Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A man aged 31 with remittent fever, leukopenia, polyuria, and splenomegaly in addition to chronic and recurrent episodes of neurologic abnormalities was examined pathologically. A chronic type of perivenous encephalomyelitis was found in the CNS, and chronic inflammatory lesions were noticed in the infundibulo-hypophyseal system and also in the peripheral nerves. Moreover, hemophagocytic lymphohistiocytosis predominated in the reticuloendothelial system. This seemed to be the first adult case of demyelinating disease with hemophagocytic lymphohistiocytosis.
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PMID:Chronic recurrent demyelinating encephalomyelitis associated with hemophagocytic lymphohistiocytosis. 683 66

A 24 year old patient with epigastric pain, polyuria, polydipsia and hypercalcemia was admitted to the hospital. Besides the frequent causes of hypercalcemia such as primary hyperparathyroidism and malignancy-related hypercalcemia we had to consider sarcoidosis because of massive splenomegaly. The interstitial lung disease shown on x-ray films of the chest, the epithelioid granulomas in lung tissue and the increased ACE confirmed the diagnosis of sarcoidosis. Hypercalcemia is found in less than 5% of all cases with sarcoidosis. After treatment with steroids, diphosphonates and diuretics all symptoms and the hypercalcemia improved.
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PMID:[Polyuria, polydipsia]. 780 Oct 19

The course of naturally acquired infection with feline immunodeficiency virus was monitored in a cat over an 18-month period after diagnosis. The cat was admitted with diarrhea, poor body condition, a bite wound abscess, gingivitis, chronic fever, and splenomegaly. The cat's condition improved after splenectomy and remained stable for approximately 15 months, then began to deteriorate, as gingivitis, polyuria, polydipsia, pyrexia, multiple cutaneous masses, and hind limb paresis developed. The in vitro response of the cat's lymphocytes to mitogens was suppressed, and absolute lymphocyte counts were low. Spinal lymphosarcoma, disseminated mastocytoma, and presumptive diabetes mellitus were diagnosed after euthanasia. Decreased immune surveillance associated with feline immunodeficiency virus-related immunosuppression possibly played a role in the development of neoplastic disease in this cat.
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PMID:Spinal lymphosarcoma and disseminated mastocytoma associated with feline immunodeficiency virus infection in a cat. 839 90

A 13-yr-old ring-tailed lemur (Lemur catta) was evaluated for depression, anorexia, polyuria, and polydipsia. The lemur was in poor body condition and was anemic, hypoalbuminemic, and hyponatremic. Cytologic examination of aspirates of the spleen, liver, and bone marrow and histopathologic examination of liver and bone marrow biopsies revealed a disseminated round cell tumor. After euthanasia, necropsy revealed hepatomegaly, splenomegaly, and mesenteric lymphadenomegaly. Neoplastic cells were present within the spleen, liver, kidneys, multiple lymph nodes, bone marrow, lung, small intestine, pancreas, and testicle and were composed of large anaplastic round cells in a background of small well-differentiated lymphocytes. Immunohistochemical analysis revealed that the small well-differentiated lymphocytes labeled for the anti-human T-cell marker, CD3, and the large anaplastic round cells labeled with the anti-human B-cell marker, CD79a. On the basis of the immunohistochemical staining results and morphologic appearance, a diagnosis of a T-cell-rich B-cell lymphoma was made.
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PMID:T-cell-rich B-cell lymphoma in a ring-tailed lemur (Lemur catta). 1155 62

Non-alcoholic steatohepatitis (NASH) is one of the most common liver disorders. This is highly prevalent in obese and diabetic subjects. Persons with central obesity are at particular risk. Other clinical predictors are age more than 40-50 years and hyperlipidemias, but none of these factors is invariable for causation of NASH. Other reported associations are, celiac disease, Wilson's Disease and few other metabolic diseases. Drugs, particularly amiodarone, tamoxifen, nucleoside analogues and methotrxate have also been linked to NASH. The disease is evenly distributed in both sexes but advanced disease is more common in women. Ethnic variation exists and African Americans are less affected than Hispanic Americans. Specific clinical features of NASH are infrequent. Patients usually come to clinical attention by elevated liver enzymes found on routine evaluation but on history, about two third of patients will admit to have mild fatigue and about half will report right upper quadrant pain. Rarely, patient may present with a complication of cirrhosis. Physical examination may reveal hepatomegaly and splenomegaly. Research in last few years has stressed that development of steatosis, stetohepatitis, fibrosis with subsequent cirrhosis are most probably the result of insulin resistance. Therefore, clinical features may reflect existence of insulin resistance. Obesity, particularly central obesity is most important of these. Patients may have sleep apnea syndrome. Hypertension and manifestations of diabetes mellitus like polyuria, polydypsia, and neurological deficits may occur. Patients may have varying combination of obesity, diabetes, hyperlipidemia, hypertension and impaired fibrinolysis (syndrome X). Children with insulin resistance may show acanthosis nigricance. Patients with polycystic ovary syndrome, which consists of insulin resistance, diabetes, obesity, hirsutism, oligo or polymenorrha and hyperlipidemia may have NASH. Other rare manifestations of insulin resistance, which can be seen in patients of NASH are lipomatosis, lipoatrophy/lipodystrophy and panniculitis. Most other rare conditions known to cause NASH like peroxisomal diseases, mitochondialpathies, Weber-Christian disease, Mauriac syndrome, Madelung's lipomatosis and abetaliopprotenemia also have insulin resistance. This is believed that primary defect underlying insulin resistance is impairment in postreceptor pathways (through tyrosine kinase activity) of insulin action. Primary defect in insulin receptors appear uncommon. This results in down regulation of insulin receptor substance 1 (IRS-1) signaling by excess free fatty acids. In muscle, activated IRS-1 promotes translocation of glucose transporter protein 4 (GLUT4) to cell membrane. As a result, monocyte glucose uptake by GLUT4 increases glucose disposal from blood and reduced need for insulin. PKC-0 is a likely candidate as serine kinase in muscle regulated by fatty acids that can impair the activation of IRS-1. Insulin resistance is usually evaluated by fasting insulin levels, Quantitative Insulin Check Index (QUICKI) and Homeostasis Model Assessment of Insulin Resistance (HOMA), C-peptid/insulin ratio oral glucose tolerance test and hyper insulinemic euglycemic clamp. The clamp technique is considered the gold standard.
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PMID:Insulin resistance and clinical aspects of non-alcoholic steatohepatitis (NASH). 1619 20

A 67-year-old trout fisherman presented with a six-week history of polyuria, polydipsia, dyspnoea on exertion and the development of subcutaneous extensor surface skin nodules. He was hypercalcaemic with acute renal impairment. Parathyroid hormone was suppressed and vitamin D levels were within normal limits. The patient had a past history of hypothyroidism, but thyroid replacement was adequate. Hypoadrenalism, myeloma and metastatic malignancy were excluded. Biopsy of a subcutaneous nodule revealed dermally based non-caseating granulomata, consistent with sarcoidosis. Serum angiotensin-converting enzyme was elevated, and computerized tomography scanning of the chest and abdomen revealed widespread lymphadenopathy with multiple lung nodules and splenomegaly. Prednisolone therapy produced rapid resolution of his skin lesions and normalization of his bone and renal biochemistry. The mechanism of hypercalcaemia in sarcoidosis is poorly understood but is thought to involve parathyroid hormone-independent 1-hydroxylation of 25-hydroxyvitamin D within sarcoid lesions. This process may be exacerbated by exposure to UV light and it is of interest that this patient developed symptoms after a period of intense trout fishing in the good weather of April and May 2007.
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PMID:A trout fisherman with hypercalcaemia and skin lesions. 2187 32