We studied the occurrence, clinical manifestations, and mechanism of hypoglycemia in patients with falciparum malaria in eastern Thailand. Hypoglycemia, which was often severe and recurrent, occurred in 17 patients, including 12 in a series of 151 patients with cerebral malaria. Thirty episodes were investigated. Plasma concentrations of insulin and C peptide were inappropriately high, and lactate and alanine concentrations were significantly higher than in patients with falciparum malaria who were normoglycemic (P less than 0.05). Sixteen patients had received quinine; plasma quinine and insulin concentrations were correlated at the time of hypoglycemia (P = 0.007). In seven healthy fasting volunteers intravenous quinine increased the mean plasma insulin concentration (+/- S.D.) from 8.9 +/- 3.1 to 17.1 +/- 8.4 mU per liter (P = 0.02) and reduced the mean plasma glucose concentration from 88 +/- 20 to 68 +/- 23 mg per deciliter (P = 0.002). Our observations indicate that in falciparum malaria quinine-induced insulin secretion may precipitate hypoglycemia, but other factors, including the large glucose requirements of the malaria parasites may also contribute. This important complication, associated with pregnancy and severe disease, must be excluded in all patients with falciparum malaria who have impaired or deteriorating consciousness.
Rabies is a fatal disease in humans, and, to date, the only survivors of the disease have received rabies vaccine before the onset of illness. The approach to management of the rabies normally should be palliative. In unusual circumstances, a decision may be made to use an aggressive approach to therapy for patients who present at an early stage of clinical disease. No single therapeutic agent is likely to be effective, but a combination of specific therapies could be considered, including rabies vaccine, rabies immunoglobulin, monoclonal antibodies, ribavirin, interferon-alpha, and ketamine. Corticosteroids should not be used. As research advances, new agents may become available in the future for the treatment of human rabies.
BackgroundIt is estimated that India has more deaths from rabies than any other
country. However, existing estimates are indirect and rely on
non-representative studies.Methods and Principal FindingsWe examined rabies deaths in the ongoing Million Death Study (MDS), a
representative survey of over 122,000 deaths in India that uses enhanced
types of verbal autopsy. We estimated the age-specific mortality rates of
symptomatically identifiable furious rabies and its geographic and
demographic distributions. A total of 140 deaths in our sample were caused
by rabies, suggesting that in 2005 there were 12,700 (99% CI 10,000
to 15,500) symptomatically identifiable furious rabies deaths in India. Most
rabies deaths were in males (62%), in rural areas (91%), and
in children below the age of 15 years (50%). The overall rabies
mortality rate was 1.1 deaths per 100,000 population (99%CI 0.9 to
1.4). One third of the national rabies deaths were found in Uttar Pradesh
(4,300) and nearly three quarters (8,900) were in 7 central and
south-eastern states: Chhattisgarh, Uttar Pradesh, Odisha, Andhra Pradesh,
Bihar, Assam, and Madhya Pradesh.Conclusions and SignificanceRabies remains an avoidable cause of death in India. As verbal autopsy is not
likely to identify atypical or paralytic forms of rabies, our figure of
12,700 deaths due to classic and clinically identifiable furious rabies
underestimates the total number of deaths due to this virus. The
concentrated geographic distribution of rabies in India suggests that a
significant reduction in the number of deaths or potentially even
elimination of rabies deaths is possible.
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