Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical characteristics were examined in 5 elderly patients whose brain showed typical features of Wernicke's encephalopathy at the autopsy. All 5 were females with a mean age of 67 +/- 4 years old. The pathological diagnosis of Wernicke's encephalopathy was based on the presence of bleeding or atrophy of bilateral mammilary bodies, proliferation of capillaries and increase of macrophages in mammilary bodies, midbrain periaqueductal gray matter and periventricular area, with relatively intact neurons. Wernicke's encephalopathy was diagnosed clinically only in one case. The remaining four had no clinical diagnosis of Wernicke's encephalopathy. Underlying diseases were varied including neurological, metabolic, gastrointestinal disorders and malignancy. The predominant symptom, consciousness disturbance, was seen in 4 cases. Two of them showed a comatose state. Ocular symptoms and ataxia were observed in 2 cases. Laboratory findings revealed leukocytosis and anemia in 3 cases, hypoproteinemia in 4 cases. One case was alcoholic, but the other four were non-alcoholics and developed the disease after prolonged malnutrition. At the onset of the disease, 4 cases were receiving glucose and electrolyte infusion without vitamins, at the onset of the disease. We propose that in elderly patients with consciousness disturbance of unknown cause, Wernicke's encephalopathy should be taken into consideration even in non-alcoholics, and thiamine infusion should be commenced at once when the disease is suspected even when typical symptoms are lacking.
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PMID:[Clinical characteristics of Wernicke's encephalopathy in the elderly]. 156 Jun 7

A 3-year-old pregnant Nubian goat that was examined because of weight loss, weakness, and change in attitude was determined to be infected with Mycobacterium paratuberculosis. Signs of depressed attitude, trembling, and ataxia were consistent with hepatic encephalopathy, which was confirmed by detection of hyperammonemia. These signs were consistent with histopathologic lesions in the liver and brain. Changes in energy balance and the hypoproteinemia that often develop in goats with paratuberculosis may lead to fat infiltration of the liver, hepatic insufficiency and, ultimately, hepatoencephalopathy.
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PMID:Hepatic encephalopathy associated with paratuberculosis in a goat. 1041 79

We report a 61-year-old man with vitamin E deficiency, presenting with, myopathy as an only clinical symptom. In 1997, at 59 years of age, he noted mild proxymal-muscle weakness and atrophy in the four extremities, nine years after he received a Billroth II partial gastrectomy for a gastric ulcer. His muscle weakness slowly exacerbated, and he was admitted to our hospital in 1999. On admission, neurological examination confirmed mild proximal-muscle weakness and atrophy in the four extremities. Intelligence, cranial nerves, coordination, sensation and tendon reflexes were all normal. Laboratory examination showed normochromic anemia (Hb 9.9 g/dl, Ht 30.9%, MCV 97.5 fl, MCHC 31.2 pg), hypoproteinemia (5.0 g/dl), and hypocholesterolemia (107 mg/dl). The levels of serum CK, lactate and pyruvate were normal. The serum vitamin E level was markedly reduced (0.17 mg/dl; normal 0.75-1.41). Cerebrospinal fluid was normal. Nerve conduction, sensory evoked potentials (SEP), electromyography (EMG), head CT and electroencephalography (EEG) were all normal. Muscle biopsy from the right deltoid muscle showed both mild myogenic and neurogenic changes. Remarkably, type 1 muscle fiber predominance and granular accumulation of autofluorescent lipofuscin granules in the muscle fibers were found. These pathological findings were compatible with those of vitamin E-deficient myopathy. Thus, he was diagnosed as having vitamin E-deficient myopathy, which was confirmed by apparent effective supplementation of vitamin E. Interestingly, our present case did not show any other neurological manifestations such as deep sensory disturbance, sensory ataxia or polyneuropathy. A long-term workload due to hard physical labor and smoking in our patient may have accelerated oxidative muscle damage, resulting in amyotrophy mainly due to vitamin E deficient myopathy.
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PMID:[A patient with vitamin E deficient, myopathy presenting with amyotrophy]. 1180 55

The medical records of 19 horses with acute hemoperitoneum were reviewed. The causes for the hemoperitoneum were idiopathic (8 horses), splenic hematoma with capsular tear (7), bleeding from the reproductive tract (3), multicentric hemangiosarcoma (1), and systemic amyloidosis (1). The affected horses were between 4 and 32 years of age (median 11.5 years). The most consistent findings on initial examination were depression, tachycardia, tachypnea, pale mucous membranes, prolonged capillary refill time, colic, and abdominal discomfort. Less common clinical signs included abdominal distention, profuse sweating, ataxia, and broad ligament mass palpated on rectal examination. Clinicopathologic abnormalities commonly detected were anemia, neutrophilia, lymphopenia, thrombocytopenia, hypoproteinemia, hypocalcemia, azotemia, increased creatinine kinase, and sorbitol dehydrogenase activity. Hemoperitoneum was diagnosed on the basis of abdominocentesis, transabdominal ultrasonography, and postmortem examination. Sixteen horses were treated, and 3 horses were euthanized at owners' request because of severe clinical signs. The treatment consisted of the administration of intravenous fluids, plasma or blood transfusion, nonsteroidal drugs, antimicrobial drugs, and antifibrinolytic and procoagulant agents. Rapid clinical deterioration was observed in 2 horses, necessitating euthanasia. The remaining 14 horses survived the abdominal bleeding (survival rate 74%) and were discharged 3-15 days (median 7.0 days) after presentation. Postmortem examination of the 6 nonsurvivors showed massive abdominal hemorrhage from splenic hematoma with capsular tear (2 horses), multicentric hemangiosarcoma with liver rupture (1), systemic amyloidosis with splenic hematoma and capsular tear (1), and bilateral ruptured ovarian hematomas (1). In one horse, no origin of the bleeding could be determined during postmortem examination.
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PMID:Acute hemoperitoneum in horses: a review of 19 cases (1992-2003). 1595 49