Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of acquired autoimmune myasthenia gravis (MG) presenting transient amenorrhea were reported. Case 1, 28 years old, developed blepharoptosis and generalized fatigability at the age of 20 years. She had been treated only by anti-cholinesterase. Amenorrhea appeared at the age of 26 years. Then, physical examinations showed normal secondary sexual development and moderate myasthenic features. On laboratory examinations, SLE findings such as leucopenia (1,600/mm3), biologically false positivity in the serological tests for syphilis, negative Mantoux reaction, positive anti-nuclear and -DNA antibodies, were noted. Anti-AChR antibody was highly positive (max.: 353 nmol/l). Decreased E2 (13-15 pg/ml) and progesterone (0.21-0.29 ng/ml) values in serum, elevated LH (110-160 mIU/ml) and FSH (78-90 mIU/ml) and highly reactive LH-RH loading test were consistent with the hypergonadotropic hypogonadism. Thymus pathology of thymectomy which was done during amenorrhea, showed hyperplasia. Bilateral ovarian biopsy revealed a number of arrested primordial follicles, but neither inflammatory changes nor fibrosis. Immune complexes were not localized in the ovarian biopsy. The Kaufmann's therapy aggravated myasthenic symptoms. Menstruation recurred after 13 months of thymectomy. Amenorrhea continued for 18 months. Case 2, 37 years old, has had anti-epileptic regimens since the age of 4 years. She has been highly myasthenic for 15 years and treated by thymectomy, steroid hormone, plasmapheresis and some other therapies for 10 years. Amenorrhea occurred at the age of 34 years. Sexual development was normal. Myasthenia was very severe. On laboratory examinations, anti-AChR antibody was positive (max.: 941 nmol/l). Transient elevation of serum LH (37 mIU/l) and FSH (14 mIU/l) values was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of myasthenia gravis associated with transient amenorrhea]. 279 17

Vascular mineralization (siderocalcinosis) in the brain of horses has been usually assumed to be an incidental age-related finding with no clinic significance. In the present study, eight 15-32-year-old horses of different breeds with cerebral siderocalcinosis were studied. Four of these horses had acute and severe central nervous system clinical signs of unknown etiology, 2 horses had neurological signs of known cause, and 2 horses did not have neurological signs. Gross examination of the brains in 4 animals revealed symmetrical foci of malacia in the cerebellar white matter. Histologically, moderate to severe mineralization of blood vessels and parenchyma were observed in all 8 horses, occasionally associated with necrosis of the adjacent tissue. Some horses were tested by virus isolation, polymerase chain reaction, immunohistochemistry, and serology to investigate Rabies virus; West Nile virus; Equid herpesvirus 1 and 4; Eastern, Western, Venezuelan, and Saint Louis encephalitis virus; and Sarcocystis neurona infection. These tests were negative in all samples analyzed. Brain cholinesterase activity and heavy metal screening were also unremarkable. The significance of the vascular and parenchymal mineralization in the brains of some of these horses remains undetermined. However, the severity of the lesions observed in the brains of some of the animals in the present study, coupled with the negative results for other common causes of neurological disease in horses, suggests a possible relationship between siderocalcinosis and the clinical signs observed.
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PMID:Vascular mineralization in the brain of horses. 2252 37