Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of refractory tuberculous meningitis which was markedly improved by intrathecal administration of isoniazid (INH). The patient was a 35-year-old woman diagnosed with systemic lupus erythematosus (SLE) at age 25, who was being managed with steroid therapy. She was admitted to another hospital due to miliary tuberculosis at age 34, and after discharge continued with a regimen of 2 anti-tuberculosis drugs (INH. Rifampicin (RFP)). She was admitted to our hospital with severe headache and fever on June 18, 2001. She showed severe meningeal irritation, and cerebrospinal fluid (CSF) examination revealed cell counts of 207/microliter (72% polynuclear cells), protein level of 300 mg/dl, glucose level of 13 mg/dl, chloride (Cl) level of 104 mEq/l, adenosine deaminase (ADA) level of 10.0 IU/l. The CSF culture was negative for Mycobacterium tuberculosis (M. tuberculosis) and direct polymerase chain reaction (PCR) for M. tuberculosis DNA was negative, but nested PCR was positive in preserved CSF samples. Marked leptomeningeal enhancement at the basilar meninges was noted by cranial MRI on gadolinium (Gd)-DTPA enhanced T1-weighted images. We diagnosed her condition as tuberculous meningitis and administered a total of 5 anti-tuberculosis drugs over about 2 months. However, during this period, both her clinical and CSF findings worsened, and she developed severe consciousness disturbance showing marked hydrocephalus on cranial MRI in August 2001. Therefore, we initiated intrathecal administration of INH 100 mg 3 times a week for progressive tuberculous meningitis. After the initiation of intrathecal therapy, both her consciousness disturbance and CSF findings were improved almost immediately. Ventriculo-peritoneal shunt operation was performed for hydrocephalus on September 26, 2001, and her clinical symptoms were further improved. To our knowledge, this is the first reported case of refractory tuberculous meningitis markedly improved by intrathecal administration of INH. Our findings suggested that intrathecal administration of INH was useful for refractory tuberculous meningitis.
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PMID:[A case of refractory tuberculous meningitis markedly improved by intrathecal administration of isoniazid (INH)]. 1282 May 46

Primary diffuse leptomeningeal gliomatosis (PDLG) is a rare condition, with only 45 cases recorded to date, characterized by infiltration of the meninges by glial cells without evidence of primary tumor in the brain or spinal cord parenchyma. Here, we describe a patient with PDLG who was managed with tuberculostatic drugs owing to multiple findings that were suggestive of tuberculous meningitis. A 19-year-old woman presented with headaches and behavioral changes. A sudden decrease in visual acuity with papilledema, bilateral sixth nerve palsies, and neck stiffness developed. Lumbar puncture showed elevated opening pressure (50 cm H2O). Cerebrospinal fluid (CSF) analysis showed glucose 30 mg/dL, protein 26.5 mg/dL, white blood cell count 150 (60% lymphocytes, 40% neutrophils). The second sample of CSF provided adenosine deaminase activity 21.9 U/L. Polymerase chain reaction for Koch's bacillus was positive in the third CSF sample. Magnetic resonance imaging revealed meningeal thickening of the quadrigeminal cistern, tentorium cerebelli, cerebral convexity, and spinal cord, with gadolinium enhancement in nodular lesions. The patient died 22 weeks after symptom onset owing to brainstem infarction. Postmortem pathologic studies revealed PDLG. This entity should be included in the differential diagnosis of tuberculous meningitis that does not respond to treatment with antituberculous drugs. Surgical biopsy should be considered in contrast-enhanced areas in magnetic resonance imaging.
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PMID:Primary diffuse leptomeningeal gliomatosis mimicking meningeal tuberculosis. 2153 87

A 76-year-old woman was admitted to our hospital because of convulsions that developed after a 1-month history of progressive right-leg palsy. MRI showed thickening of the meninges with gadolinium enhancement in the left parietal lobe and it revealed pia-subarachnoid space pattern. A lumbar puncture was performed, and cerebrospinal fluid analysis revealed no abnormality. Her serum adenosine deaminase level was elevated (28.7 IU/l). The results of serum cultures were normal. To differentially diagnose collagen disease, infection, malignancy, and inflammation of uncommon causes, we conducted brain and meningeal biopsies on the 15th hospital day. Histopathological examination of the brain tissue showed mainly necrosis and inflammation. There was severe pachymeningeal thickening without necrosis. Although it was difficult to reach a definitive diagnosis, a tissue sample taken from under the leptomeninges tested positive for mycobacterium on Ziehl-Neelsen staining. The results of polymerase chain reaction for mycobacterium were negative in the meningeal tissue. The patient received anti-tuberculous drugs, anti-nontuberculous mycobacteriosis drugs, and corticosteroids to treat Mycobacterium tuberculosis and nontuberculous mycobacterium. After starting treatment, the findings on magnetic resonance imaging improved dramatically, and no convulsions occurred during hospitalization. She was discharged on the 153rd hospital day without any neurological deficit. Because previous studies have reported that isolated mycobacterium meningitis is a diagnostically challenging condition, brain and meningeal biopsies should be considered in patients with gadolinium enhancement in the meninges.
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PMID:[A case of isolated mycobacterial focal meningitis diagnosed on brain and meningeal biopsy]. 2458 89