PubMed · 13536784
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G E BURCH. 1958. Chlorothiazide.. https://pubmed.ncbi.nlm.nih.gov/13536784/
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A series of sulfonamides has been obtained by reacting sulfanilamide or 5-amino-1,3,4-thiadiazole-2-sulfonamide with omega-chloroalkanoyl chlorides, followed by replacement of the omega-chlorine atom with secondary amines. Tails incorporating heterocyclic amines belonging to the morpholine, piperidine and piperazine ring systems have been attached to these sulfonamides, by means of an alkanoyl-carboxamido linker containing from two to five carbon atoms. The new derivatives prepared in this way were tested as inhibitors of three carbonic anhydrase (CA, EC 4.2.1.1) isozymes, the cytosolic isozymes CA I and II, and the catalytic domain of the transmembrane, tumor-associated isozyme CA IX. Several low nanomolar CA I and CA II inhibitors were detected both in the aromatic and heterocyclic sulfonamide series, whereas the best hCA IX inhibitors (inhibition constants in the range of 22-35 nM) all belonged to the acetazolamide-like derivatives.
AIMS/BACKGROUND: To analyse the effectiveness and safety of cyclodiode treatment in eyes with silicone oil-related raised intraocular pressure (IOP) and to correlate the results with clinical features of treated eyes. METHODS: Retrospective review of case notes of all eyes that underwent cyclodiode treatment following injection of silicone oil at Moorfields Eye Hospital between April 1993 and January 2003 and were followed up for at least 1 year. RESULTS: In all, 38 patients were followed up for between 13 and 113 months. Totally, 17 had silicone oil in situ at the time of first treatment. The mean pretreatment IOP was 31.4 mmHg (SD 10.9), reducing to 18.6 mmHg (SD 8.6) at 1 year and to 13.9 mmHg (SD 8.4) at the final follow-up visit (P<0.001). Before treatment, 28 (73.7%) patients were on two or more topical medications. This was reduced to 18 (47.4%) patients (P=0.013) at 1 year and 13 (34.2%) patients (P=0.0007) at final follow-up. Use of oral acetazolamide for glaucoma was reduced from 16 (42.1%) patients precyclodiode to five (13.2%) patients at 1 year (P=0.0034) and three (7.9%) patients at the final visit (P=0.001). Four patients (10.5%) at 1 year and five patients (13.2%) at the final visit had hypotony (defined as IOP of less than 5 mmHg). One patient had enucleation 75 months following first cyclodiode treatment. CONCLUSION: Diode laser photocoagulation can successfully control silicone oil-induced raised intraocular pressure where medical treatment fails. Reduction of IOP appears to be maintained long term.
BACKGROUND: Periodic paralysis is classified into hypokalemic (hypoPP) and hyperkalemic (hyperPP) periodic paralysis according to variations of blood potassium levels during attacks. OBJECTIVE: To describe new mutations in the muscle sodium channel gene SCN4A that cause periodic paralysis. METHODS: A thorough clinical, electrophysiologic, and molecular study was performed of four unrelated families who presented with periodic paralysis. RESULTS: The nine affected members had episodes of muscle weakness reminiscent of both hyperPP and hypoPP. A provocative test with potassium chloride was positive in two patients. However, repeated and carefully performed tests of blood potassium levels during attacks resulted in normal potassium levels. Remarkably, two patients experienced hypokalemic episodes of paralysis related to peculiar provocative factors (corticosteroids and thyrotoxicosis). Similarly to hyperPP, electromyography in nine patients revealed increased compound muscle action potentials after short exercise and a delayed decline during rest after long exercise as well as myotonic discharges in one patient. With use of molecular genetic analysis of the gene SCN4A, three new mutations were found affecting codon 675. They resulted in an amino acid substitution of a highly conserved arginine (R) to either a glycine (G), a glutamine (Q), or a tryptophan (W). Interestingly, hypoPP is caused by both mutations affecting nearby codons as well as the change of an arginine into another amino acid. CONCLUSION: A potassium-sensitive and normokalemic type of periodic paralysis caused by new SCN4A mutations at codon 675 is reported.