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Two patients with fibromatosis colli (congenital torticollis) presented with lytic lesions in the clavicle at the insertion of the fibrosed clavicular head of the sternocleidomastoid muscle. Biopsy of one lesion showed intraosseous fibrosis. These lesions are probably not uncommon but radiographs are rarely performed in uncomplicated cases.
In situ hybridization was performed to demonstrate hepatocyte growth factor (HGF) mRNA in two patients with normal kidney and in 23 patients with allograft nephrectomy. In situ hybridization was combined with immunohistochemistry to identify HGF-producing cells. In the two patients with normal kidney, no HGF mRNA was obtainable. In 15 of the 23 allograft patients, signals of HGF mRNA were detectable. In six of these 15 patients, the signals were present mainly at the medullocortex junction, and in the other nine patients at the cortex and/or medulla. Strong and frequent signals were present in gland-like structures in 15 cases. Some scattered signals were also present in the fibrosed glomeruli in five cases, in the thickened intimas of large arteries in three cases, and in the arterial muscle coats of two cases. Combined immunohistochemistry and in situ hybridization showed that HGF mRNA-positive cells in gland-like arrangements were also positive for cytokeratin and negative for factor VIII. Cells with HGF mRNA signal and located in the arterial media were also positive for actin. These findings suggest that HGF mRNA is transcribed both in the urinary tubular epithelium and in the mesenchymal cells (fibroblasts, and smooth muscle cells in chronic vascular rejection and endothelial cells and/or mesangial cells in transplant glomerulopathy) in human rejecting kidney.
By means of histometric, enzyme histochemical, and electron microscopic investigations it was demonstrated that the pathological changes in the spleen in vinylchloride-disease are primary. Fibroblastic cells are the only specific splenic cells involved. Fibre-associated reticulum cells of the red pulp and fibroblastic reticulum cells in white pulp are stimulated to produce excessive amounts of the extracellular elements of connective tissue, especially collagen fibrils. The newly formed connective tissue causes obliteration of extracellular blood channels in the red pulp and thus a reduction in the number of pulp-cord macrophages, and scarring of the periaterial lymphatic sheaths. The results of this fibrosing process are characteristic quantitative changes in the splenic histologic structures. These changes are different from those structural alterations occurring in spleens following extrasplenic hemodynamic changes, such as thrombosis of the splenic veins or cirrhosis of the liver.
The study compares the histotopographical lesions of two cases of endomyocardial fibrosis with those of two hearts in sleeping sickness, all of them from Uganda. There was considerable overlapping of the fibrosed zones in endomyocardial fibrosis and the corresponding sites occupied by the chronic inflammatory process in trypanosomiasis. There was a tendency towards fibrosis in the hearts of trypanosomiasis while, in endomyocardial fibrosis, there were mild focal chronic cellular infiltrations. This overlapping and to some extent similarities would suggest that the two conditions may only differ in evolution in time and intensity and that they may be the result of the same inflammatory process. Stipulating a cardiac tropism for African trypanosomes, it is suggested that some African cases of endomyocardial fibrosis may be merely burnt-out lesions of trypanosomal pancarditis. Previous descriptions of carditis in human African and American trypanosomiasis are briefly reviewed, and the present findings are discussed in view of a possible trypanosomal aetiology in some African cardiomyopathies.
A consecutive series of 28 patients (31 knees) with a symptomatic mediopatellar plica without concomitant lesions excised arthroscopically under local anaesthesia in the outpatient department is described. The results were classified as excellent or good in 26/31 cases after a median follow-up period of 15 months. It is concluded that excising a fibrosed mediopatellar plica large enough to cover the medial femoral condyle during flexion is followed by good results; local anaesthesia is sufficient and economical, and arthroscopic excision under local anaesthesia carries a low morbidity.
Tumor-like lymphoplasias of the human lung are named in different ways and differently classified according to their characteristic features: inflammatory, benign, semi-malignant, and malignant. From the cellular point of view the term "lymphocytoma" is appropriate. There are different stages in the course, each respresenting characteristic histological pictures. An early symptom is a strong lymphatic hyperplasia in the walls of small bronchia followed by a voluminous lymphoplasmacellular infiltration of the interalveolar septa with formation of follicles containing germinal centres. The interstitial infiltration may periodically become more "colored" by facultative participation of basophil stem cells, macrophages, reticular cells, eosinophiles and multinucleated giant cells. The alveolar epithelium reacts with hypertrophy and hyperplasy and finally the alveoles are totally obliterated. Fibroses and hyalinoses develop in later stages. Clinically and morphologically they bear a close relationship to the inflammatory lymphoma Saltzstein and to the lymphoid interstitial pneumonia Liebow. Probably there are transitorial stages between these diseases. The cause is to be seen in immunological reactions of the lymphoepithelial system of the lung. Antigens contact immunocompetent cells at the tonsilla pulmonis. Thus the lymphoplasia is put into action. Is the noxa not diminished it may be followed by the formation of autoantibodies, which support the chronic course. The process can become independent and in that way assume the character of a tumor. Such cases may be named immunocytoma.
Symmetrical aseptic necrosis in the marrow of the distal femur was systematically examined in 4 autopsies. According to formal analysis, the self reliant process, with a tendency toward relapse begins with two forms of destruction of the medullary fatty tissue. The consequences are fundamentally the same as those present after necrosis of the extra-medullary fatty tissue; there are only modifications caused location. These modifications include the regular calcification of non-liquifying by fatty-tissue necrosis that fibroses in a net-like manner, and of subsequent bone formation. Spongiosis in incorporated secondarily into necrosis. Medullary necrosis are not caused by vascular lesions and differ therefore from infarct-like necrosis of the bone. The etiology of the medullary steatonecrosis, which probably begins dystrophically, cannot be cleared up morphologically, and is unknown up to now. There are no definite indications for a causal relationship with cortico-steroid therapy. This form of necrosis of the marrow is therefore termed "idiopathic".
Macrophages in malakoplakia contain large amounts of immunoreactive alpha-1-antitrypsin (AAT). The amount of AAT remains unchanged during the morphogenetic stages of the pathological process (early, granulomatous, fibrosing phases), and does not correlate with the number or the presence of Michaelis-Gutmann (M.G.) bodies. Macrophages from other pathological processes, closely resembling malakoplakia cells but without M.G. bodies, did not contain AAT, except for a few macrophages in tuberculosis and xanthogranulomatous pyelonephritis. Whatever the source and the pathogenic role of AAT in malakoplakia, its presence in all macrophages seems to be specific for this disease. Immunohistochemical staining for AAT is therefore proposed as a useful test for an early and accurate differential diagnosis of malakoplakia.
Hypertrophic pachymeningitis is a rare fibrosing inflammatory process involving dura mater and tentorium. In this report we are presenting contrast enhanced MRI findings of an unusual case of pachymeningitis which presented with a periorbital mass due to dural sinuses occlusion and retrograde filling of periorbital veins through superior sagittal sinus.
In an overview of the problem of occupational muscle pain the evidence indicates that injury is more common the greater the load and the worse the posture in which the work is performed. The commonest are backstrains or ligament or joint damage due to overuse. Fatigue is associated with alterations in energy metabolites in muscle while pain is often due to microscopical damage to the cellular architecture. The progress of pathological changes in muscle following occupational injury may be similar to those seen in primary fibromyalgia (fibrositis) because of a final common pathway involving calcium-induced secondary damage. Occupational muscle pain frequently occurs in the muscles supporting the upper limb girdle and head in workers engaged in repetitively performing skilled manipulations or activities requiring high or sustained mental concentration. It is suggested that both occupational myalgia of this kind may be due to an imbalance in the use of muscles for postural activity (holding or supporting fine movements) compared to phasic use in dynamic work. While there are undoubtedly muscular indications of damage these may be secondary to alterations in (unconscious) central motor control mechanisms.
Muscle fibre degeneration and regeneration, inflammation in intramuscular connective tissue and hypoxia in resting muscle are not necessarily associated with pain. However, when sustained or dynamic muscle contractions are performed in an ischaemic muscle, severe pain develops. In the chronic muscle pain syndrome called fibromyalgia (or fibrositis) the most likely cause of the pain is a combination of muscle tension and muscle hypoxia. This conclusion is supported by the finding of a pathological distribution of tissue oxygen tension in painful muscles and a subjective feeling of muscle tension and muscle stiffness in the majority of patients. A decrease in high energy phosphates is found in biopsies from painful muscle. The most characteristic morphological finding is the so called ragged red fibre, which is a finding that can been seen in mitochondrial disorders. The morphological and chemical findings are possibly a consequence of a long standing hypoxia. The possibility that activity in muscle sympathetic nerves is important for the development of chronic muscle pain is discussed.
Considering our own data and after reviewing the literature the following conclusions can be drawn: 1. In 0.41% of all births the incidence of a chorioangioma is to be expected. 2. Small chorioangiomas are much more frequent than large ones. In most cases, they occur solitary, only sometimes multiple. 3. Most of the chorioangiomas are located centrally in placental tissue or at the fetal side in relation to the chorion. 4. A classification of five histological types can be made: Type I: Endotheliomatous chorioangioma; Type II: Capillary chorioangioma; Type III: Cavernous chorioangioma; Type IV: Fibrosing chorioangioma; Type V: Fibroma. 5. There is no significant relationship to the mother's age. The incidence is higher in primipari. The rates of gestones as well as the rates of prematurity and still birth increased with these tumors. 6. Hydramnion as well as fetal complications are entailed with large or multiple tumors.
Combination of the two drugs bleomycin (BLM) and peplomycin (PEP) may enhance their antineoplastic effects; however, it is not known as to whether this enhancement is accompanied by a concomitant increase in toxicity, especially toxic lung damage. A histologic and stereologic investigation was carried out to compare the pulmonary toxicity of BLM, PEP, and a combination of the two drugs in animals. A total of 180 female Wistar rats were randomly assigned to 4 groups: 45 animals were treated with daily i.p. injections of 4 mg/kg BLM, 45 rats received 2.5 mg/kg i.p. PEP daily, 45 animals were given i.p. injections of a combination of 2.5 mg/kg BLM and 1 mg/kg PEP, and 45 rats received 1 ml 0.9% NaCl solution. Histological examination of the lungs demonstrated varying degrees of exudative and fibrosing alveolitis in animals treated with BLM, PEP, and BLM-PEP. Stereological analysis revealed a significant thickening of the alveolar wall after 20-60 days and a significant decrease in the surface density of alveolar walls after 40-60 days in all treated groups. Both histological examination and stereological parameters indicated more pronounced inflammatory changes in the alveolar walls and a prior loss of alveolar surface after 20 and 30 days in animals receiving PEP and PEP-BLM as compared with those undergoing BLM treatment. After 40-60 days, during which time irreversible fibrotic changes prevailed, significant stereological differences between the three treated groups could not be detected. Thus, our experimental observations did not show any potentiation of the toxic pulmonary effect of BLM and PEP following their combined administration.
The pathological changes in the lungs of six patients who were treated by an artificial ventilation with a Bird or Bennett type respirator for three days to six months with oxygen concentrations of 24-100% were examined by light microscopy, studies on thick-sections, reconstruction models and vascular casts, and morphometric methods. After prolonged inhalation of high concentrations of oxygen the lungs showed thickening of the alveolar wall, marked deposition of reticulin fibers and fibroblastic proliferation in the alveolar wall, reduction in the number of capillaries, an abnormal configuration of the capillary network and hyperplasia of alveolar lining cells. These lesions are not specific to this condition, and seemed to be less marked than similar lesions in cases of chronic forms of fibrosing alveolitis, chronic interstitial pneumonia, usual interstitial pneumonia and so-called pulmonary fibrosis. Morphometric results confirm these histological observations and show not only the concentrations of oxygen but also the duration of high and pure oxygen inhalation have important roles for these pulmonary lesions. The main reasons for these lesions seemed to be repeated damage to the capillaries and loss of the normal configuration of the capillary network, accompanied by rearrangement and reconstruction of the two types of reticulin fibers.
We have investigated the interaction between granulocytes and quartz with respect to the expression of complement receptor type 1 (CR1) and the presence of normal human serum (NHS). Quartz down-regulates selectively CR1 on activated granulocytes. This down-regulation is abolished in the presence of both NHS and heat-inactivated NHS (NHS56) but not human albumin. When quartz was preincubated with NHS (quartz-NHS) before exposure to activated granulocytes, a down-regulating effect was observed in contrast to preincubation with NHS56, which did not induce a down-regulation. Preincubation with cytochalasin B reduced the down-regulation of quartz-NHS, indicating a cytoskeleton-dependent internalization of the receptor. The serine protease inhibitor PMSF partly reduced this down-regulation. Our results indicate that the presence of NHS in the alveolar space influences the interaction between quartz and recruited granulocytes with respect to CR1 expression. Since CR1 is an important opsonin receptor and soluble CR1 can modulate the inflammatory response, this may be of importance in the inflammation and fibrosing process induced by quartz in the alveolar space and lung interstitium.
Interleukin-7 (IL-7) is a growth factor for pro-B cells, pre-B cells, and thymocytes and is known to induce the proliferation of normal human peripheral T cells. Moreover, human B and T acute leukemia cells with immature surface markers proliferate in response to IL-7. Here we describe a case of T-chronic lymphocytic leukemia, in which the leukemic cells showed a proliferative response to human recombinant IL-7 in vitro. The patient was a 74-year-old woman with anemia and thrombocytopenia, whose bone marrow was fibrosed and infiltrated with pathologic cells. Surface markers of the leukemic cells were CD2(+), CD3(+), CD5(+), CD7(+), CD8(+), and CD4(-). Both T-cell receptor beta-chain and gamma-chain genes were found to be rearranged by immunogenotypic analysis. The leukemic cells proliferated in response to IL-7 dose dependently. The DNA synthesis of CLL cells was stimulated by not only IL-7 but also IL-2 and IL-4. The IL-7-induced proliferation was not inhibited by antibodies to IL-2 receptors or the anti-IL-4 antibody. These findings indicate that IL-7 may induce the proliferation of peripheral CD8+ T cells, even on its pathological counterpart.
The reparative process following left ventriculotomy was investigated immunohistochemically using anti-type I, II, III, IV, V and VI collagen antibodies, and anti-fibronectin antibody. Wound healing began with proliferation of young fibroblasts positive for type I, III and V collagens at the wound margin; vascular granulation tissue then grew into the injured myocardium followed by deposition of fibrous components immunoreactive with type I and III. At 30 days after operation when almost the entire thickness of the myocardium at the wound was replaced by fibrosing granulation tissue, a small cluster of adipocytes appeared around capillaries at the wound margin. The granulation tissue was gradually replaced by the adipose tissue with establishment of a fibrous union at the subendocardium by 90 days. In addition to type I and III collagens, type VI collagen was detected in a fine fibrillary pattern along thick collagen fibre bundles in the fibrous tissue and around the adipocytes. Fibronectin was distributed diffusely in the granulation tissue and gradually decreased with increase of the fibrous components. These results indicate that the ventriculotomy was finally repaired in the form of a fibrous scar, particularly in the endocardium. There was marked infiltration of adipose tissue in the damaged myocardium. Presumably type VI collagen, as well as type I and type III collagens, plays an important role in wound union.
Six cases of miliary pneumonia are reported, in which the marked increase in antibody titers showed that Mycoplasma pneumoniae was the probable cause. The clinical picture of these patients showed an acute and severe onset, with the appearance of diffuse alveolitis. The outcome of the disease depended on the time of initiation of treatment in relationship to the onset of symptoms. One case was seen to progress to fibrosing alveolitis with persistent impairment of diffusion. This observation suggests the possibility that some cases of pulmonary fibrosis of unknown aetiology may be due to previous mycoplasmal infection.