Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

Abuse of analgesics (AA) is a well known cause of chronic interstitial nephritis. Recently a noxious effect of AA on the pancreas has been suggested based upon case observations, and first evidence for association of AA with chronic pancreatitis was presented. In the present prospective clinical study 95 patients with chronic renal insufficiency, in 53 of them associated with AA, were investigated for evidence of chronic pancreatitis (e.g. history of pancreatitis, pancreatic calcifications, diabetes and exocrine function). The patients were divided into two groups: group A consisted of 53 patients with chronic nephropathy associated with AA, and control group B consisted of 42 patients with chronic nephropathy of other etiology. Pancreatic calcifications were observed in 5 cases of group A (10%), but in none of the patients of group B. Exocrine insufficiency was found in 2 of the 5 cases with pancreatic calcifications. Only one of the 5 patients had a history of pancreatitis in association with exocrine and endocrine insufficiency. Thus pancreatic calcifications, which are virtually pathognomonic for chronic pancreatitis, were found exclusively in the group with chronic nephropathy due to analgesic abuse. Chronic pancreatitis in this group of patients is likely to be overlooked because of the lack of clinical and laboratory evidence. The present data support our previous observations that AA may be an etiological factor in chronic calcifying pancreatitis. This first evidence for a drug-induced form of chronic pancreatitis is presented.
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PMID:[Chronic pancreatitis as a possible result of analgesic abuse]. 358 21

In the annuals of autopsy records in Japan, edited by the Japanese Society of Pathology and covering 20 years, from 1958 to 1977, 377841 autopsy cases are registered with a short summary of the pathology findings. Of these, 434 cases with idiopathic, interstitial, viral, non-specific (NSM) and giant cell (GCM) myocarditis were found. The incidences of NSM and GCM were 0.11 and 0.007%, respectively. The annual incidence of NSM showed periodic fluctuations with in 5-year intervals and increased remarkably after 1974. Incidence of GCM showed a similar fluctuation but with a one to two year delay of peaks. The male to female ratio was 1.2: 1 and the age distribution had two peaked patterns for both sexes, though these peaks were scattered widely from neonate to elderly patients. The regional distribution of NSM showed a concentration in the middle portion of Honshu and its regional annual incidence had propagation waves from the central area to peripheral areas. The same tendency was observed in GCM cases. Hokkaido was characterized by a low incidence of NSM and no GCM. Complications of myocarditis included pancreatitis, pneumonitis, interstitial nephritis, meningoencephalitis, hepatitis, hepatic cirrhosis and a considerable incidence of malignancies. Antibiotics, antineoplastic agents, steroids and irradiation therapy were the main forms of treatment applied before or after the start of myocarditis.
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PMID:Twenty year autopsy statistics of myocarditis incidence in Japan. 382 May 37

Systemic pathological alterations were studied in thirty-seven autopsied patients with Kawasaki disease. Systemic vasculitis was the most characteristic pathological finding and was present in all the patients. In addition to the vasculitis, there was a high incidence of inflammatory lesions in various organs and tissues: in the heart, endocarditis, myocarditis, and pericarditis; in the digestive system, stomatitis, sialoduct-adenitis, catarrhal enteritis, hepatitis, cholangitis, pancreatitis, and pancreas ductitis; in the respiratory system, bronchitis and segmental interstitial pneumonia; in the urinary system, focal interstitial nephritis, cystitis, and prostatitis; in the nervous system, aseptic leptomeningitis, choriomeningitis, gangliontis, and neuritis; in the hematopoietic system, lymphadenitis, splenitis, and thymitis. Dermatitis, panniculitis or myositis were also observed in some patients. Therefore, Kawasaki disease is a systemic inflammatory disease which mainly affects the cardiovascular system. These systemic inflammatory lesions are considered to correspond to the variegated clinical manifestaitions. The relationship between Kawasaki disease and infantile polyarteritis nodosa (IPN) were discussed, based on the clinicopathological characteristics.
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PMID:General pathology of Kawasaki disease. On the morphological alterations corresponding to the clinical manifestations. 744 9

The aim of our study was to analyze the clinical course and outcome of acute renal failure (ARF) in patients with hemorrhagic fever with renal syndrome (HFRS). From 1983 to 1995, we treated 33 patients (27 males, 6 females) aged from 16 to 71 years. Half of patients were connected with work at a farm or in a forest. The disease was confirmed serologically with indirect immunofluorescence test (IFT) and enzyme-linked immunosorbent assay (ELISA). In 18 patients percutaneous kidney needle biopsies were analyzed. In 85% of the cases, the disease broke out from June to October. The most frequently expressed clinical signs and symptoms were fever, nausea/vomiting, headache, backache, abdominal pain, myalgia, diarrhea, conjunctival injection, and hemorrhages. Four patients had concomitant pancreatitis. In 25 patients, oliguria was present, and transient hemodialysis treatment was needed in 19 patients. Infection with Hantaan virus was established in 20 patients and with Puumala virus in 13 patients. At renal biopsy, acute interstitial nephritis accompanied with hemorrhages and necrosis was found, and at a later biopsy there were also signs of interstitial fibrosis. All patients were cured, but renal function was not completely recovered in some. We conclude that ARF is a serious complication in patients with HFRS. Although not lethal in our group of patients, many of them showed severe signs and symptoms of illness. Transient hemodialysis was necessary in two-thirds of the patients. Some degree of functional defects and morphological changes might persist.
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PMID:Acute renal failure due to hemorrhagic fever with renal syndrome. 887 90

The study was undertaken to study the frequency, causes, and efficiency of treatment for acute renal failure (ARF) at the intensive nephrological care unit. The data on 117 patients with ARF of various etiology were studied. In them, ARF was caused by acute interstitial nephritis in 18.8%, by urosepsis in 18.8%, by non-urological sepsis in 19%, by destructive pancreatitis in 18%, in 13% rapidly progressive glomerulonephritis was present in systemic vasculitis. In 8.5% of the patients, ARF developed as a complication of severe pneumonias along with respiratory failure. Only single cases were presented with ARF of other intoxication etiology, crush syndrome, or acute vascular diseases. Renal replacement therapy was used in all cases. Its mode (intermittent or low-flow continuous) was determined by the severity of renal failure and the general condition of patients. The overall mortality was 38% in the whole group. It was 55% in sepsis, 33% in destructive pancreatis, 8.3% in urosepsis, 8% in acute interstitial nephritis, 64.7% in rapidly progressive glomerulonephritis. According to the type of therapy, there were no significant differences in mortality rates. There was also a correlation of the mortality rates and the APACHE score.
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PMID:[The structure of causes of acute renal failure and the efficacy of its treatment according to the materials of an intensive nephrological care unit]. 1593 98

A 52-year-old male was admitted with autoimmune pancreatitis (AIP), showing mononuclear cell infiltration in both the pancreas and salivary glands with both normal sialography and anti-SS-A/SS-B antibodies. Although the AIP improved with glucocorticoid treatment, subsequent abdominal computed tomography (CT) revealed a nodular shadow in the bilateral kidneys, which was confirmed as interstitial nephritis by renal biopsy. The patient's serum immunoglobulin G4 (IgG4) level was 10 times higher than the upper limit of the normal range. IgG4-positive mononuclear cell infiltration was detected in the salivary gland, pancreas, and kidney. A new entity proposed as 'IgG4-related autoimmune disease' was considered.
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PMID:A case of IgG4-related autoimmune disease with multiple organ involvement. 1646 47

Lymphoplasmacytic sclerosing pancreatitis ("autoimmune" pancreatitis) is the best-known manifestation of an unusual corticosteroid-sensitive systemic fibrosclerotic disease that is associated with high plasma immunoglobulin G4 (IgG4) and tissue infiltration with IgG4-secreting plasma cells. Pancreatic and biliary manifestations of this condition are well-reported, but reports of other systemic involvement are few. We report here a case of initially unrecognized autoimmune pancreatitis followed 5 years later by a focal sclerosing lymphoplasmacytic tubulointerstitial nephritis and concurrent membranous nephropathy. The patient presented with hypertension, a raised serum creatinine, proteinuria, elevated serum IgG4, and eosinophilia. Immunolabeling of renal tissue showed numerous IgG4 positive plasma cells with peritubular and glomerular subepithelial IgG4 deposition. On steroid therapy serum IgG4 levels normalized, the eosinophilia resolved, and there was improvement in symptomatic wheeze, dry eyes, serum creatinine, and liver function tests. This case highlights a distinctive and potentially treatable form of interstitial nephritis manifesting from a systemic immune disorder, and provides circumstantial evidence to support the notion that dysregulated IgG4 can precipitate the development of a form of membranous nephropathy.
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PMID:Nephropathy in IgG4-related systemic disease. 1706 91

We report a case of chronic tubulointerstitial nephritis associated with multiple nodular lesions of the kidneys in a patient with autoimmune pancreatitis. Serum immunoglobulin G4 (IgG4) level was increased, and immunohistochemical staining for IgG4 on the renal biopsy specimen showed positive staining of plasma cells and tubular basement membrane within areas of chronic tubulointerstitial nephritis. There are a few reports of nodular lesions of kidneys or interstitial nephritis associated with autoimmune pancreatitis. Our case is unique in that all 3 conditions presented together and suggests that interstitial nephritis can present as nodular lesions.
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PMID:Chronic tubulointerstitial nephritis presenting as multiple renal nodules and pancreatic insufficiency. 1718 38

Paramyxovirus-1 (PMV-1) infection was diagnosed in racing pigeons in Ontario during 1985, but it was not until January 1989, that the virus was isolated from feral pigeons (Columba livia) in this province. During an 18 month period beginning January 1988, a total of 43 feral pigeons was submitted to the Wildlife Diseases Laboratory, Pathology Department, Ontario Veterinary College. A history of neurological signs accompanied most of the birds. Tissues from 29 birds were submitted for PMV-1 isolation. Allantoic inoculation of embryonated chicken eggs yielded PMV-1 in 10 of the pigeons submitted. On the basis of histological criteria, we believe that 12 other birds were also infected with PMV-1.Gross pathological changes were unremarkable. Lymphplasmacytic interstitial nephritis was observed histologically in all birds from which PMV-1 was isolated. Other lesions seen, in decreasing frequency of occurrence, were lymphoplasmacytic interstitial hepatitis and multifocal hepatic necrosis, lymphoplasmacytic interstitial pancreatitis, nonsuppurative encephalitis and myelitis.The existence of PMV-1 in feral pigeons poses a potential threat to the poultry population since there is ample opportunity for mingling with poultry under open housing management. There is also a concern that pigeons may harbor the virus, perhaps in the kidney, and become chronic carriers and potential long-term disseminators of the disease.
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PMID:Paramyxovirus-1 in feral pigeons (Columba livia) in Ontario. 1742 32


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