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PubMed1991

[Current problems in the diagnosis and treatment of small intestinal diseases].

Based on the data obtained during clinical examination of 1,026 patients with small intestinal diseases the authors provide the portion of laboratory and instrumental methods employed in the diagnosis of different disease entities. The clinical picture of small intestinal diseases is mainly determined by the gravity of malabsorption. Histological examination of the small intestinal mucosa is a method of choice in the diagnosis of gluten enteropathy, Whipple's disease, primary lymphangiectasis and amyloidosis. Immunoassays play the key role in recognition of variable immunodeficiencies and disease of heavy alpha-chains. Meanwhile in differential diagnosis of Crohn's disease, small intestinal tumors, congenital abnormalities of rotation and in some others, the leading part is played by x-ray methods. The authors describe the treatment schedule based on the pathogenetic approach, that makes it possible to reach a stable clinical remission and recovery of the working capacity even in part of patients with stage III malabsorption.

Diagnosis, Differential↗
PubMed2000

[Structural changes in the ileal mucosa of urinary conduits].

OBJECTIVES: To study the changes found in the terminal ileum mucosa in contact with urine in patients with skin ureteroileostomy following cystectomy due to infiltrant carcinoma of the bladder. MATERIAL AND METHODS: 21 biopsies of gut mucosa were performed in as many patients. Measurements included height of intestinal villi (average values -AV-: 350-300 mu), height of crypts (AV: 70-100 mu), crypt/villus ratio (AV: 0.2), goblet cells/enterocytes ratio, presence of lymphangiectasis and inflammatory infiltrate. Also the existence of lab changes were measured with ionogram and venous gasometry. RESULTS: Mean age of patients was 65.2 years +/- 7.4 SD. Males 66.7%. Time of evolution with urinary by-pass was 59.5 months +/- 53.2 SD. Mean height of villi 178.2 mu +/- 70.2 SD, mean height of crypts 290.9 mu +/- 114.4 SD and mean crypt/villus ratio 4.2 +/- 9.2 SD. Submucous inflammatory infiltrate was mild in 57.1%, moderate in 23.8%, and severe in 19.0%. Only 2 cases had lymphangiectasis images. Goblet cells/enterocytes ratio was 3.3 +/- 1.3 SD. No correlation was seen between time of evolution of urinary by-pass with the various changes in gut mucosa or between degree of mucosal atrophy and existence of metabolic disorders. CONCLUSIONS: Changes in the terminal ileum mucosa in patients with skin ureteroileostomy-like urinary by-pass are characterised by a marked atrophy of intestinal villi with increased crypt length, increased crypt/villus ratio and presence of mild-to-moderate inflammatory infiltrate. There is also an increase of goblet cells in detriment of enterocytes. All these changes are independent from the time of evolution of patients with urinary by-pass.

Aged↗
PubMed1990

Generalized lymphangiectasis in a dog with subcutaneous chyle and lymphangioma.

A 2 1/2-year-old spayed Great Dane was evaluated for large, fluctuant, chyle-containing swellings on the ventral portion of the left side of the abdomen. Multiple abnormalities of the lymphatic system were diagnosed, including thoracic duct obstruction, lymphangioma, subcutaneous chyle reflux, intestinal lymphangiectasia, and dilatation of hepatic, mesenteric, and pleural lymphatic vessels. Mesenteric lymphangiography revealed leakage of contrast medium into the subcutaneous tissues adjacent and to the left of the second lumbar vertebral body. Dietary and surgical management to control the chylous reflux were unsuccessful, and the dog died approximately one year after the skin lesions were first observed.

Animals↗
PubMed1988

Intracellular iron storage and the pathogenesis of paratuberculosis. Comparative studies with other mycobacterial, parasitic or infectious conditions of veterinary importance.

The distribution of iron and mycobacteria was examined in the intestinal tract of ruminants with naturally-occurring M. paratuberculosis infection and compared with mycobacterial infections in several species. This distribution was compared with that of iron in chronic lesions caused by other microbial or parasitic agents. In the clinical form of paratuberculosis in cattle, sheep and goats there was marked lymphangiectasis and a high proportion of the granulomatous lesions contained siderotic macrophages with a high mycobacterial content. In cattle with preclinical lesions of granulomatous enteropathy, the greatest number of acid-fast organisms was present in siderotic, non-differentiated, ileo-caecal macrophages; concurrent mast cell-associated allergic enteropathy was also apparent in the duodenum, proximal and mid-ileum of most animals. In paratuberculosis-affected herds, a high proportion of non-productive cows were without classical granulomatous change but had cultural or immunological evidence of M. paratuberculosis infection and similar allergic catarrhal enteropathy of the upper intestinal tract. Interstitial haemorrhage of the ileocaecal valve, with the accumulation of haemosiderin and ferritin in undifferentiated macrophages was observed in some of these cattle and also in others with experimentally-induced copper deficiency and acute ostertagiasis. Colonisation of the ileo-caecal or caecal glandular crypts by large, apparently saprophytic acid-fast organisms indicated regional tolerance to such organisms in all cattle. In other mycobacterioses such as bovine or avian tuberculosis, undifferentiated, siderotic macrophages containing mycobacteria were also seen in early granulomas, but epithelioid and giant cell differentiation invariably led to the disappearance of intracellular iron and a reduction in mycobacterial numbers. In possums in which epithelioid and giant cells did not occur in response to M. bovis infection, siderosis persisted in many macrophages and overwhelming mycobacterial multiplication occurred. These studies indicate that, in most infections with mycobacteria, differentiation of macrophages radically reverses their iron acquisitive properties, creating an intracellular environment unsuitable for mycobacterial multiplication. It seems likely that allergically mediated microvascular haemorrhage, local tolerance of commensal mycobacteria and attenuation of the macrophage siderosis reversal mechanism provide unique conditions for early, uninhibited, intracellular multiplication of M. paratuberculosis in the ileo-caecal valve of certain mature ruminants.

Animals↗
PubMed2002

Primary Sjögren's syndrome with protein-losing gastroenteropathy: report of two cases.

Protein-losing gastroenteropathy is a rare complication in autoimmune diseases, especially in Sjögren's syndrome. We report two cases of primary Sjögren's syndrome, one in a 37-year-old female and another in a 50-year-old female, both of whom presented with peripheral edema. Protein-losing gastroenteropathies of the stomach and small intestine in the first patient and of the small intestine only in the second patient were demonstrated by abdominal Tc-99m labeled albumin abdominal scintigraphy and pathologic findings. Results of gastrointestinal tract biopsies from both patients showed chronic inflammatory cell infiltrations without lymphangiectasis or vasculitis. The patients were successfully treated with corticosteroids. Results of follow-up Tc-99m labeled albumin scintigraphy were well correlated with clinical improvement and the increase in serum albumin. Sjögren's syndrome should be considered as a cause of protein-losing enteropathy. Tc-99m labeled albumin abdominal scintigraphy is helpful in diagnosing the condition, locating the protein-losing sites, and monitoring the treatment outcome, especially in cases where protein loss occurs in the stomach.

Adult↗
PubMed1983

Apolipoprotein B subspecies in chylomicrons isolated from a patient with chyluria.

The diagnosis and the clinical course of a 17-year-old white male with chyluria are reported. Cloudy, milky urine appeared spontaneously, in the absence of edema or any signs or symptoms of parasitic infection. Pedal lymphangiography demonstrated the presence of a lymphatic renal fistula, and digital subtraction angiography showed aneurysmal dilatation of the aorta at the level of the renal arteries. This case provided an opportunity to ascertain which of the forms of apolipoprotein B were present in lymph chylomicrons. Apolipoprotein B is needed for chylomicron secretion. It exists in several forms--B-100, B-74, B-48, and B-26. After a meal consisting of fat, chylomicrons in which apolipoprotein B-48 was virtually the only apolipoprotein B present appeared in the urine, while apolipoprotein B-100 was the only apolipoprotein B present in the plasma very low-density lipoproteins. Chyluria disappeared two weeks after institution of a low-fat diet. This case illustrates an interesting, rare cause of chyluria. Because of the presence of chyluria, it was also demonstrated that chylomicrons in which apolipoprotein B-48 is virtually the only apolipoprotein B present are a physiologically normal product of the intestine.

Adolescent↗
PubMed1967

Measurement of gastrointestinal protein loss using ceruloplasmin labeled with copper.

Ceruloplasmin labeled with (67)copper and administered intravenously to dogs, control human subjects, and patients with excessive gastrointestinal loss was shown to fulfill the requirements for a label for quantification of gastrointestinal protein loss. The radiocopper moiety was poorly absorbed from the gastrointestinal tract, not actively secreted into the intestinal tract, and did not alter significantly the metabolism of ceruloplasmin. Approximately 70% of the body pool of ceruloplasmin in both dog and man was within the intravascular space. In control human subjects the mean ceruloplasmin concentration was 30 mg per 100 ml with total circulating and total body ceruloplasmin pools of 15.5 and 22 mg per kg, respectively. In patients with excessive gastrointestinal protein loss secondary to intestinal lymphangiectasia, the serum ceruloplasmin concentration was reduced to 16 mg per 100 ml with a comparable reduction in the total circulating and total body ceruloplasmin pools to 8.8 and 12 mg per kg. The survival half-time of ceruloplasmin was 6.1 days in normal human subjects and 4.5 days in normal dogs. From 1.0 to 1.9% of the intravascular pool of ceruloplasmin was lost into the gastrointestinal tract of the dog per day, representing less than 11% of the over-all metabolism of this protein. In control human subjects from 1.9 to 3.9% of the intravascular pool was lost into the gastrointestinal tract each day, representing a maximum of from 11 to 22% of the over-all metabolism of this molecule. In contrast, patients with intestinal lymphangiectasia had a markedly shortened ceruloplasmin survival of 3.1 days, with from 15 to 40% of the intravascular pool of ceruloplasmin cleared into the gastrointestinal tract daily. This represented 76% of the over-all metabolism of this protein. Thus, although bulk loss of serum proteins into the gastrointestinal tract does not normally appear to be a significant factor in protein metabolism in normal dogs and men, such loss is a major factor in the pathogenesis of the hypoceruloplasminemia noted in patients with intestinal lymphangiectasia.

Animals↗
PubMed2000

Familial congenital pulmonary lymphangectasia, non-immune hydrops fetalis, facial and lower limb lymphedema: confirmation of Njolstad's report.

We report on four cases, three familial and one sporadic, with congenital pulmonary lymphangectasia and facial and lower limb lymphedema. Hydrops fetalis was observed in three cases and death occurred in one of those. This is the third report describing inherited pulmonary lymphangectasia with a clinical phenotype very similar to that described by Njolstad et al. [1998: Eur J Pediatr 157: 498-501], who reported three sibs with non-immune hydrops fetalis (NIHF), chylothorax, pulmonary lymphangectasia, distal lymphedema, and swelling of the face. We think that the present report and that of Njolstad et al. describe a new condition very similar to Hennekam syndrome, which is characterized by autosomal recessive inheritance, intestinal lymphangiectasia, lymphedema of the lower limbs and facial anomalies (flat face, hypertelorism, flat, broad nasal bridge, lymphedema, tooth anomalies, and ear defects). Similarity with our cases and Hennekam syndrome will be discussed.

Child↗
PubMed1990

[Hemangiomatous lesions with lymphangiectasias in the large intestine].

We present the case of a 16 year-old male who presented intestinal hemorrhages since childhood; he was operated in emergency for microhemangiomas located in sigmoid colon and rectum. This lesion can be considered as a complex vascular hamartoma. We review the literature and discuss the differences between this lesion and angiodysplasia.

Adolescent↗
PubMed1992

Rectal hemorrhage associated with vascular ectasia in a young dog.

Rectal bleeding in a 7-month-old 13-kg sexually intact female mixed-breed dog was determined to be associated with vascular ectasia of the small intestine, descending colon, rectum, and anus. Microscopically, the telangiectasia was associated with lymphangiectasia and focal ulceration. Surgical intervention resulted in incomplete resection of the lesion and only temporary amelioration of clinical signs. The dog's age was compatible with a congenital origin for the defect, but an acquired cause could not be excluded.

Angiodysplasia↗
PubMed2003

Hennekam syndrome presenting as nonimmune hydrops fetalis, congenital chylothorax, and congenital pulmonary lymphangiectasia.

We report a female infant with congenital lymphedema, facial anomalies, intestinal lymphangiectasia consistent with a diagnosis of Hennekam syndrome. At birth the patient presented with severe respiratory distress due to nonimmune hydrops fetalis, a congenital chylothorax (CC), and pulmonary lymphangiectasia. Hydrops fetalis may be present in newborns with the Hennekam syndrome. Lymphoscintigraphy can be useful in explaining pleural-pulmonary involvement of this generalized lymph vessel malformation syndrome.

Abnormalities, Multiple↗
PubMed1996

Penetration of M cells and destruction of Peyer's patches by Yersinia enterocolitica: an ultrastructural and histological study.

Yersinia enterocolitica is enteropathogenic for man and rodents. Previous studies provided evidence that Y. enterocolitica invades the lymphoid follicles of the Peyer's patches (PP) of the small intestine. In this study Y. enterocolitica-induced tissue alterations of the follicle-associated epithelium (FAE) and the underlying PP tissue were analysed by scanning (SEM) and transmission electron microscopy (TEM) as well as by conventional histological examination. For this purpose, an experimental mouse infection model including orogastric infections as well as ileal loop experiments were used. A rapid and selective colonisation of the FAE after orogastric yersinia infection was observed by SEM. TEM studies confirmed that Y. enterocolitica adhered closely to the FAE including M cells and enterocytes. Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE. One day after Y. enterocolitica infection the FAE was altered and small micro-abscesses comprising yersiniae expressing the major outer-membrane protein YadA were observed immediately beneath the FAE. Adjacent villi were dilated from lymphangiectasis and transmigrating polymorphonuclear leucocytes (PMNL) were found within the epithelium. At 5-7 days after infection the FAE and parts of PP were destroyed. Profound alterations of the cyto-architecture of the PP were due to the enormous recruitment of PMNL. By day 5 after infection, abscesses were found in the mesenteric lymph nodes. However, TEM studies revealed evidence that Y. enterocolitica may disseminate from the PP not only via the lymphatics but also by invasion of blood vessels. Taken together, the results of this study demonstrate that the FAE is the primary site of host-pathogen interaction in Y. enterocolitica infection and that this pathogen penetrates M cells and subsequently induces destruction of the PP.

Animals↗
PubMedDate not supplied

[Alpha 1-antitrypsin as an endogenous marker of protein-losing enteropathies].

A novelty of the present studies is the use of alpha 1-antitrypsin (A-1--AT) as an endogenous marker of enteric protein loss. Enteric clearance of alpha 1-antitrypsin was determined in 10 patients with the symptoms of PLE, and in 6 healthy individuals. Alpha 1-Antitrypsin concentration has been assayed in single, random samples of feces collected from 42 patients and 12 healthy individuals (normal values: 1.31 +/- 0.72 mg/g of feces). Markedly increased enteric clearance and A-1-AT concentrations in single, random samples of feces have been found in patients with enteric lymphangiectasis, Crohn's disease, ulcerative colitis, and constrictive pericarditis, slightly lower in coeliac, chronic diarrhoea, nonspecific hemorrhagic colitis, esophagitis, lambliasis, hypogammaglobulinemia, Wiskott-Aldrich syndrome, Rendu-Osler-Weber syndrome, hepatitis in newborn, and Gilbert's disease. Statistically significant positive clearance has been noted (r = 0.997; p less than .001). A single assay of A-1-AT in feces is simple, repeatable, and sensitive technique in the diagnosis and evaluation of these diseases in which the symptoms of enteric protein loss are seen.

Adolescent↗
PubMed2006

Oesophageal tuberculosis mimicking oesophageal carcinoma.

Tuberculous involvement of the oesophagus is rare, and is usually caused by direct spread from adjacent afflicted structures. We report an 83-year-old male patient with oesophageal tuberculosis secondary to tuberculous mediastinal lymphadenitis who presented with non-specific symptoms of anorexia and lethargy. Upper gastro-intestinal endoscopy revealed an ulcerative tumour-like lesion in the mid-oesophagus suggesting oesophageal carcinoma. Repeated endoscopic biopsies revealed a non-specific acute-on-chronic inflammation consisting of non-caseating granulomas, with no evidence of malignancy. Endoscopic ultrasonography demonstrated that the oesophageal lesion was secondary to direct extension of mediastinal lymphadenopathy. The diagnosis of tuberculosis was eventually confirmed by histological and microbiological analysis of a surgically excised cervical lymph node. The patient responded promptly to treatment with antituberculous drugs. We suggest that oesophageal tuberculosis has to be kept in mind in the differential diagnosis of oesophageal ulcerohypertrophic lesions.

Aged↗
PubMed2002

Lymphedema-lymphangiectasia-mental retardation (Hennekam) syndrome: a review.

The Hennekam syndrome is an infrequently reported heritable entity characterized by lymphedema, lymphangiectasia, and developmental delay. Here we add an additional 8 patients, and compare their findings to the 16 cases from the literature. The lymphedema is usually congenital, can be markedly asymmetrical, and, often, gradually progressive. Complications such as erysipelas are common. The lymphangiectasias are present in the intestines, but have also been found in the pleura, pericardium, thyroid gland, and kidney. Several patients have demonstrated congenital cardiac and blood vessel anomalies, pointing to a disturbance of angiogenesis in at least some of the patients. Facial features are variable, and are chiefly characterized, in a typical patient, by a flat face, flat and broad nasal bridge, and hypertelorism. Facial features are thought to mirror the extent of intrauterine facial lymphedema, or may be caused by lymphatic obstruction that affects the early migration of neural crest tissue. Other anomalies have included glaucoma, dental anomalies, hearing loss, and renal anomalies. The psychomotor development varies widely, even within a single family, from almost normal development to severe mental retardation. Convulsions are common. The existence of 10 familial cases, equal sex ratio, increased parental consanguinity rate (4/20 families), and absence of vertical transmission are consistent with an autosomal recessive pattern of inheritance. It seems likely that most (but not all) manifestations of the entity can be explained as sequences of impaired prenatal and postnatal lymphatic flow, suggesting that the causative gene(s) should have a major function in lymphangiogenesis.

Abnormalities, Multiple↗