Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bilateral renal dysplasia and nephron hypoplasia was diagnosed in a Quarter Horse foal with clinical signs of lethargy, convulsions, and diarrhea. Laboratory evaluation revealed anemia, hypoproteinemia, leukopenia, hyponatremia, hypochloremia, and hyposmolality. The foal also had high concentrations of serum creatinine, BUN, and phosphorus. Evaluation of urinary indices revealed a high ratio of urinary gamma-glutamyl-transferase activity to concentration of creatinine, as well as a high fractional clearance ratio of sodium and potassium. Intravenous treatment with saline solution (0.9% NaCl) and antimicrobials provided only temporary resolution of some of the abnormalities. Diagnosis was partly established by histologic evaluation of renal tissue obtained via an ultrasonographically guided biopsy and was confirmed at necropsy. Pathologic changes in the kidney were unique in that the size of the kidneys, along with the appearance and number of glomeruli, were essentially normal despite marked hypoplasia of nephron tubules in the medulla.
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PMID:Bilateral renal dysplasia with nephron hypoplasia in a foal. 236 27

A case of an aneurysm on the persistent primitive trigeminal artery (PPTA) is reported. A seventy-five-year-old woman with subarachnoid hemorrhage was admitted to the Hospital six hours after the onset. She was lethargic and had stiffness of her neck with severe headache and vomiting. Computed tomographic examination showed marked subarachnoid hemorrhage in the basal cisterns, especially in the ambient cistern on the right side. Cerebral angiogram revealed the right PPTA having a saccular aneurysm on the trunk. Her advanced age and the special location of the aneurysm did not allow direct operation in the acute stage. She died of rebleeding of the aneurysm thirty days after admission. Pathological study showed that the PPTA was originated from the cavernous portion of the right internal carotid artery and joined to the cephalad portion of the basilar artery. The aneurysm, 10 X 7 mm in size, was located at the curved midportion of PPTA, 9 mm proximal to the basilar artery. The proximal portion of the PPTA to the aneurysm had severe arteriosclerosis, whereas the distal portion showed less sclerotic change. However, there were no evidences of developmental anomaly in the wall of the PPTA. Eighteen cases of PPTA with the aneurysm arisen from PPTA itself or at its junction with internal carotid artery have been previously reported. PPTA in any case has not been examined pathologically. It has been speculated that dysplasia of the PPTA wall contributes to initiating the aneurysm on the PPTA. However our histopathological examination of the PPTA revealed no evidence of dysplasia in the PPTA wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of a persistent primitive trigeminal artery aneurysm]. 328 32

A 12-month-old neutered male golden retriever was presented with a history of lethargy and exercise intolerance. Clinical examination, electrocardiography, radiography and echocardiography supported a diagnosis of fixed subvalvular aortic stenosis with a Doppler pressure gradient of 77.5 mmHg. Surgical inspection also revealed gross structural abnormalities of the mitral valve consistent with mitral dysplasia. Intervention consisted of resection of the dysplastic mitral valve and the subvalvular aortic stenosis. The mitral valve was replaced with a bioprosthetic valve. Total cardiopulmonary bypass time was 65 minutes and aortic cross-clamp time was 55 minutes. A full recovery was made and 11 months postoperatively the aortic transvalvular gradient was 30 mmHg. At the time of writing, 12 months after surgery, the dog was clinically normal and requires no medication.
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PMID:Surgical management of subvalvular aortic stenosis and mitral dysplasia in a golden retriever. 920 Jan 15

A term male newborn, appropriate for gestational age, developed hypothermia, severe cardiac dysrrhythmia, and nonoliguric hyperkalemia within 24 hours of birth. Despite the prenatal identification of cystic renal dysplasia without oligohydramnios, at birth, a solitary left leg vascular hemangioma and large palpable kidneys were the only anomalies. Gradually hypotonia, lethargy, and poor feeding developed and by 20 hours of age recurrent cardiac dysrrhythmias, myocardial dysfunction, and renal insufficiency with intermittent hyperkalemia were apparent. Episodes of apnea developed on day 7 followed by respiratory failure, recurrent cardiac dysrrhythmias, and death on day 12. Eventually laboratory and autopsy findings confirmed the diagnosis of lethal neonatal carnitine palmitoyltransferase II deficiency.
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PMID:Lethal neonatal carnitine palmitoyltransferase II deficiency: an unusual presentation of a rare disorder. 1263 78

A 4-year-old, spayed female, domestic shorthair cat was presented for lethargy, nonregenerative anemia, and inappetence. Results of a CBC included macrocytic, normochromic, nonregenerative anemia and a glucocorticoid-associated leukogram. On blood smear examination, neutrophils had abnormal features including hyposegmentation and a diffuse chromatin pattern with nuclear filament formation and nuclear blebbing. Microscopic examination of a roll preparation of bone marrow revealed hypolobulated megakaryocytes with asynchronous maturation of nuclei. The granulocytic to erythrocyte (G:E) ratio was 76. Segmented neutrophils had asynchronous maturation and dysplastic features. The entire erythroid lineage was markedly decreased for the degree of anemia and rare dysplastic features were noted in erythroid precursor cells. The interpretation of bone marrow findings was erythroid hypoplasia, megakaryocytic dysplasia, and granulocytic hyperplasia with dysplasia. Histopathologic examination of a bone marrow core sample also revealed myeloid hyperplasia and erythroid hypoplasia. The result of a direct immunofluorescence assay for FeLV performed on the bone marrow roll preparation was positive. A diagnosis of dysmyelopoiesis associated with FeLV infection was made. This case was unique in that the dysplastic changes occurred in cell lines that did not have associated cytopenias. The dysmyelopoiesis most closely resembled myelodysplastic syndrome with refractory cytopenia (MDS-RC); however, secondary dysmyelopoiesis could not be ruled out.
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PMID:Blood smear from a cat: features to "dys"cover. 1712 56

A 58-year-old man was admitted with symptoms of lethargy and easy bruising for four months duration. Peripheral blood (PB) analysis revealed a white blood cell count (WBC) of 15.9 x 10(9)/l with monocytes 5.4 x 10(9)/l. Bone marrow (BM) was hypercellular with 15% blasts, monocytosis and trilineage dysplasia. Conventional cytogenetic analysis (G-banding) detected an apparently normal male karyotype (46,XY). A diagnosis of chronic myelomonocytic leukaemia (CMML) was made. After 3 years, PB analysis revealed a WBC count of 22 x 10(9)/l and a predominance of blasts. BM aspirate analysis also revealed 89% myeloid blasts and G-banding detected the emergence of an abnormal clone harbouring an extra copy of chromosomes 13 and 15. A diagnosis of disease transformation to acute myeloid leukaemia (AML) was made. Post chemotherapy BM aspirate was very hypocellular and the abnormal +13, +15 clone was still present suggesting primary refractory disease. A second course of chemotherapy was only administered for 24 hours due to complications. The abnormal +13, +15 clone was still present and it was decided that no further treatment apart from palliative care could be offered. The patient died 11 weeks later, five months after AML transformation. This is the first description of a cytogenetically normal CMML patient transforming to AML with the emergence of a unique +13, +15 double trisomy resulting in an adverse outcome.
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PMID:Transformation of cytogenetically normal chronic myelomonocytic leukaemia to an acute myeloid leukaemia and the emergence of a novel +13, +15 double trisomy resulting in an adverse outcome. 1785 37

An 18-year-old female alpaca was presented to the Colorado State University Veterinary Teaching Hospital for chronic ill thrift over a 1-year period. Six weeks previously, an infected left mandibular cheek tooth was removed by oral extraction. On physical examination the patient was cachectic, lethargic, and weak. Abnormalities on the CBC included neutropenia, thrombocytosis, and severe nonregenerative, macrocytic, hypochromic anemia. Dysplastic nucleated erythrocytes and micromegakaryocytes were observed on the peripheral blood smear. Neutrophils, bands, and metamyelocytes appeared markedly toxic. Numerous blasts containing variable numbers of fine azurophilic granules were also observed. Based on their morphology, the cells were interpreted to be progranulocytes and myeloblasts, and a presumptive diagnosis of acute myeloid leukemia (AML) was made. The blast cells accounted for 60% of the nucleated cell population on bone marrow aspirates, further supporting a diagnosis of AML with multilineage dysplasia. Post mortem examination showed infiltration of the neoplastic cells into spleen, liver, kidney, and lymph nodes. Based on histologic findings, the morphologic diagnoses were disseminated myeloid neoplasia, chronic regionally extensive tooth root abscess, and membranous glomerulonephritis. The neoplastic cells were CD172a-positive on flow cytometry, chloroacetate esterase-positive by cytochemistry, and myeloperoxidase-positive by immunohistochemistry, confirming myeloid origin. To our knowledge, this is the first case of AML with multilineage dysplasia in an alpaca, with only one other case of myelodysplasia described previously in this species.
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PMID:Acute myeloid leukemia with multilineage dysplasia in an alpaca. 1876 21

A 14-year-old female had repeated vomiting, headache, abdominal pain, visual field deficit and lethargy at the onset of hypertensive encephalopathy. Cerebrospinal fluid (CSF) test revealed a high level of IgG and protein. MRI demonstrated no supratentorial cerebral lesions but hyperintense lesions were observed from the lower pons to the Th8 level of spinal cord and cerebellar cortex on T2 weighted and FLAIR images without contrast enhancement. The two antihypertensive drugs stabilized to control her blood pressure and improved her clinical symptoms. Reexamination of MRI and cerebrospinal fluid test also revealed clear improvement of the above abnormalities. The abnormal findings on abdominal CT and renography led us to suspect renal infarction. Abdominal angiography demonstrated multifocal stenoses of renal interlobar arteries, which were supposed to supply the renal infarcted regions. These suggested that the renal infarctions due to fibromuscular dysplasia caused systemic hypertension. There have been only two reports that demonstrated spinal cord lesions in reversible posterior leukoencephalopathy syndrome (RPLES). We report extensive spinal lesions on MRI and a high level of IgG in CSF at the subacute phase in a young female with RPLES associated with hypertensive (brainstem) encephalopathy.
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PMID:A case of hypertensive encephalopathy with extensive spinal lesions on MRI. 1973 90

A 4-year-old male Shih Tzu died suddenly with the only history being slight lethargy during the previous 2 days. Gross and histopathological examination of the heart revealed severe segmental stenosis of the epicardial coronary artery branches and extensive areas of acute myocardial necrosis interspersed with areas of fibrosis. The segmental coronary artery stenosis was due to smooth muscle and myofibroblast proliferation in the tunica media. The smooth muscle cells and myofibroblasts disrupted the internal elastic lamina and extended into the tunica intima. Thickening of the intima and media was accompanied by fibrosis, consistent with fibromuscular dysplasia. The resulting stenosis led to myocardial infarction and cardiac insufficiency. This report details for the first time the vascular lesions in a case of sudden cardiac death in a dog afflicted with fibromuscular dysplasia of the coronary arteries.
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PMID:Epicardial coronary artery fibromuscular dysplasia, myocardial infarction and sudden death in a dog. 2053 84

An ultrasonographic reproductive health examination of a 26-yr-old female African elephant (Loxodonta africana) revealed bilateral ureteral wall thickening and dilatation. On ultrasonographic examination, the bladder and both ureters were normal near the trigone; however, the cranial-most aspect of each ureter was dilated and thickened for a length of 30-50 cm. The same month, elevated blood creatinine (3.0 mg/dl), and urine protein-creatinine ratio (4.0) were observed. Chronic renal failure was diagnosed based on these abnormalities, and the persistent ureteral dilatation was seen on subsequent ultrasound examinations. Complete blood cell counts, serum chemistries, and urinalyses remained relatively unchanged until 24 mo after diagnosis, at which time azotemia, hypophosphatemia, and hypercalcemia (including elevated ionized calcium) developed. Hydronephrosis of both kidneys and prominent sacculation of the left ureter were noted on ultrasonographic examination. Lethargy, ventral edema, and oral mucosal ulceration acutely developed 30 mo after diagnosis. Although blood urea nitrogen remained elevated, creatinine, total calcium, and ionized calcium returned to within reference ranges at that time. Due to rapid clinical decline and grave prognosis, humane euthanasia was elected. Bilateral ureteral dilatation, dysplasia of the right kidney, and chronic nephritis of the left kidney were identified postmortem.
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PMID:Dilated ureters, renal dysplasia, and chronic renal failure in an African elephant (Loxodonta africana). 2244 23


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