Literature watch. Peritumor Lymphatics Induced by Vascular Endothelial Growth Factor-C Exhibit Abnormal Function.
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Animals↗
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LYMPHATICS AND THE GUT.
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Congenital Abnormalities↗
Vascular permeability factor/vascular endothelial growth factor induces lymphangiogenesis as well as angiogenesis.
Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF, VEGF-A) is a multifunctional cytokine with important roles in pathological angiogenesis. Using an adenoviral vector engineered to express murine VEGF-A(164), we previously investigated the steps and mechanisms by which this cytokine induced the formation of new blood vessels in adult immunodeficient mice and demonstrated that the newly formed blood vessels closely resembled those found in VEGF-A-expressing tumors. We now report that, in addition to inducing angiogenesis, VEGF-A(164) also induces a strong lymphangiogenic response. This finding was unanticipated because lymphangiogenesis has been thought to be mediated by other members of the VPF/VEGF family, namely, VEGF-C and VEGF-D. The new "giant" lymphatics generated by VEGF-A(164) were structurally and functionally abnormal: greatly enlarged with incompetent valves, sluggish flow, and delayed lymph clearance. They closely resembled the large lymphatics found in lymphangiomas/lymphatic malformations, perhaps implicating VEGF-A in the pathogenesis of these lesions. Whereas the angiogenic response was maintained only as long as VEGF-A was expressed, giant lymphatics, once formed, became VEGF-A independent and persisted indefinitely, long after VEGF-A expression ceased. These findings raise the possibility that similar, abnormal lymphatics develop in other pathologies in which VEGF-A is overexpressed, e.g., malignant tumors and chronic inflammation.
Adenoviridae↗
Molecular mechanisms of lymphangiogenesis.
Although the process of vascular development has been well documented, little is understood about lymphatic vasculature formation, despite its importance in normal and pathologic conditions. The dysfunction or abnormal growth of lymphatic vessels is associated with lymphedema and cancer metastasis. The recent discovery of lymphangiogenic growth factors vascular endothelial growth factor (VEGF)-C and VEGF-D and of their receptor, VEGFR-3, on lymphatic endothelial cells has started to provide an understanding of the molecular mechanisms of lymphangiogenesis. In addition, other genes that participate in the specification of lymphatic endothelial cells and the modulation of lymphatic vascular development have been identified. The capacity to induce or inhibit lymphangiogenesis by the manipulation of such molecules offers new opportunities to understand the function of the lymphatic system and to develop novel treatments for lymphatic disorders. This review describes the main players in lymphangiogenesis that have been identified so far and the attempts to shed some light on the mysteries surrounding this process.
Animals↗
Lymphatic and venous examination of the ulcerated leg: a preliminary report.
BACKGROUND: It has been widely accepted that deep venous thrombosis and venous incompetence initiate a series of events resulting in various ulcerations. The role of the lymphatic system in the progression of these events has not been extensively studied. METHODS: Twenty-three patients with nonarterial ulcerations of the legs were examined by phlebography and lymphangiography. All had recurrent ulcerations associated with nonpitting edema, brawny induration, and dermatitis characteristic of the postphlebitic syndrome. Arterial circulation was normal in all patients. RESULTS: Phlebographic abnormalities found were the presence of communicating vein incompetence in all 23 patients, varicose veins in six, and deep venous occlusion in one. Lymphatic abnormalities were also present in all patients. Extravasation in the area of the ulcer was seen in eight patients, dermal backflow in six, tortuosity and irregularity of the channels in four, and retention of contrast agent for more than 24 hours in seven. CONCLUSIONS: Significant abnormalities of the lymphatic system exist in patients with leg ulcers caused by the postthrombotic syndrome.
Humans↗
Cutaneous oozing of lymphatic fluid after interventional cardiac catheterization in a patient with Noonan syndrome.
A 15-year-old girl with Noonan syndrome, intestinal lymphangiectasia and severe valvar pulmonary stenosis had an abnormal lymphangioscintigram that showed intense activity in the inguinal regions bilaterally. Cutaneous oozing of lymphatic fluid from the groin wound complicated percutaneous balloon pulmonary valvoplasty. This previously unreported complication highlights the risk of damage to abnormal lymphatic channels in patients with Noonan syndrome who undergo interventional catheterization.
Adolescent↗
[Chylous reflux and chylous ascites in lymphatic dysplasia, with the lymphographic demonstration of mediastinal and retroperitoneal lymphatic cysts].
Two patients with congenital dysplasia of the lymphatic system and with chylous ascites are described. In one 24-year old woman with this rare condition, it was possible to demonstrate for the first time numerous mediastinal lymphatic cysts during lymphangiography. Both patients showed an abnormality of the retroperitoneal lymphatics, consisting of lymphatic dilatation and cysts. In the investigation of chylous ascites, direct lymphangiography must be regarded as a valuable and necessary investigation.
Adult↗
Primary lymphatic dysplasia in children: chylothorax, chylous ascites, and generalized lymphatic dysplasia.
Primary lymphatic "dysplasia", a congenital maldevelopment, interferes with function of the lymphatic system and causes effusion of chyle or lymph into the limbs and pleural or peritoneal cavity. Between 1955 and 1982, 38 Mayo Clinic patients were found to have a chylous effusion or dysplasia of the lymphatic system. In 22, the condition was secondary to surgery or other medical problems and in 16 it was primary. These cases were separated into three categories: chylothorax, chylous ascites, and generalized lymphatic dysplasia. Conservative therapy, such as a restricted fat diet or total parenteral nutrition with repeated thoracentesis or paracentesis, was effective in the children with isolated abnormalities of the lymphatic system (75% resolution rate, no deaths). All five children with documented generalized dysplasia reported in the literature had died; of the three reported here, one has died and two have become progressively worse.
Adolescent↗
Total parenteral nutrition as a primary therapeutic modality for congenital chylous ascites: report of one case.
Congenital chylous ascites in the neonatal period is a rare entity. It is primarily related to congenital abnormalities of the lymphatics. We present a case in which ascites was detected by prenatal ultrasonogram. No evidence of congenital cytomegalovirus infection, intrauterine meconium peritonitis, or intestinal or genitourinary system abnormalities was found. Congenital chylous ascites was confirmed via an abdominal sonogram and diagnostic paracentesis. After 26 days of NPO and total parenteral nutrition, the newborn hadfully recovered.
Chylous Ascites↗
Congenital lymphatic oedema in Ayrshire calves.
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Animals↗
Chylothorax and lymphangiomas of bone: unusual manifestations of lymphatic disease.
A patient with chylothorax, mediastinal lymphangiomatous malformation of the thoracic duct, and multiple lymphangiomas of bone is reported. If a patient has radiographic findings of increased pleural fluid with multiple lucent lesions of the skeleton, the possibility of a generalized abnormality in the lymphatic system should be considered. Early diagnosis and treatment can prevent a protracted course and wasting of the body due to the loss of essential body nutrients in the chylous fluid.
Adolescent↗
Congenital malformations of the cervicothoracic lymphatic system: embryology and pathogenesis.
Familiarity with the embryology of the lymphatic system is helpful in understanding the pathogenesis and radiologic appearance of lymphangiomas of the cervicothoracic region. By considering anatomic location and radiologic appearance, one can predict the type of lymphangioma present, the primordial lymph sac from which the malformation arose, and when it formed in embryonic life. Cystic hygromas are composed of large, dilated lymphatic spaces. They form when a primordial lymph sac fails to reestablish communication with the central venous system from which it arose. These lesions may also result from an aberrant bud arising from a primordial lymph sac. Cavernous and capillary lymphangiomas are composed of smaller lymphatic channels. They form from abnormally sequestered buds of the developing lymphatic mesenchyme responsible for the fine meshwork of terminal branches in the periphery of the embryo. Their growth may be inhibited by the relatively tougher tissues in the periphery (eg, skin and muscle) compared with the relatively loose fatty connective tissue in which cystic hygromas form. Not only can all types of lymphangioma occur in one lesion, but lymphatic and vascular malformations may also coexist.
Humans↗
Lymphoedema: pathophysiology and classification.
This paper reviews current knowledge and hypotheses about the physiology of lymph production and lymph flow and the aetiology and classification of lymphoedema. One of the earlier contributions in the 1930's by Allen suggested that primary lymphoedema was caused by congenital underdevelopment of lymph vessels. At that time he described two clinical varieties (congenital and praecox) but later suggested a further subdivision into inflammatory and non-inflammatory types of lymphoedema. Kinmonth in 1957 produced the first clinical classification dividing all cases into primary or secondary lymphoedema but at that time gave no indication as to the cause of the primary variety. In the 1950's Kinmonth also developed a radiological classification which has contributed considerably to our knowledge of the anatomical abnormalities of the lymphatic system in primary lymphoedema. However, despite the widespread use of Kinmonth's classification the lymphographic appearances in primary lymphoedema give little or no clue to the aetiology of the disease process. The aetiology of primary lymphoedema is not known. There are various descriptive classifications based on age of onset and radiological findings for instance, but none attempts to explain the pathophysiology of the disease. We have therefore described our current knowledge of the known physiology and the potential abnormalities of the collection and passage of lymph from the interstitial space to the blood system. Based on this we have presented a simple classification of the aetiology of lymphoedema. Thus primary lymphoedema may be defined as lymphoedema caused by a primary abnormality or disease of the lymph conducting elements of the lymph vessels or lymph nodes. Secondary lymphoedema is oedema caused by disease in the nodes or vessels that began elsewhere (e.g., neoplasia or filariasis), or lymphocytic proliferative disorders such as Hodgkin's disease or following surgical extirpation of lymph nodes or vessels. There are three groups of primary lymphoedema in which the functional abnormality and its cause are known; namely (a) large vessel abnormalities such as congenital aplasia of the thoracic duct or cysterna chyli, (b) congenital lymphatic valvular incompetence or congenital aplasia and (c) lymph node fibrosis. The remainder are characterised by a reduced number of lymphatics on lymphography. Such patients can be described as having obliterated lymphatics. If they present within a few years of birth they were probably born with too few lymphatics. However, those who present later in life may have acquired obliterative disease, the cause of which is still obscure.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Lymphatic distribution of the stomach in normal, inflammatory, hyperplastic, and neoplastic tissue.
Prompted by the lack of knowledge of the distribution of gastric lymphatics and the discrepancy between the incidence of lymph node metastases from intramucosal gastric carcinoma versus intramucosal colonic carcinoma, we undertook a study of the distribution of lymphatics in normal, abnormal non-neoplastic, and neoplastic gastric mucosas. The study involved the histologic, immunocytochemical, and electron microscopic evaluation of a total of 47 gastric biopsy, polypectomy, and resection specimens and showed that the gastric lymphatics normally begin as a plexus of vessels immediately superficial to, within, and below the muscularis mucosae. The upper two-thirds of the gastric lamina propria is normally devoid of lymphatics. This distribution is maintained throughout the cardia, fundus, and antrum and is also maintained in hyperplastic and neoplastic tissues. However, in patients with severe atrophic gastritis in which the overall height of the gastric mucosa is markedly decreased, lymphatic capillaries may be found near the surface epithelium. The relevance of these findings to the behavior of early gastric cancer is discussed.
Gastric Mucosa↗
Lymphatic filling during knee arthrography.
Six cases of lymphatic filling during knee arthrography have been recorded in literature, all of which have had advanced rheumatoid arthritis. We report a case of lymph vessel filling from a popliteal cyst in a young male nonrheumatoid patient. It is concluded that abnormal synovial-lymphatic connection in the knee joint may occur also in other forms of synovial pathology and such a finding does not indicate rheumatoid inflammation.
Adult↗
Further delineation of Hennekam syndrome.
We report four children from four inbred Arab families with varying manifestations of Hennekam syndrome and additional features that have not been previously reported. These include abnormalities of the middle ear, anomalous pulmonary venous drainage, interrupted inferior vena cava, polysplenia, crossed renal ectopia, median position of the liver and multiple cavernous haemangiomas. In addition, in one case lymphoedema was absent and oedema due to hypoproteinaemia appeared at 6 years of age. Since anomalies of the veins and the consequent developmental abnormalities of the lymphatics might lead to alterations in the fluid balance of the embryo, we hypothesize that altered fluid dynamics due to defective vascular and lymphatic development might disrupt critical events in craniofacial morphogenesis resulting in Hennekam syndrome.
Abnormalities, Multiple↗
Bronchogenic carcinoma associated with chronic lymphatic leukemia.
This report pertains to the development of bronchogenic carcinoma in 4 elderly patients with chronic lymphatic leukemia. The abnormal radiologic shadows in the lung (confined to the upper lobes and hili) were noted 30-60 months after recognition of the hematologic abnormality. Spread to ipsilateral or contralateral lymph nodes was common. After the appearance of lung carcinoma, the patient's course was downhill, with an average survival period of 2 months. The development of a new pulmonary lesion in any patient with chronic lymphatic leukemia should arouse the suspicion of malignancy and lead to prompt investigation.
Aged↗
The clinical significance of proteinuria in patients with nonparasitic chyluria.
Five patients with heavy proteinuria and nonparasitic chyluria due to congenital abnormalities of the lymphatic system are described. Renal biopsies confirmed the clinical suspicion of an underlying glomerulonephritis. The coexistence of glomerulonephritis and chyluria in these patients was thought coincidental. Tests of value in detecting a concomitant glomerulonephritis in these patients with chyluria include urinary RBC morphology, quantitation of 24-hour urinary protein, and immunoelectrophoresis of serum and urinary proteins. Contrary to previous reports, the present study suggests that chyluria does not produce proteinuria of enough severity to cause hypoproteinemia.
Adult↗