receiving repeated somatostatin infu¬ sions suggests the possible inhibition of the thrombopoietin system by
somatostatin. These observations must be consid¬ ered preliminary and should be inter¬ preted with caution since (1) we do not have appropriate controls to be certain that the mortality and patho¬ logic findings relate specifically to re¬
peated
exposure to somatostatin, (2) the transient effects of somatostatin on platelet aggregation appear to be indirect rather than direct, and (3) thrombocytopenia has not been clear¬ ly demonstrated to be a consequence of repeated somatostatin adminis¬ tration. To settle the question of chronic effects of somatostatin on hemostasis, a prospective study would have to be done with suitable con¬ trols. To date, no bleeding problems have been reported in human subjects
receiving single
or
even
repeated
doses of somatostatin. The intra¬ venous dose used in our baboons is about seven to eight times higher on a body-weight basis than the dose used in the reported clinical studies and may account for the differences between the clinical experience and our observations in the baboon. If,
however, thrombocytopenia proves
to
be related to long-term adminis¬ tration of somatostatin, it will be im¬ portant to determine the associated cumulative dose-response relation¬ ships in designing human therapeutic trials. On the basis of our studies and of the negative observations on the hemostatic system in human subjects reported to us by Gerich, we conclude that studies limited to brief expo¬ sures using currently approved doses of somatostatin would involve little or no risk to human subjects but that human studies involving long-term exposure to somatostatin should prob¬ ably be suspended until appropriate long-term toxicity studies are com¬
pleted.
Donna J. Koerker, PhD Lawrence Harker, MD Charles J. Goodner, MD John Ensinck, MD Department of Medicine University of Washington School of Medicine
Seattle
St. Louis
Encephalitis
To the Editor.\p=m-\InJuly,
and
August, September 1974, twenty-three laboratory-confirmed cases of St. Louis encephalitis (SLE) occurred in Mis-
sissippi. Attack
rates
were
greatest
in the northwest corner of the state and in persons more than 50 years old. Attack rates were similar for residents of urban and rural areas. Signs and symptoms of the patients were similar to those reported in previous epidemics.1-3 Six months after the onset of illness, 9 of the 23 patients were still unable to resume their usual activities. In the same period, 43 laboratory-confirmed cases of SLE occurred in Memphis and western Tennessee, and five cases in Arkansas. The summer reservoirs of SLE virus are birds, and the vectors for epidemic SLE are usually Culex pipiens or C quinquefasciatus mosquitoes. Man is an accidental host and is the only species in which serious symptomatic illness develops. Clinical illness due to SLE is usually more frequent and more severe in persons more than 50 years old. Nineteen seventy-four was the first year since 1966 in which ap¬ preciable SLE virus activity was re¬ ported.4 Past experience suggests that increased SLE virus activity fre¬ quently occurs several years in suc¬ cession. Therefore, more cases may occur in 1975 or 1976. The geographic location of cases cannot be predicted. Outbreaks may again occur primarily in the southeastern United States, or they may be as widespread as in 1964, when focal outbreaks were reported from Texas to New Jersey.5 Diagnos¬ tic assistance and environmental con¬ trol measures are available through many city, county, state, and federal health agencies. Kenneth E. Powell, MD DURWARD L. Blakey, MD Mississippi State Board of Health Jackson
1. Quick DT, Thompson JM, Bond JO: The 1962 epidemic of St. Louis encephalitis in Florida. Am J Epide-
miol 81:415-427, 1965. 2. Riggs S, Smith DL, Phillips CA: St. Louis encephalitis in adults during the 1964 Houston epidemic. JAMA 193:104-108, 1965. 3. Southern PM, Smith JW, Luby JP, et al: Clinical and laboratory features of epidemic St. Louis encephalitis. Ann Intern Med 71:681-689, 1969. 4. Neurotropic Viral Disease Surveillance\p=m-\Encephalitis: Annual summary. Atlanta, Center for Disease Control, 1971. 5. Luby JP, Sulkin SE, Sanford JP: The epidemiology of St. Louis encephalitis: A review. Ann Rev Med 20:329\x=req-\ 359, 1969.
Clinitest and Acetest Ketodiasticks
vs
To the Editor.\p=m-\Indealing with the reasons for changing from Clinitest and Acetest tablets to Keto-
possible
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 06/10/2015
diasticks your QUESTIONS AND ANSWERS consultant (230:1584, 1974) does not mention that Acetest tablets contain a strong alkali and that this has been the cause of severe poisoning when the tablets were accidentally swallowed. I believe that possible health hazards should be taken into account when considering diagnostic procedures such as this, intended for use by laymen as well as professionals. S. Erill, MD
Universidad Aut\l=o'\noma de Barcelona
Barcelona, Spain
Nonremoval of Dentures During Anesthesia To the Editor.\p=m-\Theseveral letters to the editor on "Nonremoval of Dentures During Anesthesia" (230:822, 1974) omitted a very important consideration. There are dentures and there are dentures. I believe the anesthesiologist would be courting danger if he failed to determine in advance the adherence of each denture. Many full lowers are easily dislodged and become candidates for aspiration. Even full uppers may have insufficient grip and may drop to become a problem. Why not a simple testing in advance of anesthesia induction? Mezz, MD, DDS Hollywood, Fla
David
Drug and Reference Errors. \p=m-\Inthe EDITORIAL
"Da Costa
Syndrome
Revisited," published in the April 14 issue (232:164,1975), three errors occurred. The second sentence in the fifth paragraph should read "Epinephrine, which is predominantly \g=b\-adrenergic in its action, has a chronotropic and inotropic effect on the myocardium and a dilating effect on the peripheral vasculature." As published, that sentence incorrectly began "Isoproterenol, which is almost completely \g=b\-adrenergic. ." Also, the superscript 3 should not have appeared in the next sentence in the editorial. In the list of references, the third one should indicate that the article by Holmgren et al was published in .
1957,
not 1975.
.
somatostatin. These observations must be consid¬ ered preliminary and should be inter¬ preted with caution since (1) we do not have appropriate controls to be certain that the mortality and patho¬ logic findings relate specifically to re¬
peated
exposure to somatostatin, (2) the transient effects of somatostatin on platelet aggregation appear to be indirect rather than direct, and (3) thrombocytopenia has not been clear¬ ly demonstrated to be a consequence of repeated somatostatin adminis¬ tration. To settle the question of chronic effects of somatostatin on hemostasis, a prospective study would have to be done with suitable con¬ trols. To date, no bleeding problems have been reported in human subjects
receiving single
or
even
repeated
doses of somatostatin. The intra¬ venous dose used in our baboons is about seven to eight times higher on a body-weight basis than the dose used in the reported clinical studies and may account for the differences between the clinical experience and our observations in the baboon. If,
however, thrombocytopenia proves
to
be related to long-term adminis¬ tration of somatostatin, it will be im¬ portant to determine the associated cumulative dose-response relation¬ ships in designing human therapeutic trials. On the basis of our studies and of the negative observations on the hemostatic system in human subjects reported to us by Gerich, we conclude that studies limited to brief expo¬ sures using currently approved doses of somatostatin would involve little or no risk to human subjects but that human studies involving long-term exposure to somatostatin should prob¬ ably be suspended until appropriate long-term toxicity studies are com¬
pleted.
Donna J. Koerker, PhD Lawrence Harker, MD Charles J. Goodner, MD John Ensinck, MD Department of Medicine University of Washington School of Medicine
Seattle
St. Louis
Encephalitis
To the Editor.\p=m-\InJuly,
and
August, September 1974, twenty-three laboratory-confirmed cases of St. Louis encephalitis (SLE) occurred in Mis-
sissippi. Attack
rates
were
greatest
in the northwest corner of the state and in persons more than 50 years old. Attack rates were similar for residents of urban and rural areas. Signs and symptoms of the patients were similar to those reported in previous epidemics.1-3 Six months after the onset of illness, 9 of the 23 patients were still unable to resume their usual activities. In the same period, 43 laboratory-confirmed cases of SLE occurred in Memphis and western Tennessee, and five cases in Arkansas. The summer reservoirs of SLE virus are birds, and the vectors for epidemic SLE are usually Culex pipiens or C quinquefasciatus mosquitoes. Man is an accidental host and is the only species in which serious symptomatic illness develops. Clinical illness due to SLE is usually more frequent and more severe in persons more than 50 years old. Nineteen seventy-four was the first year since 1966 in which ap¬ preciable SLE virus activity was re¬ ported.4 Past experience suggests that increased SLE virus activity fre¬ quently occurs several years in suc¬ cession. Therefore, more cases may occur in 1975 or 1976. The geographic location of cases cannot be predicted. Outbreaks may again occur primarily in the southeastern United States, or they may be as widespread as in 1964, when focal outbreaks were reported from Texas to New Jersey.5 Diagnos¬ tic assistance and environmental con¬ trol measures are available through many city, county, state, and federal health agencies. Kenneth E. Powell, MD DURWARD L. Blakey, MD Mississippi State Board of Health Jackson
1. Quick DT, Thompson JM, Bond JO: The 1962 epidemic of St. Louis encephalitis in Florida. Am J Epide-
miol 81:415-427, 1965. 2. Riggs S, Smith DL, Phillips CA: St. Louis encephalitis in adults during the 1964 Houston epidemic. JAMA 193:104-108, 1965. 3. Southern PM, Smith JW, Luby JP, et al: Clinical and laboratory features of epidemic St. Louis encephalitis. Ann Intern Med 71:681-689, 1969. 4. Neurotropic Viral Disease Surveillance\p=m-\Encephalitis: Annual summary. Atlanta, Center for Disease Control, 1971. 5. Luby JP, Sulkin SE, Sanford JP: The epidemiology of St. Louis encephalitis: A review. Ann Rev Med 20:329\x=req-\ 359, 1969.
Clinitest and Acetest Ketodiasticks
vs
To the Editor.\p=m-\Indealing with the reasons for changing from Clinitest and Acetest tablets to Keto-
possible
Downloaded From: http://jama.jamanetwork.com/ by a University of Iowa User on 06/10/2015
diasticks your QUESTIONS AND ANSWERS consultant (230:1584, 1974) does not mention that Acetest tablets contain a strong alkali and that this has been the cause of severe poisoning when the tablets were accidentally swallowed. I believe that possible health hazards should be taken into account when considering diagnostic procedures such as this, intended for use by laymen as well as professionals. S. Erill, MD
Universidad Aut\l=o'\noma de Barcelona
Barcelona, Spain
Nonremoval of Dentures During Anesthesia To the Editor.\p=m-\Theseveral letters to the editor on "Nonremoval of Dentures During Anesthesia" (230:822, 1974) omitted a very important consideration. There are dentures and there are dentures. I believe the anesthesiologist would be courting danger if he failed to determine in advance the adherence of each denture. Many full lowers are easily dislodged and become candidates for aspiration. Even full uppers may have insufficient grip and may drop to become a problem. Why not a simple testing in advance of anesthesia induction? Mezz, MD, DDS Hollywood, Fla
David
Drug and Reference Errors. \p=m-\Inthe EDITORIAL
"Da Costa
Syndrome
Revisited," published in the April 14 issue (232:164,1975), three errors occurred. The second sentence in the fifth paragraph should read "Epinephrine, which is predominantly \g=b\-adrenergic in its action, has a chronotropic and inotropic effect on the myocardium and a dilating effect on the peripheral vasculature." As published, that sentence incorrectly began "Isoproterenol, which is almost completely \g=b\-adrenergic. ." Also, the superscript 3 should not have appeared in the next sentence in the editorial. In the list of references, the third one should indicate that the article by Holmgren et al was published in .
1957,
not 1975.
.
