Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mycoplasma-like organisms (MLO) are non-cultivated intracellular cell-wall deficient pathogenic bacteria with a distinctive ultrastructural appearance. Diagnosis of MLO disease depends on finding the organisms in parasitized cells using a transmission electron microscope. MLO are a well studied cause of transmissible chronic plant disease responsive to antibiotics. MLO have recently been found to cause human chronic uveitis, orbital, and retinal disease with autoimmune features. Ophthalmic leucocytes in these patients display MLO parasitization. Inoculation of human uveitis MLO into mouse eyelids produced chronic uveitis. MLO also disseminated to produce randomly distributed lethal systemic disease including chronic hepatitis. MLO parasitized leucocytes were present in all disease sites. Direct intrahepatic inoculation of human hepatic pathogens is a simple and efficient technique to produce murine hepatitis. This report describes the delayed onset widespread inflammatory liver disease produced by direct intrahepatic inoculation of human chronic uveitis MLO in 12 of 20 mice versus 0 in 40 controls (P < 0.05). The liver disease was accompanied by elevated serum SGOT levels, splenomegaly, and accelerated mortality. All 12 inflamed livers displayed MLO parasitized leucocytes versus 0 of 10 control livers. The resemblance of human chronic active hepatitis, massive hepatic necrosis, and post-necrotic cirrhosis to the MLO induced murine liver disease, the role of molecular biologic techniques in the detection and classification of those bacteria, and in therapy of MLO disease are discussed.
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PMID:Experimental murine chronic hepatitis: results following intrahepatic inoculation of human uveitis mycoplasma-like organisms. 839 4

In dogs, hepatocutaneous syndrome (superficial necrolytic dermatitis) belongs to a group of syndromes in which cutaneous signs signal the presence of systemic disease. It is characterized by parakeratosis, superficial necrolysis, and basilar hyperplasia of the epidermis, in association with an unusual hepatopathy accompanied by certain metabolic derangements. Hepatocutaneous syndrome was diagnosed in 3 dogs on the basis of typical dermatologic changes and clinicopathologic findings. Hepatic ultrasonography revealed a hyperechoic network surrounding hypoechoic areas of parenchyma, resulting in a Swiss cheese-like appearance. The ultrasonographic image corresponded to the pathological findings. The liver had a nodular appearance, both grossly and microscopically; this was attributed to collapse of the areas of parenchyma surrounding the nodules, rather than to the cirrhosis and/or nodular hyperplasia reported previously.
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PMID:Hepatic ultrasonography and pathological findings in dogs with hepatocutaneous syndrome: new concepts. 855 87

The causes of abnormal uterine bleeding include a wide spectrum of diseases of the reproductive system and nongynecologic causes as well. The differential diagnosis of abnormal excessive uterine bleeding includes organic causes that may be subdivided into reproductive tract disease, iatrogenic causes, and systemic disease. Reproductive tract disease that may result in abnormal uterine bleeding comprises the complications of pregnancy (threatened, incomplete, or missed abortion, ectopic pregnancy, trophoblastic disease, placental polyp, and subinvolution of the placental site), malignant tumors (endometrial, cervical, vaginal, vulvar, and oviduct malignancies and granulosa theca cell ovarian tumors), infection (endometritis, salpingitis), and other benign pelvic disorders (traumatic lesions of the vagina, severe vaginal infections, foreign bodies, cervical polyps, cervical erosion, cervicitis, submucous uterine leiomyomas, adenomyosis, endometriosis, and endometrial polyps). Iatrogenic causes of abnormal uterine bleeding include sex steroids, hypothalamic depressants, digitalis, phenytoin, anticoagulants, and intrauterine contraceptive devices. Systemic diseases that may cause abnormal uterine bleeding include hypothyroidism, cirrhosis, and coagulation disorders. Abnormal uterine bleeding that occurs in a woman of reproductive age should be considered the result of complication of pregnancy until proved otherwise. Abnormal uterine bleeding occurring in a woman of perimenopausal or postmenopausal age should be considered the result of a malignancy until proved otherwise. Menorrhagia occurring in an adolescent should be attributed to a coagulopathy until proved otherwise. When an organic cause of abnormal uterine bleeding cannot be found, then by exclusion the diagnosis of dysfunctional uterine bleeding is assumed. Coagulation disorders, particularly von Willebrand disease, are more common than many physicians realize. Women with a history of high-risk factors, all adolescents with menorrhagia, women with anovulatory dysfunctional uterine bleeding who fail medical or surgical therapy, and women with ovulatory dysfunctional uterine bleeding without an anatomic uterine lesion should be screened for a coagulopathy.
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PMID:Differential diagnosis of abnormal uterine bleeding. 882 59

Fifty cirrhotic patients with portal hypertension but without colonic or systemic disease underwent lower gastrointestinal endoscopy in order to investigate the effects, if any, of portal hypertension on the colon. Fifty patients without liver or systemic disease, examined by colonoscopy because of irritable bowel syndrome in the same period served as controls. Rectosigmoid varices were observed in 34% of the cirrhotic patients and 2% of the controls. Hemorrhoids were observed in 70% of the cirrhotic patients and 48% of the controls. Multiple vascular-appearing lesions were found in 16% of the cirrhotic patients and 6% of the controls. Nonspecific inflammatory changes were noted in 10% of the cirrhotic patients and 4% of the controls. Simultaneous presence, in the same patient, of rectosigmoid varices, hemorrhoids, multiple vascular-appearing lesions, and nonspecific inflammatory changes, was observed in only five (10%) of the cirrhotic patients. We found polyps in 12% of the cirrhotic patients and 14% of the controls, and a malignant tumor in 4% of the cirrhotic patients. The patients with normal colonoscopic findings were 8% of the cirrhotic patients and 36% of the controls. All patients and controls were followed up for 1 year; there was no gastrointestinal hemorrhage among controls, whereas 34% of the cirrhotic patients had an upper gastrointestinal hemorrhage (88% from esophageal varices, 12% from the stomach) and 4% had a lower gastrointestinal hemorrhage (one from rectosigmoid varices and one from nonspecific inflammatory lesions). Colonic lesions were significantly more frequent in the cirrhotic patients (92%) than in the control group (64%); however, such lesions did not seem specific to the disease and were not statistically correlated with the degree of esophageal varices by Child's grading, the etiology of cirrhosis, or the bleeding risk from the lower gastrointestinal tract.
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PMID:Colonic disease in cirrhotic patients with portal hypertension: an endoscopic and clinical evaluation. 960 Mar 75

Functional and morphological alterations of microvascular endothelial cells (ECs) would lead to microcirculatory disturbances, thereby providing a basis for the development of a disease state. Clinically endotoxemia frequently encountered in a variety of diseases is considered to be a trigger to develop the microcirculatory disorders such as disseminated intravascular coagulation (DIC) and multiple organ failure (MOF), both of which feature the end stage of severe systemic disease. Experimentally intravital microscopy reveals that continuous venous infusion of endotoxin (LPS) causes a low flow state in the rat mesenteric microcirculatory unit. By vital stain with monastral blue B (MBB), the microvascular ECs are focally positive for MBB at the postcapillary venular site, where leukocytes adhere and extravasate. As shown in the histamine-induced diapedesis by transmission electron microscopy, the MBB-positve venular ECs may correspond to the contracted ECs, enabling the polymorphonuclear leukocytes and erythrocytes to extravasate through the widened gaps between the contracted ECs. Actin filaments proven in the microvascular ECs by electron microscopy may play a modulating role in this neutrophil diapedesis. In the process of gastric ulcer formation under restrained stress to the rat, the ECs of microvessels in the gastric mucosa, particularly of the mucosal capillaries and postcapillary venules directly innervated by the cholinergic nerves, are altered by the stress-induced overstimulation of the autonomic nerves, inducing the diapedesis of leukocytes and erythrocytes followed by hemorrhagic and ischemic injuries in the gastric mucosa. Liver cirrhosis also accompanies endotoxemia. The most prominent electron microscopic alterations of hepatic microvasculature are a decrease of hepatic sinusoidal endothelial fenestrae (SEF) both in diameter and in number, and the formation of basement membranes beneath the hepatic sinusoidal ECs. These ultrastructural changes would be induced by a most potent vasoconstrictor endothelin (ET)-1 through the overexpressed ET(A) and ET(B) receptors on the hepatic stellate cells and the sinusoidal ECs, contributing to the development of portal hypertension as well as to the disturbance in excretion of endotoxin into the bile canaliculi via the hepatocytes from the circulating sinusoidal blood to prevent endotoxemia.
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PMID:Endothelial cell dysfunction in microvasculature: relevance to disease processes. 1132 41

Background: Essential mixed cryoglobulinemia (EMC) is a systemic disease frequently associated with chronic viral hepatitis. This study was conducted in order to assess the prevalence of EMC in patients with hepatitis B virus (HBV) or hepatitis C virus (HCV) infections. We also evaluated the possible associations of EMC with (1) the clinical, virological, and histological status of liver disease; (2) the presence of EMC-related symptoms; and (3) the response rate to interferon-alpha (IFN-alpha) treatment, in an attempt to address whether EMC is a major problem in hepatitis patients. Methodology: A total of 154 consecutive patients (104 with HBV and 50 with HCV infection) were investigated for the presence of rheumatoid factor (RF), cryoglobulins, and EMC-related manifestations. Sixty-two HBV patients were chronic carriers of hepatitis B surface antigen, 29 had chronic hepatitis B, and 13 HBV cirrhosis. Thirty-five HCV patients had chronic hepatitis C and 15 HCV cirrhosis. HCV genotyping was performed in 44 patients. Results: The prevalence of cryoglobulins was significantly higher (P<0.001) in HCV patients (46%) than in HBV patients (13.4%). EMC was associated with a high frequency of RF detection, older age, and longer duration of viral diseases. Weakness or malaise, arthralgias, and purpura were significantly more frequent in cryoglobulin-positive patients. These manifestations, however, were mild in most of the patients. The EMC-related symptoms were significantly associated with the presence of HCV infection, increased levels of cryoglobulins, and RF detection (P<0.01, P<0.05, and P<0.000005, respectively). Worse liver histology was unrelated to a higher prevalence or increased levels of cryoglobulins in both HBV and HCV infection. There was no relationship between EMC and a specific HCV genotype. IFN-alpha therapy led to the disappearance of cryoglobulins and EMC-related manifestations in most cases. The response rate to IFN-alpha was similar in both groups of patients (with and without EMC). Conclusions: A higher prevalence of EMC was observed in HCV patients than in HBV patients. However, this finding was unrelated to overt clinical manifestations of EMC, a specific HCV genotype, or worse liver histology. The latter suggests that EMC does not contribute to liver injury and vice versa, that EMC pathogenesis is rather unrelated to the degree of liver injury. From a clinical point of view, testing for cryoglobulins seems reasonable only for HCV patients with EMC-related manifestations, since this may have therapeutic consequences. RF detection could be used primarily as a surrogate marker for the existence of cryoglobulins.
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PMID:Cryoglobulinemia due to chronic viral hepatitis infections is not a major problem in clinical practice. 1155 30

Nodular regenerative hyperplasia of the liver (NRHL) is an uncommon non-malignant finding typically associated with haematological or auto-immune disease. The main clinical symptom is portal hypertension in the absence of underlying liver cirrhosis. The pathogenesis of NRHL remains unknown. We report a case of NRHL with cholestasis and progression to liver insufficiency without any underlying disease and no association with systemic disease or drug intake. Cholestasis and liver function tests improved significantly during treatment with ursodeoxycholic acid (750 mg per day). Based on this case, it may be concluded that treatment with ursodeoxycholic acid might be beneficial in patients with NRHL and progression to liver insufficiency.
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PMID:Nodular regenerative hyperplasia of the liver: a rare differential diagnosis of cholestasis with response to ursodeoxycholic acid. 1266 46

Brucella infection is a systemic disease, but the microorganism rarely causes infections in the gastrointestinal system such as hepatitis, cholecystitis, colitis and pancreatitis. Spontaneous bacterial peritonitis due to Brucella is extremely rare. Herein, we report a case of cirrhosis complicated with nongranulomatous hepatitis and peritonitis, both due to Brucella. A 63 year-old man with diabetes mellitus was admitted to hospital with complaints of weakness, backache, abdominal pain and abdominal swelling. On the basis of physical examination and laboratory findings, cryptogenic cirrhosis and spontaneous bacterial peritonitis were diagnosed. Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture. Liver biopsy findings revealed cirrhosis and a nongranulomatous hepatitis which was thought might be due to Brucella infection. Doxycycline and rifampicin, in addition to diuretics were administered for spontaneous ascites infection due to Brucella. A week later, the patient's condition improved and he became afebrile. After two months of therapy, the ascites had almost disappeared.
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PMID:Spontaneous bacterial peritonitis due to Brucella infection. 1461 44

Needle biopsy of the liver provides concrete diagnostic information that cannot be as readily obtained in any other way. This report reviews 401 liver biopsies in 312 patients. THE MAJOR INDICATIONS FOR USE OF THIS PROCEDURE ARE: To determine the cause of an obscure liver enlargement; to establish the cause of jaundice; to distinguish between malignant disease and cirrhosis of the liver; to determine when hepatitis has subsided; and to evaluate the results of treatment. At times, systemic disease that has not been recognized by other means may be diagnosed by this technique. There is risk in performing this test, and the 0.25 per cent mortality in this series compares favorably with that reported from other clinics. Where the diagnosis by biopsy could be compared with observations at operation or autopsy, the correct diagnosis was made by biopsy in 85 per cent of cases. Greater accuracy was obtained by two or more biopsic examinations in one case then by single biopsy. In several cases in which surgical operation was considered, biopsic information made it unnecessary, and vice versa.
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PMID:Needle biopsy of the liver; general considerations. 1488 54

GH hypersecretory states include organic and functional causes. Among functional GH hypersecretory states, enhanced somatotroph secretion physiologically occurs at birth associated with reduced IGF-I levels reflecting the still immature sensitivity of liver to circulating GH levels; this may also occur in women exposed to oral extrogens. Pathophysiological conditions of GH hypersecretion are generally associated with congenital or acquired/functional conditions of peripheral GH insensitivity. Genetic alterations of the GH receptor lead to the so called Laron's syndrome. On the other hand, a relevant number of clinical conditions (malnutrition, malabsorption, anorexia nervosa, liver cirrhosis, renal failure, Type 1 diabetes mellitus) are associated with acquired GH insensitivity and a more or less pronounced GH hypersecretion. Both organic and acquired conditions of GH insensitivity show low IGF-I synthesis and release and therefore lack the negative IGF-I feedback action on somatotroph function. GH hypersecretion may be associated with renal failure; however, in this case, the alteration in the metabolic clearance rate of GH would also have a role; moreover, IGF-I levels are generally normal in this condition. Hyperthyroidism is another condition connoted by elevated GH levels that reflects a true GH hypersecretory state and is, in fact, associated with high-normal IGF-I levels; this peculiar condition is likely to be reflecting the stimulatory effect of thyroid hormones on both GH and IGF-I secretion and is promptly reversed by treatment-induced euthyroidism. Apart from these "functional" hypersecretory state, the classic organic GH hypersecretory state is represented by acromegaly or giantism. In these conditions GH hypersecretion is generally sustained by a pituitary adenoma hypersecreting GH alone or together with another pituitary hormone, mostly PRL; less frequently GH hypersecretion may be due to ectopic GHRH hypersection. Exaggerated GH secretion elicits exaggerated IGF-I synthesis and secretion that is, in turn, responsible for the large majority of endocrine signs and symptoms. In the appropriate clinical context of acromegalic features, evidence of concomitant marked GH and IGF-I hypersecretion at baseline demonstrates active acromegaly or giantism and indicates the need for magnetic resonance imaging in order to verify the presence of a pituitary tumor. However, as random measurement of basal GH levels is not reliable for definite diagnosis of acromegaly, it is considered mandatory to rely on the lack of GH suppression below 1 microg/l during oral glucose tolerance test (OGTT) coupled with elevated IGF-I levels. The same criteria are assumed, at present, to define true cure of the disease after (or under) treatment. There is consensus about the assumption that concomitant normalization or persistent abnormality of both OGTT-induced GH nadir and IGF-I levels define a successfully or a poorly controlled disease status, respectively. On the other hand, acromegalic patients with GH nadir above 1 microg/l or IGF-I levels persistently elevated are inadequately controlled and their disease should not be considered inactive. It has been clearly demonstrated that an extended exposure to GH and IGF-I excess level, even if slight, has a very harmful effect on patients; therefore early diagnosis of acromegaly and appropriate definition of its cure are of fundamental extreme in order to plan a prompt and appropriate therapeutic intervention(s) guaranteed also by the continuous improvement in the therapeutic tools available to treat this systemic disease.
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PMID:Hormonal diagnosis of GH hypersecretory states. 1549 57


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