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At least 19 recordsLinked to original sources

The triple cold syndrome. Cold hyperalgesia, cold hypoaesthesia and cold skin in peripheral nerve disease.

A syndrome of cold hyperalgesia associated with cold hypoaesthesia is described in 28 patients with peripheral polyneuropathy or mononeuropathy of various aetiologies. A mechanism of sensory disinhibition, where diminished cold-specific A delta input releases cold pain input carried by C nociceptors, is proposed to explain the hyperalgesia. In most patients, the symptomatic skin is abnormally cold. This is a likely consequence of vasospasm, due to sympathetic denervation supersensitivity, caused by dropout of sympathetic efferents as part of the small caliber nerve fibre insult. The term 'triple cold syndrome' is coined to describe this specific pathophysiological condition. Descriptively it is a mirror image of erythralgia, as described by Sir Thomas Lewis (1936) and updated by one of the present authors, a human condition also centred around anomalous primary nociceptor input, in which there is heat hyperalgesia and hot symptomatic skin due to C nociceptor sensitization and vasodilatation from antidromic discharge. Thus, like the latter condition, the triple cold syndrome emerges as an independent clinical entity with definable abnormal mechanisms which should be retrieved out of the all-embracing, descriptive, diagnostic category 'reflex sympathetic dystrophy--causalgia'.

Adult↗

Detection of cold pain, cold allodynia and cold hyperalgesia in freely behaving rats.

BACKGROUND: Pain is elicited by cold, and a major feature of many neuropathic pain states is that normally innocuous cool stimuli begin to produce pain (cold allodynia). To expand our understanding of cold induced pain states we have studied cold pain behaviors over a range of temperatures in several animal models of chronic pain. RESULTS: We demonstrate that a Peltier-cooled cold plate with +/- 1 degrees C sensitivity enables quantitative measurement of a detection withdrawal response to cold stimuli in unrestrained rats. In naïve rats the threshold for eliciting cold pain behavior is 5 degrees C. The withdrawal threshold for cold allodynia is 15 degrees C in both the spared nerve injury and spinal nerve ligation models of neuropathic pain. Cold hyperalgesia is present in the spared nerve injury model animals, manifesting as a reduced latency of withdrawal response threshold at temperatures that elicit cold pain in naïve rats. We also show that following the peripheral inflammation produced by intraplantar injection of complete Freund's adjuvant, a hypersensitivity to cold occurs. CONCLUSION: The peltier-cooled provides an effective means of assaying cold sensitivity in unrestrained rats. Behavioral testing of cold allodynia, hyperalgesia and pain will greatly facilitate the study of the neurobiological mechanisms involved in cold/cool sensations and enable measurement of the efficacy of pharmacological treatments to reduce these symptoms.

Afferent Pathways↗

Clinical characteristics of cold-induced systemic reactions in acquired cold urticaria syndromes: recommendations for prevention of this complication and a proposal for a diagnostic classification of cold urticaria.

The acquired cold urticaria (ACU) syndromes consists of nonfamilial heterogeneous disorders characterized by urticaria, angioedema, and occasionally symptoms of hypotension after cold exposure. In a study of 50 consecutive patients with ACU syndromes, it was observed that 70% experienced cold-induced systemic reactions, most frequently with aquatic activities. Patients with ACU syndromes were categorized by their response to an experimental cold-stimulation time test (CSTT) i.e., minimum time threshold of cold stimulation required to induce a coalescent wheal. One subpopulation of patients with ACU syndromes with positive CSTTs of 3 minutes or less experienced the highest incidence (68%; 13/19) of severe systemic reactions with hypotensive symptoms after natural cold exposure. However, 32% of patients with ACU syndromes (6/19) who experienced cold-induced systemic reactions with hypotension had a negative CSTT or a positive test of greater than 3 minutes. These observations indicate that all patients with ACU with active histories of cold urticaria are at risk to develop systemic reactions to cold and should therefore refrain from participating in aquatic activities. In addition, high-risk patients should receive prophylactic medications (i.e., cyproheptadine or doxepin) that are effective in suppressing this disorder. A diagnostic classification of cold urticaria is presented. This classification permits a more specific definition of the various cold urticaria disorders that comprise the ACU syndromes.

Adolescent↗

Angina pectoris in the cold. Effects of cold environment and cold air inhalation at exercise test.

Patients with effort angina and a history of cold intolerance performed brief submaximal exercise bicycle test in various temperatures with separation of inspiration and room air. Exposure to a cold room (-10 degrees C) and inhalation of very cold air(- 35 degrees C) in a normal room caused a significant decrease in maximal workload. Heart rate, systolic blood pressure, and rate-pressure product were significantly higher during exercise when compared with findings in the normal room. The decrease in maximal workload correlated significantly to the increase in heart rate and rate pressure product during exercise in both conditions, and to the increase in systolic blood pressure at exposure to a cold room. Exposure to 10 and 0 degree C environmental temperature and inhalation of moderately cold air (- 10 degrees C) did not cause any significant changes in maximal workload, heart rate, blood pressure, or rate pressure product during exercise, compared to the findings in the normal room. In conclusion, skin cooling seems to be far more important in its effect on heart load and the working capacity in patients with effort angina than inhalation of moderately cold air; inhalation of very cold air, however, does cause changes in working capacity similar to those of exposure to a cold environment. Increase in heart work during exercise is likely to cause the decrease in working capacity observed both with skin cooling and cold air inhalation.

Angina Pectoris↗

Expression of a new cold shock protein of 21.5 kDa and of the major cold shock protein by Streptococcus thermophilus after cold shock.

Streptococcus thermophilus is widely used in food fermentations; it commonly suffers diverse stress challenges during manufacturing. This study investigated the cold shock response of S. thermophilus when the cell culture temperature shifted from 42 degrees C to 15 degrees C or 20 degrees C. The growth of cells was affected more drastically after cold shock at 15 degrees C than at 20 degrees C. The generation time was increased by a factor of 19 when the temperature was lowered from 42 degrees to 20 degrees C, and by a factor of 72 after a cold shock at 15 degrees C. The two-dimensional electrophoretic protein patterns of S. thermophilus under cold shock conditions were compared with the reference protein pattern when cells were grown at optimal temperature. Two proteins of 21.5 and 7.5 kDa synthesized in response to cold shock were characterized. N-terminal sequencing and sequence homology searches have shown that the 7.5-kDa protein belonged to the family of the major cold shock proteins, while no homology was found for the new cold shock protein of 21.5 kDa.

Amino Acid Sequence↗

Unusual cold-induced disorders: cold-dependent dermatographism and systemic cold urticaria.

Two patients are described in whom new cold-induced disorders were defined. The patients presented with histories suggesting either dermatographism or typical cold urticaria; however, standard tests for each disorder failed to reproduce the patients' symptoms. One patient had dermatographism that was observable only upon chilling the skin subsequent to scratching it. The reaction was associated with detectable elevation of venous histamine levels coincident with the development of urticaria. The second patient had generalized urticaria that was induced by systemic rather than local cold challenge. The reaction was anaphylactoid in nature and was associated with systemic elevation of histamine levels. This patient was also mildly dermatographic, and skin reactivity was markedly augmented during an episode of generalized hives. These cold-dependent disorders should be included in the differential diagnosis of patients with histories suggestive of cold urticaria with or without a dermatographic component. Further evaluation is indicated when the standard tests for either of these disorders are negative.

Adolescent↗

Cold-induced putative DEAD box RNA helicases CshA and CshB are essential for cold adaptation and interact with cold shock protein B in Bacillus subtilis.

The nucleic acid binding cold shock proteins (CSPs) and the cold-induced DEAD box RNA helicases have been proposed separately to act as RNA chaperones, but no experimental evidence has been reported on a direct cooperation. To investigate the possible interaction of the putative RNA helicases CshA and CshB and the CSPs from Bacillus subtilis during cold shock, we performed genetic as well as fluorescence resonance energy transfer (FRET) experiments. Both cshA and cshB genes could be deleted only in the presence of a cshB copy in trans, showing that the presence of one csh gene is essential for viability. The combined gene deletion of cshB and cspD resulted in a cold-sensitive phenotype that was not observed for either helicase or csp single mutants. In addition to the colocalization of the putative helicases CshA and CshB with CspB and the ribosomes in areas surrounding the nucleoid, we detected a strong FRET interaction in vivo between CshB and CspB that depended on active transcription. In contrast, a FRET interaction was not observed for CshB and the ribosomal protein L1. Therefore, we propose a model in which the putative cold-induced helicases and the CSPs work in conjunction to rescue misfolded mRNA molecules and maintain proper initiation of translation at low temperatures in B. subtilis.

Adaptation, Physiological↗

Cold urticaria. Dissociation of cold-evoked histamine release and urticara following cold challenge.

Nine patients with acquired cold urticaria were studied to assess the effects of beta-adrenergic agents, xanthines, and corticosteroids on cold-evoked histamine release from skin in vivo. The patients, in all of whom an immediate urticarial response developed after cooling of the forearm, demonstrated release of histamine into the venous blood draining that forearm. Following treatment with aminophylline and albuterol in combination or prednisone alone, suppression of histamine release occurred in all but one patient. In some patients, this was accompanied by a subjective diminution in pruritus or buring, but there was no significant improvement in the ensuing edema or erythema. In one patient, total suppression of histamine release was achieved without any effect on whealing and erythema in response to cold challenge. Our results suggest that histamine is not central to the pathogenesis of vascular changes in acquired cold urticaria.

Adolescent↗

Liver metabolism in cold hypoxia: a comparison of energy metabolism and glycolysis in cold-sensitive and cold-resistant mammals.

The effects of cold hypoxia were examined during a time-course at 2 degrees C on levels of glycolytic metabolites: glycogen, glucose, glucose-1-phosphate, glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-bisphosphate, phosphoenolpyruvate, pyruvate, lactate and energetics (ATP, ADP, AMP) of livers from rats and columbian ground squirrels. Responses of adenylate pools reflected the energy imbalance created during cold hypoxia in both rat and ground squirrel liver within minutes of organ isolation. In rat, ATP levels and energy charge values for freshly isolated livers were 2.54 mumol.g-1 and 0.70, respectively. Within 5 min of cold hypoxia, ATP levels had dropped well below control values and by 8 h storage, ATP, AMP, and energy charge values were 0.21 mumol.g-1, 2.01 mumol.g-1, and 0.17, respectively. In columbian ground squirrels the patterns of rapid ATP depletion and AMP accumulation were similar to those found in rat. In rat liver, enzymatic regulatory control of glycolysis appeared to be extremely sensitive to the decline in cellular energy levels. After 8 h cold hypoxia levels of fructose-6-phosphate decreased and fructose-1,6-bisphosphate increased, thus reflecting an activation of glycolysis at the regulatory step catalysed by phosphofructokinase fructose-1,6-bisphosphatase. Despite an initial increase in flux through glycolysis over the first 2 min (lactate levels increased 3.7 mumol.g-1), further flux through the pathway was not permitted even though glycolysis was activated at the phosphofructokinase/fructose-1,6-bisphosphatase locus at 8 h, since supplies of phosphorylated substrate glucose-1-phosphate or glucose-6-phosphate remained low throughout the duration of the 24-h period.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

[Results of the treatment in cases of cold urticaria, cold pruritus and cold rhinitis with peritol (zyproheptadinhydrochlorid) (author's transl)].

19 patients with cold urticaria, 5 with cold pruritus and 2 with cold rhinitis were successfully treated with peritol with the exception of one patient who suffered from a symptomatic pruritus due to polycythemia vera. Even in cases of recurrence the treatment was at once successful. Therefore peritol seems to be useful in the treatment of diseases due to cold.

Cold Temperature↗

Cold-adaptive modifications in man induced by repeated short-term cold-exposures and during a 10-day and-night cold-exposure.

Two types of cold exposures were carried out in humans. A. Fourteen subjects were exposed 4-7 times within 2 weeks to the following conditions: ambient temperature was decreased from 28 degrees C to between plus and minus 5 degrees C; the subjects wore a bathing suit and remained in a resting position during the exposure which lasted for 1h. B. Nine conscripts were studied before and after a 10-day exercise, during which they were exposed to moderately cold conditions during day and night. The exercise did not require increased physical activity. In two thirds of the subjects A, metabolic reactions and shivering threshold were shifted to a lower weighted mean body temperature as well as a lower esophageal temperature ("hypothermic" type of adaptation). This modification in the thermoregulatory system was linked with a reduction in thermal discomfort and cold sensation. No change was found in the resting metabolic rate nor was there any indication of the development of non-shivering thermogenesis. Similar modifications were found in 4 of the 9 soldiers (study B). These 4, however, had particularly high shivering thresholds before the 10-day exercise and the values found thereafter were no lower than those found in the remaining five and in the subjects of group A before the cold-exposure regimen.

Acclimatization↗

Cold-adapted variants of influenza A virus: evaluation in adult seronegative volunteers of A/Scotland/840/74 and A/Victoria/3/75 cold-adapted recombinants derived from the cold-adapted A/Ann Arbor/6/60 strain.

Influenza A/Scotland/74 (H3N2) and A/Victoria/75 (H3N2) cold-adapted (ca) recombinant viruses, prepared by mating the A/Ann Arbor/6/60 (H2N2) ca donor virus and influenza A wild-type virus, were evaluated in adult seronegative volunteers (serum hemagglutination-inhibiting antibody titer, </=1:8) for level of attenuation, antigenicity, and genetic stability of the temperature-sensitive and ca phenotypes. At 10(7.0) to 10(7.5) 50% tissue culture infective doses the A/Scotland/74 and A/Victoria/75 ca recombinant viruses were clearly attenuated and antigenic. However, one of eight vaccinees infected with 10(7.5) 50% tissue culture infective doses of the A/Scotland/74 ca recombinant had a febrile reaction (39 degrees C). At a 10-fold higher dose (10(8.5) 50% tissue culture infective doses), 4 of 12 A/Scotland/74 vaccinees had a febrile and/or systemic reaction. Febrile reactions were not observed in volunteers who received the A/Victoria/75 ca recombinant virus, whereas 3 of the 12 vaccinees had mild upper respiratory tract symptoms, in one instance associated with mild systemic manifestations. Significantly, the serum hemagglutination- and neuraminidase-inhibiting antibody responses were comparable to those induced by wild-type virus. Both ca recombinant viruses were shed in low titer for a short period of time. Each isolate retained the temperature-sensitive phenotype. However, there was evidence of genetic instability of the ca marker in that 7 of 24 isolates exhibited some loss of the ca property, and one isolate completely lost the capacity to produce plaques at 25 degrees C. The retention of a low level of residual reactogenicity in the A/Scotland/74 ca recombinant suggests that acquisition of the ca and temperature-sensitive phenotypes by a ca recombinant virus may not always bring about a satisfactory level of attenuation for individuals lacking hemagglutinin immunity.

Adaptation, Physiological↗

Human vascular fluid responses to cold stress are not altered by cold acclimation.

Repeated cold water immersion can induce the development of an insulative type of cold acclimation in man. This investigation determined if repeated cold water immersion produced changes in vascular fluid responses to cold stress in addition to the previously reported changes in thermoregulation. Seven male subjects performed a standardized cold air and cold water exposure before and again after a cold acclimation program. The cold acclimation program consisted of daily immersion (90 min) in cold water (18 degrees C, stirred) repeated 5 times/wk for 5 consecutive wk. Cold acclimation did not alter the responses of plasma volume or electrolyte concentrations, nor urinary flow or electrolyte excretion during either cold air or cold water exposure. The percent reduction in plasma volume was larger (P less than 0.01) in cold water (-17%) than in cold air (-12%). Cold water immersion resulted in greater (P less than 0.01) diuresis than cold air exposure. Plasma K+ concentration increased (P less than 0.01) during cold (both air and water) exposure, whereas plasma Na+ concentration was unchanged. Calculated renal clearance and urinary excretion rate of both Na+ and K+ increased during cold (both air and water) exposure. The magnitude of plasma volume reduction during cold exposure was not correlated with either the degree of body cooling or diuresis. It is concluded that a) insulative cold acclimation does not influence vascular fluid responses to cold stress, and b) although vascular fluid shifts, body cooling and diuresis are all greater in cold water than in air, a consistent relationship among these parameters could not be established for an individual's response.

Acclimatization↗

Identification and expression analysis of cold-regulated genes from the cold-hardy Citrus relative Poncirus trifoliata (L.) Raf.

Citrus is a cold-sensitive genus and most commercially important varieties of citrus are susceptible to freezes. On the other hand, Poncirus trifoliata (L.) Raf. is an interfertile Citrus relative that can tolerate temperatures as low as -26 degrees C when fully cold acclimated. Therefore, it has been used for improving cold tolerance in cold-sensitive commercial citrus rootstock varieties and in attempts to improve scion varieties. In this study, cDNA libraries were constructed from both 2-day cold-acclimated and from non-acclimated Poncirus seedlings using a subtractive hybridization method with the objective of identifying cold-regulated genes. A total of 192 randomly picked clones, 136 from the cold-induced library and 56 from the cold-repressed library, were sequenced. The majority of these clones showed sequence homology to previously identified cold-induced and/or environmental stress-regulated genes in Arabidopsis. In addition, some of them shared homology with cold and/or environmental stress-induced genes previously identified in other herbaceous and woody perennial plants and some showed no homology with sequences in GenBank. When these 192 cDNAs were analyzed by reverse northern blot with cold-acclimated and non-acclimated probes, 92 of the cDNAs displayed significantly increased expression, ranging from 2 to 49-fold, during cold acclimation; all 92 were from the cold-induced library. Surprisingly no clones displayed significantly repressed expression in response to cold. Analysis of a number of selected genes individually in northern blots of mRNA from cold-acclimated and non-acclimated plants largely confirmed the reverse northern analysis, verifying induction of expression of selected cDNAs in response to cold. The results showed that subtractive hybridization is an efficient method for identification of cold-induced genes in plants with limited sequence information available. This study also revealed that genes induced during cold acclimation of the cold-hardy citrus relative P. trifoliata are similar to those in Arabidopsis, indicating that similar pathways may be present and activated during cold acclimation in woody perennial plants.

Acclimatization↗

Recycling of cold-stable microtubules: evidence that cold stability is due to substoichiometric polymer blocks.

A substantial subpopulation of mammalian brain crude extract microtubules is resistant to cold-temperature disassembly. We propose here that microtubules are rendered cold stable by rare substoichiometric blocks. Mild shearing of rat brain cold-stable microtubules makes them largely cold labile. In addition, cold-stable microtubules can be destabilized by exposure to low concentrations of calmodulin (5 microM) in the presence of calcium at 0 degree C. Cold-disassembled microtubule protein, obtained from sheared or calmodulin-treated cold-stable preparations, re-forms a cold-stable subpopulation upon reassembly. These observations allow strategies for the recycling purification of cold-stable microtubules. Comparison of purified cold-labile and cold-stable material by gel electrophoresis shows enrichment for a few unique polypeptides, of 135, 70-82, and 56 kilodaltons, in the cold-stable preparation. The 64-kilodalton "switch protein", previously identified as uniquely dephosphorylated in cold-stable microtubules, is equally represented in recycled cold-stable and cold-labile microtubule preparations. Furthermore, when disassembled, cold-stable microtubule proteins are passed through a calmodulin affinity column on which the polypeptides characteristic of cold-stable microtubules are specifically retained, the breakthrough (unbound) material repolymerizes into cold-labile microtubules only. Based on the above data, a model is presented in which microtubules are rendered cold stable by the presence of substoichiometric, calmodulin-sensitive blocks that randomly reshuffle upon reassembly of cold-stable microtubules.

Animals↗

A cold- and menthol-activated current in rat dorsal root ganglion neurones: properties and role in cold transduction.

Skin temperature is sensed by peripheral thermoreceptors. Using the neuronal soma in primary culture as a model of the receptor terminal, we have investigated the mechanisms of cold transduction in thermoreceptive neurones from rat dorsal root ganglia. Cold-sensitive neurones were pre-selected by screening for an increase in [Ca(2+)](i) on cooling; 49 % of them were also excited by 0.5 microM capsaicin. Action potentials and voltage-gated currents of cold-sensitive neurones were clearly distinct from those of cold-insensitive neurones. All cold-sensitive neurones expressed an inward current activated by cold and sensitised by (-)-menthol, which was absent from cold-insensitive neurones. This current was carried mainly by Na(+) ions and caused a depolarisation on cooling accompanied by action potentials, inducing voltage-gated Ca(2+) entry; a minor fraction of Ca(2+) entry was voltage-independent. Application of (-)-menthol shifted the threshold temperatures of the cold-induced depolarisation and the inward current to the same extent, indicating that the cold- and menthol-activated current normally sets the threshold temperature for depolarisation during cooling. The action of menthol was stereospecific, with the (+)-isomer being a less effective agonist than the (-)-isomer. Extracellular Ca(2+) modulated the cold- and menthol-activated current in a similar way to its action on intact cold receptors: lowered [Ca(2+)](o) sensitised the current, while raised [Ca(2+)](o) antagonised the menthol-induced sensitisation. During long cooling pulses the current showed adaptation, which depended on extracellular Ca(2+) and was mediated by a rise in [Ca(2+)](i). This adaptation consisted of a shift in the temperature sensitivity of the channel. In capsaicin-sensitive neurones, capsaicin application caused a profound depression of the cold-activated current. Inclusion of nerve growth factor in the culture medium shifted the threshold of the cold-activated current towards warmer temperatures. The current was blocked by 50 microM capsazepine and 100 microM SKF 96365. We conclude that the cold- and menthol-activated current is the major mechanism responsible for cold-induced depolarisation in DRG neurones, and largely accounts for the known transduction properties of intact cold receptors.

Action Potentials↗

Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension.

Chronic cold exposure causes hypertension and diuresis. The aim of this study was to determine whether vasopressin (AVP) plays a role in cold-induced hypertension and diuresis. Two groups of Long-Evans (LE) and two groups of homozygous AVP-deficient Brattleboro (VD) rats were used. Blood pressure (BP) was not different among the four groups during a 2-wk control period at room temperature (25 degrees C, warm). After the control period, one LE group and one VD group were exposed to cold (5 degrees C); the remaining groups were kept at room temperature. BP and body weight were measured weekly during exposure to cold. Food intake, water intake, urine output, and urine osmolality were measured during weeks 1, 3, and 5 of cold exposure. At the end of week 5, all animals were killed and blood was collected for measurement of plasma AVP. Kidneys were removed for measurement of renal medulla V2 receptor mRNA and aquaporin-2 (AQP-2) protein expression. BP of LE and VD rats increased significantly by week 2 of cold exposure and reached a high level by week 5. BP elevations developed at approximately the same rate and to the same degree in LE and VD rats. AVP deficiency significantly increased urine output and solute-free water clearance and decreased urine osmolality. Chronic cold exposure increased urine output and solute-free water clearance and decreased urine osmolality in LE rats, indicating that cold exposure caused diuresis in LE rats. Cold exposure failed to affect these parameters in VD rats, suggesting that the AVP system is responsible for cold-induced diuresis. Cold exposure did not alter plasma AVP in LE rats. Renal medulla V2 receptor mRNA and AQP-2 protein expression levels were decreased significantly in the cold-exposed LE rats, suggesting that cold exposure inhibited renal V2 receptors and AVP-inducible AQP-2 water channels. We conclude that 1) AVP may not be involved in the pathogenesis of cold-induced hypertension, 2) the AVP system plays a critical role in cold-induced diuresis, and 3) cold-induced diuresis is due to suppression of renal V2 receptors and the associated AQP-2 water channels, rather than inhibition of AVP release.

Angiotensin II↗

An open-label, single-center, phase IV clinical study of the effectiveness of zinc gluconate glycine lozenges (Cold-Eeze) in reducing the duration and symptoms of the common cold in school-aged subjects.

Each year, more than 62 million cases of the common cold in the United States require medical attention and more than 80% affect school-aged children. The objective of this prospective, intent-to-treat, phase IV study was to determine the therapeutic and prophylactic effectiveness of zinc gluconate glycine lozenges (Cold-Eeze) for the common cold. Zinc lozenges were administered once daily during the cold season for prophylaxis. For therapeutic purposes, lozenges were given 4 times per day. The primary objective of the study was the treatment effect on cold duration, and the secondary objective was the effect on the number of common colds. A putative control from our previous study was used for comparison. A total of 178 children, ages 12 to 18 years, was enrolled, of which 134 met criteria for efficacy analysis. The average cold duration with therapeutic lozenge use was 6.9 +/- 3.1 days, significantly shorter than the 9.0 +/- 3.5 days found in the control group (P < 0.001). The mean number of colds was 1.28 +/- 1.03 with zinc lozenge prophylaxis versus 1.7 +/- 1.91 without prophylaxis (P < 0.05), a 25% reduction. With prophylaxis, 25% of the subjects did not experience a cold and two-thirds never had a cold or only had 1 cold. There was no antibiotic use for any cold, and there were no adverse events reported. Results of this study are consistent with those from our previous retrospective study showing significantly shorter cold duration and fewer colds with the use of zinc gluconate glycine lozenges. The zinc gluconate glycine lozenges are well tolerated and are an easy-to-administer therapy that has the potential to substantially reduce cold-related school absences and antibiotic use and misuse as well as to provide a cost saving.

Adolescent↗