Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 59-year-old man was admitted to our hospital on May 17, 1991 because of dizziness and a sense of abdominal fullness. Physical examination on admission showed splenomegaly without hepatomegaly or lymphadenopathy, and blood examination revealed normocytic anemia, thrombocytopenia and marked leukocytosis of 16,800/microliters with 87% lymphoid cells. Prolymphocytoid cells formed 28% of the lymphoid cells. Bone marrow aspiration revealed massive infiltration of lymphoid cells. Surface marker analysis showed that the lymphoid cells were positive for anti-HLA-DR, CD 5, CD19, CD20, CD21, SmIgM and SmIgD. The patient was diagnosed as having B-CLL/PL, according to the classification advocated by Melo in 1986, and initially treated with vindesine + prednisolone + pirarubicin (VP-THP). However, the prolymphocyte count increased, so we changed to VP-THP + cyclophosphamide (VEP-THP), and remission was obtained. CLL/PL is a rare disease in Japan but we obtained a good response to chemotherapy.
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PMID:[A case of B-chronic lymphocytic leukemia/prolymphocytic leukemia (CLL/PL)]. 842 81

Of 43 elderly patients who were suspected to have polycythemia between October 1990 and July 1998, 12 patients showed an increased red cell volume measured by 51Cr-labeled red blood cells. We analyzed the clinical characteristics of the 12 patients consisted of 7 men and 5 women, with a median age of 71 (range: 57-92). Chief complaints were headaches and dizziness (3 cases), symptoms of other conditions than polycythemia (4 cases). Five patients had no symptoms. Five of 6 patients over 70 years old had no symptoms due to polycythemia. Seven cases (58%) showed splenomegaly and three cases (25%) showed hepatomegaly. Laboratory findings were as follows: WBC 9.7 +/- 3.9 x 10(3)/microliter (mean +/- SD, p < 0.02 vs normal control), Hb 17.9 +/- 4.2 g/dl (p < 0.001), Plt 39.7 +/- 26.0 x 10(4)/microliter, EPO 13.8 +/- 5.2 mU/ml (p < 0.0001), NAP score 258 +/- 114, Vit. B12 1,686 +/- 2,156 pg/ml, arterial O2 saturation more than 92% in all cases. The diagnosis of all cases was polycythemia vera according to the diagnostic criteria of Polycythemia Vera Study Group. Associated conditions included 8 cases of thrombosis (cerebral thrombosis 4, thrombophrebitis 2, myocardial infarction 1, ischemic colitis 1) and 3 cases of malignancy (esophageal cancer 1, breast cancer 1, renal cancer 1), none of which was therapy-related cancer. Six patients (50%) had only phlebotomy, three (25%) only chemotherapy, and three (25%) both phlebotomy and chemotherapy. Patients over 80 years old needed neither intensive nor continuous treatment. Only one patient died due to esophageal cancer at age 89.
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PMID:[Clinical characteristics of polycythemia vera in the elderly]. 1041 May 70

The authors reported a case of niclofolan intoxication occurred during the trial of clonorchiasis treatment. The case, a 15 years old Korean schoolboy, took niclofolan(Bilevon(R)) of total 473 mg(11 mg/kg) in 11 divided doses during 20 days. And the case suffered from neurologic symptoms such as severe headache, dizziness, nausea, vomiting, blurred vision, papilledema, retinal hemorrhage, an epsiode of seizure attack and elevated intracranial pressure, and hepatotoxic symptoms such as hepatomegaly, increased serum transaminases, and shoulder pain, excessive sweating and weight loss. Therapy was concentrated to the management of the elevated intracranial pressure. Hepatotoxic manifestations subsided within one month. The clinical signs related to elevated intracranial pressure persisted two months. Body weight regained after 2 months. And the symptoms of headache, dizziness and vomiting were complained intermittently until 4 months after onset. However, no subsequent clinical problems related with this episode has been noted until this record.
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PMID:A Case Of Niclofolan (Bilevon(R)) Intoxication. 1290

Amyloidoses are a heterogeneous group of multisystem disorders, which are characterized by an extracellular deposition of amyloid fibrils. Typically affected are the heart, liver, kidneys, and nervous system. More than half of the patients die due to cardiac involvement. Clinical signs of cardiac amyloidosis are edema of the lower limbs, hepatomegaly, ascites and elevated jugular vein pressure, frequently in combination with dyspnea. There can also be chest pain, probably due to microvessel disease. Dysfunction of the autonomous nervous system or arrhythmias may cause low blood pressure, dizziness, or recurrent syncope. The AL amyloidosis caused by the deposition of immunoglobulin light chains is the most common form. It can be performed by monoclonal gammopathy. The desirable treatment therapy consists of high-dose melphalan therapy twice followed by autologous stem cell transplantation. Due to the high peritransplantation mortality, selection of appropriate patients is mandatory. The ATTR amyloidosis is an autosomal dominant disorder caused by the amyloidogenic form of transthyretin, a plasmaprotein that is synthesized in the liver. Therefore, liver transplantation is the only curative therapy. The symptomatic treatment of cardiac amyloidosis is based on the current guidelines for chronic heart failure according to the patient's New York Heart Association (NYHA) state. Further types of amyloidosis with possible cardiac involvement comprise the senile systemic amyloidosis caused by the wild-type transthyretin, secondary amyloidosis after chronic systemic inflammation, and the beta(2)-microglobulin amyloidosis after long-term dialysis treatment.
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PMID:[Cardiac amyloidosis]. 1834 65

Glycogen storage diseases (GSDs) comprise a large, heterogeneous group of disorders characterized by abnormal glycogen deposition. Multiple cases in the literature have demonstrated an association between GSD type I and pulmonary arterial hypertension (PAH). We now also report on two patients with GSD type III and PAH, a novel association. The first patient was a 16-year-old girl of Nicaraguan descent with a history of hepatomegaly and growth retardation. Molecular testing identified a homozygous 17delAG mutation in AGL consistent with GSD type IIIb. At the age of 16, she was found to have PAH and was started on medical therapy. Two years later, she developed acute chest pain and died shortly thereafter. The second patient is a 13-year-old girl of Colombian descent homozygous for the c.3911dupA mutation consistent with GSD IIIa. An echocardiogram at age 2 showed left ventricular hypertrophy, which resolved following the institution of a high protein, moderate carbohydrate diet during the day and continuous gastric-tube feeding overnight. At the age of 12, she was found to have pulmonary hypertension. She was started on sildenafil, and her clinical status has shown marked improvement including normalization of her elevated transaminases. PAH may be a rare association in patients with GSD IIIa and IIIb and should be evaluated with screening echocardiograms for cardiac hypertrophy or if they present with symptoms of right-sided heart failure such as shortness of breath, chest pain, cyanosis, fatigue, dizziness, syncope, or edema. Early diagnosis of PAH is important as increasingly effective treatments are now available.
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PMID:Two Cases of Pulmonary Hypertension Associated with Type III Glycogen Storage Disease. 2343 Aug 32