other pulmonary diseases, especially pulmonary tuberculosis (TB), we measured the serum SP-D levels in active pulmonary TB (smear and/or culture: positive), acute interstitial pneumonia (AIP), IPF, acute exacerbation of IPF, hypersensitivity pneumonitis (HP), pneumoconiosis, bronchiectasis, and bacterial pneumonia by an enzyme-linked immunosorbent assay using monoclonal antibodies to human lung SP-D, and compared them with those of healthy elderly subjects over 50 years of age. The SP-D level in the healthy elderly subjects was 57.6 +/- 38.4 ng/ml (mean +/- SD, n = 287). The levels in patients with active pulmonary TB (140.6 +/- 18.2 ng/ml, n = 49), AIP (1,021 ng/ml, n = 1), IPF (307.0 +/- 180.7 ng/ml, n = 42), acute exacerbation of IPF (817.7 +/- 283.6 ng/ml, n = 3), and HP (716.6 +/- 548.8 ng/ml, n = 4) were significantly higher than those in the healthy elderly controls (p < 0.05), whereas those of pneumoconiosis, bronchiectasis, and bacterial pneumonia, 121.9 +/- 92.8 ng/ml (n = 8), 93.9 +/- 72.9 ng/ml (n = 11), and 72.7 +/- 3.4 ng/ml (n = 4), respectively, showed no significant difference with the controls. In active pulmonary TB, the percentage of patients whose serum SP-D levels were over 134.6 ng/ml (mean + 2SD of healthy elderly controls) was 34.7%, and therefore we considered the serum SP-D level was not useful for the diagnosis of pulmonary TB. However, it was significantly higher in the patients with cavity formation than in those without (p < 0.05), and there was a significant positive correlation between the serum SP-D level and the number of tubercle bacilli in the sputum (r = 0.416, p = 0.00165), erythrocyte sedimentation rate at 1 hr (r = 0.489, p < 0.01), and CRP level (r = 0.383, p = 0.003). These findings suggest that the serum SP-D level is a useful indicator of the disease activity in pulmonary TB.

Aged↗

Platelets enhance contractility in perfused rat mesenteric arteries: involvement of endothelin-1.

We investigated the effects of platelet supernatant on pressor responses to norepinephrine in isolated perfused rat mesenteric arteries. Perfusion of the arteries with platelet supernatant for 2 h markedly enhanced the pressor responses to norepinephrine (10(-6) and 3 x 10(-6) M). This enhancement was significantly inhibited by phosphoramidon (10(-4) M), an endothelin converting enzyme inhibitor. Both BQ788 [N-cis-2,6-dimethylpiperidinocarbonyl-L-gamma-methylleucyl-D -1-methoxycarbonyltryptophanyl-D-norleucine] (10(-6) M), an endothelin ET(B) receptor antagonist, and bosentan (Ro47-0203, 4-tert-butyl-N-[6-(2-hydroxy-ethoxy)-5-(2-methoxy-phenoxy)-2,2-bipyri midin-4-yl]-benzenesulfonamide) (10(-5) M), a nonselective endothelin receptor antagonist, also prevented the potentiation of responses to norepinephrine evoked by platelet supernatant, but FR 139317 ((R)2-[(R)-2-[(S)-2-[[1-(hexahydro-1H-azepinyl)]carbonyl]amino-4-+ ++methylpentanoyl] amino-3-[3-(1-methyl-1H-indoyl)]propionyl]amino-3-(2-pyridyl) propionic acid) (10-6 M), an endothelin ET(A) receptor antagonist, had little effect. Suppressor doses of endothelin-1 (3 x 10(-10) M) or sarafotoxin S6c (S6c) (3 x 10(-10) M) potentiated significantly the norepinephrine-induced vasoconstriction, in the same preparation. Moreover, supernatant-induced enhancement of pressor responses to norepinephrine was markedly suppressed by TGF-beta1 neutralizing antibody. Transforming growth factor-beta1 (TGF-beta1) (40 pM) also significantly enhanced the pressor responses to norepinephrine (10(-6) M) and this enhancement was significantly inhibited by phosphoramidon. These results suggest that platelet-derived TGF-beta1 stimulates the vascular production of endothelin-1 and thereby enhances vasoconstrictor responses to norepinephrine. Platelet-induced enhancement of vasoconstrictor responses to norepinephrine seems to be mainly mediated by endothelin ET(B) receptor, in rat mesenteric arteries.

Animals↗

Regulation of the gp80 and gp130 subunits of the IL-6 receptor by sex steroids in the murine bone marrow.

Both estrogen and androgen exert their antiosteoporotic effects, at least in part, by inhibiting IL-6 production, thereby suppressing osteoclastogenesis. Several observations, however, suggest that besides increased IL-6 production, sensitivity of the osteoclastogenic process to this cytokine is altered after ovariectomy. Based on this and evidence that the ligand-binding subunit of the IL-6 receptor (gp80) is a limiting factor for the actions of IL-6 on bone, we hypothesized that sex steroids regulate expression of the IL-6 receptor as well. We report that 17beta-estradiol or dihydrotestosterone in vitro decreased the abundance of the gp80 mRNA as well as the mRNA of the signal-transducing subunit of the IL-6 receptor (gp130) in cells of the bone marrow stromal/osteoblastic lineage, and also decreased gp130 protein levels. These effects did not require new protein synthesis. In contrast to sex steroids, parathyroid hormone stimulated gp130 expression; this effect was opposed by sex steroids. Consistent with these findings, ovariectomy in mice caused an increase in expression of gp80, gp130, and IL-6 mRNAs in ex vivo bone marrow cell cultures as determined by quantitative reverse transcription (RT)-PCR, and confirmed on an individual cell basis using in situ RT-PCR. The demonstration of increased expression of the IL-6 receptor after loss of sex steroids provides an explanation for why IL-6 is important for skeletal homeostasis in the sex steroid-deficient, but not replete, state.

Animals↗

Amino acid substitutions in the first transmembrane domain (TM1) of P-glycoprotein that alter substrate specificity.

Recently, we showed that the amino acid at position 61 in TM1 of human P-glycoprotein is important in deciding the substrate specificity of this protein. In this work, we investigated whether the amino acids other than His61 in TM1 of P-glycoprotein are also essential in the function of this protein. Nine amino acids residues, from Ala57 to Leu65 in TM1, were independently substituted to Arg, and analyzed the drug resistance of cells stably expressing each of these mutant P-glycoproteins. The mutant P-glycoproteins Ile60 --> Arg, His61 --> Arg, Ala63 --> Arg, Gly64 --> Arg, and Leu65 --> Arg were normally processed and expressed in the plasma membrane. Substrate specificities of mutant P-glycoproteins Gly64 --> Arg and Leu65 --> Arg were quite different from that of the wild type, and similar to that of the His61 --> Arg mutant, while the Ile60 --> Arg and Ala63 --> Arg mutant P-glycoproteins showed similar substrate specificities to that of the wild-type P-glycoprotein, suggesting that not only the amino acid residue at position 61 but also those at position 64 and 65 are also important in deciding the substrate specificity of P-glycoprotein. These three amino acids His61, Gly64, and Leu65 would form a compact region on an alpha-helix arrangement of TM1. These results suggest that a region consisting of His61, Gly64, and Leu65 in TM1 would participate in the formation of the recognition site for substrates of P-glycoprotein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Alteration of substrate specificity by mutations at the His61 position in predicted transmembrane domain 1 of human MDR1/P-glycoprotein.

In CFTR, a member of the ABC superfamily and a chloride channel, amino acid substitutions in its transmembrane domains 1 and 6 (TM1, TM6) have been reported to modulate the anion selectivity or ion conductance of the ion channel. In P-glycoprotein, no amino acid substitution in TM1, but some in TM6, have been reported to modify the substrate specificity of this protein. In this work, we demonstrated the involvement of His61, which is in the middle of the predicted TM1, in the function of P-glycoprotein. His61 was replaced by all other amino acid residues, and each of the mutant cDNAs was introduced into drug-sensitive human carcinoma cells, KB3-1. The drug-resistance profile of cells stably expressing each mutated P-glycoprotein was investigated by comparing their relative resistance to vinblastine, colchicine, VP16, and adriamycin. The resistance to vinblastine was increased by replacing His61 by amino acids with smaller side chains, while it was lowered by replacing by amino acids with bulkier side chains. The reverse effect was observed for resistance to colchicine and VP16. The resistance to adriamycin was increased by replacing by amino acids with bulkier side chains except Lys or Arg, which have a basic side chain. We also showed that the replacement of His61 by Phe and Lys greatly impaired the efflux of calcein AM, while the replacement had no effect on the efflux of rhodamine 123. These results suggest that an amino acid residue at position 61 in TM1 is important in deciding the substrate specificity of P-glycoprotein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Clonal selection of HIV type 1 variants associated with resistance to foscarnet in vitro: confirmation by molecular evolutionary analysis.

Foscarnet (trisodium phosphonoformate, PFA) is an effective inhibitor of retroviral reverse transcriptase (RT) and is known to block the replication of human immunodeficiency virus type 1 (HIV-1). In this article we analyzed the evolutionary process in generating HIV-1 strains related to drug resistance, using PFA as a selective pressure. PFA inhibited virus replication and protected the virus-induced cell killing, but it did not completely eliminate HIV-1 during the course of 7 weeks of treatment. The nucleotide sequence of the 859-bp DNA fragment spanning the core region of the HIV-1 pol gene was determined for 51 clones obtained from genomic DNA of the HIV-1-infected cells at different time points during PFA treatment. The nucleotide sequence analysis documented the presence of a minor HIV-1 variant prior to the PFA treatment. Molecular evolutionary techniques were utilized to analyze how the minor HIV-1 clones became predominant during this evolutionary process under the selective pressure of PFA. A phylogenetic tree analysis divided these 51 HIV-1 clones into 3 groups. One of the groups consisted of the clones associated with the resistance to PFA. The clones belonging to this group became predominant over time during the course of PFA treatment. Thus, the acquisition of PFA resistance by HIV-1 was considered to be due to clonal selection. Furthermore, among the various amino acid substitutions observed, the substitution of arginine at position 172 by lysine (Arg172Lys) clearly distinguished this group from the others. Since the consistent amino acid substitution observed here has not been identified in the HIV-1 strains resistant to other RT inhibitors, PFA in combination with other RT inhibitors is considered to be a feasible candidate for a convergent combined chemotherapy against HIV-1 in the treatment of patients with AIDS and related conditions.

Amino Acid Sequence↗

Anti-cancer drugs and glutathione stimulate vanadate-induced trapping of nucleotide in multidrug resistance-associated protein (MRP).

Multidrug resistance-associated protein (MRP), a member of the ABC superfamily transporters, functions as an ATP-dependent efflux pump that extrudes cytotoxic drugs from the cells. Although glutathione has been considered to play an important role in the function of MRP, there is no convincing evidence that glutathione directly interacts with MRP. Here we demonstrate that vanadate-induced trapping of 8-azido-ATP in MRP was stimulated in the presence of glutathione, oxidized glutathione and the anti-cancer drugs VP-16 and vincristine. MRP in membrane from a human MRP cDNA transformant was specifically photolabeled with 8-azido-[alpha-32P]ATP by the vanadate-trapping technique. Vanadate and Mg2+ were required for trapping of nucleotides, and vanadate trapping of nucleotides was inhibited by excess ADP as well as ATP. These results suggest that a stable inhibitory complex MRP x MgADP x Vi, an analog of the MRP x MgADP x Pi transition state complex, is formed in the presence of vanadate. Glutathione as well as anti-cancer drugs would directly interact with MRP, and stimulate the formation of the transition state of the ATPase reaction of MRP.

ATP-Binding Cassette Transporters↗

Nitric oxide production by superficial and deep articular chondrocytes.

OBJECTIVE: Chondrocytes have been shown to produce large amounts of nitric oxide (NO) when appropriately stimulated with proinflammatory cytokines or bacterial lipopolysaccharide (LPS). In view of recent observations underscoring profound phenotypic differences between superficial and deep articular chondrocytes, these studies investigated NO production, inducible NO synthase (iNOS) activity, and messenger RNA (mRNA) expression of superficial and deep cartilage explants and cells. METHODS: Superficial and deep bovine and human articular cartilage explants and isolated bovine chondrocytes were cultured in the presence of stimulating cytokines or LPS. NO was measured by the Griess reagent. Inducible NOS activity was quantitated by conversion of L-14 C-arginine to L-14C-citrulline. Inducible NOS mRNA expression was quantitated by reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. RESULTS: Superficial bovine cartilage explants stimulated with interleukin-1 alpha, LPS, or tumor necrosis factor alpha for 24 and 48 hours produced significantly more NO than did deep explants with all stimulants and at both times. Similar results were obtained with stimulated isolated superficial and deep cells. NO synthase activity, measured by the conversion of L-14C-arginine to L-14C-citrulline, paralleled NO production. Comparable results were obtained using explants from a normal human donor. Semiquantitation of iNOS mRNA by RT-PCR showed significantly larger amounts of PCR products in superficial cells and superficial explants. These results were confirmed by in situ hybridization of explants and isolated cells. CONCLUSION: Increased NO production at the cartilage surface-synovial fluid interface may play an important role in the modulation of cartilage damage in inflammatory arthritis.

Animals↗

How does P-glycoprotein recognize its substrates?

We review how P-glycoprotein recognizes a wide variety of compounds and how it carries its substrates across membranes. Amino acid substitutions that affect the substrate specificity of P-glycoprotein have been found scattered throughout the molecule. In particular, some amino acid residues in the putative transmembrane domain (TM) 1 together with TM5-6 and TM11-12 may help to govern substrate specificity. The features that substrates for P-glycoprotein share are also discussed. The amphipathy of a substrate may decide whether the substrate can be intercalated into the lipid bilayer of the membrane. In addition, only certain molecular volumes and tertiary structures may make it possible for the substrate to fit into the substrate-binding site(s) of P-glycoprotein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Specific changes of urinary excretion of cross-linked N-telopeptides of type I collagen in pre- and postmenopausal women: correlation with other markers of bone turnover.

Urinary excretion of cross-linked N-telopeptide of type I collagen (NTx) has been reported to be a specific marker of bone resorption [18]. We assessed a new immunoassay for NTx as an indicator of changes in bone resorption caused by spontaneous menopause and compared cross-sectionally the levels of urinary NTx, hydroxylysylpyridinoline (HP), lysylpyridinoline (LP), hydroxyproline (OH-Pr), other serum biochemical indices, and lumbar spine and proximal femur bone mineral density (BMD). Eighty-one Japanese women aged 22-77 participated in this study; 36 were premenopausal and 45 were postmenopausal. Urinary HP, LP, and NTx stayed at low levels in the premenopausal period and rose 21%, 30%, and 67% in the postmenopausal period, respectively. The rise in LP and NTx was statistically significant (P < 0.01), suggesting that NTx is mostly released from bone matrix when bone resorption is accelerated. When premenopausal women were divided into two age groups and postmenopausal women were divided into two groups according to years since menopause (YSM) there were significant differences in LP and NTx between women <4 YSM and women aged <40 and those women aged 41+ (P < 0.01 and P < 0.05, respectively). A significant 110% increase in urinary NTx and a 48% increase in urinary LP were observed in postmenopausal women compared with age-matched premenopausal women aged 45-55. All biochemical markers other than serum PTH correlated significantly with each other (r = 0. 243-0.858, P < 0.05-0.0001). Urinary NTx inversely correlated with lumbar spine BMD. When postmenopausal women were divided into three groups, the correlation between bone resorption and formation markers in women 0-1 YSM was greater than in women 2-10 YSM and in women 11 + YSM, indicating that resorption and formation are coupled at the early postmenopausal period. We conclude that urinary NTx is responsive to changes in bone metabolism caused by estrogen deficiency and may be a more sensitive and specific marker than HP, LP, or OH-Pr in the early postmenopausal years.

Adult↗

Efficacy of interferons in treating children with chronic hepatitis C.

UNLABELLED: Twenty-two children with chronic hepatitis serologically positive for hepatitis C virus (HCV) were treated with interferon-alpha (IFN-alpha). Liver biopsy showed chronic active hepatitis in 13 and chronic persistent hepatitis in 9 patients. A sustained clearance of HCV was observed in 8/22 children 12 months after the administration of IFN-alpha for 26 weeks, associated with normalization of HCV core antibody. Of these eight patients six had HCV genotype III and two HCV genotype II or IV. Hepatitis relapsed in seven other patients after completion of IFN-alpha with an increase in HCV core antibody titre, five with HCV genotype II, and two with HCV genotype III or IV. A second course of IFN-alpha suppressed the reactivation of HCV in all seven patients. Three of seven responders who relapsed after the first course remained negative for HCV RNA 12 months after their second course of IFN-alpha. However, the remaining four patients with HCV genotype II again relapsed after completing their second course of IFN-alpha. Seven children with the HCV genotype II resistant to IFN, including 8 weeks of IFN-beta administration, and showed no significant reduction in HCV core antibody titre. CONCLUSION: The genotype of HCV (III) and a reduction in the core antibody titre appear to be useful parameters for predicting the response to IFN-alpha therapy.

Adolescent↗

Growth inhibition of Helicobacter pylori by a polyamine synthesis inhibitor, methylglyoxal bis(cyclopentylamidinohydrazone).

The anti-proliferative effect of methylglyoxal bis(cyclopentylamidino-hydrazone) (MGBCP), a multi-enzyme inhibitor of polyamine biosynthesis, on the growth of Helicobacter pylori was investigated. MGBCP inhibited the cell growth of H. pylori in a dose-dependent manner. The inhibition was partially reversed by the addition of spermidine. Synthesis of macromolecules, DNA, RNA and protein, was inhibited in the spermidine-depleted H. pylori cells. These findings suggest that MGBCP exhibits an anti-proliferative effect on H. pylori by suppression of macromolecule synthesis.

Anti-Bacterial Agents↗

[Determination of cutoff value of serum anti-Legionella antibody titer--microplate agglutination test (MPAT)].

In order to promote the serological diagnosis of legionellosis in the clinical laboratory, the cutoff values of serum anti-Legionella antibody titers for microplate agglutination (MPAT) test were determined. Antibody levels were tested for 178 serum specimens including 98 healthy persons, 22 ordinally workers having either metabolic or renal failure, definitely diagnosed patients of 17 mycoplasmal and 9 chlamydial pneumonia, 32 patients of other bacterial pneumonia. Heat killed unstained cell suspension of each strain of Legionella pneumophila serogroup (SG) 1a, 1b, SGs 2 to 6, L. bozemanii, L. dumoffii, L. gormanii, and L. micdadei were used as antigens. Strains of L. pneumophila SG 1b were mainly isolated from environmental specimens. However, in some Legionella pneumonia cases, etiologic agents were determined as L. pneumophila SG 1 b. Thus the representative strain of SG 1b was used as an antigen for the determination of the patient's antibody titer. Quantitative agglutination was performed by using a 96-well U-bottom microplate for each antigen. Test sera were diluted from 1:16 to 1:256. Results were read after 20 h at 25 degrees C. Cutoff values for 11 antigens were determined, at this moment, as 4-fold or greater increase in level to > or = 1:128 in paired sera, and > or = 1:256 in single serum. However, final diagnosis should be given by over-all coordination of serological results and clinical symptoms together with other laboratory findings. Two culture-positive Legionella pneumonia cases due to either SG3 or 6 in which significant rise of serum antibody titers against organisms of corresponding SG estimated by MPAT method were discussed.

Agglutination Tests↗

Mechanism of the acceleration of CO2 production from pyruvate in liver mitochondria by HCO3-.

To investigate the mechanism by which HCO3- accelerates pyruvate metabolism in guinea pig liver mitochondria, we measured continuously, at pH 7.4 and 37 degrees C, 13C16O2 production from [1-13C]pyruvate by mass spectrometry and NADH concentration by fluorescence and analyzed total malate, citrate, and beta-hydroxybutyrate produced by standard biochemical methods. When [1-13C]pyruvate is added to the mitochondrial suspension, 13C16O2 concentration rises steeply in the first seconds and then slows to a steady lower rate. Carbonic anhydrase (CA) eliminates this initial phase, which shows that decarboxylation of pyruvate produces CO2, not HCO3-, and it does this more rapidly than it can equilibrate without CA. HCO3- (25 mM) increased 13C16O2 production, O2 consumption and total malate and citrate production and decreased NADH concentration and total beta-hydroxybutyrate production. After obtaining the total amount of 13C16O2, malate, citrate, and beta-hydroxybutyrate produced, we calculated that the addition of 25 mM HCO3- to the suspension medium increased the amount of pyruvate decarboxylated by pyruvate dehydrogenase (PDH) 16% and increased the amount carboxylated by pyruvate carboxylase 300%. This supports our initial proposal that HCO3- accelerates the pyruvate carboxylation, which in turn consumes ATP directly and NADH and acetyl CoA secondarily, all of which increase PDH activity. However, we found no acceleration of pyruvate decarboxylation by 0.5 and 1 microM free Ca2+ concentration, unless the mitochondria were uncoupled and ATP was added.

3-Hydroxybutyric Acid↗

Osteopontin expression by osteoclast and osteoblast progenitors in the murine bone marrow: demonstration of its requirement for osteoclastogenesis and its increase after ovariectomy.

Osteoclast development requires cell-to-cell contact between hematopoietic osteoclast progenitors and bone marrow stromal/osteoblastic support cells. Based on this, we hypothesized that osteopontin, an adhesion protein produced by osteoclasts and osteoblasts, plays a role in osteoclastogenesis. Using in situ hybridization, we demonstrate that cells expressing the osteopontin messenger RNA (mRNA) appear after 3 days of culturing murine bone marrow cells. The number of these cells increases thereafter, reaching a peak on day 5. In the same cultures, cells expressing alkaline phosphatase (AP) or tartrate resistant acid phosphatase (TRAP), phenotypic markers for osteoblastic and osteoclast-like cells, respectively, appeared subsequent to the appearance of the osteopontin-positive cells. By means of a combination of in situ hybridization and histostaining, it was shown that the osteopontin mRNA was localized in 30-50% of the AP-positive or the TRAP-positive, as well as in nonspecific esterase (NSE)-positive, cells. The number of cells expressing both the osteopontin mRNA and either one of the three phenotypic markers was significantly increased in bone marrow cultures from estrogen-deficient mice, as compared with controls. Conversely, the number of all three populations of double positive cells was decreased in cultures treated with a specific antimouse rabbit osteopontin antibody or an RGD peptide. These findings indicate that osteopontin is expressed during the early stages of the differentiation of osteoclast and osteoblast progenitors in the bone marrow and that its cell adhesion properties are required for osteoclastogenesis.

Animals↗

Pulmonary involvement in polymyositis and dermatomyositis: sequential evaluation with CT.

OBJECTIVE: The characteristic findings of pulmonary involvement in polymyositis (PM) or dermatomyositis (DM) and the change in findings before and after treatment were evaluated with sequential high-resolution CT studies. MATERIALS AND METHODS: CT images of pulmonary involvement in 19 patients with PM or DM were reviewed. During a period of 2-61 months, 17 of these patients underwent sequential CT before and after treatment with corticosteroids, immunosuppressants, or both. RESULTS: Findings of the initial CT studies included pleural irregularities and prominent interlobular septa (n = 19), ground-glass attenuation (n = 19), patchy consolidation (n = 19), parenchymal bands (n = 15), irregular peribronchovascular thickening (n = 15), and subpleural lines (n = 7). Honeycombing was not detected on any CT images. These findings were more remarkable in the lower portion and the subpleural area of the lungs. In 16 of the 17 patients who underwent sequential CT conditions such as patchy consolidation, parenchymal bands, and irregular peribronchovascular thickening improved, becoming pleural irregularities and prominent interlobular septa, ground-glass attenuation, and subpleural lines on follow-up CT scans. CONCLUSION: Consolidation with patchy and subpleural distribution, parenchymal bands, and irregular peribronchovascular thickening were characteristic and reversible CT findings in patients with PM or DM.

Adult↗