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)

Ten patients, suffering from affective disorders, were treated with carbamazepine for polyuria and polydipsia associated with long-term lithium therapy. Oral carbamazepine (300--600 mg daily for six weeks) was observed to have no beneficial effect in alleviating these symptoms when compared with placebo tablets in a double blind crossover study. Plasma and urinary osmolality were observed to be within normal range in these patients and there was no antidiuretic response following subcutaneous Pitressin injection. There was 50% drop-out due to severe side-effects like ataxia, dizziness, restlessness and confusional states. It appears that lithium exacerbates carbamazepine induced CNS side-effects or vice versa, the mechanism of which is not very clear. It may be due to their mutual effect on sodium metabolism or on nervous conduction velocity. Hence, simultaneous administration of these two drugs should preferably be avoided.
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PMID:Effect of carbamazepine in polyuria associated with lithium therapy. 36 Feb 49

The majority of cases of acute, nonspecific diarrhea are of short duration, can be treated symptomatically with nonprescription medications and adequate hydration, and do not require a visit to the physician's office. If the family practitioner can determine via telephone that the patient, or the caller's child, is not experiencing certain signs and symptoms often associated with diarrheal illness that may indicate a more severe condition (e.g., high fever, vomiting, persistent diarrhea, or diarrhea accompanied by blood or severe abdominal or rectal pain), self-treatment may be allowed without an office visit. In addition, if the physician determines that the patient is not suffering from diarrheal dehydration, indicated by dry mouth, excessive thirst (or for children, inadequate fluid intake), wrinkled skin, little or no urination, dizziness, or lightheadedness, the physician may also allow the patient to be treated without an office visit. If, however, the patient is experiencing any of these symptoms, an office visit is required to facilitate further evaluation by the physician.
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PMID:Family practitioner's guide to patient self-treatment of acute diarrhea. 235 47

Data is reviewed on premenstrual symptoms which have been related to high suicide and accident rates, employment absentee rates, poor academic performance and acute psychiatric problems. A recent study of healthy young women indicated that 39% had troublesome premenstrual symptoms, 54% passed clots in their menses, 70% had cyclical localized acneiform eruptions and only 17% failed to experience menstrual pain. Common menstrual disorders are classified as either dysmenorrhea or the premenstrual syndrome. Symptoms for the latter usually begin 2-12 days prior to menstruation and include nervous tension, irritability, anxiety, depression, bloated breasts and abdomen, swollen fingers and legs, headaches, dizziness, occasional hypersomia, excessive thirst and appetite. Some women may display an increased susceptibility to migraine, vasomotor rhinitis, asthma, urticaria and epilepsy. Symptoms are usually relieved with the onset of menses. While a definitive etiological theory remains to be substantiated, symptomatic relief has been reported with salt and water restriction and simple diuretics used 7 to 10 days premenstrually. Diazapam or chlordiazepoxide treatment is recommended before oral contraceptive therapy. The premenstrual syndrome may persist after menopause, is unaffected by parity, and sufferers score highly on neuroticism tests. Primary or spasmodic dysmenorrhea occurs in young women, tends to decline with age and parity and has no correlation with premenstrual symptoms or neuroticism. Spasmodic or colicky pain begins and is most severe on the first day of menstruation and may continue for 2-3 days. Treatment of dysmenorrhea with psychotropic drugs or narcotics is discouraged due to the risk of dependence and abuse. Temporary relief for disabling pain may be obtained with oral contraceptives containing synthetic estrogen and progestogen but the inherent risks should be acknowledged. Both disorders have been correlated to menstrual irregularity. Amenorrhea in many women may be precipitated by simple psychological events such as leaving home, while severely stressful events produce a higher incidence. Unless a physiological factor such as malnutrition is operating, menses usually recur spontaneously within a few months. Amenorrhea is a constant feature of anorexia nervosa and may precede related attitudes toward eating and body weight. This syndrome is best regarded as a chronic and often severe neurotic disorder requiring combined physiological and psychological treatment, although some evidence exists to indicate an endocrine disorder. Extensive basic research is needed on the complex relationship between the neuroendocrine system and emotion.
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PMID:Premenstrual symptoms. 473 36

We report a 29-year-old man with diabetes insipidus and cerebellar ataxia who developed spinal cord swelling 15 years after the onset. He was well until 14 years of the age when he noted dizziness. Two years after there was an onset of gait disturbance and slurred speech. He also noted polydipsia and polyuria. He was evaluated at the neurosurgery service of our hospital when he was 17 years of the age. Neurologic examination at that time revealed memory loss, horizontal nystagmus, cerebellar ataxic gait, dysmetria and decomposition more on the left. Cranial CT scan revealed a mass lesion involving the left subthalamic region and the head of the caudate area. Spinal fluid was unremarkable, however, human chorionic gonadotropin was increased to 27 mIU/ml. He was treated by radiation therapy (3,000 rads for total brain area and 5,460 rads for focal region). His CT scan and memory loss improved, however, cerebellar ataxia was unchanged. Three years after the radiation, he started to show choreic movement in his neck and left upper extremity. He was admitted to our service in August 14, 1995 when he was 29 years of the age. On admission, he was alert but disoriented to time; calculation was also poor. Higher cerebral functions were intact. The optic fundi were normal without papilledema. Visual field appeared intact. Gaze nystagmus was observed in all the directions, but more prominent in the horizontal direction. Speech was slurred. Otherwise, cranial nerves were unremarkable. Motor wise, he showed marked truncal and gait ataxia; he was unable to walk because of ataxia. Muscle atrophy and marked weakness was noted in both upper extremities more on the left side. Deep tendon reflexes were diminished in the upper extremities but active in the lower extremities. He was polyuric; urinary specific gravity was low. Spinal fluid contained 6 cells/cmm and 113 mg/ dl of protein; Queckenstedt was positive. MRI revealed swelling of the cervical cord; in addition, the entire cervical region and the medullar oblongata appeared as high signal intensity areas. No mass lesion was noted in the supratentorial structures but the third ventricle was markedly enlarged. Surgical biopsy was performed on the cervical lesion. The patient was discussed in neurologic CPC, and the chief discussant arrived at the conclusion that the patient had germinoma with syncytiotrophoblastic giant cells in the diencephalic region which appeared to have been cured by radiation therapy; he thought that the cervical lesion was the seeding of germinoma. Cerebellar ataxia was ascribed to the remote effect of germinoma. Most of the participants thought that the original tumor was germinoma and the cervical lesion was its spread. Some participants thought that his ataxia was caused by germinoma cells involving the medulla and the inferior cerebellar peduncles. Histologic observation of the biopsied tissue from the spinal cord revealed the typical two cell patterned germinoma. Most of the tumor cells were not stained for an antibody against HCG, but some tumor cells were positively stained. Germinoma is very radio-sensitive; this patient showed T2 high signal lesion involving the medulla oblongata and cervical cord continuously. Probably, tumor cells in the lower brain stem escaped radiation, and gradually spread to the spinal cord over many years. At the time of operation, the surface of the spinal cord was free from tumor cells. Therefore, tumor cells invaded the spinal cord continuously from the medulla oblongata. He was treated with cervical radiation, and his neurologic as well as radiologic findings showed marked improvement.
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PMID:[A 29-year-old man with diabetes insipidus and cerebellar ataxia and development of spinal cord swelling 15 years after the onset]. 916 63

Starr County, Texas, a Texas-Mexico border community, was the site of a study involving culturally-appropriate education and group support for Mexican Americans with type 2 diabetes. Data were collected from 63 subjects on frequency of diabetes-related symptoms during the previous month and on self-care symptom treatments. On average, subjects were 57-year-old females, diagnosed with diabetes for 10 years, and exhibiting HbA1c levels of 12.5%. Almost 50% experienced excessive urination, excessive thirst, shakiness/nervousness, and numbness and/or tingling in their extremities. More than 50% of those who experienced symptoms did not view them as serious. Only one subject checked blood sugar levels when symptoms occurred. Significantly higher mean glycosylated hemoglobin levels were found for individuals who experienced dizziness and/or chest pain compared with those who did not. A variety of self-care treatments were employed, including over-the-counter medications and home remedies.
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PMID:Symptom-related self-care of Mexican Americans with type 2 diabetes: preliminary findings of the Starr County Diabetes Education Study. 967 51

Intracranial aneurysms (ICA) are a well-known feature of autosomal dominant polycystic kidney disease. There is only one report about ICA in an adult patient with autosomal recessive polycystic kidney disease (ARPKD). We observed a 2-year, 6-month old girl with ARPKD and multiple ICA. The family history is negative for kidney disease. The diagnosis of ARPKD was based on the typical findings in ultrasonography and computed tomography. Cystic ectasia of biliary ducts 6.3/4.8 cm in diameter was found in the liver. Arterial hypertension in a range of 140/100-170/120 mm Hg was registered. The child has polyuria, polydipsia and enuresis. Blood urea was 15 mmol/l, creatinine in a range of 120 to 75 micromol/l. One episode of vomiting, dizziness and lethargy was the reason for a brain magnetic resonance imaging. Multiple fusiform and saccular aneurysms in the branches of middle and posterior cerebral arteries were seen bilaterally. The girl is growing well without neurological symptoms during an observation period of 1.5 years. Blood pressure is well controlled with an ACE inhibitor (Enalapril 2.5 mg daily). It was concluded that ICA can be found in patients with ARPKD. Blood pressure control is essential to reduce the risk of intracranial hemorrhage.
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PMID:Intracranial aneurysms in a child with autosomal recessive polycystic kidney disease. 1179 94

The prevalence of schizophrenia is about 1% worldwide. Individuals with schizophrenia are at increased risk for osteoporosis and fractures for several reasons, including poor diet, lack of exercise, cigarette smoking, and polydipsia. Some antipsychotic medications may further increase the risk of fractures by causing dizziness, orthostatic hypotension, and falls. Studies in women with hyperprolactinemia resulting from pituitary tumors have demonstrated high rates of osteoporosis believed to result from hypoestrogenism. Similarly, hyperprolactinemia in men results in hypogonadism and bone loss. Preliminary surveys have indicated that schizophrenia patients also may have elevated rates of osteoporosis and pathological fractures, possibly resulting in part from the long-term administration of antipsychotic agents that produce hyperprolactinemia and secondarily lower estrogen and testosterone levels. This potential complication of treatment with certain antipsychotic agents requires careful study and could represent a serious public health problem.
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PMID:Hyperprolactinemia and bone mineral density: the potential impact of antipsychotic agents. 1265 Jun 84

Brown tumor is a focal lesion of the bone caused by primary or, less commonly, secondary or tertiary hyperparathyroidism (HPT). While the mandible is the most frequently involved bone in the head and neck region, atypical involvement of the cranium in the area of the sphenoid sinus is exceedingly rare. In the literature, a unique case of brown tumor of the sphenoid sinus was reported in a patient with primary HPT. We present a case of sphenoid sinus and occipital bone brown tumor associated with primary HPT. A 47-yr-old woman presented a 2-yr history of headaches, dizziness, diffuse body and articular pain, fatigue, and a 6-month history of intermittent nausea and vomiting, polydipsia, and polyuria. Magnetic resonance imaging (MRI) demonstrated an expansive mass lesion in the sphenoid sinus with erosion of the sellar floor and medial wall of the right orbit, and expansion in the medulla of bone. Examination of biopsy specimens obtained from sphenoid sinus mass confirmed the diagnosis of brown tumor. The biochemical laboratory studies showed elevation of parathyroid hormone and confirmed the diagnosis of primary HPT. Excision of a parathyroid adenoma affected the metabolic status into normalizing. At the follow-up of 12 months postoperatively, the size of sphenoid sinus brown tumor decreased and the mass of occipital bone disappeared. In conclusion, this is a first report of primary HPT masquerading as a destructive fibrous sphenoid sinus brown tumor associated with a mass lesion of occipital bone and hypercalcemia in the literature.
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PMID:Sphenoid sinus brown tumor, a mass lesion of occipital bone and hypercalcemia: an unusual presentation of primary hyperparathyroidism. 1523 58

Diabetes mellitus develops in about 10% of acromegalic patients, usually secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. Here, we present one case of this disorder. A 57-year-old man came to the emergency room due to 2 weeks of dizziness. He also had polyuria, polydipsia, nausea, diplopia, blurred vision and dysarthria. His plasma glucose level was 32.06 mmol/L, plasma osmolarity was 322 mOsm/L, arterial pH was 7.30, level of bicarbonates was 18 mmol/L, urine ketones was 4+, and HbA1c was 14.1%. No specific cause for the development of this metabolic derangement could be found. He displayed clinical features of acromegaly during admission, which was confirmed by an elevated growth hormone level and pituitary macroadenoma shown on magnetic resonance imaging. The patient underwent total transsphenoid tumor removal 2 weeks later; plasma glucose levels became normal thereafter.
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PMID:Diabetic ketoacidosis in a patient with acromegaly. 1790 70

A 63-year-old man was admitted because of dizziness, polydipsia, polyuria, and diminished libido. His brain MRI showed swelling of the pituitary gland. Because of panhypopituitarism suggested by hormonal examination, hydrocortisone, desmopressin and levothyroxine sodium were started as hormone replacement therapy. He was given a clinical diagnosis of central neurosarcoidosis with panhypopituitarism because of the presence of an abnormal lung shadow, positive gallium scintigram in bilateral hilar lymph nodes, negative tuberculin skin test, lymphocytosis and a high CD4/8 ratio in bronchoalveolar lavage fluid. After prednisolone therapy, his lung shadow and pituitary swelling reduced significantly. Anti-diuretic hormones and anterior pituitary hormones tended to increase, and his urine volume also decreased. This case suggested that endocrinological abnormalities in central neurosarcoidosis might be improved by prednisolone therapy even if the initiation of treatment is delayed.
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PMID:[Case of central neurosarcoidosis with panhypopituitalism]. 1904 32


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