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The purpose of this project was t o investigate the clinical forms of acquired myasthenia gravis in dogs. The medical records from 25 dogs with seropositive acquired myasthenia gravis were reviewed, and the following data were recorded for each patient: signalment, history, clinical findings; results of IV edrophonium chloride administration, repetitive nerve stimulation, and presence or absence of muscle membrane staining by immunocytochemical methods; serum acetylcholine receptor antibody concentration; treatment; and outcome. Several clinical forms of acquired myasthenia gravis were identified. Nine of the 25 patients (36%) had no historical or clinical evidence of appendicular muscle weakness, and were designated as focalmyasthenics. These dogs exhibited focal weakness in one or more of the following muscle groups: facial (3 of 9). pharyngeal (3 of 9). and laryngeal (3 of 9). The remaining 16 dogs (64%) exhibited appendicular muscle weakness. Four of these 16 dogs had acute onset and rapid development of clinical signs, and were designated as acute fulminating myasthenics. The remaining 12 dogs were classified as generalized myasthenics. All 4 dogs with acute fulminating myasthenia gravis had megaesophagus, 2 had facial muscle weakness, and 1 had pharyngeal muscle weakness. Ten of the 12 dogs with generalized myascquired myasthenia gravis (MG) is an immune-medi-A ated disorder in which autoantibodies against nicotinic acetylcholine (ACh) receptors of skeletal muscle are produced, resulting in impairment of action potential transmission from nerve to muscle.'-6 The mechanisms proposed for the antibody impairment of neuromuscular transmission include accelerated endocytosis of antibody cross-linked ACh receptors, complement-mediated destruction of postsynaptic muscle cell membrane in the vicinity of the ACh receptors, decreased synthesis and membrane incorporation of new ACh receptors, and direct interference of ACh receptor function by bound antib~dy.'.~ Myasthenia gravis is well documented in dogs, and exhibits many similarities to the corresponding disorder of people. 1~3,S,7,x The "classic" clinical presentation of a dog with acquired MG is episodic, generalized muscle weakness, most obvious in the appendicular muscles, that is worsened by activity and ameliorated with rest.'.i.' Megaesophagus is a common finding in dogs with acquired MG because of the large proportion of skeletal muscle in the esophagus of dogs.'," In people, several clinical forms of acquired MG have been described, which has prompted the development of a number of classification schemes.2.4.6. Io.i2-i7 M ost of the classification schemes describe a focal ocular form (involving extraocular muscles) and a generalized form characterized by appendicular muscle weakness,6.~n. I Z M . IS. 17.1 n The latter is subdivided into mild, moderate, and severe forms.'"~'Z.14.1'~'7 The subdivision of generalized MG in human beings is based upon the presence and degree of bulbar and respiratory muscle involvement, and the rate of progression of clinica...

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This report describes the presentation and clinical course of a 40-year-old woman who had an emergency admission for eclampsia. During routine investigations, she was found to have profound hypercalcaemia, the cause of which was identified as milk-alkali syndrome, caused by self-medication with antacid tablets for dyspepsia. Treatment with aggressive rehydration, bisphosphonates and discontinuation of antacid tablets restored normocalcaemia. The patient made a full recovery with no long-term side-effects. Her male infant was safely delivered with no deleterious effects of exposure to high calcium concentrations in utero.

Through the use of two internal controls, we have developed an improved method of quantitating ribonuclease protection assay (RPA) results. A truncated sense RNA fragment and an antisense RNA fragment for the gene of interest were transcribed from PCR fragments containing T7 bacterial promoters. An 18S ribosomal RNA fragment was also used. When radiolabeled antisense and 18S probes, along with sense fragment and sample RNA, were hybridized, digested with RNase A/T1 and gel-electrophoresed, three distinct bands resulted. The antisense RNA fragment bound to the sense RNA fragment confirmed the integrity of the reaction. The antisense RNA fragment bound to endogenous mRNA measured the amount of specific gene expression in the sample. The 18S RNA fragment bound to endogenous mRNA determined the actual amount of sample added to the gel. Using the specific activities of the antisense and 18S transcripts, and scintillation counts of the protected fragments, we calculated the amounts of message and total RNA on the gel, determining picogram of message per microgram of total RNA. Final results were not based on assumed original amounts of RNA placed in the assay nor were they biased by lane-to-lane variations. Through the described adaptations, we have developed a well-controlled RPA that accurately and reproducibly quantifies gene expression.