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PubMed1999

Plasma pharmacokinetics and tissue distribution in CD2F1 mice of Pc4 (NSC 676418), a silicone phthalocyanine photodynamic sensitizing agent.

PURPOSE: Pc4 is a silicone phthalocyanine photosensitizing agent that is entering clinical trials. Studies were undertaken in mice to develop a suitable formulation and analytical methodology for use in pharmacokinetic studies and to define the plasma pharmacokinetics, tissue distribution, and urinary excretion of Pc4 after i.v. delivery. METHODS: An HPLC method suitable for separation and quantification of Pc4 was developed and validated for use in mouse plasma, tissues, and urine. The stability of Pc4 was characterized in a variety of formulations as well as in mouse plasma. Before pursuing pharmacokinetic studies, preliminary toxicity studies were undertaken. These studies utilized Pc4 formulated in diluent 12:0. 154 M NaCl (1:3, v:v). Pharmacokinetic studies involved Pc4 doses of 40 mg/kg, 10 mg/kg and 2 mg/kg administered as i.v. boluses to female, CD2F1 mice. Doses of 40 mg/kg, 10 mg/kg, and 2 mg/kg were studied with drug formulated in diluent 12:0.154 M NaCl (1:3, v:v). Doses of 10 mg/kg and 2 mg/kg were also studied with drug formulated in a vehicle consisting of polyethylene glycol:Tween 80:0. 01 M sodium phosphate buffer, pH 7.0 (40:0.2:59.8, v:v:v). Compartmental and non-compartmental analyses were applied to the plasma concentration-versus-time data. Concentrations of Pc4 were also determined in a variety of tissues, including brain, lung, liver, kidney, skeletal muscle, skin, heart, spleen, and abdominal fat. Urine was collected from animals treated with each of the doses of Pc4 mentioned above, and daily, as well as cumulative drug excretion was calculated until 168 h after treatment. RESULTS: At a dose of 80 mg/kg, two of five male and two of five female mice were dead by 24 h after injection. Pathologic examination revealed gross findings of blue discoloration affecting many tissues, with lungs that were grossly hemorrhagic and very blue-black. Microscopic examination of the lungs revealed mild acute interstitial pneumonia, with perivascular edema and inflammation, and a detectable margination of neutrophils around larger pulmonary blood vessels. Animals sacrificed 14 days after treatment showed mild granulomatous pneumonia, characterized by clusters of multi-nucleated giant cells, with fewer macrophages and neutrophils. The giant cells frequently contained phagocytized particles, which were clear and relatively fusiform. All mice treated with 40 mg/kg or 20 mg/kg survived and returned to pretreatment weight during the 14 days after treatment. Intravenous bolus delivery of Pc4, at a dose of 40 mg/kg, produced "peak" plasma Pc4 concentrations between 7.81 and 8.92 microg/ml in mice killed at 5 min after injection (the earliest time studied after drug delivery). Sequential reduction of the Pc4 dose to 10 mg/kg in diluent 12:0.154 M NaCl (1:3, v:v), 10 mg/kg in polyethylene glycol:Tween 80:sodium phosphate buffer (40:0.2:59.8, v:v:v), 2 mg/kg in diluent 12:0.154 M NaCl (1:3, v:v), and, finally, 2 mg/kg in polyethylene glycol:Tween 80:sodium phosphate buffer (40:0.2:59.8, v:v:v) resulted in "peak" plasma Pc4 concentrations between 2.07 and 3.24, 0.68 and 0.98 microg/ml, and 0.29 and 0.41 microg/ml, respectively. Pc4 persisted in plasma for prolonged periods of time (72-168 h). Non-compartmental analysis of plasma Pc4 concentration-versus-time data showed an increase in area under the plasma Pc4 concentration-versus-time curve (AUC) when the dose of Pc4 increased from 2 mg/kg to 40 mg/kg. Across the 20-fold range of doses studied, total body clearance (CL(tb)) varied from 376 to 1106 ml h(-1) kg(-1). Compartmental modeling of plasma Pc4 concentration versus time data showed the data to be fit best by a two-compartment, open, linear model. Minimal amounts of Pc4 were detected in the urine of mice. After i.v. bolus delivery to mice, Pc4 distributed rapidly to all tissues and persisted in most tissues for the duration of each pharmacokinetic study. Tissue exposure, as measured by AUC, increased in a dose-dependent fash

Animals↗
PubMed2002

Pharmacokinetics of a benzodithiin (RD3-0028) following aerosol treatment in rat.

1. RD3-0028, a benzodithiin compound, has potent antiviral activity against respiratory syncytial virus (RSV) in cell culture. The compound also inhibits growth of RSV and improves pathologic changes of interstitial pneumonia in the immunosuppressed mouse when delivered by small-particle aerosol. 2. In the present study, the absorption, distribution and excretion of 14C-RD3-0028 were compared in rat following either a single aerosol treatment or oral administration. 3. The plasma concentration was maintained at the same level from 5 min to 1 h, and decreased with a half-life of 2.2 +/- 0.1 h for 1-8 h. 4. The excretion of radioactivity in the urine and faeces at 24 h after aerosol treatment was 89.3 and 4.5%, respectively, indicating that almost all the radioactivity was rapidly excreted in the urine. The excretion of total radioactivity was 98.9% within 168 h. 5. The concentrations of radioactivity in the lung and trachea following aerosol treatment were higher than those in other tissues, and were detected even at 72 h. 6. These results suggest that the aerosol treatment might be useful for delivering RD3-0028 to the respiratory tract of RSV-infected patients.

Administration, Oral↗
PubMed1985

Mononuclear-cell pulmonary vasculitis in NZB/W mice. I. Histopathologic evaluation of spontaneously occurring pulmonary infiltrates.

This report describes the spontaneous occurrence of pulmonary vasculitis in NZB/W mice, a well-characterized autoimmune strain of mice. These mice develop pulmonary vasculitis in an age-related fashion. Mild perivascular and peribronchiolar lymphoid hyperplasia is first seen at 4 months of age and progresses into severe hyperplasia by 8 months. This precedes the development of angiodestructive lesions, which are first noticeable at 10 months. By 12 months of age all mice show multilobe disease characterized by transmural infiltration of the vascular walls by plasma cells, histiocytes, and mature lymphocytes. Mitotic figures and necrosis are rare to absent. Vessel lumens are markedly narrowed and obliterated in severe cases, with focal disruption of the limiting elastic membranes. In mice older than 10 months of age, there is extension of the infiltrate into the interstitium in a manner similar to that of lymphoid interstitial pneumonia. Arteries and veins are equally affected. The cellular infiltrates and pattern of involvement bears similarity to various pulmonary vasculitides in humans. This is the first report of spontaneous pulmonary vasculitis in NZB/W mice.

Aging↗
PubMed1977

Polymyositis and polyarthritis associated with systemic lupus erythematosus in a dog.

Systemic lupus erythematosus with polymyositis and polyarthritis was diagnosed in a 7-year-old female Standard Poodle. Pertinent clinical signs included extreme muscular weakness, muscle wasting, atrial fibrillation, and dysphagia due to megaesophagus. Aspiration pneumonia secondary to the megaesophagus contributed to the death of the dog. Serum muscle enzyme activities were increased. Electromyographic findings included fibrillation potentials, positive sharp waves, increased insertional activity, and bizarre high-frequency repetitive potentials. Histopathologic findings in skeletal muscle included myofiber necrosis and phagocytosis; regeneration of myofibers; perivascular and interstitial infiltrations of macrophages, lymphocytes, and plasma cells; and type I and II myofiber degeneration and vacuolation.

Animals↗
PubMed2005

Reversed halo sign in pulmonary paracoccidioidomycosis.

OBJECTIVE: The purpose of this study was to evaluate the prevalence of the reversed halo sign in pulmonary paracoccidioidomycosis. MATERIALS AND METHODS: The high-resolution CT scans (1- or 2-mm collimation scans) of 148 consecutive patients with proven pulmonary paracoccidioidomycosis were reviewed to determine the prevalence of the reversed halo sign in these patients. The reversed halo sign was defined as central ground-glass opacity surrounded by a crescent or ring of consolidation. The images were reviewed by two radiologists who reached a decision by consensus. RESULTS: A reversed halo sign was found in 15 patients (10%), including 13 men and two women ranging in age from 20 to 58 years (mean, 48 years). Three patients had only one reversed halo sign, one had two lesions, and the remaining had multiple lesions. The size of the sign ranged from 10 to 50 mm (average, 20 mm). In two cases the reversed halo sign was the only finding on CT. The most common associated findings seen in the remaining 13 patients included bilateral patchy areas of ground-glass attenuation (n = 10), parenchymal bands (n = 8), and small centrilobular nodules (n = 8). Three patients underwent surgical lung biopsy. Histologically the central area of the lesions consisted of an inflammatory infiltrate in the alveolar septa, composed of macrophages, lymphocytes, plasma cells, and some giant cells, with relative preservation of the alveolar spaces. The periphery of the lesion consisted of dense and homogeneous intraalveolar cellular infiltrate. There was no evidence of organizing pneumonia. CONCLUSION: The reversed halo sign is seen in approximately 10% of patients with paracoccidioidomycosis. In these patients, this sign reflects the presence of a central area of predominantly interstitial inflammation surrounded by predominantly air-space infiltration.

Female↗
PubMed2005

[Lymphocytic interstitial pneumonia in primary Sjögren syndrome].

Ljmphocytic interstitial pneumonia (LIP) is a rare form of interstitial pneumonia. It can occur as a idiopathic disease however most frequently associated with other diseases, particularly Sjogren syndrome. We present a 58 years old woman, with primary Sjögren syndrome who developed after 7 years interstitial lung disease. LIP was diagnosed on the basis of histological examinations of specimens obtained by open lung biopsy. Diffuse infiltrations composed of small polyclonal lymphocytes, plasma cells with reactive follicules were found. Infiltrates observed in bronchial and bronchiolar walls expanded into interlobular and alveolar septae. Prednisone in a dose of 40 mg per day was introduced and clinical, radiological, spirometric and gasometric improvement was observed. The dose of prednisone was gradually reduced but is still continued.

Collagen Diseases↗
PubMed1999

[Autoimmune hepatitis with drug-induced pneumonia due to Sho-saiko-to].

A 71-year-old woman was being treated with Sho-saiko-to for chronic hepatitis. On the 14th day, she complained of dyspnea; chest X-ray films and CT scans revealed ground-glass shadows in both lung fields. Under a suspected diagnosis of drug-induced pneumonia, Sho-saiko-to was discontinued and the patient was started on prednisolone. After several days, her laboratory data and chest X-ray findings were markedly improved. Cell analysis of bronchoalveolar lavage fluid disclosed an increase in the lymphocyte fraction and a depressed CD 4/CD 8 count. Lymphocyte stimulation tests of Sho-saiko-to and its ingredients, Ohgon and Hange, were positive in the case of peripheral lymphocytes, but not bronchoalveolar lavage lymphocytes. These findings yielded a diagnosis of drug-induced pneumonia caused by Sho-saiko-to. A histologic examination of needle biopsy specimens from the liver revealed severe lymphocytic infiltration into the tissues of Glisson's capsule and liver parenchyma, and mild infiltration by plasma cells into tissues surrounding Glisson's capsule. To our knowledge, this is the first case of autoimmune hepatitis with Sho-saiko-to-induced pneumonia to be reported.

Aged↗
PubMed1986

[Interstitial pneumopathies during amiodarone treatment. Determination of serum amiodarone, typing of lymphocytes from bronchiolo-alveolar lavage].

We report 6 cases of diffuse interstitial pneumonia complicating therapy. The patients' study included the determination of amiodarone plasma level by high performance liquid chromatography (HPLC) and a study of lymphocyte subpopulations in alveolar lavage (wash cut). The mean cumulative dosage of amiodarone was 229 g; clinical symptoms were mainly weight loss, asthenia, dyspnea and dry cough. Bronchiolo-alveolar lavage fluids contained numerous lymphocytes, of which were T cells with a predominance of T8 lymphocytes. This is compatible with an immunoallergic mechanism as suggested in allergic alveolitis and in other drug induced pulmonary diseases. The determination of plasma amiodarone level performed after amiodarone withdrawal consistently showed a level inferior to the toxic one. These data confirm the lack of correlation between the pneumonitis outbreak and the amiodarone plasma level. Study of the red cell concentration of amiodarone and its major metabolites seems to be of greater interest.

Aged↗
PubMed1978

Anchoring fibrils. A new connective tissue structure in fibrotic lung disease.

Electron microscopic studies of lung were made and compared in 17 patients with lung disease (10 with idiopathic pulmonary fibrosis, 3 with collagen--vascular diseases, 3 with sarcoidosis, and 1 with chronic eosinophilic pneumonia) and in 5 control patients. In control patients, the alveolar epithelial cells were normal, and no hemidesmosomes were present between the plasma membranes and the basal laminae. In comparison, cuboidal alveolar epithelial cells were present in 15 of the patients with fibrotic lung disease; in 9 of these the alveolar epithelial cells were multilayered. In 7 of the latter 9 patients (5 with idiopathic pulmonary fibrosis and 2 with collagen-vascular diseases), the basal laminae of the alveolar epithelial cells were attached to the plasma membranes by hemidesmosomes and to the underlying interstitial connective tissue by "anchoring fibrils." These fibrils measured from 4000 to 6000 A in length and from 200 to 600 A in width. One or both ends of the anchoring fibrils inserted into thebasal lamina, often forming arcs through which collagen fibrils and connective tissue microfibrils penetrated. Anchoring fibrils showed a complex pattern of transverse banding, which differed from that of collagen and appeared to be symmetric about the center of the fibril. These anchoring fibrils, which resemble those in normal skin and other tissues, were not found in lungs of control patients. In addition, there was a significant correlation between the severity of the pulmonary fibrosis and the presence of anchoring fibrils. These observations suggest that in severe fibrotic lung disease, anchoring fibrils reinforce the attachment of the basal lamina of multilayered alveolar epithelial cells to interstitial connective tissue.

Adult↗
PubMed1983

Ultrastructural pathology of 3-methylindole-induced pneumotoxicity in cattle. I. Glycogen accumulation in the alveolar type II cells and tubular myelin accumulation in the alveoli.

3-Methylindole (3MI) was orally administered as a single dose of 0.1-0.2 gm/kgm which then produced acute pulmonary edema in cattle. Electronmicroscopic examination of lung tissue collected after 72 hours revealed vesiculation and desquamation of alveolar type I cells as well as hyperplasia of the alveolar type II cells. Hyaline membrane formation, along with massive accumulation of tubular myelin in the alveolar spaces, was observed. Pulmonary capillaries were occluded with microthrombi and leukocytes infiltrated the interstitium as well as the alveoli. Accumulation of large aggregates of glycogen in the alveolar type II cells were the most unusual changes seen in the experimental animals. It is suggested that accumulation of tubular myelin is a structural manifestation of surfactant inactivation by the plasma proteins. Furthermore, the disease process may be complicated by a compositional or quantitative defect in the surfactant produced by the alveolar type II cells, which are pathologically loaded with glycogen.

Animals↗
PubMed2004

Expression of glutaredoxin is highly cell specific in human lung and is decreased by transforming growth factor-beta in vitro and in interstitial lung diseases in vivo.

Glutaredoxins (Grx) are thiol-disulfide oxidoreductases with antioxidant capacity and catalytic functions closely associated with glutathione, an antioxidant abundantly present in human lung. The present study investigated the expression of both human glutaredoxins in cultured human lung cells and lung homogenates by reverse-transcription polymerase chain reaction and Western blotting. Immunohistochemical studies were conducted with 38 human lung specimens, including healthy lung, parenchymal sarcoidosis, extrinsic allergic alveolitis, and usual interstitial pneumonia (UIP). The ultrastructural localization of Grx1 was assessed by immunoelectron microscopy. In addition, cultured airway epithelial cells were exposed to tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta. Both Grx1 and Grx2 could be detected at the mRNA and protein level in cultured human lung cells, but only Grx1 was prominently expressed in lung homogenates and alveolar macrophages. Immunohistochemically, Grx1 was highly concentrated to alveolar macrophages and weakly positive in the bronchial epithelium. Grx1 was ultrastructurally localized to the plasma membrane, cytoplasmic vacuoles, and nucleus. The expression of Grx1 decreased in alveolar macrophages of sarcoidosis and allergic alveolitis compared with the case for controls (P < 0.001), and bronchial epithelium of these diseases revealed no Grx1 immunoreactivity. Fibroblast foci and other fibrotic areas in UIP were mainly negative. In A549 cells, Grx1 was down-regulated by TGF-beta, whereas TNF-alpha caused no clear effect. Overall, high expression of Grx1 in alveolar macrophages suggests its importance in the primary defense of human lung. Decreased expression of Grx1 further suggests the impairment of this system both in inflammatory and fibrotic lung diseases, consistent with the down-regulation of Grx1 by TGF-beta in vitro.

Blotting, Western↗
PubMed1994

[A case report of light and heavy chain deposition disease (IgG2 lambda)].

A 73-year-old male was admitted to the renal division of our hospital because of hypertension, proteinuria and bilateral pretibial edema. Eight years previously, he was diagnosed as being afflicted with interstitial pneumonia on the basis of a chest X-ray examination. Laboratory tests conducted during the current admission showed normocytic normochromic anemia, renal dysfunction and mild proteinuria. Total IgG was normal, but a high proportion of IgG2 was observed. M-protein in the serum was positive for both IgG lambda and Bence Jones protein (lambda type). A bone marrow biopsy showed the proportion of plasma cells to be 10.6%, but atypical cells were not found. We diagnosed the patient's condition as plasma cell dyscrasia. Light microscopy examination of a renal biopsy specimen showed moderate mesangial proliferation with a deposition of PAS-positive and Congo red negative materials in the mesangial area: nodular gomerulonephritis was seen in some glomeruli. Immunofluorescence revealed IgG and lambda light chains, strong linear staining along the glomerular basement membrane and tubular basement membrane and positivity in the mesangial area. Results of staining for IgA, IgM, fibrinogen and C3 were weakly positive in the mesangium area, while those for C4, Clq and free kappa were negative. Positive staining of IgG2 was seen by immunoperoxidase study, but the tissue was negative for IgG1, IgG3, IgG4. Electron microscopy demonstrated a dense granular deposition in the mesangial, subendothelial and peritubular area and a microfibrillar structure in the mesangial area. The diameter of the microfibrillar structure was 14 nm on the average.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Changes in lung morphology and cell number in radiation pneumonitis and fibrosis: a quantitative ultrastructural study.

We used stereologic-morphometric techniques to obtain a detailed quantitative picture of the changes in lung ultrastructure of rats at 12 and 26 weeks after unilateral thoracic irradiation with 3000 cGy. At 12 weeks post-radiation, the total number type 1 epithelial cells, type 2 epithelial cells and capillary endothelial cells were decreased 50-70%, total type 1 epithelial and capillary surface areas were decreased 55-60%, and the total volume of intracapillary blood was decreased 75%. The interstitial cells and matrix together accounted for more than 9% of the peripheral lung tissue volume including air, compared to 3% in controls. The numerical density of interstitial cells was increased to 3-fold the control value. The numerical density of interstitial cells was increased to 3-fold the control value. Although fibroblasts still comprised the largest interstitial cell subgroup, the numerical density of mast cells was increased over 150-fold and other inflammatory and immune cells were increased to a lesser extent. At 26 weeks post-radiation, the number, volume, and surface area of the type 1 epithelium and capillary endothelium had further decreased to only 5-10% of control values. The total number of type 2 epithelial cells was reduced by 75% but the volume density was actually increased because of a 4-fold increase in the mean cell volume. The interstitial cells and matrix now comprised over 77% of total peripheral lung tissue volume including air as compared to 6% in controls. Mast cells and plasma cells comprised 11% and 19% of all interstitial cells respectively and the densities of these cells were 540 and 180-fold the control value respectively. The relation of these morphometric findings to the results of previous morphologic studies is discussed.

Animals↗
PubMed1985

[Lymphocytic interstitial pneumopathy and primary pulmonary lymphoma. Differential diagnosis].

Two cases of lymphoid interstitial pneumonia, diagnosed according to Liebow's criteria, are reported. In both cases an extra-thoracic lymphoma developed 3 and 6 years respectively after the interstitial pneumonia was diagnosed. Simultaneously, the radiological images of the lungs became more pronounced. Only a few similar cases have been published. This raises the question of whether lymphoid interstitial pneumonia and lymphomas are distinct entities, especially since the histological and immunopathological discriminating criteria seem to be discussed.

Diagnosis, Differential↗
PubMed1971

Fatal encephalopathy complicating lymphoid interstitial pneumonia.

The case is reported of a young woman who suffered from lymphoid interstitial pneumonia. Involvement of the brain by what appeared to be an identical pathological process led to her death, and the orbital tissues were also involved at one stage. The cause of this condition is unknown, but the hypotheses are put forward that it may represent one facet of delayed hypersensitivity or that a slow virus is the responsible aetiological agent. Although lymphoid interstitial pneumonia has previously been reported as an isolated entity, the evidence from this case suggests that it might represent part of pluri-systemic disease.

Adult↗
PubMed1988

Lymphocytic interstitial pneumonia.

Lymphocytic interstitial pneumonia is a common complication of HIV infection in children, but uncommon in adults. It is characterized clinically by the presence of cough and dyspnea, diffuse pulmonary infiltrates on chest x-ray, restrictive pulmonary dysfunction, and hypoxemia. This constellation of findings usually erroneously suggests PCP, and a lung biopsy is necessary to establish the diagnosis. Typical microscopic findings include diffuse infiltration of the pulmonary interstitium with a mixture of lymphocytes and plasma cells; immunohistologic studies reveal that in association with HIV infection, these lymphocytes are T cells. The pathogenesis of LIP in patients with HIV infection is not known. It is believed that it represents a tissue response to EBV infection, HIV infection of the lung, or both. Although patients with LIP may respond dramatically to corticosteroid therapy, others may improve with no treatment. Unfortunately, most patients eventually succumb to other complications of HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed2006

[A case of interstitial pneumonia accompanying SIADH].

A 75-year-old man was transferred to our hospital on November 28, 2003 because of acute aggravation while being treated for interstitial pneumonia superimposed on pneumoconiosis at a local hospital. Upon admission, oxygen inhalation therapy and antimicrobial chemotherapy were started for the interstitial pneumonia. In addition, since he showed hyponatremia from admission, a saline load was administered and the clinical course was observed. However, disturbance of consciousness developed on January 5, 2004. At that time, the serum sodium was 115mEq/l. Since secretion of antidiuretic hormone (SIADH) had continued despite a low plasma osmolarity, we diagnosed syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We initiated treatment with water restriction and saline load, but no remarkable improvement was observed. From February 7, 40mg /day prednisolone was started because of aggravation of interstitial pneumonia. As a result, the respiratory status and image findings improved, and serum sodium level was normalized. This case was considered to be SIADH secondary to interstitial pneumonia. Among respiratory tract diseases, SIADH is often caused by small cell lung carcinoma, although it may also occur concurrently with other respiratory tract diseases. Since hyponatremia may manifest grave disturbance of consciousness, investigation of the cause is important.

Aged↗