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	<title>Horse &#8211; LABOGEN</title>
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		<title>Hypertriglyceridemia-induced pancreatitis (HIP) in the Freiberger</title>
		<link>https://labogen.com/en/2025/11/28/hypertriglyceridemia-induced-pancreatitis-hip-in-the-freiberger/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Fri, 28 Nov 2025 13:11:26 +0000</pubDate>
				<category><![CDATA[Horse]]></category>
		<category><![CDATA[Genetic test]]></category>
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					<description><![CDATA[Hypertriglyceridemia-induced pancreatitis (HIP) in the Freiberger We offer a new genetic test for Freiberger that can be used to identify carriers and affected animals of hypertriglyceridemia-induced pancreatitis (HIP). The disease is a hereditary metabolic defect. The HIP gene variant causes the loss of function of an important enzyme in fat metabolism, which ensures that absorbed [&#8230;]]]></description>
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							<h2>Hypertriglyceridemia-induced pancreatitis (HIP) in the Freiberger</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>We offer a new genetic test for Freiberger that can be used to identify carriers and affected animals of hypertriglyceridemia-induced pancreatitis (HIP).</p><p>The disease is a hereditary metabolic defect. The HIP gene variant causes the loss of function of an important enzyme in fat metabolism, which ensures that absorbed fats are processed. Without this enzyme, there is a harmful accumulation of fat in the blood, which in turn leads to acute inflammation of the pancreas.</p><p>Affected foals suffer from loss of appetite, diarrhea, fever and apathy. As a rule, foals die in the first few weeks of life or have to be euthanized.</p><p>HIP is inherited in an autosomal recessive manner. This means that a foal is only affected if it has received an affected gene from both its sire and dam. This means that both the sire and dam must carry the mutated gene. Carrier animals themselves are clinically completely inconspicuous, but have a 50% probability of passing on the inherited trait to their offspring. When mating two carriers, there is a risk that the offspring will be affected by the disease (25%). Therefore, a carrier should never be mated with another carrier. Genetic testing is the only way to avoid such mating.</p></div>						</div>
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		<title>Attention sycamore maple &#8211; danger to life from hypoglycin A in horses</title>
		<link>https://labogen.com/en/2025/11/28/attention-sycamore-maple-danger-to-life-from-hypoglycin-a-in-horses/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Fri, 28 Nov 2025 13:07:45 +0000</pubDate>
				<category><![CDATA[Horse]]></category>
		<guid isPermaLink="false">https://labogen.com/2025/11/28/attention-sycamore-maple-danger-to-life-from-hypoglycin-a-in-horses/</guid>

					<description><![CDATA[Which genetic test suits my dog? Individual test, breed package or XXL screening - targeted or broad analysis?...]]></description>
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							<h2 style="box-sizing: inherit;">Attention sycamore maple – danger to life from hypoglycin A in horses</h2>						</div>
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							<p>Due to current events, we would like to draw your attention to the danger of poisoning your grazing horses: In recent weeks, there have been repeated cases of sycamore poisoning in Germany. Horses that have access to areas with or near sycamore maples (Acer pseudoplatanus) are particularly at risk.</p><p>The toxic substance hypoglycin A is found in seeds (the typical wing fruits), seedlings and young shoots of various maple species. Horses usually eat these plant parts when there is not enough grass in the pasture, for example in the fall.</p><p>The toxic amino acid hypoglycine A leads to so-called atypical pasture myopathy in horses, a severe and sometimes fatal disease. After ingestion of the toxin, there is massive damage to the muscles, which manifests itself in significantly increased muscle values (CK, LDH, AST) and leads to pronounced myoglobinuria (red-brown urine).</p><p>You should look out for the following symptoms: generalized weakness, stiffness, colic, rapid breathing (tachypnoea) and increased pulse rate (tachycardia), altered urine color.</p><p>Unfortunately, the disease is often fatal in horses with pronounced symptoms; 60-70% of affected animals do not survive despite intensive treatment.</p><p>Hypoglycine A can be detected directly from the serum (1 ml) and provides important diagnostic information. In peracute cases of pasture myopathy, values of over 1000 nmol/L were found. If the values are below 100 nmol/L, it is possible that only small amounts of the toxin have been absorbed or that the absorption took place several days ago. It should be noted that the toxin is usually broken down in the animal within a few days.</p><p>An evaluation of the samples sent to our laboratory in 2025 shows a significant increase in the number of cases since October: <strong>around 87%</strong> of the samples sent in for hypoglycine A analysis were <strong>positive</strong>, and of these, around <strong>35%</strong> showed <strong>extremely high concentrations</strong> of between <strong>2000 and 8000 nmol/L</strong>, while the majority of the others showed <strong>double-digit values</strong>.</p><p>Prevention is crucial: Horses should not be put on pastures with or near sycamore, especially in fall (seed fall) and spring (seedlings). As the wing fruits in particular can be spread far and wide by the wind, haystacks and standing water should also be checked. The poison is water-soluble and can therefore contaminate the drinking water. A good supply of feed in the pasture and regular checks are the best protective measures.</p>						</div>
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		<title>Reliable laboratory results for responsible decisions</title>
		<link>https://labogen.com/en/2025/11/03/reliable-laboratory-results-for-responsible-decisions/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Mon, 03 Nov 2025 11:22:50 +0000</pubDate>
				<category><![CDATA[Cat]]></category>
		<category><![CDATA[Dog]]></category>
		<category><![CDATA[Horse]]></category>
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					<description><![CDATA[Reliable laboratory results for responsible decisions Laboklin’s laboratory results are sent exclusively as PDF files, which are digitally signed and protected against editing. This ensures that the content cannot be changed unnoticed after it has been created. The digital signature confirms the authenticity of the document and proves that it actually originates from Laboklin. These [&#8230;]]]></description>
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							<h2>Reliable laboratory results for responsible decisions</h2><div class="x11i5rnm xat24cr x1mh8g0r x1vvkbs xtlvy1s x126k92a"><p>Laboklin’s laboratory results are sent exclusively as <strong>PDF files</strong>, which are <strong>digitally signed</strong> and <strong>protected against editing</strong>. This ensures that the content cannot be changed unnoticed after it has been created. The digital signature confirms the <strong>authenticity of the document</strong> and proves that it actually originates from Laboklin.</p><p>These security measures meet <strong>high technical standards</strong> and offer reliable protection against manipulation. So you can be sure: When you receive a signed PDF, it has been transmitted unchanged and truthfully.</p><p>Despite these high security precautions, <strong>fraud</strong> can unfortunately never be completely ruled out. We therefore recommend that you only accept findings from <strong>trustworthy sources</strong> and, <strong>if in doubt</strong>,<strong> contact</strong> Laboklin directly. Especially when it comes to important decisions on health care, mating or the purchase of an animal, it is crucial that you can rely on the accuracy and authenticity of the findings.</p><p>For data protection reasons, we are not permitted to provide information about the findings of other customers or clients. However, we can confirm the authenticity of an existing finding if there is reasonable doubt.</p><p>With these measures, we want to offer you the greatest possible <strong>security </strong>and<strong> transparency</strong> – so that you can rely on the accuracy of the results.</p></div>						</div>
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		<title>(W)FFS gene variant in the Haflinger in Germany</title>
		<link>https://labogen.com/en/2022/11/15/wffs-gene-variant-in-the-haflinger-in-germany/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Tue, 15 Nov 2022 16:05:00 +0000</pubDate>
				<category><![CDATA[Horse]]></category>
		<guid isPermaLink="false">https://staging.laboklin.com/labogen/labogen_wp/index.php/2022/11/15/wffs-gene-variant-in-the-haflinger-in-germany/</guid>

					<description><![CDATA[(W)FFS gene variant in the Haflinger in Germany WFFS, Warmblood Fragile Foal Syndrome, is a recessive hereditary disease that was initially only described in warmbloods. Classic symptoms are extremely stretchy and brittle, cracked skin, as well as extremely overstretched joints, especially the fetlock joints are affected. Other possible symptoms are incomplete closure of the abdominal [&#8230;]]]></description>
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							<h2 style="box-sizing: inherit;">(W)FFS gene variant in the Haflinger in Germany</h2>
<p>WFFS, Warmblood Fragile Foal Syndrome, is a recessive hereditary disease that was initially only described in warmbloods. Classic symptoms are extremely stretchy and brittle, cracked skin, as well as extremely overstretched joints, especially the fetlock joints are affected. Other possible symptoms are incomplete closure of the abdominal wall, deformation of the spinal column, intracranial hemorrhage and others.<br />Affected foals are not viable and, if they were not already stillborn or died shortly after birth, have to be euthanized due to the poor prognosis.<br />In 2020, various studies were published showing the presence of the WFFS gene variant in various other horse breeds such as the Thoroughbred, the Knabstrupper, the Quarter Horse, the Paint Horse, the Mustang, the Appaloosa and also the Haflinger. The hereditary disease originally known as Warmblood Fragile Foal Syndrome is therefore now also referred to as Fragile Foal Syndrome (FFS).  <br />As part of a study conducted internally at LABOKLIN, the question was to be answered as to what extent the (W)FFS gene variant can also be found in Haflingers in Germany. For this purpose, 448 samples from Haflinger horses from Germany, which were available at LABOKLIN, were analyzed. The genotype N/N (free) was determined for 443 animals; these animals do not carry the gene variant that causes FFS. 5 animals (1.1 %) showed the N/WFFS genotype, i.e. these animals are carriers for the FFS gene variant and can therefore pass it on to their offspring.</p>
<p>The study shows that the FFS gene variant also occurs in Haflinger horses in Germany, but the carrier frequency of 1.1% is significantly lower than in warmbloods, where various studies postulate a carrier frequency of between 12% and 15%. The exact extent to which the German Haflinger breeding population is affected cannot be deduced from this study, as it was not checked whether the animals examined were bred in Germany or imported from abroad.</p>
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		<title>Spread of PSSM in different breeds</title>
		<link>https://labogen.com/en/2019/08/14/spread-of-pssm-in-different-breeds/</link>
		
		<dc:creator><![CDATA[Fabian Keller]]></dc:creator>
		<pubDate>Wed, 14 Aug 2019 08:27:00 +0000</pubDate>
				<category><![CDATA[Horse]]></category>
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					<description><![CDATA[Spread of PSSM in different breeds Polysaccharide storage myopathy type 1 is a hereditary disorder of sugar metabolism. The clinical symptoms are “cross-flap-like” and cover the entire spectrum from reluctance to move, muscle tremors, muscle stiffness, sweating, alternating lameness to immobility. PSSM is inherited in an autosomal dominant manner.This means that heterozygous carriers (genotype N/PPSM) [&#8230;]]]></description>
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							<h2 style="box-sizing: inherit;">Spread of PSSM in different breeds</h2>
<p style="box-sizing: inherit; margin-bottom: 20px; color: #4c4c4c; font-size: 16px;">Polysaccharide storage myopathy type 1 is a hereditary disorder of sugar metabolism. The clinical symptoms are “cross-flap-like” and cover the entire spectrum from reluctance to move, muscle tremors, muscle stiffness, sweating, alternating lameness to immobility. PSSM is inherited in an autosomal dominant manner.<br />This means that heterozygous carriers (genotype N/PPSM) also have an increased risk of developing the disease, while homozygotes (genotype PSSM/PSSM) are more severely affected than heterozygotes. The genetic test can also be used to confirm a suspected diagnosis.<br />The PSSM test was developed at the University of Minnesota and is patented in Europe. Laboklin is the exclusive license holder.<br />PSSM was initially regarded as a disease of Western horses (Quarter Horse, Paint Horse and Appaloosa), but the causative mutation goes back a long way, so that this gene variant occurs in many different horse breeds. In warmblood horses, for example, it has been shown in recent years that approx. 5% of the horses tested were heterozygous carriers (N/PPSM) and just under 1% were homozygous (PSSM/PSSM).</p>
<p style="box-sizing: inherit; margin-bottom: 20px; color: #4c4c4c; font-size: 16px;">In the overall population, the allele frequency is probably somewhat lower in some breeds where the test is not mandatory, as some horses may only have been tested due to clinical suspicion.</p>
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