Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 44-year-old man with hepatitis C-associated liver cirrhosis, cyanosis, digital clubbing, and platypnea presented with left-side hemiplegia found to be due to a brain abscess. Hepatopulmonary syndrome was diagnosed after demonstration of the presence of a massive intrapulmonary shunt. Although the anomalous vascular channel never was defined anatomically, follow-up studies confirmed the presence of a functional shunt. Culture of a sample from the abscess yielded Streptococcus intermedius. It was hypothesized that the patient's pulmonary vascular pathology was due, in large part, to chronic elevated levels of nitric oxide (a potent vasodilator thought to be generated by endotoxin absorbed from the gut). Treatment with oral norfloxacin was initiated on the basis of data that this antibiotic reduces endotoxemia and concomitant nitric oxide production in patients with cirrhosis. Four months after initiation of treatment, the patient's hypoxia had resolved.
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PMID:Novel presentation and approach to management of hepatopulmonary syndrome with use of antimicrobial agents. 1131 64

Familial hemiplegic migraine type 1 (FHM-1) is a dominantly inherited subtype of migraine with aura and transient hemiplegia associated with mutations in the CACNA1A gene. FHM-1 shares many phenotypical similarities with common types of migraine, indicating common neurobiological pathways. Experimental studies have established that activation of the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway plays a crucial role in migraine pathophysiology. Therefore, we tested the hypothesis that CACNA1A mutations in patients with FHM-1 are associated with hypersensitivity to NO-cGMP pathway. We included eight FHM-1 patients with R583Q and C1369Y mutations and nine healthy controls, who received intravenous infusions of 0.5 microg kg(-1) min(-1) glyceryl trinitrate (GTN) over 20 min. We recorded: headache intensity on a verbal rating scale; mean flow velocity in the middle cerebral artery (V(meanMCA)) by transcranial Doppler; diameter of the superficial temporal artery (STA) by Dermascan. One patient reported migraine without aura 5 h after start of the GTN infusion. No aura was reported. The AUC(headache) in the immediate phase was more pronounced in patients than in controls (P = 0.01). In the 14 h following GTN infusion, there was no difference in the AUC(headache) between patients and controls (P = 0.17). We found no difference in the AUC(VmeanMCA) (P = 0.12) or AUC(STA) (P = 0.71) between FHM-1 patients and controls. None of the control persons reported migraine-like headache. FHM-1 patients do not show hypersensitivity of the NO-cGMP pathway, as characteristically seen in migraine patients with and without aura. This indicates that the pathophysiological pathways underlying migraine headache in FHM-1 may be different from the common types of migraine.
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PMID:Familial hemiplegic migraine type 1 shows no hypersensitivity to nitric oxide. 1838 18