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At least 469 records · Page 26Linked to original sources
PubMed1984

Occult papillary carcinoma of the thyroid with distant metastases.

It is well established that small clinically undetected thyroid carcinomas can produce extensive lymphatic metastases. However, occult papillary carcinoma of the thyroid presenting as a large blood-borne metastasis and occult papillary carcinoma of the thyroid leading to death are both uncommon. The authors report two unusual cases of clinically occult carcinoma of the thyroid. The first case is a 2.4 mm microscopic carcinoma presenting as a large solitary pulmonary metastasis, and is one of the smallest reported primary papillary thyroid carcinomas presenting as a distant hematogenous metastasis. The second case represents a lethal carcinoma with extensive metastases not diagnosed until autopsy. These two cases effectively illustrate that the absence of a clinically detectable thyroid abnormality does not exclude the possibility of extensive hematogenous and lymphatic metastases from a minute or undetected carcinoma of the thyroid.

Bone Marrow↗
PubMed2007

Postnatal lymphatic partitioning from the blood vasculature in the small intestine requires fasting-induced adipose factor.

Lymphatic vessels develop from specialized venous endothelial cells. Using knockout mice, we found that fasting-induced adipose factor (Fiaf) is required for functional partitioning of postnatal intestinal lymphatic and blood vessels. In wild-type animals, levels of intestinal Fiaf expression rise during the first postnatal day and peak at day 2, which coincides with the onset of the lymphatico-venous partitioning abnormality in Fiaf-/- mutants on a mixed 129/SvJ:C57BL/6 genetic background. Fiaf deficiency is not associated with disruption of the blood vasculature or with lymphatic endothelial recruitment of smooth muscle cells. We identified Prox1, a critical regulator of lymphangiogenesis, as a downstream target for Fiaf signaling in the intestinal lymphatic endothelium. This organ-specific lymphovascular abnormality can be rescued by allowing embryonic Fiaf-/- intestinal isografts to develop in Fiaf+/+ recipients.

Angiopoietin-Like Protein 4↗
PubMed2002

Prostaglandin E(1) inhibits abnormal follicle rupture and restores ovulation in indomethacin-treated rats.

In the presence of indomethacin, an inhibitor of prostaglandin (PG) synthesis, the gonadotropin surge induces abnormal follicle rupture at the basolateral follicle sides, thus preventing effective ovulation in rats. This study was undertaken to analyze whether exogenous prostaglandin administration can overcome the antiovulatory action of indomethacin. Cycling rats were treated with vehicle (olive oil) or indomethacin (1 mg/rat) on the morning of proestrus. Rats treated with indomethacin were injected with different doses (50, 250, or 500 micro g/rat) of PGE(1), PGE(2), PGF(2alpha), or vehicle (saline) at 1900 h in proestrus. The ovulatory response was analyzed on the morning of estrus by evaluating follicle rupture and the location of the oocytes in serially sectioned ovaries. The number of oocytes in the oviducts was also counted in rats treated with the highest prostaglandin doses. In indomethacin-treated rats, most newly formed corpora lutea showed abnormal follicle rupture at the basolateral sides. In addition, invasion of the ovarian stroma and blood and lymphatic vessels by granulosa cells and follicular fluid was observed. Prostaglandins of the E series, and especially PGE(1), inhibited abnormal follicle rupture and restored ovulation, although the number of oocytes in the oviducts were significantly decreased. PGF(2alpha) was only partially effective in inhibiting abnormal follicle rupture and restoring ovulation. These data suggest that prostaglandins of the E series, and particularly PGE(1), play a crucial role in ovulation by determining the targeting of follicle rupture at the apex, thus allowing release of oocytes to the periovarian space.

Alprostadil↗
PubMedDate not supplied

[New development in Crohn's disease: ++unravelling the mystery and its reinstatement as a surgically treatable condition. Part 2. Potential etiopathogenesis of "terminal ileitis" and extension of the disease to mesenteric small intestine and the colon].

INTRODUCTION: The aetiopathogenesis of terminal ileitis is still unknown, as is the cause of its spread to the small and large bowel. The aim of this study was to shed light on these unknown aspects of Crohn's disease. CONCLUSIONS: The lack of patency of the ileal branch of the ileocolic lymphatic collector which causes terminal ileitis, usually in the earlier part of life, is likely to occur in the foetus around the 10th week of pregnancy as a result of a minor abnormality of the physiological regression of the vitelline duct. Excessive atrophy of the lymphatic network seems to occur, also affecting the rudimentary lymphatic vessels in the midgut destined to become the terminal ileum. The terminal ileitis spreads to the large bowel in an increasing percentage of cases and is directly related to duration of the disease, causing first ileitis plus right colitis, and then ileitis plus total colitis (which, however, does not include the rectum). It may also include the jejunum, causing skip lesions. This spread of lesions is not due to any genetic predisposition (that is to say, it is not predetermined in empirical terms), but rather to the extent of the lymphatic obstruction caused by the spread of immunocomplexes via the lymphatic network. This is shown by the fact that secondary lesions of the jejunum and large bowel are also typical of lymphoedema and that their spread is segmentary. In the light of these pathogenetic mechanisms, it is reasonable to assume that the spread of the process from the ileum to the colon might be prevented by prompt surgery during the initial phase of the ileitis. If these views are correct, the traditional subdivision of Crohn's disease forms into ileitis, ileocolitis and solitary colitis should be replaced by a very simple scheme showing the spread of the primary ileitis very often to ileocolitis, first confined to the right colon and then total. We cannot include either solitary colitis (not clearly defined in the literature) or anorectal Crohn's disease (whose forms have yet to be fully acknowledged) in this scheme.

Colonic Diseases↗
PubMed1985

Chylous metrorrhea.

A nine-year-old girl with primary (idiopathic) chylous metrorrhea is described. Extravasation from retroperitoneal lymphatics into the vaginal vault was seen on dorsal pedal lymphangiography. Bony abnormalities were also present in the lumbosacral vertebrae. Nineteen months after transperitoneal lymphangiectomy she is asymptomatic.

Child↗
PubMed1996

[Intermittent chyluria in a young man].

Chyluria is the passage of chylus into urine resulting in fistulization through the lymphatic system and the urinary system. This rare condition is usually caused by filaria infestation or malformations, neoplasia or trauma. We report a case of a 18-year-old man. The patient presented milky urine which had appeared after angiography following minor leg trauma. Physical examination revealed asymmetry of the face and cutaneous dyschromia. Blood tests revealed hypogammaglobulinemia and altered CD4/CD8 ratio (0.6). Urine tests showed proteinuria (30 mg/dl), lipiduria (triglycerides 750 mg/dl) and density of 1025. Renal function was normal. Abdomen computed tomography and urography were normal. Cystoscopy revealed the presence of milky urine in the bladder and selective catheterization revealed that the origin was the right ureter alone. Ascendent pyelography did not reveal any malformation of the urinary tract; but after this the chyluria spontaneously disappeared. The patient was rehospitalized 3 months later for recurrence. Lymphography was then performed and revealed a dilated lymphatic network with minute lacunar images projecting into the right kidney. Chyluria again disappeared spontaneously and recurred sporadically over the next two years in a patient who remained in good physical condition. The etiology of chyluria in a patient without filaria infestation is problematic, particularly when the most common causes (tuberculosis, neoplasia, trauma) are excluded as in our case. The asymmetry of the face, together with cutaneous dyschromia and the presence of a subarachnoidea cyst in the right temporal region suggested our patient had multiple congenital malformations.

Abnormalities, Multiple↗
PubMed1978

Congenital hereditary lymphedema in the pig.

A histopathological investigation was performed in newborn pigs with congenital hereditary lymphedema. The edema varied greatly in degree and extension. Although mostly confined to the hind legs it may involve other parts of the body, and even attain a most severe generalized distribution. It was found due to malformations of the lymphatic system which were general in character in all animals irrespective the grade in their edema. Parallel to the grade of edema however, these lymphvascular abnormalities varied from minor hypoplasia and localized aplasia to a complete agenesis of the whole lymphatic system.

Animals↗
PubMed1992

[Changes in lymph microcirculation in appendicular peritonitis].

When studied in experiment (63 dogs) and in clinical settings (116 patients), microlymphatic channel in appendicular peritonitis (AP) was found impaired, while lymphatic drainage of large-molecular substances and metabolites coming from the abdominal cavity appeared activated. Methods of correction of AP-induced abnormalities in microlymphocirculation have been developed which imply three levels of the impact: microcirculation, affected organ, lymphatic system. The clinical trial of the methods proved their efficacy even in the most severe AP forms.

Animals↗
PubMed2002

The TSC-2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma.

AIMS: Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex-2 gene (TSC-2) have been described in LAM cells and angiomyolipomas. The TSC-2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression. METHODS AND RESULTS: Tissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti-tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin. CONCLUSIONS: Our results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism.

Adult↗
PubMed1980

Pathological and pathophysiological study on intestinal lymphatic system in fat absorption.

Pathological and pathophysiological study on the intestinal lymphatics was carried out clinically and experimentally. Jejunal biopsy study revealed marked dilatation of intestinal lymphatics in liver cirrhosis with ascites and Behçet's disease as well as protein-losing enteropathy. Lymphangiographic study showed also abnormal findings in above-mentioned diseases. In cases of McKee dogs in which mechanism of blockade of lymphatic flow was already clarified, McKee dogs showed marked malabsorptive of fat. When lymphatic flow was blocked mechanically at the thoracic duct, fat accumulation was seen in the absorptive cells as well as in dilated intestinal lymphatics. In administration of colchicine to rats, fat accumulation was seen in the matrix of absorptive cells as well as in the endoplasmic reticulums and Golgi apparatus. However, amorphous substances instead of chylomicrons were seen in dilated intestinal lymphatics. These studies suggested that a tract of fat transportation from intestinal cells to the thoracic duct should be considered as a functional unit in fat absorption.

Animals↗
PubMed2003

Reproductive/developmental toxicity and immunotoxicity assessment in the nonhuman primate model.

Nonhuman primates are being used increasingly as a non-rodent animal model during preclinical toxicology and safety assessment on the basis of proven similarity and comparability between nonhuman primates and humans. The validity of the nonhuman primate models applies to many aspects of toxicological testing and holds particularly true for the evaluation of reproductive toxicology and developmental toxicology. More recently, the advent of humanized antibodies and vaccines imposed further demand on nonhuman primate models since many immunotherapeutics do not interact with rodent receptors but frequently only cross-react with primate tissue. In this paper we discuss the suitability of primate models for reproductive, developmental and immunotoxicology testing, and present our initial data on the development of lymphatic organs and immune system in a nonhuman primate model.

Abnormalities, Drug-Induced↗
PubMed2006

Hyperfibrinogenemia is associated with lymphatic as well as hematogenous metastasis and worse clinical outcome in T2 gastric cancer.

BACKGROUND: Abnormal hemostasis in cancer patients has previously been described, however the correlation between the plasma fibrinogen level and cancer metastasis and prognosis has not been reported in a large-scale clinical study. METHODS: Preoperative plasma fibrinogen levels were retrospectively examined in 405 patients who underwent surgery for advanced gastric cancer. The association of fibrinogen levels with clinical/pathological findings and clinical outcome was evaluated. RESULTS: There was a positive correlation between plasma fibrinogen levels and the depth of invasion (p < 0.05). Hyperfibrinogenemia (>310 mg/dl) was independently associated with lymph node (Odds Ratio; 2.342, P = 0.0032) and liver (Odds Ratio; 2.933, P = 0.0147) metastasis, not with peritoneal metastasis in this series. Patients with hyperfibrinogenemia showed worse clinical outcome in T2 gastric cancer, however, there was no correlation of plasma fibrinogen level with prognosis in T3/T4 gastric cancer. CONCLUSION: Our results might support the idea that hyperfibrinogenemia can augment lymphatic and hematogeneous metastasis of advanced gastric cancer, which is major determinant of the prognosis in T2 gastric cancer. Therefore, in the situation without peritoneal involvement, hyperfibrinogenemia is a useful biomarker to predict the possible metastasis and worse clinical outcome in T2 gastric cancer.

Aged↗