The Black Death and Other Pandemics
Scott M. Jackson in Skin Disease and the History of Dermatology, 2023
Toxicity from consumption of substantial amounts of ergotamine can manifest as severe limb pain and peripheral vasoconstriction (gangrenous ergotism), or seizures, muscle spasms, delusion, confusion, and hallucinations (convulsive ergotism). The prevalence of ergotism among the poor is explained by the tendency of the poor to consume spurred rye. The dissimilarity in the manifestations of ergotism east and west of the Rhine remains somewhat of a mystery. Modern researchers suggest that it was variability in the concentration of ergot alkaloids in the grain due to various reasons: regional differences in the strains of C. purpurea, differences in the soil or habitat where the grain was grown and stored, and degradation of the ergot over time after prolonged storage.66 Less rye was grown in Italy in the Middle Ages; hence, St. Anthony's Fire was not mentioned in medieval Italian chronicles.67
Valve Disease
Mary N. Sheppard in Practical Cardiovascular Pathology, 2022
Serotonergic drugs previously used in Parkinson's disease, such as pergolide, have been associated with valvular myxoid thickening and regurgitation in both mitral and aortic valves. Use of fenfluramines, either alone or co-administered with phentermine (‘fen-phen’) as anorexic agents in obesity, has been associated with similar changes. Ergotamine used in treating migraines gives a similar picture. Macroscopic changes include irregular leaflet thickening, accompanied by chordal fusion in the mitral valve, with no commissural fusion or evidence of annular dilation. The heart valves have a glistening white appearance. Histopathological findings show plaque-like encasement of the leaflets and chords with intact valve architecture. The histopathological features are identical to those seen in carcinoid-induced valve disease.
Migraine: diagnosis and treatment
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby in Headache in Clinical Practice, 2018
We sometimes use ergotamine65 to treat moderate to severe migraine if analgesics do not provide satisfactory headache relief or if they produce significant side-effects and cost is a factor. However, with time and experience, the triptans are preferred to ergots for most patients. Some patients still respond preferentially to rectal ergotamine. Patients who cannot tolerate ergotamine because of nausea are pretreated with an antiemetic. Ergotamine tartrate, originally derived from a rye fungus (Claviceps purpurea), is an ergopeptide, which consists of a natural D-lysergic acid linked to a tricyclic peptide moiety by a peptide bond. Ergotamine tartrate is still available as a sublingual preparation and, in combination with caffeine, as an oral tablet and a suppository. The evidence to support ergotamine’s efficacy for migraine treatment is inconsistent. For individual attacks, patients can take up to six 1 mg tablets or two suppositories over 24 hours. Use should not exceed 2 dosage days per week.66–67 In certain circumstances, these limits may be liberalized (e.g. cluster headache, intractable menstrual migraine).
Direct cost and healthcare resource utilization of patients with migraine before treatment initiation with calcitonin gene-related peptide monoclonal antibodies by the number of prior preventive migraine medication classes
Published in Current Medical Research and Opinion, 2022
Shonda A. Foster, Margaret Hoyt, Wenyu Ye, Oksana Mason, Janet H. Ford
The Charlson Comorbidity Index (CCI) was defined as a score based on the presence or absence of 17 chronic conditions identified from claims data for each cohort. The score was calculated for the diagnoses during the 24-month pre-index period, to help characterize the health severity of patients19. Acute medication overuse was defined as class-level average acute medication use per month during the study period. For each class, acute medication overuse was 8+ days/month for opioids, triptans, or ergotamines, 15+ days/month for prescription nonsteroidal anti-inflammatory drugs (NSAIDs), 5+ days/month for barbiturates, and 10+ days/month for any combination of ergotamine, triptans, analgesics, and/or opioids without overuse of a single class20,21. Medication overuse headache presented the proportion of patients having a diagnostic claim (G44.40) during the pre-index period.
Current advances in the management of cluster headaches
Published in Expert Opinion on Pharmacotherapy, 2021
Theodoros Mavridis, Marianthi Breza, Christina Deligianni, Dimos D. Mitsikostas
Ergot derivatives such as oral ergotamine and intranasal or intravenous dihydroergotamine (DHE) have been used as a treatment for CH bouts but with little evidence of clear efficacy. The initial dose of oral ergotamine is 2 mg sublingual and can be repeated every 30 minutes with a max dose of 6 mg daily. Intranasal DHE has a level U recommendation from the AHS [29], denoting insufficient evidence to make. Intravenous DHE has shown better results for inpatient management of the refractory episodic CH [40]. The initial dose of DHE is 1 mg IV bolus and can be repeated after 1 hour with a max dose of 3 mg per day. Ergots can also induce medication overuse headache (MOH) with very low doses and their use must be limited to less than 10 days per month. Contraindications are coronary artery disease due to the constriction of the coronal vessels [41], arterial hypertension, and cerebrovascular diseases. Due to their impact on the vascular system, they should not be used in combination with other vasoconstrictor drugs. Other contraindications include Raynaud disease, renal or hepatic failure, pregnancy, and lactation [27,36].
Are 5-HT1 receptor agonists effective anti-migraine drugs?
Published in Expert Opinion on Pharmacotherapy, 2021
Masaru Tanaka, Nóra Török, László Vécsei
The ergot alkaloid ergotamine is an antimigraine drug isolated from the ergot fungus in 1918, which targets 5-HT1/2-, adrenaline-, and dopamine receptors (Figure 1). Dihydroergotamine relieves migraine headache through the activation of 5-HT1D receptors of intracranial blood vessels, which leads to vasoconstriction, and increase of 5-HT1D receptor expression of the trigeminal sensory nerve endings, which leads to the inhibition of the release of inflammatory neuropeptides, such as CGRP (Table 1 and Table 2). Furthermore, ergotamine targets 5-HT1B receptor, 5-HT2A receptor, and adrenergic receptors alpha (α) 1A/B/D subtypes, prolonging vasoconstriction through the inhibition of norepinephrine uptake and stimulation of α -adrenergic receptors. Generally, ergotamine is not considered as the first-line treatment for migraine [3].
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