Background Cannabinoid hyperemesis syndrome is a condition characterized by chronic cannabis use and cyclic episodes of nausea, vomiting, and abdominal pain, relieved by compulsive bathing. The syndrome is likely to be underdiagnosed in pregnant women due to its similarity with hyperemesis gravidarum in the presentation. Case We report a 20-year-old pregnant woman with multiple admissions for recurrent nausea and vomiting who was observed to be taking frequent hot showers. Without other identifiable causes, she was diagnosed with cannabinoid hyperemesis syndrome and managed with antiemetics and abstinence. Conclusion Abstinence from cannabis use is highly recommended in pregnant women due to its potential harm in fetal development and stimulation of intractable nausea and vomiting. Recognizing the symptoms and proper history taking prompt early diagnosis, allowing timely and adequate treatment.
Two cases will be presented in which hyperlactatemia occurred without acidosis and the degree of lactatemia decreased significantly when CO, was administered as therapy.H~c k a b e e , ' .~ Eichenholz and collaborators,' and others' have shown that lactatemia occurs with hyperventilation, both in man and in dogs. Huckabee states that this is a form of lactatemia in which "excess lactate" does not occur, i.e., the lactate/pyruvate ratio would remain normal. I t is inferred that the condition in man is usually benign and passes off when the cause of hyperventilation is controlled. We would not disagree with the latter part of this statement but have evidence that the benign nature of these states leaves something to be desired. Whether this form of lactatemia should be considered as "a compensatory mechanism" or not is a matter of opinion. Eichenholz et al.' have shown that the primary respiratory alkalosis may lead, through secondary lactatemia, to an eventual acidosis. This suggests that the mechanism is not truly compensatory.Primary hyperventilation giving rise to an initial respiratory alkalosis occurs in man in a number of diseased states: (1) voluntary or hysterical hyperventilation; (2) CNS lesions, e.g., cerebrovascular accidents; (3) anoxemia, especially a t altitude6 and possibly also in pneumonic stiffness of lung (in these instances the lactatemia may be partly due to the effects of anoxemia as well as hyperventilation, i.e., mixed cases); (4) hepatic coma;' (5) salicylate poisoning; and (6) excessive ventilation by artificial means on a respirator or under anesthesia. We believe that acute Wernicke's encephalopathy (as will be described in one of the patients below) may also be associated with a pathological disorder of acid base homeostasis on the basis of hyperventilation.Eichenholz' has emphasized an important facet of lactatemia that occurs with primary hyperventilation, namely, that if five per cent CO, in air or oxygen is used as the respiratory gas, hyperlactatemia is prevented and will not occur despite continuation of hyperventilation. Further, if the gas mixture is changed from air to the Con mixture after hyperlactatemia has been induced by either salicylate or passive hyperventilation, the level of lactate will fall and the serum bicarbonate concentration will rise, concomitantly.The fact that several observers have noticed that hyperlactatemia occurs with hyperventilation of the passive type refutes the theory that this mechanism is due to the work involved in hyperventilation itself.
Objective: To report a case of worsening myasthenia gravis after the initiation of gabapentin for treatment of essential tremor. Case Summary: A 69-year-old man experienced minor ptosis of the left eyelid, slight neck weakness, and transient difficulties in chewing food on day 6 of a slow gabapentin dosage titration. As the titration continued, the myasthenia symptoms progressed to bilateral ptosis, and there was dramatic worsening of weakness by day 23. He was taking gabapentin 1500 mg daily at the time; the drug was then tapered to discontinuation. All myasthenia gravis symptoms were reported as resolved 3 days after discontinuation of gabapentin. The initiation and discontinuation of gabapentin also coincided with improvement, then worsening of the patient's tremor. Discussion: Three published case reports describe worsening of myasthenia gravis during use of gabapentin for the treatment of various neuropathies. To the best of our knowledge, this is the first case report of a patient experiencing worsening of myasthenia gravis upon initiation of gabapentin for essential tremor. The Naranjo probability scale suggests a probable association between gabapentin and worsening of myasthenia gravis symptoms in our patient. Several myasthenia-like symptoms are listed in the gabapentin mongraph as low-frequency adverse events, increasing the possibility that gabapentin may have been unmasking or worsening myasthenia gravis in clinical trials. However, myasthenia gravis is not identified as a contraindication or caution for gabapentin use. Conclusions: Gabapentin should be used with caution in patients with myasthenia gravis, and clinicians must be aware of the potential risks of this therapy.
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